A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.
The active metabolite of FOLIC ACID. Leucovorin is used principally as an antidote to FOLIC ACID ANTAGONISTS.
Antimetabolites that are useful in cancer chemotherapy.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.
Organic compounds which contain platinum as an integral part of the molecule.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
An enzyme of the transferase class that catalyzes the reaction 5,10-methylenetetrahydrofolate and dUMP to dihydrofolate and dTMP in the synthesis of thymidine triphosphate. (From Dorland, 27th ed) EC 2.1.1.45.
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA TOPOISOMERASES, TYPE I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
Uracil is a nitrogenous base, specifically a pyrimidine derivative, which constitutes one of the four nucleobases in the nucleic acid of RNA (ribonucleic acid), pairing with adenine via hydrogen bonds during base-pairing. (25 words)
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.
Drug therapy given to augment or stimulate some other form of treatment such as surgery or radiation therapy. Adjuvant chemotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.
A malignant epithelial tumor with a glandular organization.
An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.
5-Fluoro-2'-deoxyuridylate. An inhibitor of thymidylate synthetase. Formed from 5-fluorouracil or 5-fluorodeoxyuridine.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
Tumors or cancer of the COLON.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
Congener of FLUOROURACIL with comparable antineoplastic action. It has been suggested especially for the treatment of breast neoplasms.
An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.
Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
4-Methyl derivative of LOMUSTINE; (CCNU). An antineoplastic agent which functions as an alkylating agent.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
Tumors or cancer of the STOMACH.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
Tumors or cancer of the RECTUM.
Deoxycytidine is a nucleoside consisting of the pentose sugar deoxyribose linked to the nitrogenous base cytosine, which plays a crucial role in DNA replication and repair processes within cells.
An antihelminthic drug that has been tried experimentally in rheumatic disorders where it apparently restores the immune response by increasing macrophage chemotaxis and T-lymphocyte function. Paradoxically, this immune enhancement appears to be beneficial in rheumatoid arthritis where dermatitis, leukopenia, and thrombocytopenia, and nausea and vomiting have been reported as side effects. (From Smith and Reynard, Textbook of Pharmacology, 1991, p435-6)
Substances that inhibit or prevent the proliferation of NEOPLASMS.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Tumors or cancer of the human BREAST.
The proportion of survivors in a group, e.g., of patients, studied and followed over a period, or the proportion of persons in a specified group alive at the beginning of a time interval who survive to the end of the interval. It is often studied using life table methods.
Regional infusion of drugs via an arterial catheter. Often a pump is used to impel the drug through the catheter. Used in therapy of cancer, upper gastrointestinal hemorrhage, infection, and peripheral vascular disease.
INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.
Tumors or cancer of the LIVER.
A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.
5-Bromo-2,4(1H,3H)-pyrimidinedione. Brominated derivative of uracil that acts as an antimetabolite, substituting for thymine in DNA. It is used mainly as an experimental mutagen, but its deoxyriboside (BROMODEOXYURIDINE) is used to treat neoplasms.
Agents counteracting or neutralizing the action of POISONS.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A fluorinated cytosine analog that is used as an antifungal agent.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The adaptation of therapeutic approaches such as pharmacological (DRUG CHRONOTHERAPY), surgical, radiological, or physical to the known variations in biological RHYTHMICITY, such as CIRCADIAN RHYTHMS. The treatment is aimed at supporting normal rhythms, or modifying the timing of therapy to achieve maximal efficacy and minimal adverse effect.
A group of diterpenoid CYCLODECANES named for the taxanes that were discovered in the TAXUS tree. The action on MICROTUBULES has made some of them useful as ANTINEOPLASTIC AGENTS.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
A compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)
Tumors or cancer of the ESOPHAGUS.
The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.
Leukopenia is a condition characterized by an abnormally low white blood cell count (less than 4,000 cells per microliter of blood) in peripheral blood, increasing the risk of infection due to decreased immune defense.
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
An INFLAMMATION of the MUCOSA with burning or tingling sensation. It is characterized by atrophy of the squamous EPITHELIUM, vascular damage, inflammatory infiltration, and ulceration. It usually occurs at the mucous lining of the MOUTH, the GASTROINTESTINAL TRACT or the airway due to chemical irritations, CHEMOTHERAPY, or radiation therapy (RADIOTHERAPY).
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
A decrease in the number of NEUTROPHILS found in the blood.
Preliminary cancer therapy (chemotherapy, radiation therapy, hormone/endocrine therapy, immunotherapy, hyperthermia, etc.) that precedes a necessary second modality of treatment.
An enzyme that catalyzes the transfer of 2-deoxy-D-ribose from THYMIDINE to orthophosphate, thereby liberating thymidine.
An enzyme which catalyzes the deamination of CYTOSINE resulting in the formation of URACIL. It can also act on 5-methylcytosine to form THYMIDINE.
Any process by which toxicity, metabolism, absorption, elimination, preferred route of administration, safe dosage range, etc., for a drug or group of drugs is determined through clinical assessment in humans or veterinary animals.
Injections made into a vein for therapeutic or experimental purposes.
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).
Antagonist of urate oxidase.
An autosomal recessive disorder affecting DIHYDROPYRIMIDINE DEHYDROGENASE and causing familial pyrimidinemia. It is characterized by thymine-uraciluria in homozygous deficient patients. Even a partial deficiency in the enzyme leaves individuals at risk for developing severe 5-FLUOROURACIL-associated toxicity.
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.
The local recurrence of a neoplasm following treatment. It arises from microscopic cells of the original neoplasm that have escaped therapeutic intervention and later become clinically visible at the original site.
A branch of the celiac artery that distributes to the stomach, pancreas, duodenum, liver, gallbladder, and greater omentum.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Uracil nucleotides which contain deoxyribose as the sugar moiety.
Uridine is a nucleoside, specifically a derivative of pyrimidine, that is composed of a uracil molecule joined to a ribose sugar molecule through a β-N1 glycosidic bond, and has significant roles in RNA synthesis, energy transfer, and cell signaling.
A simple organophosphorus compound that inhibits DNA polymerase, especially in viruses and is used as an antiviral agent.
One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells. In addition to antiviral activity, it activates NATURAL KILLER CELLS and B-LYMPHOCYTES, and down-regulates VASCULAR ENDOTHELIAL GROWTH FACTOR expression through PI-3 KINASE and MAPK KINASES signaling pathways.
A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against PNEUMOCYSTIS PNEUMONIA in AIDS patients. Myelosuppression is its dose-limiting toxic effect.
An enzyme that catalyzes the transfer of ribose from uridine to orthophosphate, forming uracil and ribose 1-phosphate.
The highest dose of a biologically active agent given during a chronic study that will not reduce longevity from effects other than carcinogenicity. (from Lewis Dictionary of Toxicology, 1st ed)
The giving of drugs, chemicals, or other substances by mouth.
A group of methylazirinopyrroloindolediones obtained from certain Streptomyces strains. They are very toxic antibiotics used as ANTINEOPLASTIC AGENTS in some solid tumors. PORFIROMYCIN and MITOMYCIN are the most useful members of the group.
A cell line derived from cultured tumor cells.
Radiotherapy given to augment some other form of treatment such as surgery or chemotherapy. Adjuvant radiotherapy is commonly used in the therapy of cancer and can be administered before or after the primary treatment.
A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as flouride (FLUORIDES) to prevent dental caries.
2'-Deoxyuridine. An antimetabolite that is converted to deoxyuridine triphosphate during DNA synthesis. Laboratory suppression of deoxyuridine is used to diagnose megaloblastic anemias due to vitamin B12 and folate deficiencies.
Elements of limited time intervals, contributing to particular results or situations.
Tumors or cancer of the GASTROINTESTINAL TRACT, from the MOUTH to the ANAL CANAL.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.
The penultimate step in the pathway of histidine biosynthesis. Oxidation of the alcohol group on the side chain gives the acid group forming histidine. Histidinol has also been used as an inhibitor of protein synthesis.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)
Transfer of a neoplasm from its primary site to lymph nodes or to distant parts of the body by way of the lymphatic system.
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
The enzyme catalyzing the formation of orotidine-5'-phosphoric acid (orotidylic acid) from orotic acid and 5-phosphoribosyl-1-pyrophosphate in the course of pyrimidine nucleotide biosynthesis. EC 2.4.2.10.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Thiophenes are aromatic heterocyclic organic compounds containing a five-membered ring with four carbon atoms and one sulfur atom, which are found in various natural substances and synthesized for use in pharmaceuticals and agrochemicals.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The total amount of radiation absorbed by tissues as a result of radiotherapy.
Leukemia L1210 is a designation for a specific murine (mouse) leukemia cell line that was originally isolated from a female mouse with an induced acute myeloid leukemia, which is widely used as a model in cancer research, particularly for in vivo studies of drug efficacy and resistance.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
Treatment that combines chemotherapy with radiotherapy.
The area covering the terminal portion of ESOPHAGUS and the beginning of STOMACH at the cardiac orifice.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
Therapeutic act or process that initiates a response to a complete or partial remission level.
Any surgical procedure for treatment of glaucoma by means of puncture or reshaping of the trabecular meshwork. It includes goniotomy, trabeculectomy, and laser perforation.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The forcible expulsion of the contents of the STOMACH through the MOUTH.
A subnormal level of BLOOD PLATELETS.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
The administration of liquid medication, nutrient, or other fluid through some other route than the alimentary canal, usually over minutes or hours, either by gravity flow or often by infusion pumping.
Catalyze the hydrolysis of nucleosides with the elimination of ammonia.
An amino acid formed in vivo by the degradation of dihydrouracil and carnosine. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. A rare genetic disorder, hyper-beta-alaninemia, has been reported.
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Tumors or cancer of the ANAL CANAL.
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.
Human colonic ADENOCARCINOMA cells that are able to express differentiation features characteristic of mature intestinal cells such as the GOBLET CELLS.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Derivatives of acetic acid with one or more fluorines attached. They are almost odorless, difficult to detect chemically, and very stable. The acid itself, as well as the derivatives that are broken down in the body to the acid, are highly toxic substances, behaving as convulsant poisons with a delayed action. (From Miall's Dictionary of Chemistry, 5th ed)
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
Disorders of the blood and blood forming tissues.
An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase.
Enzymes of the transferase class that catalyze the transfer of a pentose group from one compound to another.

Intensive weekly chemotherapy is not effective in advanced pancreatic cancer patients: a report from the Italian Group for the Study of Digestive Tract Cancer (GISCAD). (1/6112)

Twenty-two patients, with locally advanced unresectable and/or metastatic pancreatic carcinoma, received weekly administration of cisplatin 40 mg m(-2), 5-fluorouracil 500 mg m(-2), epidoxorubicin 35 mg m(-2), 6S stereoisomer of leucovorin 250 mg m(-2) and glutathione 1.5 mg m(-2), supported by a daily administration of lenograstim at a dose of 5 microg kg(-1). Nineteen patients were men and three were women. Median age was 63 years (range 47-70). At study entry, pain was present in 15 out of 22 patients (68%) with a mean value of Scott-Huskisson scale of 27.6+/-23.8, whereas a weight loss >10% was present in 15 patients. After eight weekly treatments, three partial responses were achieved for a response rate of 13% (95% CI 0-26%), five patients had stable disease and 14 progressed on therapy. Pain was present in 9 out of 22 patients (40%) with a mean value of Scott-Huskisson scale of 12.3+/-18.4. Eight patients (36%) (three partial response and five stable disease) had a positive weight change. Toxicity was mild: WHO grade III or IV toxicity was recorded in terms of anaemia in 7 out of 188 cycles (3.7%), of neutropenia in 9 out of 188 cycles (4.7%) and of thrombocytopenia in 3 out of 188 cycles (1.5%). Median survival of all patients was 6 months. The outcome of this intensive chemotherapy regimen does not support its use in pancreatic cancer.  (+info)

Is early post-operative treatment with 5-fluorouracil possible without affecting anastomotic strength in the intestine? (2/6112)

Early post-operative local or systemic administration of 5-fluorouracil (5-FU) is under investigation as a means to improve outcome after resection of intestinal malignancies. It is therefore quite important to delineate accurately its potentially negative effects on anastomotic repair. Five groups (n = 24) of rats underwent resection and anastomosis of both ileum and colon: a control group and four experimental groups receiving daily 5-FU, starting immediately after operation or after 1, 2 or 3 days. Within each group, the drug (or saline) was delivered either intraperitoneally (n = 12) or intravenously (n = 12). Animals were killed 7 days after operation and healing was assessed by measurement of anastomotic bursting pressure, breaking strength and hydroxyproline content. In all cases, 5-FU treatment from the day of operation or from day 1 significantly (P<0.025) and severely suppressed wound strength; concomitantly, the anastomotic hydroxyproline content was reduced. Depending on the location of the anastomosis and the route of 5-FU administration, even a period of 3 days between operation and first dosage seemed insufficient to prevent weakening of the anastomosis. The effects of intravenous administration, though qualitatively similar, were quantitatively less dramatic than those observed after intraperitoneal delivery. Post-operative treatment with 5-FU, if started within the first 3 days after operation, is detrimental to anastomotic strength and may compromise anastomotic integrity.  (+info)

Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (3/6112)

Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency.  (+info)

Dihydropyrimidine dehydrogenase deficiency and fluorouracil-related toxicity. (4/6112)

Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme of 5-fluorouracil (5-FU) catabolism. We report lymphocytic DPD data concerning a group of 53 patients (23 men, 30 women, mean age 58, range 36-73), treated by 5-FU-based chemotherapy in different French institutions and who developed unanticipated 5-FU-related toxicity. Lymphocyte samples (standard collection procedure) were sent to us for DPD determination (biochemical method). Among the whole group of 53 patients, 19 had a significant DPD deficiency (DD; below 150 fmol min(-1) mg(-1) protein, i.e. less than 70% of the mean value observed from previous population study). There was a greater majority of women in the DD group (15 out of 19, 79%) compared with the remaining 34 patients (15 out of 34, 44%, P<0.014). Toxicity was often severe, leading to patient death in two cases (both women). The toxicity score (sum of WHO grading, theoretical range 0-20) was twice as high in patients with marked DD (below 100 pmol min(-1) mg(-1) protein, n = 11, mean score = 13.2) compared with patients with moderate DD (between 150 and 100 pmol min(-1) mg(-1) protein, n = 8, mean score = 6.8), P = 0.008. In the DD group, there was a high frequency of neurotoxic syndromes (7 out of 19, 37%). The two deceased patients both had severe neurotoxicity. The occurrence of cardiac toxicity was relatively rare (1 out of 19, 5%). These data suggest that women are particularly prone to DPD deficiency and allow a more precise definition of the DD toxicity profile.  (+info)

Antitumor agents. I. Effect of 5-fluorouracil and cyclophosphamide on liver microsomes and thymus of rat. (5/6112)

Effects of antitumor agents on rat liver microsomal drug-metabolizing enzyme activities and thymus lymphocytes were studied in male Wistar rats. High doses of 5-fluorouracil (5-FU) and cyclophosphamide (CP) given parenterally for 6 days caused a partial decrease in whole body weight and the microsomal enzyme content such as cytochrome P-450 and cytochrome b5. Aniline p-hydroxylase and aminopyrine N-demethylase activities also decreased in rats dosed for 5 days decreased compared with the control. Both compounds in the high concentrations produced spectral change of "modified type II". However, the magnitude of the spectral changes observed was independent of the the concentration of substrate added. The addition of NADPH to the microsomes-substrate mixture modified the spectral change. Both drugs caused a considerable decrease in thymus weight and the number of thymus lymphocytes, while the alkaline phosphatase activity was enhanced in 5-FU groups, indicating that the agents cause a significant involution of the thymus. Decrease in the total number of the lymphocytes was greater than that in the blood leucocytes.  (+info)

Persistent induction of apoptosis and suppression of mitosis as the basis for curative therapy with S-1, an oral 5-fluorouracil prodrug in a colorectal tumor model. (6/6112)

In an effort to improve the therapeutic selectivity of 5-fluorouracil (FUra) against colorectal cancer, S-1, a combination agent including a prodrug of FUra with two modulators, was recently developed by Taiho Pharmaceuticals Co. S-1 is a combination of tegafur (FT), 5-chloro-2,4-hydroxypyridine, and potassium oxonate in the molar ratio of 1.0:0.4:1.0, with the latter two components as inhibitors of dihydropyrimidine dehydrogenase and phosphoribosylpyrophosphate transferase, respectively. In this study, the therapeutic selectivity and efficacy of S-1 (oral) was compared with FT (oral) and FUra (i.v. infusion) in rats bearing advanced colorectal cancer by using clinically relevant schedules. The maximum tolerated doses (MTDs) of S-1, FT, and FUra were 31.5, 200, and 25 mg/kg/d for 7 days and 22.5, 150, and 12.5 mg/kg/d for 28 days, respectively. The therapeutic index of S-1 was 4- to 5-fold higher than that of either FT or FUra. S-1 achieved 100% complete tumor regression (CR) at its MTD in both 7-day and 28-day schedules. Furthermore, the high incidences of stomatitis, alopecia, and diarrhea observed with FUra and FT, were not observed with S-1. In an attempt to understand the basis for the observed superior therapeutic selectivity with S-1, we studied pharmacokinetic analysis of FUra, drug-induced apoptosis, suppression of mitosis, and inhibition of thymidylate synthase (TS) after S-1, FUra, or FT administration. The peak plasma FUra concentrations derived from FUra or S-1 (FT) at comparable MTDs were similar, but the plasma level of FUra was higher with S-1 than with FUra. Induction of high and sustained apoptosis was achieved with S-1. Although the initial level of apoptosis induced by FUra was comparable to S-1, it was not sustained. The sustained level of apoptosis appears to correlate with tumor growth inhibition. Mitotic figures were more greatly suppressed with S-1 treatment than with FUra. Studies on TS inhibition indicated that, although both S-1 and FUra caused a 4- to 6-fold induction of total TS protein, single oral administration of S-1 was superior to 24-h infusion of FUra in suppressing free TS. The data are consistent with the observation that the therapeutic efficacy of S-1 (100% cure) over FUra is associated with high and sustained levels of drug-induced apoptosis, greater suppression of mitosis, and inhibition of free TS in tumor tissues.  (+info)

Phase I study of eniluracil, a dihydropyrimidine dehydrogenase inactivator, and oral 5-fluorouracil with radiation therapy in patients with recurrent or advanced head and neck cancer. (7/6112)

5-Fluorouracil (5-FU) is an effective enhancer of radiation therapy (RT) in head and neck cancers. Due to rapid, predominantly hepatic metabolism by dihydropyrimidine dehydrogenase (DPD) and suggested clinical benefit from prolonged drug exposure, 5-FU is commonly given by continuous infusion. Eniluracil is a novel DPD-inactivator designed to prolong the half-life of 5-FU and provide sustained plasma concentrations of 5-FU with oral dosing. We conducted a Phase I study of the safety and efficacy of eniluracil given with oral 5-FU in patients receiving concurrent RT for recurrent or advanced squamous cell carcinomas of the head and neck. Thirteen patients with recurrent, metastatic, or high-risk (defined as an expected 2-year survival rate of <10%) head and neck cancer were enrolled and treated with concomitant chemoradiotherapy on an every-other-week schedule. Eniluracil at a fixed dose [20 mg twice a day (BID)] was given for 7 consecutive days (days 1-7). 5-FU and RT were given on 5 consecutive days (days 2-6). One patient was treated with once-daily RT (2.0 Gy fractions). The remaining patients received hyperfractionated RT (1.5-Gy fractions BID). The initial dose of 5-FU was 2.5 mg/m2 given BID. Dose escalation in patient cohorts was scheduled at 2.5-mg/m2 increments, with intrapatient dose escalation permitted. Lymphocyte DPD activity and serum 5-FU and uracil concentrations were monitored during two cycles. DPD activity was completely or nearly completely inactivated in all patients. Sustained, presumed therapeutic concentrations of 5-FU were observed at a dose of 5.0 mg/m2 given BID. Cumulative dose-limiting myelosuppression (both neutropenia and thrombocytopenia) was observed during the fourth and fifth cycles following administration of 5.0 mg/m2 5-FU BID. One patient died of neutropenic sepsis during cycle 4. Other late cycle toxicities included diarrhea, fatigue, and mucositis. Grade 3 mucositis was observed in 4 patients, but no grade 4 mucositis or grade 3 or 4 dermatitis was observed. A second patient death occurred during cycle 1 of treatment. No specific cause of death was identified. The study was subsequently discontinued. Cumulative myelosupression was the significant dose-limiting toxicity of oral 5-FU given with the DPD-inactivator eniluracil on an every-other-week schedule. Clinical radiation sensitization was not observed, based on the absence of dose-limiting mucositis and dermatitis. Alternative dosing schedules need to be examined to determine the most appropriate use of eniluracil and 5-FU as radiation enhancers.  (+info)

A Fas-dependent component in 5-fluorouracil/leucovorin-induced cytotoxicity in colon carcinoma cells. (8/6112)

We have shown previously (J. A. Houghton et al., Proc. Natl. Acad. Sci. USA, 94: 8144-8149, 1997) that thymineless death in thymidylate synthase-deficient (TS-) colon carcinoma cells is mediated via Fas/FasL interactions after deoxythymidine (dThd) deprivation, and that Fas-dependent sensitivity of human colon carcinoma cell lines may be dependent upon the level of Fas expressed. The objective of this study was to elucidate whether a Fas-dependent component exists in 5-fluorouracil (FUra)/leucovorin (LV)-induced cytotoxicity of colon carcinoma cells, and whether this may be potentiated by IFN-gamma-induced elevation in Fas expression, using the HT29 cell line as a model. The cytotoxic activity of FUra/LV was inhibited by dThd in HT29 cells and also, in part, by NOK-1+NOK-2 MoAbs that prevent Fas/FasL interactions. FUra/LV-induced cytotoxicity was significantly potentiated by IFN-gamma, reversed by exposure to NOK-1+NOK-2 antibodies, and correlated with a 4-fold induction of Fas expression in the presence of IFN-gamma and significant elevation in expression of FasL. Using five additional human colon carcinoma cell lines, FUra/LV-induced cytotoxicity was dThd-dependent in GC3/c1, VRC5/c1, and Caco2 but not in HCT8 or HCT116 cells. Like HT29 cells, this cytotoxicity was potentiated by IFN-gamma in GC3/c1 and VRC5/c1 but not in Caco2, which fails to express Fas, nor in HCT8 and HCT116, in which no dThd-dependent FUra-induced cytotoxicity was demonstrated. Data suggest that a Fas-dependent component, potentiated by IFN-gamma, exists in FUra/LV-induced cytotoxicity but requires FUra/LV-induced DNA damage for IFN-gamma-induced potentiation to occur.  (+info)

Fluorouracil is a antineoplastic medication, which means it is used to treat cancer. It is a type of chemotherapy drug known as an antimetabolite. Fluorouracil works by interfering with the growth of cancer cells and ultimately killing them. It is often used to treat colon, esophageal, stomach, and breast cancers, as well as skin conditions such as actinic keratosis and superficial basal cell carcinoma. Fluorouracil may be given by injection or applied directly to the skin in the form of a cream.

It is important to note that fluorouracil can have serious side effects, including suppression of bone marrow function, mouth sores, stomach and intestinal ulcers, and nerve damage. It should only be used under the close supervision of a healthcare professional.

Leucovorin is the pharmaceutical name for a form of folic acid, also known as folinic acid. It is used in medicine as a medication to reduce the toxic effects of certain chemotherapy drugs, such as methotrexate, that work by blocking the action of folic acid in the body. Leucovorin is able to bypass this blockage and restore some of the necessary functions of folic acid, helping to prevent or reduce the severity of side effects like nausea, vomiting, and damage to the mucous membranes.

Leucovorin may also be used in combination with fluorouracil chemotherapy to enhance its effectiveness in treating certain types of cancer. It is important to note that leucovorin should only be used under the supervision of a healthcare professional, as it can interact with other medications and have potentially serious side effects if not used properly.

Antimetabolites are a class of antineoplastic (chemotherapy) drugs that interfere with the metabolism of cancer cells and inhibit their growth and proliferation. These agents are structurally similar to naturally occurring metabolites, such as amino acids, nucleotides, and folic acid, which are essential for cellular replication and growth. Antimetabolites act as false analogs and get incorporated into the growing cells' DNA or RNA, causing disruption of the normal synthesis process, leading to cell cycle arrest and apoptosis (programmed cell death).

Examples of antimetabolite drugs include:

1. Folate antagonists: Methotrexate, Pemetrexed
2. Purine analogs: Mercaptopurine, Thioguanine, Fludarabine, Cladribine
3. Pyrimidine analogs: 5-Fluorouracil (5-FU), Capecitabine, Cytarabine, Gemcitabine

These drugs are used to treat various types of cancers, such as leukemias, lymphomas, breast, ovarian, and gastrointestinal cancers. Due to their mechanism of action, antimetabolites can also affect normal, rapidly dividing cells in the body, leading to side effects like myelosuppression (decreased production of blood cells), mucositis (inflammation and ulceration of the gastrointestinal tract), and alopecia (hair loss).

Antineoplastic combined chemotherapy protocols refer to a treatment plan for cancer that involves the use of more than one antineoplastic (chemotherapy) drug given in a specific sequence and schedule. The combination of drugs is used because they may work better together to destroy cancer cells compared to using a single agent alone. This approach can also help to reduce the likelihood of cancer cells becoming resistant to the treatment.

The choice of drugs, dose, duration, and frequency are determined by various factors such as the type and stage of cancer, patient's overall health, and potential side effects. Combination chemotherapy protocols can be used in various settings, including as a primary treatment, adjuvant therapy (given after surgery or radiation to kill any remaining cancer cells), neoadjuvant therapy (given before surgery or radiation to shrink the tumor), or palliative care (to alleviate symptoms and prolong survival).

It is important to note that while combined chemotherapy protocols can be effective in treating certain types of cancer, they can also cause significant side effects, including nausea, vomiting, hair loss, fatigue, and an increased risk of infection. Therefore, patients undergoing such treatment should be closely monitored and managed by a healthcare team experienced in administering chemotherapy.

Organoplatinum compounds are a group of chemical substances that contain at least one carbon-platinum bond. These compounds have been widely studied and used in the field of medicine, particularly in cancer chemotherapy. The most well-known organoplatinum compound is cisplatin, which is a platinum-based drug used to treat various types of cancers such as testicular, ovarian, bladder, and lung cancers. Cisplatin works by forming crosslinks with the DNA of cancer cells, disrupting their ability to replicate and ultimately leading to cell death. Other examples of organoplatinum compounds used in cancer treatment include carboplatin and oxaliplatin.

A "Drug Administration Schedule" refers to the plan for when and how a medication should be given to a patient. It includes details such as the dose, frequency (how often it should be taken), route (how it should be administered, such as orally, intravenously, etc.), and duration (how long it should be taken) of the medication. This schedule is often created and prescribed by healthcare professionals, such as doctors or pharmacists, to ensure that the medication is taken safely and effectively. It may also include instructions for missed doses or changes in the dosage.

Colorectal neoplasms refer to abnormal growths in the colon or rectum, which can be benign or malignant. These growths can arise from the inner lining (mucosa) of the colon or rectum and can take various forms such as polyps, adenomas, or carcinomas.

Benign neoplasms, such as hyperplastic polyps and inflammatory polyps, are not cancerous but may need to be removed to prevent the development of malignant tumors. Adenomas, on the other hand, are precancerous lesions that can develop into colorectal cancer if left untreated.

Colorectal cancer is a malignant neoplasm that arises from the uncontrolled growth and division of cells in the colon or rectum. It is one of the most common types of cancer worldwide and can spread to other parts of the body through the bloodstream or lymphatic system.

Regular screening for colorectal neoplasms is recommended for individuals over the age of 50, as early detection and removal of precancerous lesions can significantly reduce the risk of developing colorectal cancer.

Thymidylate synthase (TS) is an essential enzyme in the metabolic pathway for DNA synthesis and repair. It catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), which is a crucial building block for DNA replication and repair. This reaction also involves the methylation of dUMP using a methyl group donated by N5,N10-methylenetetrahydrofolate, resulting in the formation of dihydrofolate as a byproduct. The regeneration of dihydrofolate to tetrahydrofolate is necessary for TS to continue functioning, making it dependent on the folate cycle. Thymidylate synthase inhibitors are used in cancer chemotherapy to interfere with DNA synthesis and replication, leading to cytotoxic effects in rapidly dividing cells.

Cisplatin is a chemotherapeutic agent used to treat various types of cancers, including testicular, ovarian, bladder, head and neck, lung, and cervical cancers. It is an inorganic platinum compound that contains a central platinum atom surrounded by two chloride atoms and two ammonia molecules in a cis configuration.

Cisplatin works by forming crosslinks between DNA strands, which disrupts the structure of DNA and prevents cancer cells from replicating. This ultimately leads to cell death and slows down or stops the growth of tumors. However, cisplatin can also cause damage to normal cells, leading to side effects such as nausea, vomiting, hearing loss, and kidney damage. Therefore, it is essential to monitor patients closely during treatment and manage any adverse effects promptly.

Intravenous (IV) infusion is a medical procedure in which liquids, such as medications, nutrients, or fluids, are delivered directly into a patient's vein through a needle or a catheter. This route of administration allows for rapid absorption and distribution of the infused substance throughout the body. IV infusions can be used for various purposes, including resuscitation, hydration, nutrition support, medication delivery, and blood product transfusion. The rate and volume of the infusion are carefully controlled to ensure patient safety and efficacy of treatment.

Camptothecin is a topoisomerase I inhibitor, which is a type of chemotherapeutic agent used in cancer treatment. It works by interfering with the function of an enzyme called topoisomerase I, which helps to uncoil DNA during cell division. By inhibiting this enzyme, camptothecin prevents the cancer cells from dividing and growing, ultimately leading to their death.

Camptothecin is found naturally in the bark and stem of the Camptotheca acuminata tree, also known as the "happy tree," which is native to China. It was first isolated in 1966 and has since been developed into several synthetic derivatives, including irinotecan and topotecan, which are used clinically to treat various types of cancer, such as colon, lung, and ovarian cancers.

Like other chemotherapeutic agents, camptothecin can have significant side effects, including nausea, vomiting, diarrhea, and myelosuppression (suppression of bone marrow function). It is important for patients receiving camptothecin-based therapies to be closely monitored by their healthcare team to manage these side effects effectively.

Methotrexate is a medication used in the treatment of certain types of cancer and autoimmune diseases. It is an antimetabolite that inhibits the enzyme dihydrofolate reductase, which is necessary for the synthesis of purines and pyrimidines, essential components of DNA and RNA. By blocking this enzyme, methotrexate interferes with cell division and growth, making it effective in treating rapidly dividing cells such as cancer cells.

In addition to its use in cancer treatment, methotrexate is also used to manage autoimmune diseases such as rheumatoid arthritis, psoriasis, and inflammatory bowel disease. In these conditions, methotrexate modulates the immune system and reduces inflammation.

It's important to note that methotrexate can have significant side effects and should be used under the close supervision of a healthcare provider. Regular monitoring of blood counts, liver function, and kidney function is necessary during treatment with methotrexate.

Uracil is not a medical term, but it is a biological molecule. Medically or biologically, uracil can be defined as one of the four nucleobases in the nucleic acid of RNA (ribonucleic acid) that is linked to a ribose sugar by an N-glycosidic bond. It forms base pairs with adenine in double-stranded RNA and DNA. Uracil is a pyrimidine derivative, similar to thymine found in DNA, but it lacks the methyl group (-CH3) that thymine has at the 5 position of its ring.

Floxuridine is a chemotherapeutic antimetabolite medication that is primarily used in the treatment of colon cancer. It is a fluorinated pyrimidine nucleoside analogue, which means it is similar in structure to the building blocks of DNA and RNA, and can be incorporated into these molecules during cell division, disrupting their normal function and preventing cell replication.

Floxuridine works by inhibiting the enzyme thymidylate synthase, which is necessary for the synthesis of thymidine, a nucleoside that is essential for DNA replication. By blocking this enzyme, floxuridine can prevent the growth and proliferation of cancer cells.

Floxuridine is often used in combination with other chemotherapy drugs as part of a treatment regimen for colon cancer. It may be administered intravenously or via continuous infusion, depending on the specific treatment plan. As with all chemotherapy drugs, floxuridine can have significant side effects, including nausea, vomiting, diarrhea, and myelosuppression (suppression of bone marrow function), which can lead to anemia, neutropenia, and thrombocytopenia.

Adjuvant chemotherapy is a medical treatment that is given in addition to the primary therapy, such as surgery or radiation, to increase the chances of a cure or to reduce the risk of recurrence in patients with cancer. It involves the use of chemicals (chemotherapeutic agents) to destroy any remaining cancer cells that may not have been removed by the primary treatment. This type of chemotherapy is typically given after the main treatment has been completed, and its goal is to kill any residual cancer cells that may be present in the body and reduce the risk of the cancer coming back. The specific drugs used and the duration of treatment will depend on the type and stage of cancer being treated.

Adenocarcinoma is a type of cancer that arises from glandular epithelial cells. These cells line the inside of many internal organs, including the breasts, prostate, colon, and lungs. Adenocarcinomas can occur in any of these organs, as well as in other locations where glands are present.

The term "adenocarcinoma" is used to describe a cancer that has features of glandular tissue, such as mucus-secreting cells or cells that produce hormones. These cancers often form glandular structures within the tumor mass and may produce mucus or other substances.

Adenocarcinomas are typically slow-growing and tend to spread (metastasize) to other parts of the body through the lymphatic system or bloodstream. They can be treated with surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these treatments. The prognosis for adenocarcinoma depends on several factors, including the location and stage of the cancer, as well as the patient's overall health and age.

Epirubicin is an anthracycline antibiotic used in cancer chemotherapy. It works by interfering with the DNA in cancer cells and preventing them from dividing and growing. Epirubicin is often used to treat breast cancer, lung cancer, stomach cancer, and ovarian cancer.

Like other anthracyclines, epirubicin can cause side effects such as hair loss, nausea and vomiting, mouth sores, and increased risk of infection due to damage to the bone marrow. It can also cause heart problems, including congestive heart failure, especially when given in high doses or when combined with other chemotherapy drugs that can also harm the heart.

Epirubicin is usually given by injection into a vein (intravenously) and is typically administered in cycles, with breaks between treatment periods to allow the body to recover from any side effects. The dose and schedule of epirubicin may vary depending on the type and stage of cancer being treated, as well as other factors such as the patient's overall health and any other medical conditions they may have.

Fluorodeoxyuridylate (FdU) is not a medical term itself, but it is a chemical compound that plays a role in the mechanism of action of certain chemotherapeutic drugs. FdU is a thymidine analogue, which means it is a synthetic molecule similar to one of the building blocks of DNA called thymidine.

FdU can be incorporated into DNA during replication, leading to the inhibition of DNA synthesis and ultimately cell death. This mechanism of action is shared by several chemotherapeutic drugs, such as fluorouracil (5-FU) and capecitabine, which are converted into FdU in the body.

Therefore, while Fluorodeoxyuridylate itself is not a medical term, it is an important concept in understanding how certain chemotherapeutic drugs work to inhibit cancer cell growth and division.

Combined modality therapy (CMT) is a medical treatment approach that utilizes more than one method or type of therapy simultaneously or in close succession, with the goal of enhancing the overall effectiveness of the treatment. In the context of cancer care, CMT often refers to the combination of two or more primary treatment modalities, such as surgery, radiation therapy, and systemic therapies (chemotherapy, immunotherapy, targeted therapy, etc.).

The rationale behind using combined modality therapy is that each treatment method can target cancer cells in different ways, potentially increasing the likelihood of eliminating all cancer cells and reducing the risk of recurrence. The specific combination and sequence of treatments will depend on various factors, including the type and stage of cancer, patient's overall health, and individual preferences.

For example, a common CMT approach for locally advanced rectal cancer may involve preoperative (neoadjuvant) chemoradiation therapy, followed by surgery to remove the tumor, and then postoperative (adjuvant) chemotherapy. This combined approach allows for the reduction of the tumor size before surgery, increases the likelihood of complete tumor removal, and targets any remaining microscopic cancer cells with systemic chemotherapy.

It is essential to consult with a multidisciplinary team of healthcare professionals to determine the most appropriate CMT plan for each individual patient, considering both the potential benefits and risks associated with each treatment method.

Colonic neoplasms refer to abnormal growths in the large intestine, also known as the colon. These growths can be benign (non-cancerous) or malignant (cancerous). The two most common types of colonic neoplasms are adenomas and carcinomas.

Adenomas are benign tumors that can develop into cancer over time if left untreated. They are often found during routine colonoscopies and can be removed during the procedure.

Carcinomas, on the other hand, are malignant tumors that invade surrounding tissues and can spread to other parts of the body. Colorectal cancer is the third leading cause of cancer-related deaths in the United States, and colonic neoplasms are a significant risk factor for developing this type of cancer.

Regular screenings for colonic neoplasms are recommended for individuals over the age of 50 or those with a family history of colorectal cancer or other risk factors. Early detection and removal of colonic neoplasms can significantly reduce the risk of developing colorectal cancer.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

Cyclophosphamide is an alkylating agent, which is a type of chemotherapy medication. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. This helps to stop the spread of cancer in the body. Cyclophosphamide is used to treat various types of cancer, including lymphoma, leukemia, multiple myeloma, and breast cancer. It can be given orally as a tablet or intravenously as an injection.

Cyclophosphamide can also have immunosuppressive effects, which means it can suppress the activity of the immune system. This makes it useful in treating certain autoimmune diseases, such as rheumatoid arthritis and lupus. However, this immunosuppression can also increase the risk of infections and other side effects.

Like all chemotherapy medications, cyclophosphamide can cause a range of side effects, including nausea, vomiting, hair loss, fatigue, and increased susceptibility to infections. It is important for patients receiving cyclophosphamide to be closely monitored by their healthcare team to manage these side effects and ensure the medication is working effectively.

Tegafur is an antineoplastic agent, which is a type of drug used to treat cancer. It is a prodrug of 5-fluorouracil (5-FU), meaning that it is converted into 5-FU in the body after administration. 5-FU is a chemotherapeutic agent that interferes with DNA and RNA synthesis, ultimately leading to the death of cancer cells.

Tegafur is used alone or in combination with other antineoplastic agents to treat various types of cancers, including colon, rectal, gastric, breast, and head and neck cancers. It works by disrupting the growth of cancer cells, which are rapidly dividing cells.

Like all chemotherapeutic agents, Tegafur has potential side effects, including nausea, vomiting, diarrhea, mouth sores, and hair loss. Additionally, it can cause myelosuppression, a condition in which the production of blood cells in the bone marrow is decreased, leading to an increased risk of infection, anemia, and bleeding. Therefore, patients receiving Tegafur require regular monitoring of their blood counts and other laboratory tests to ensure that they are tolerating the treatment well.

Mitomycin is an antineoplastic antibiotic derived from Streptomyces caespitosus. It is primarily used in cancer chemotherapy, particularly in the treatment of various carcinomas including gastrointestinal tract malignancies and breast cancer. Mitomycin works by forming cross-links in DNA, thereby inhibiting its replication and transcription, which ultimately leads to cell death.

In addition to its systemic use, mitomycin is also used topically in ophthalmology for the treatment of certain eye conditions such as glaucoma and various ocular surface disorders. The topical application of mitomycin can help reduce scarring and fibrosis by inhibiting the proliferation of fibroblasts.

It's important to note that mitomycin has a narrow therapeutic index, meaning there is only a small range between an effective dose and a toxic one. Therefore, its use should be closely monitored to minimize side effects, which can include myelosuppression, mucositis, alopecia, and potential secondary malignancies.

Antimetabolites are a class of drugs that interfere with the normal metabolic processes of cells, particularly those involved in DNA replication and cell division. They are commonly used as chemotherapeutic agents to treat various types of cancer because many cancer cells divide more rapidly than normal cells. Antimetabolites work by mimicking natural substances needed for cell growth and division, such as nucleotides or amino acids, and getting incorporated into the growing cells' DNA or protein structures, which ultimately leads to the termination of cell division and death of the cancer cells. Examples of antimetabolites include methotrexate, 5-fluorouracil, and capecitabine.

Survival analysis is a branch of statistics that deals with the analysis of time to event data. It is used to estimate the time it takes for a certain event of interest to occur, such as death, disease recurrence, or treatment failure. The event of interest is called the "failure" event, and survival analysis estimates the probability of not experiencing the failure event until a certain point in time, also known as the "survival" probability.

Survival analysis can provide important information about the effectiveness of treatments, the prognosis of patients, and the identification of risk factors associated with the event of interest. It can handle censored data, which is common in medical research where some participants may drop out or be lost to follow-up before the event of interest occurs.

Survival analysis typically involves estimating the survival function, which describes the probability of surviving beyond a certain time point, as well as hazard functions, which describe the instantaneous rate of failure at a given time point. Other important concepts in survival analysis include median survival times, restricted mean survival times, and various statistical tests to compare survival curves between groups.

Semustine is not a medical term itself, but it's a brand name for the chemical compound called lomustine. Here is the medical definition of Lomustine:

Lomustine: A nitrosourea alkylating agent used in cancer chemotherapy. It is classified as an antineoplastic agent and works by preventing the growth of cancer cells through inhibiting DNA replication. Lomustine is used to treat various types of cancers, including Hodgkin's lymphoma, brain tumors, and non-Hodgkin's lymphoma. Common side effects include nausea, vomiting, and bone marrow suppression leading to anemia, leukopenia, and thrombocytopenia.

Disease-free survival (DFS) is a term used in medical research and clinical practice, particularly in the field of oncology. It refers to the length of time after primary treatment for a cancer during which no evidence of the disease can be found. This means that the patient shows no signs or symptoms of the cancer, and any imaging studies or other tests do not reveal any tumors or other indications of the disease.

DFS is often used as an important endpoint in clinical trials to evaluate the effectiveness of different treatments for cancer. By measuring the length of time until the cancer recurs or a new cancer develops, researchers can get a better sense of how well a particular treatment is working and whether it is improving patient outcomes.

It's important to note that DFS is not the same as overall survival (OS), which refers to the length of time from primary treatment until death from any cause. While DFS can provide valuable information about the effectiveness of cancer treatments, it does not necessarily reflect the impact of those treatments on patients' overall survival.

Stomach neoplasms refer to abnormal growths in the stomach that can be benign or malignant. They include a wide range of conditions such as:

1. Gastric adenomas: These are benign tumors that develop from glandular cells in the stomach lining.
2. Gastrointestinal stromal tumors (GISTs): These are rare tumors that can be found in the stomach and other parts of the digestive tract. They originate from the stem cells in the wall of the digestive tract.
3. Leiomyomas: These are benign tumors that develop from smooth muscle cells in the stomach wall.
4. Lipomas: These are benign tumors that develop from fat cells in the stomach wall.
5. Neuroendocrine tumors (NETs): These are tumors that develop from the neuroendocrine cells in the stomach lining. They can be benign or malignant.
6. Gastric carcinomas: These are malignant tumors that develop from the glandular cells in the stomach lining. They are the most common type of stomach neoplasm and include adenocarcinomas, signet ring cell carcinomas, and others.
7. Lymphomas: These are malignant tumors that develop from the immune cells in the stomach wall.

Stomach neoplasms can cause various symptoms such as abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. The diagnosis of stomach neoplasms usually involves a combination of imaging tests, endoscopy, and biopsy. Treatment options depend on the type and stage of the neoplasm and may include surgery, chemotherapy, radiation therapy, or targeted therapy.

Doxorubicin is a type of chemotherapy medication known as an anthracycline. It works by interfering with the DNA in cancer cells, which prevents them from growing and multiplying. Doxorubicin is used to treat a wide variety of cancers, including leukemia, lymphoma, breast cancer, lung cancer, ovarian cancer, and many others. It may be given alone or in combination with other chemotherapy drugs.

Doxorubicin is usually administered through a vein (intravenously) and can cause side effects such as nausea, vomiting, hair loss, mouth sores, and increased risk of infection. It can also cause damage to the heart muscle, which can lead to heart failure in some cases. For this reason, doctors may monitor patients' heart function closely while they are receiving doxorubicin treatment.

It is important for patients to discuss the potential risks and benefits of doxorubicin therapy with their healthcare provider before starting treatment.

Rectal neoplasms refer to abnormal growths in the tissues of the rectum, which can be benign or malignant. They are characterized by uncontrolled cell division and can invade nearby tissues or spread to other parts of the body (metastasis). The most common type of rectal neoplasm is rectal cancer, which often begins as a small polyp or growth in the lining of the rectum. Other types of rectal neoplasms include adenomas, carcinoids, and gastrointestinal stromal tumors (GISTs). Regular screenings are recommended for early detection and treatment of rectal neoplasms.

Deoxycytidine is a chemical compound that is a component of DNA, one of the nucleic acids in living organisms. It is a nucleoside, consisting of the sugar deoxyribose and the base cytosine. Deoxycytidine pairs with guanine via hydrogen bonds to form base pairs in the double helix structure of DNA.

In biochemistry, deoxycytidine can also exist as a free nucleoside, not bound to other molecules. It is involved in various cellular processes related to DNA metabolism and replication. Deoxycytidine can be phosphorylated to form deoxycytidine monophosphate (dCMP), which is an important intermediate in the synthesis of DNA.

It's worth noting that while deoxycytidine is a component of DNA, its counterpart in RNA is cytidine, which contains ribose instead of deoxyribose as the sugar component.

Levamisole is an anthelmintic medication used to treat parasitic worm infections. It works by paralyzing the worms, allowing the body to remove them from the system. In addition, levamisole has been used in veterinary medicine as an immunomodulator, a substance that affects the immune system.

In human medicine, levamisole was previously used in the treatment of colon cancer and autoimmune disorders such as rheumatoid arthritis. However, its use in these areas has largely been discontinued due to side effects and the availability of more effective treatments.

It is important to note that levamisole has also been identified as a common adulterant in cocaine, which can lead to various health issues, including agranulocytosis (a severe decrease in white blood cells), skin lesions, and neurological symptoms.

Antineoplastic agents are a class of drugs used to treat malignant neoplasms or cancer. These agents work by inhibiting the growth and proliferation of cancer cells, either by killing them or preventing their division and replication. Antineoplastic agents can be classified based on their mechanism of action, such as alkylating agents, antimetabolites, topoisomerase inhibitors, mitotic inhibitors, and targeted therapy agents.

Alkylating agents work by adding alkyl groups to DNA, which can cause cross-linking of DNA strands and ultimately lead to cell death. Antimetabolites interfere with the metabolic processes necessary for DNA synthesis and replication, while topoisomerase inhibitors prevent the relaxation of supercoiled DNA during replication. Mitotic inhibitors disrupt the normal functioning of the mitotic spindle, which is essential for cell division. Targeted therapy agents are designed to target specific molecular abnormalities in cancer cells, such as mutated oncogenes or dysregulated signaling pathways.

It's important to note that antineoplastic agents can also affect normal cells and tissues, leading to various side effects such as nausea, vomiting, hair loss, and myelosuppression (suppression of bone marrow function). Therefore, the use of these drugs requires careful monitoring and management of their potential adverse effects.

Neoplasm metastasis is the spread of cancer cells from the primary site (where the original or primary tumor formed) to other places in the body. This happens when cancer cells break away from the original (primary) tumor and enter the bloodstream or lymphatic system. The cancer cells can then travel to other parts of the body and form new tumors, called secondary tumors or metastases.

Metastasis is a key feature of malignant neoplasms (cancers), and it is one of the main ways that cancer can cause harm in the body. The metastatic tumors may continue to grow and may cause damage to the organs and tissues where they are located. They can also release additional cancer cells into the bloodstream or lymphatic system, leading to further spread of the cancer.

The metastatic tumors are named based on the location where they are found, as well as the type of primary cancer. For example, if a patient has a primary lung cancer that has metastasized to the liver, the metastatic tumor would be called a liver metastasis from lung cancer.

It is important to note that the presence of metastases can significantly affect a person's prognosis and treatment options. In general, metastatic cancer is more difficult to treat than cancer that has not spread beyond its original site. However, there are many factors that can influence a person's prognosis and response to treatment, so it is important for each individual to discuss their specific situation with their healthcare team.

Breast neoplasms refer to abnormal growths in the breast tissue that can be benign or malignant. Benign breast neoplasms are non-cancerous tumors or growths, while malignant breast neoplasms are cancerous tumors that can invade surrounding tissues and spread to other parts of the body.

Breast neoplasms can arise from different types of cells in the breast, including milk ducts, milk sacs (lobules), or connective tissue. The most common type of breast cancer is ductal carcinoma, which starts in the milk ducts and can spread to other parts of the breast and nearby structures.

Breast neoplasms are usually detected through screening methods such as mammography, ultrasound, or MRI, or through self-examination or clinical examination. Treatment options for breast neoplasms depend on several factors, including the type and stage of the tumor, the patient's age and overall health, and personal preferences. Treatment may include surgery, radiation therapy, chemotherapy, hormone therapy, or targeted therapy.

Medical survival rate is a statistical measure used to determine the percentage of patients who are still alive for a specific period of time after their diagnosis or treatment for a certain condition or disease. It is often expressed as a five-year survival rate, which refers to the proportion of people who are alive five years after their diagnosis. Survival rates can be affected by many factors, including the stage of the disease at diagnosis, the patient's age and overall health, the effectiveness of treatment, and other health conditions that the patient may have. It is important to note that survival rates are statistical estimates and do not necessarily predict an individual patient's prognosis.

Intra-arterial infusion is a medical procedure in which a liquid medication or fluid is delivered directly into an artery. This technique is used to deliver drugs directly to a specific organ or region of the body, bypassing the usual systemic circulation and allowing for higher concentrations of the drug to reach the target area. It is often used in cancer treatment to deliver chemotherapeutic agents directly to tumors, as well as in other conditions such as severe infections or inflammation.

Intra-arterial infusions are typically administered through a catheter that is inserted into an artery, usually under the guidance of imaging techniques such as fluoroscopy, CT, or MRI. The procedure requires careful monitoring and precise control to ensure proper placement of the catheter and accurate delivery of the medication.

It's important to note that intra-arterial infusions are different from intra venous (IV) infusions, where medications are delivered into a vein instead of an artery. The choice between intra-arterial and intra-venous infusion depends on various factors such as the type of medication being used, the location of the target area, and the patient's overall medical condition.

Stomatitis is a medical term that refers to inflammation of the mucous membrane of any of the soft tissues in the mouth, including the lips, gums, tongue, palate, and cheek lining. It can cause discomfort, pain, and sores or lesions in the mouth. Stomatitis may result from a variety of causes, such as infection, injury, allergic reaction, or systemic diseases. Treatment depends on the underlying cause and may include medications, mouth rinses, or changes in oral hygiene practices.

Liver neoplasms refer to abnormal growths in the liver that can be benign or malignant. Benign liver neoplasms are non-cancerous tumors that do not spread to other parts of the body, while malignant liver neoplasms are cancerous tumors that can invade and destroy surrounding tissue and spread to other organs.

Liver neoplasms can be primary, meaning they originate in the liver, or secondary, meaning they have metastasized (spread) to the liver from another part of the body. Primary liver neoplasms can be further classified into different types based on their cell of origin and behavior, including hepatocellular carcinoma, cholangiocarcinoma, and hepatic hemangioma.

The diagnosis of liver neoplasms typically involves a combination of imaging studies, such as ultrasound, CT scan, or MRI, and biopsy to confirm the type and stage of the tumor. Treatment options depend on the type and extent of the neoplasm and may include surgery, radiation therapy, chemotherapy, or liver transplantation.

Levoleucovorin is the pharmaceutical form of the active isomer of folinic acid, which is a reduced and readily usable form of folate. It is used in medicine as a medication to reduce the toxic effects of methotrexate, an antifolate chemotherapeutic agent, when high-dose methotrexate therapy is used.

Methotrexate works by blocking the action of an enzyme called dihydrofolate reductase, which is necessary for the production of thymidine, one of the four nucleosides in DNA. By inhibiting this enzyme, methotrexate prevents the synthesis of DNA and RNA, thereby interfering with cell division and growth. However, methotrexate can also block the action of other enzymes that require reduced folates as cofactors, leading to toxicity in normal cells.

Levoleucovorin is a form of folate that can bypass the blocked enzyme and provide the necessary cofactor for these other enzymes, thereby reducing the toxic effects of methotrexate on normal cells. It is usually given 24 hours after the start of high-dose methotrexate therapy, and its administration is continued until the serum concentration of methotrexate falls below a certain level.

It's important to note that levoleucovorin should not be given at the same time as methotrexate, as it can reduce the efficacy of methotrexate in killing cancer cells.

Bromouracil is a chemical compound that is used in the synthesis of DNA. It is a brominated derivative of uracil, which is one of the nucleobases found in RNA. Bromouracil can be incorporated into DNA during replication in place of thymine, another nucleobase. This can lead to mutations in the DNA because bromouracil behaves differently from thymine in certain chemical reactions.

Bromouracil is not typically found in living organisms and is not considered to be a normal part of the genetic material. It may be used in research settings to study the mechanisms of DNA replication and mutation. In clinical medicine, bromouracil has been used in the treatment of psoriasis, a skin condition characterized by red, scaly patches. However, its use in this context is not common.

It is important to note that bromouracil can have toxic effects and should be handled with care. It can cause irritation to the skin and eyes, and prolonged exposure may lead to more serious health problems. If you have any questions about bromouracil or its use, it is best to speak with a healthcare professional or a qualified scientist.

An antidote is a substance that can counteract the effects of a poison or toxin. It works by neutralizing, reducing, or eliminating the harmful effects of the toxic substance. Antidotes can be administered in various forms such as medications, vaccines, or treatments. They are often used in emergency situations to save lives and prevent serious complications from poisoning.

The effectiveness of an antidote depends on several factors, including the type and amount of toxin involved, the timing of administration, and the individual's response to treatment. In some cases, multiple antidotes may be required to treat a single poisoning incident. It is important to note that not all poisons have specific antidotes, and in such cases, supportive care and symptomatic treatment may be necessary.

Examples of common antidotes include:

* Naloxone for opioid overdose
* Activated charcoal for certain types of poisoning
* Digoxin-specific antibodies for digoxin toxicity
* Fomepizole for methanol or ethylene glycol poisoning
* Dimercaprol for heavy metal poisoning.

Drug synergism is a pharmacological concept that refers to the interaction between two or more drugs, where the combined effect of the drugs is greater than the sum of their individual effects. This means that when these drugs are administered together, they produce an enhanced therapeutic response compared to when they are given separately.

Drug synergism can occur through various mechanisms, such as:

1. Pharmacodynamic synergism - When two or more drugs interact with the same target site in the body and enhance each other's effects.
2. Pharmacokinetic synergism - When one drug affects the metabolism, absorption, distribution, or excretion of another drug, leading to an increased concentration of the second drug in the body and enhanced therapeutic effect.
3. Physiochemical synergism - When two drugs interact physically, such as when one drug enhances the solubility or permeability of another drug, leading to improved absorption and bioavailability.

It is important to note that while drug synergism can result in enhanced therapeutic effects, it can also increase the risk of adverse reactions and toxicity. Therefore, healthcare providers must carefully consider the potential benefits and risks when prescribing combinations of drugs with known or potential synergistic effects.

Flucytosine is an antifungal medication used to treat serious and life-threatening fungal infections, such as cryptococcal meningitis and candidiasis. It works by interfering with the production of DNA and RNA in the fungal cells, which inhibits their growth and reproduction.

The medical definition of Flucytosine is:

A synthetic fluorinated pyrimidine nucleoside analogue that is converted to fluorouracil after uptake into susceptible fungal cells. It is used as an antifungal agent in the treatment of serious systemic fungal infections, particularly those caused by Candida and Cryptococcus neoformans. Flucytosine has both fungistatic and fungicidal activity, depending on the concentration achieved at the site of infection and the susceptibility of the organism.

Flucytosine is available in oral form and is often used in combination with other antifungal agents to increase its effectiveness and prevent the development of resistance. Common side effects include nausea, vomiting, diarrhea, and bone marrow suppression. Regular monitoring of blood counts and liver function tests is necessary during treatment to detect any potential toxicity.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Chronotherapy is a medical treatment strategy that involves adjusting the timing of medication or other treatments based on the body's internal clock or circadian rhythms. The goal of chronotherapy is to optimize the effectiveness and minimize the side effects of treatments by administering them at specific times when they are most likely to be beneficial and well-tolerated.

For example, certain medications may be more effective when given at night because the body's metabolism slows down during sleep, allowing the drug to remain in the system longer. Similarly, some cancer treatments may be more effective when administered in the morning or evening based on the patient's circadian rhythms.

Chronotherapy can also involve adjusting lifestyle factors such as diet, exercise, and light exposure to help regulate the body's internal clock and improve overall health. This approach has been shown to be effective in treating a variety of conditions, including insomnia, depression, asthma, and cardiovascular disease.

Taxoids are a class of naturally occurring compounds that are derived from the bark of the Pacific yew tree (Taxus brevifolia) and other species of the genus Taxus. They are known for their antineoplastic (cancer-fighting) properties and have been used in chemotherapy to treat various types of cancer, including ovarian, breast, and lung cancer.

The most well-known taxoid is paclitaxel (also known by the brand name Taxol), which was first discovered in the 1960s and has since become a widely used cancer drug. Paclitaxel works by stabilizing microtubules, which are important components of the cell's skeleton, and preventing them from disassembling. This disrupts the normal function of the cell's mitotic spindle, leading to cell cycle arrest and ultimately apoptosis (programmed cell death).

Other taxoids that have been developed for clinical use include docetaxel (Taxotere), which is a semi-synthetic analogue of paclitaxel, and cabazitaxel (Jevtana), which is a second-generation taxoid. These drugs have similar mechanisms of action to paclitaxel but may have different pharmacokinetic properties or be effective against cancer cells that have developed resistance to other taxoids.

While taxoids have been successful in treating certain types of cancer, they can also cause significant side effects, including neutropenia (low white blood cell count), anemia (low red blood cell count), and peripheral neuropathy (nerve damage). As with all chemotherapy drugs, the use of taxoids must be carefully balanced against their potential benefits and risks.

Squamous cell carcinoma is a type of skin cancer that begins in the squamous cells, which are flat, thin cells that form the outer layer of the skin (epidermis). It commonly occurs on sun-exposed areas such as the face, ears, lips, and backs of the hands. Squamous cell carcinoma can also develop in other areas of the body including the mouth, lungs, and cervix.

This type of cancer usually develops slowly and may appear as a rough or scaly patch of skin, a red, firm nodule, or a sore or ulcer that doesn't heal. While squamous cell carcinoma is not as aggressive as some other types of cancer, it can metastasize (spread) to other parts of the body if left untreated, making early detection and treatment important.

Risk factors for developing squamous cell carcinoma include prolonged exposure to ultraviolet (UV) radiation from the sun or tanning beds, fair skin, a history of sunburns, a weakened immune system, and older age. Prevention measures include protecting your skin from the sun by wearing protective clothing, using a broad-spectrum sunscreen with an SPF of at least 30, avoiding tanning beds, and getting regular skin examinations.

A prodrug is a pharmacologically inactive substance that, once administered, is metabolized into a drug that is active. Prodrugs are designed to improve the bioavailability or delivery of a drug, to minimize adverse effects, or to target the drug to specific sites in the body. The conversion of a prodrug to its active form typically occurs through enzymatic reactions in the liver or other tissues.

Prodrugs can offer several advantages over traditional drugs, including:

* Improved absorption: Some drugs have poor bioavailability due to their chemical properties, which make them difficult to absorb from the gastrointestinal tract. Prodrugs can be designed with improved absorption characteristics, allowing for more efficient delivery of the active drug to the body.
* Reduced toxicity: By masking the active drug's chemical structure, prodrugs can reduce its interactions with sensitive tissues and organs, thereby minimizing adverse effects.
* Targeted delivery: Prodrugs can be designed to selectively release the active drug in specific areas of the body, such as tumors or sites of infection, allowing for more precise and effective therapy.

Examples of prodrugs include:

* Aspirin (acetylsalicylic acid), which is metabolized to salicylic acid in the liver.
* Enalapril, an angiotensin-converting enzyme (ACE) inhibitor used to treat hypertension and heart failure, which is metabolized to enalaprilat in the liver.
* Codeine, an opioid analgesic, which is metabolized to morphine in the liver by the enzyme CYP2D6.

It's important to note that not all prodrugs are successful, and some may even have unintended consequences. For example, if a patient has a genetic variation that affects the activity of the enzyme responsible for converting the prodrug to its active form, the drug may not be effective or may produce adverse effects. Therefore, it's essential to consider individual genetic factors when prescribing prodrugs.

Head and neck neoplasms refer to abnormal growths or tumors in the head and neck region, which can be benign (non-cancerous) or malignant (cancerous). These tumors can develop in various sites, including the oral cavity, nasopharynx, oropharynx, larynx, hypopharynx, paranasal sinuses, salivary glands, and thyroid gland.

Benign neoplasms are slow-growing and generally do not spread to other parts of the body. However, they can still cause problems if they grow large enough to press on surrounding tissues or structures. Malignant neoplasms, on the other hand, can invade nearby tissues and organs and may also metastasize (spread) to other parts of the body.

Head and neck neoplasms can have various symptoms depending on their location and size. Common symptoms include difficulty swallowing, speaking, or breathing; pain in the mouth, throat, or ears; persistent coughing or hoarseness; and swelling or lumps in the neck or face. Early detection and treatment of head and neck neoplasms are crucial for improving outcomes and reducing the risk of complications.

Esophageal neoplasms refer to abnormal growths in the tissue of the esophagus, which is the muscular tube that connects the throat to the stomach. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant esophageal neoplasms are typically classified as either squamous cell carcinomas or adenocarcinomas, depending on the type of cell from which they originate.

Esophageal cancer is a serious and often life-threatening condition that can cause symptoms such as difficulty swallowing, chest pain, weight loss, and coughing. Risk factors for esophageal neoplasms include smoking, heavy alcohol consumption, gastroesophageal reflux disease (GERD), and Barrett's esophagus. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Phosphoribosyl Pyrophosphate (PRPP) is defined as a key intracellular nucleotide metabolite that plays an essential role in the biosynthesis of purine and pyrimidine nucleotides, which are the building blocks of DNA and RNA. PRPP is synthesized from ribose 5-phosphate and ATP by the enzyme PRPP synthase. It contributes a phosphoribosyl group in the conversion of purines and pyrimidines to their corresponding nucleotides, which are critical for various cellular processes such as DNA replication, repair, and gene expression. Abnormal levels of PRPP have been implicated in several genetic disorders, including Lesch-Nyhan syndrome and PRPP synthetase superactivity.

Leukopenia is a medical term used to describe an abnormally low white blood cell (WBC) count in the blood. White blood cells are crucial components of the body's immune system, helping to fight infections and diseases. A normal WBC count ranges from 4,500 to 11,000 cells per microliter (μL) of blood in most laboratories. Leukopenia is typically diagnosed when the WBC count falls below 4,500 cells/μL.

There are several types of white blood cells, including neutrophils, lymphocytes, monocytes, eosinophils, and basophils. Neutropenia, a specific type of leukopenia, refers to an abnormally low neutrophil count (less than 1,500 cells/μL). Neutropenia increases the risk of bacterial and fungal infections since neutrophils play a significant role in combating these types of pathogens.

Leukopenia can result from various factors, such as viral infections, certain medications (like chemotherapy or radiation therapy), bone marrow disorders, autoimmune diseases, or congenital conditions affecting white blood cell production. It is essential to identify the underlying cause of leukopenia to provide appropriate treatment and prevent complications.

Neoplasm staging is a systematic process used in medicine to describe the extent of spread of a cancer, including the size and location of the original (primary) tumor and whether it has metastasized (spread) to other parts of the body. The most widely accepted system for this purpose is the TNM classification system developed by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC).

In this system, T stands for tumor, and it describes the size and extent of the primary tumor. N stands for nodes, and it indicates whether the cancer has spread to nearby lymph nodes. M stands for metastasis, and it shows whether the cancer has spread to distant parts of the body.

Each letter is followed by a number that provides more details about the extent of the disease. For example, a T1N0M0 cancer means that the primary tumor is small and has not spread to nearby lymph nodes or distant sites. The higher the numbers, the more advanced the cancer.

Staging helps doctors determine the most appropriate treatment for each patient and estimate the patient's prognosis. It is an essential tool for communication among members of the healthcare team and for comparing outcomes of treatments in clinical trials.

Mucositis is a common side effect of cancer treatment, particularly chemotherapy and radiation therapy. It's defined as the inflammation and damage to the mucous membranes that line the digestive tract, from the mouth to the anus. This condition can cause symptoms such as pain, redness, swelling, and ulcers in the mouth, throat, esophagus, stomach, and intestines.

Mucositis can make it difficult for patients to eat, drink, and swallow, which can lead to dehydration, malnutrition, and weight loss. It can also increase the risk of infection, as the damaged mucous membranes provide an entry point for bacteria and other microorganisms.

The severity of mucositis can vary depending on the type and dose of chemotherapy or radiation therapy, as well as individual patient factors such as age, overall health status, and genetic makeup. Mucositis typically occurs within a few days to a week after starting cancer treatment and may persist for several weeks or even months after treatment has ended.

Management of mucositis typically involves a combination of strategies, including pain relief, oral hygiene measures, nutritional support, and infection prevention. In severe cases, hospitalization and intravenous fluids may be necessary to prevent dehydration and manage infection.

Drug resistance in neoplasms (also known as cancer drug resistance) refers to the ability of cancer cells to withstand the effects of chemotherapeutic agents or medications designed to kill or inhibit the growth of cancer cells. This can occur due to various mechanisms, including changes in the cancer cell's genetic makeup, alterations in drug targets, increased activity of drug efflux pumps, and activation of survival pathways.

Drug resistance can be intrinsic (present at the beginning of treatment) or acquired (developed during the course of treatment). It is a significant challenge in cancer therapy as it often leads to reduced treatment effectiveness, disease progression, and poor patient outcomes. Strategies to overcome drug resistance include the use of combination therapies, development of new drugs that target different mechanisms, and personalized medicine approaches that consider individual patient and tumor characteristics.

Neutropenia is a condition characterized by an abnormally low concentration (less than 1500 cells/mm3) of neutrophils, a type of white blood cell that plays a crucial role in fighting off bacterial and fungal infections. Neutrophils are essential components of the innate immune system, and their main function is to engulf and destroy microorganisms that can cause harm to the body.

Neutropenia can be classified as mild, moderate, or severe based on the severity of the neutrophil count reduction:

* Mild neutropenia: Neutrophil count between 1000-1500 cells/mm3
* Moderate neutropenia: Neutrophil count between 500-1000 cells/mm3
* Severe neutropenia: Neutrophil count below 500 cells/mm3

Severe neutropenia significantly increases the risk of developing infections, as the body's ability to fight off microorganisms is severely compromised. Common causes of neutropenia include viral infections, certain medications (such as chemotherapy or antibiotics), autoimmune disorders, and congenital conditions affecting bone marrow function. Treatment for neutropenia typically involves addressing the underlying cause, administering granulocyte-colony stimulating factors to boost neutrophil production, and providing appropriate antimicrobial therapy to prevent or treat infections.

Neoadjuvant therapy is a treatment regimen that is administered to patients before they undergo definitive or curative surgery for their cancer. The main goal of neoadjuvant therapy is to reduce the size and extent of the tumor, making it easier to remove surgically and increasing the likelihood of complete resection. This type of therapy often involves the use of chemotherapy, radiation therapy, or targeted therapy, and it can help improve treatment outcomes by reducing the risk of recurrence and improving overall survival rates. Neoadjuvant therapy is commonly used in the treatment of various types of cancer, including breast, lung, esophageal, rectal, and bladder cancer.

Thymidine phosphorylase (TP) is an enzyme that plays a role in the metabolism of nucleosides, specifically thymidine. The medical definition of thymidine phosphorylase is:

An enzyme that catalyzes the conversion of thymidine to thymine and deoxyribose-1-phosphate. Thymidine phosphorylase has been identified as a key enzyme in the angiogenic (formation of new blood vessels) pathway, where it facilitates the release of pro-angiogenic factors such as vascular endothelial growth factor (VEGF).

In addition to its role in nucleoside metabolism and angiogenesis, thymidine phosphorylase has been implicated in cancer biology. Increased levels of thymidine phosphorylase have been found in various human cancers, including colorectal, breast, lung, and pancreatic cancers. These high levels of thymidine phosphorylase are associated with poor prognosis and increased angiogenesis, contributing to tumor growth and metastasis.

Thus, thymidine phosphorylase is a crucial enzyme in nucleoside metabolism, angiogenesis, and cancer biology, making it an important target for the development of novel anti-cancer therapies.

Cytosine deaminase is an enzyme that catalyzes the hydrolytic deamination of cytosine residues in DNA or deoxycytidine residues in RNA, converting them to uracil or uridine, respectively. This enzyme plays a role in the regulation of gene expression and is also involved in the defense against viral infections in some organisms. In humans, cytosine deamination in DNA can lead to mutations and has been implicated in the development of certain diseases, including cancer.

"Drug evaluation" is a medical term that refers to the systematic process of assessing the pharmacological, therapeutic, and safety profile of a drug or medication. This process typically involves several stages, including preclinical testing in the laboratory, clinical trials in human subjects, and post-marketing surveillance.

The goal of drug evaluation is to determine the efficacy, safety, and optimal dosage range of a drug, as well as any potential interactions with other medications or medical conditions. The evaluation process also includes an assessment of the drug's pharmacokinetics, or how it is absorbed, distributed, metabolized, and eliminated by the body.

The findings from drug evaluations are used to inform regulatory decisions about whether a drug should be approved for use in clinical practice, as well as to provide guidance to healthcare providers about how to use the drug safely and effectively.

Intravenous injections are a type of medical procedure where medication or fluids are administered directly into a vein using a needle and syringe. This route of administration is also known as an IV injection. The solution injected enters the patient's bloodstream immediately, allowing for rapid absorption and onset of action. Intravenous injections are commonly used to provide quick relief from symptoms, deliver medications that are not easily absorbed by other routes, or administer fluids and electrolytes in cases of dehydration or severe illness. It is important that intravenous injections are performed using aseptic technique to minimize the risk of infection.

Pancreatic neoplasms refer to abnormal growths in the pancreas that can be benign or malignant. The pancreas is a gland located behind the stomach that produces hormones and digestive enzymes. Pancreatic neoplasms can interfere with the normal functioning of the pancreas, leading to various health complications.

Benign pancreatic neoplasms are non-cancerous growths that do not spread to other parts of the body. They are usually removed through surgery to prevent any potential complications, such as blocking the bile duct or causing pain.

Malignant pancreatic neoplasms, also known as pancreatic cancer, are cancerous growths that can invade and destroy surrounding tissues and organs. They can also spread (metastasize) to other parts of the body, such as the liver, lungs, or bones. Pancreatic cancer is often aggressive and difficult to treat, with a poor prognosis.

There are several types of pancreatic neoplasms, including adenocarcinomas, neuroendocrine tumors, solid pseudopapillary neoplasms, and cystic neoplasms. The specific type of neoplasm is determined through various diagnostic tests, such as imaging studies, biopsies, and blood tests. Treatment options depend on the type, stage, and location of the neoplasm, as well as the patient's overall health and preferences.

I'm sorry for any confusion, but "Oxonic Acid" is not a recognized term in medical or clinical sciences. It is, however, a chemical compound with the formula C5H7NO5. It is a type of organic acid that is used in research and industrial settings, particularly as a precursor in the synthesis of other chemicals.

If you have any questions related to medical terminology or health-related topics, I would be happy to help answer them for you!

Dihydropyrimidine dehydrogenase (DPD) deficiency is a genetic disorder that affects the metabolism of certain chemicals in the body. DPD is an enzyme that helps break down pyrimidines, which are building blocks of DNA, including the chemicals uracil and thymine.

People with DPD deficiency have reduced levels or completely lack DPD activity, leading to an accumulation of pyrimidines and their metabolites in the body. This can cause a range of symptoms, including neurological problems, gastrointestinal issues, and skin abnormalities.

DPD deficiency is often discovered in individuals who experience severe toxicity after receiving fluorouracil (5-FU) chemotherapy, which is metabolized by DPD. In these cases, the accumulation of 5-FU can cause life-threatening side effects such as neutropenia, sepsis, and mucositis.

DPD deficiency is inherited in an autosomal recessive manner, meaning that an individual must inherit two copies of the mutated gene (one from each parent) to have the condition. It is estimated that DPD deficiency affects approximately 1 in 1000 individuals, but many people with the disorder may not experience any symptoms.

Nausea is a subjective, unpleasant sensation of discomfort in the stomach and upper gastrointestinal tract that may precede vomiting. It's often described as a feeling of queasiness or the need to vomit. Nausea can be caused by various factors, including motion sickness, pregnancy, gastrointestinal disorders, infections, certain medications, and emotional stress. While nausea is not a disease itself, it can be a symptom of an underlying medical condition that requires attention and treatment.

Local neoplasm recurrence is the return or regrowth of a tumor in the same location where it was originally removed or treated. This means that cancer cells have survived the initial treatment and started to grow again in the same area. It's essential to monitor and detect any local recurrence as early as possible, as it can affect the prognosis and may require additional treatment.

The hepatic artery is a branch of the celiac trunk or abdominal aorta that supplies oxygenated blood to the liver. It typically divides into two main branches, the right and left hepatic arteries, which further divide into smaller vessels to supply different regions of the liver. The hepatic artery also gives off branches to supply other organs such as the gallbladder, pancreas, and duodenum.

It's worth noting that there is significant variability in the anatomy of the hepatic artery, with some individuals having additional branches or variations in the origin of the vessel. This variability can have implications for surgical procedures involving the liver and surrounding organs.

Paclitaxel is a chemotherapeutic agent derived from the bark of the Pacific yew tree (Taxus brevifolia). It is an antimicrotubule agent that promotes the assembly and stabilization of microtubules, thereby interfering with the normal dynamic reorganization of the microtubule network that is essential for cell division.

Paclitaxel is used in the treatment of various types of cancer including ovarian, breast, lung, and pancreatic cancers. It works by inhibiting the disassembly of microtubules, which prevents the separation of chromosomes during mitosis, leading to cell cycle arrest and apoptosis (programmed cell death).

Common side effects of paclitaxel include neutropenia (low white blood cell count), anemia (low red blood cell count), alopecia (hair loss), peripheral neuropathy (nerve damage causing numbness or tingling in the hands and feet), myalgias (muscle pain), arthralgias (joint pain), and hypersensitivity reactions.

Deoxyuracil nucleotides are chemical compounds that are the building blocks of DNA. Specifically, they are the form of nucleotides that contain the sugar deoxyribose and the nucleobase deoxyuracil. In DNA, deoxyuracil nucleotides pair with deoxyadenosine nucleotides through base pairing.

Deoxyuracil is a nucleobase that is similar to thymine, but it lacks a methyl group. Thymine is the usual nucleobase that pairs with adenine in DNA, while uracil is typically found in RNA paired with adenine. However, in certain circumstances, such as during DNA repair or damage, deoxyuracil can be incorporated into DNA instead of thymine.

Deoxyuracil nucleotides are important for understanding DNA replication, repair, and mutation. Abnormalities in the incorporation or removal of deoxyuracil nucleotides can lead to genetic disorders, cancer, and other diseases.

Uridine is a nucleoside that consists of a pyrimidine base (uracil) linked to a pentose sugar (ribose). It is a component of RNA, where it pairs with adenine. Uridine can also be found in various foods such as beer, broccoli, yeast, and meat. In the body, uridine can be synthesized from orotate or from the breakdown of RNA. It has several functions, including acting as a building block for RNA, contributing to energy metabolism, and regulating cell growth and differentiation. Uridine is also available as a dietary supplement and has been studied for its potential benefits in various health conditions.

Phosphonoacetic acid (PAA) is not a naturally occurring substance, but rather a synthetic compound that is used in medical and scientific research. It is a colorless, crystalline solid that is soluble in water.

In a medical context, PAA is an inhibitor of certain enzymes that are involved in the replication of viruses, including HIV. It works by binding to the active site of these enzymes and preventing them from carrying out their normal functions. As a result, PAA has been studied as a potential antiviral agent, although it is not currently used as a medication.

It's important to note that while PAA has shown promise in laboratory studies, its safety and efficacy have not been established in clinical trials, and it is not approved for use as a drug by regulatory agencies such as the U.S. Food and Drug Administration (FDA).

Interferon-alpha (IFN-α) is a type I interferon, which is a group of signaling proteins made and released by host cells in response to the presence of viruses, parasites, and tumor cells. It plays a crucial role in the immune response against viral infections. IFN-α has antiviral, immunomodulatory, and anti-proliferative effects.

IFN-α is produced naturally by various cell types, including leukocytes (white blood cells), fibroblasts, and epithelial cells, in response to viral or bacterial stimulation. It binds to specific receptors on the surface of nearby cells, triggering a signaling cascade that leads to the activation of genes involved in the antiviral response. This results in the production of proteins that inhibit viral replication and promote the presentation of viral antigens to the immune system, enhancing its ability to recognize and eliminate infected cells.

In addition to its role in the immune response, IFN-α has been used as a therapeutic agent for various medical conditions, including certain types of cancer, chronic hepatitis B and C, and multiple sclerosis. However, its use is often limited by side effects such as flu-like symptoms, depression, and neuropsychiatric disorders.

Trimetrexate is a antifolate drug, which means it interferes with the use of folic acid in the body. It is primarily used in the treatment of certain types of cancer and parasitic infections. Trimetrexate works by blocking the action of an enzyme called dihydrofolate reductase, which is necessary for the production of DNA and RNA, the genetic material found in cells. By inhibiting this enzyme, trimetrexate can help to stop the growth and multiplication of cancer cells or parasites.

In medical terms, Trimetrexate is classified as an antineoplastic agent and an antiprotozoal agent. It may be used to treat certain types of cancer such as non-Hodgkin's lymphoma, and it may also be used to treat parasitic infections caused by Pneumocystis jirovecii (formerly known as Pneumocystis carinii) in patients with weakened immune systems.

It is important to note that Trimetrexate can have significant side effects and should only be used under the close supervision of a healthcare provider.

Uridine phosphorylase is an enzyme that plays a role in the metabolism of nucleosides, specifically uridine. The medical definition of 'uridine phosphorylase' is:

An enzyme (EC 2.4.2.3) involved in the reversible phosphorolysis of uridine to uracil and ribose-1-phosphate. This enzyme also catalyzes the phosphorolytic cleavage of other pyrimidine nucleosides, such as cytidine and thymidine, into their respective bases and ribose-1-phosphate. Uridine phosphorylase has a role in the salvage pathway of pyrimidine nucleotide biosynthesis and is found in various tissues, including the liver, intestines, and blood cells. Deficiency or dysfunction of uridine phosphorylase can lead to impaired nucleotide metabolism and may be associated with certain medical conditions, such as hereditary orotic aciduria.

The Maximum Tolerated Dose (MTD) is a term used in medical research, particularly in clinical trials of new drugs or treatments. It refers to the highest dose of a medication or treatment that can be given without causing unacceptable or severe side effects or toxicity to the patient.

Determining the MTD is an important step in developing new medications, as it helps researchers establish a safe and effective dosage range for future use. This process typically involves gradually increasing the dose in a group of subjects (often healthy volunteers in early phase trials) until intolerable side effects occur, at which point the previous dose is considered the MTD.

It's important to note that the MTD may vary between individuals and populations, depending on factors such as age, sex, genetic makeup, and overall health status. Therefore, individualized dosing strategies may be necessary to ensure safe and effective treatment with new medications.

Oral administration is a route of giving medications or other substances by mouth. This can be in the form of tablets, capsules, liquids, pastes, or other forms that can be swallowed. Once ingested, the substance is absorbed through the gastrointestinal tract and enters the bloodstream to reach its intended target site in the body. Oral administration is a common and convenient route of medication delivery, but it may not be appropriate for all substances or in certain situations, such as when rapid onset of action is required or when the patient has difficulty swallowing.

Mitomycin is an antineoplastic antibiotic derived from Streptomyces caespitosus. It is used in cancer chemotherapy, particularly for the treatment of gastrointestinal tumors, head and neck cancers, and sensitive skin cancers like squamous cell carcinoma. Mitomycin works by forming cross-links in DNA, which prevents DNA replication and transcription, ultimately leading to cell death. It is often administered through intravenous injection or topically during surgery for local treatment of certain cancers. Common side effects include nausea, vomiting, diarrhea, and potential myelosuppression (decrease in blood cells).

A cell line that is derived from tumor cells and has been adapted to grow in culture. These cell lines are often used in research to study the characteristics of cancer cells, including their growth patterns, genetic changes, and responses to various treatments. They can be established from many different types of tumors, such as carcinomas, sarcomas, and leukemias. Once established, these cell lines can be grown and maintained indefinitely in the laboratory, allowing researchers to conduct experiments and studies that would not be feasible using primary tumor cells. It is important to note that tumor cell lines may not always accurately represent the behavior of the original tumor, as they can undergo genetic changes during their time in culture.

Adjuvant radiotherapy is a type of cancer treatment that uses radiation therapy as an adjunct to a primary surgical procedure. The goal of adjuvant radiotherapy is to eliminate any remaining microscopic cancer cells that may be present in the surrounding tissues after surgery, thereby reducing the risk of local recurrence and improving the chances of cure.

Radiotherapy involves the use of high-energy radiation to destroy cancer cells and shrink tumors. In adjuvant radiotherapy, the radiation is usually delivered to the tumor bed and regional lymph nodes in order to target any potential sites of residual disease. The timing and dosing of adjuvant radiotherapy may vary depending on the type and stage of cancer being treated, as well as other factors such as patient age and overall health status.

Adjuvant radiotherapy is commonly used in the treatment of various types of cancer, including breast, colorectal, lung, head and neck, and gynecologic cancers. Its use has been shown to improve survival rates and reduce the risk of recurrence in many cases, making it an important component of comprehensive cancer care.

Fluorine is not a medical term itself, but it is a chemical element that is often discussed in the context of dental health. Here's a brief scientific/chemical definition:

Fluorine is a chemical element with the symbol F and atomic number 9. It is the most reactive and electronegative of all elements. Fluorine is never found in its free state in nature, but it is abundant in minerals such as fluorspar (calcium fluoride).

In dental health, fluoride, which is a compound containing fluorine, is used to help prevent tooth decay. It can be found in many water supplies, some foods, and various dental products like toothpaste and mouthwash. Fluoride works by strengthening the enamel on teeth, making them more resistant to acid attacks that can lead to cavities.

Deoxyuridine is a chemical compound that is a component of DNA. It is a nucleoside, which means it consists of a sugar (deoxyribose) linked to a nitrogenous base (uracil). In the case of deoxyuridine, the uracil is not methylated, which differentiates it from thymidine.

Deoxyuridine can be converted into deoxyuridine monophosphate (dUMP) by the enzyme thymidine kinase. The dUMP can then be converted into deoxythymidine triphosphate (dTTP), which is a building block of DNA, through a series of reactions involving other enzymes.

Deoxyuridine has been used in research and medicine as a marker for DNA synthesis and repair. It can also be used to inhibit the growth of certain types of cells, such as cancer cells, by disrupting their DNA synthesis.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Gastrointestinal (GI) neoplasms refer to abnormal growths in the gastrointestinal tract, which can be benign or malignant. The gastrointestinal tract includes the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus.

Benign neoplasms are non-cancerous growths that do not invade nearby tissues or spread to other parts of the body. They can sometimes be removed completely and may not cause any further health problems.

Malignant neoplasms, on the other hand, are cancerous growths that can invade nearby tissues and organs and spread to other parts of the body through the bloodstream or lymphatic system. These types of neoplasms can be life-threatening if not diagnosed and treated promptly.

GI neoplasms can cause various symptoms, including abdominal pain, bloating, changes in bowel habits, nausea, vomiting, weight loss, and anemia. The specific symptoms may depend on the location and size of the neoplasm.

There are many types of GI neoplasms, including adenocarcinomas, gastrointestinal stromal tumors (GISTs), lymphomas, and neuroendocrine tumors. The diagnosis of GI neoplasms typically involves a combination of medical history, physical examination, imaging studies, and biopsy. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or immunotherapy.

Antineoplastic agents, phytogenic, also known as plant-derived anticancer drugs, are medications that are derived from plants and used to treat cancer. These agents have natural origins and work by interfering with the growth and multiplication of cancer cells, helping to slow or stop the spread of the disease. Some examples of antineoplastic agents, phytogenic include paclitaxel (Taxol), vincristine, vinblastine, and etoposide. These drugs are often used in combination with other treatments such as surgery, radiation therapy, and other medications to provide a comprehensive approach to cancer care.

Diarrhea is a condition in which an individual experiences loose, watery stools frequently, often exceeding three times a day. It can be acute, lasting for several days, or chronic, persisting for weeks or even months. Diarrhea can result from various factors, including viral, bacterial, or parasitic infections, food intolerances, medications, and underlying medical conditions such as inflammatory bowel disease or irritable bowel syndrome. Dehydration is a potential complication of diarrhea, particularly in severe cases or in vulnerable populations like young children and the elderly.

Histidinol is not typically considered a medical term, but it is a biochemical concept. Histidinol is an intermediate in the metabolic pathway for the synthesis of the amino acid histidine. It is a reduced form of histidine, where a hydroxyl group replaces the imidazole ring's double-bonded nitrogen atom.

In clinical or medical contexts, Histidinol may be mentioned in relation to inborn errors of metabolism, such as histidinemia, which is characterized by an accumulation of histidine and its metabolites, including histidinol, due to a deficiency in the enzyme histidase. However, it's worth noting that histidinemia is typically asymptomatic or associated with mild symptoms, such as delayed development, learning difficulties, or speech problems.

Antibiotics are a type of medication used to treat infections caused by bacteria. They work by either killing the bacteria or inhibiting their growth.

Antineoplastics, also known as chemotherapeutic agents, are a class of drugs used to treat cancer. These medications target and destroy rapidly dividing cells, such as cancer cells, although they can also affect other quickly dividing cells in the body, such as those in the hair follicles or digestive tract, which can lead to side effects.

Antibiotics and antineoplastics are two different classes of drugs with distinct mechanisms of action and uses. It is important to use them appropriately and under the guidance of a healthcare professional.

Carcinoma is a type of cancer that develops from epithelial cells, which are the cells that line the inner and outer surfaces of the body. These cells cover organs, glands, and other structures within the body. Carcinomas can occur in various parts of the body, including the skin, lungs, breasts, prostate, colon, and pancreas. They are often characterized by the uncontrolled growth and division of abnormal cells that can invade surrounding tissues and spread to other parts of the body through a process called metastasis. Carcinomas can be further classified based on their appearance under a microscope, such as adenocarcinoma, squamous cell carcinoma, and basal cell carcinoma.

Lymphatic metastasis is the spread of cancer cells from a primary tumor to distant lymph nodes through the lymphatic system. It occurs when malignant cells break away from the original tumor, enter the lymphatic vessels, and travel to nearby or remote lymph nodes. Once there, these cancer cells can multiply and form new tumors, leading to further progression of the disease. Lymphatic metastasis is a common way for many types of cancer to spread and can have significant implications for prognosis and treatment strategies.

Prognosis is a medical term that refers to the prediction of the likely outcome or course of a disease, including the chances of recovery or recurrence, based on the patient's symptoms, medical history, physical examination, and diagnostic tests. It is an important aspect of clinical decision-making and patient communication, as it helps doctors and patients make informed decisions about treatment options, set realistic expectations, and plan for future care.

Prognosis can be expressed in various ways, such as percentages, categories (e.g., good, fair, poor), or survival rates, depending on the nature of the disease and the available evidence. However, it is important to note that prognosis is not an exact science and may vary depending on individual factors, such as age, overall health status, and response to treatment. Therefore, it should be used as a guide rather than a definitive forecast.

Orotate phosphoribosyltransferase (OPRT) is an enzyme that catalyzes the conversion of orotate to oximine monophosphate (OMP), which is a key step in the biosynthesis of pyrimidines, a type of nucleotide. This enzyme plays a crucial role in the metabolism of nucleic acids, which are the building blocks of DNA and RNA.

The reaction catalyzed by OPRT is as follows:

orotate + phosphoribosyl pyrophosphate (PRPP) -> oximine monophosphate (OMP) + pyrophosphate

Defects in the gene that encodes for OPRT can lead to orotic aciduria, a rare genetic disorder characterized by an accumulation of orotic acid and other pyrimidines in the urine and other body fluids. Symptoms of this condition may include developmental delay, mental retardation, seizures, and megaloblastic anemia.

Cell survival refers to the ability of a cell to continue living and functioning normally, despite being exposed to potentially harmful conditions or treatments. This can include exposure to toxins, radiation, chemotherapeutic drugs, or other stressors that can damage cells or interfere with their normal processes.

In scientific research, measures of cell survival are often used to evaluate the effectiveness of various therapies or treatments. For example, researchers may expose cells to a particular drug or treatment and then measure the percentage of cells that survive to assess its potential therapeutic value. Similarly, in toxicology studies, measures of cell survival can help to determine the safety of various chemicals or substances.

It's important to note that cell survival is not the same as cell proliferation, which refers to the ability of cells to divide and multiply. While some treatments may promote cell survival, they may also inhibit cell proliferation, making them useful for treating diseases such as cancer. Conversely, other treatments may be designed to specifically target and kill cancer cells, even if it means sacrificing some healthy cells in the process.

Thiophenes are organic compounds that contain a heterocyclic ring made up of four carbon atoms and one sulfur atom. The structure of thiophene is similar to benzene, with the benzene ring being replaced by a thiophene ring. Thiophenes are aromatic compounds, which means they have a stable, planar ring structure and delocalized electrons.

Thiophenes can be found in various natural sources such as coal tar, crude oil, and some foods like onions and garlic. They also occur in certain medications, dyes, and pesticides. Some thiophene derivatives have been synthesized and studied for their potential therapeutic uses, including anti-inflammatory, antiviral, and antitumor activities.

In the medical field, thiophenes are used in some pharmaceuticals as building blocks to create drugs with various therapeutic effects. For example, tipepidine, a cough suppressant, contains a thiophene ring. Additionally, some anesthetics and antipsychotic medications also contain thiophene moieties.

It is important to note that while thiophenes themselves are not typically considered medical terms, they play a role in the chemistry of various pharmaceuticals and other medical-related compounds.

Monoclonal antibodies are laboratory-produced proteins that mimic the immune system's ability to fight off harmful antigens such as viruses and cancer cells. They are created by fusing a single B cell (the type of white blood cell responsible for producing antibodies) with a tumor cell, resulting in a hybrid cell called a hybridoma. This hybridoma can then be cloned to produce a large number of identical cells, all producing the same antibody, hence "monoclonal."

Humanized monoclonal antibodies are a type of monoclonal antibody that have been genetically engineered to include human components. This is done to reduce the risk of an adverse immune response in patients receiving the treatment. In this process, the variable region of the mouse monoclonal antibody, which contains the antigen-binding site, is grafted onto a human constant region. The resulting humanized monoclonal antibody retains the ability to bind to the target antigen while minimizing the immunogenicity associated with murine (mouse) antibodies.

In summary, "antibodies, monoclonal, humanized" refers to a type of laboratory-produced protein that mimics the immune system's ability to fight off harmful antigens, but with reduced immunogenicity due to the inclusion of human components in their structure.

Follow-up studies are a type of longitudinal research that involve repeated observations or measurements of the same variables over a period of time, in order to understand their long-term effects or outcomes. In medical context, follow-up studies are often used to evaluate the safety and efficacy of medical treatments, interventions, or procedures.

In a typical follow-up study, a group of individuals (called a cohort) who have received a particular treatment or intervention are identified and then followed over time through periodic assessments or data collection. The data collected may include information on clinical outcomes, adverse events, changes in symptoms or functional status, and other relevant measures.

The results of follow-up studies can provide important insights into the long-term benefits and risks of medical interventions, as well as help to identify factors that may influence treatment effectiveness or patient outcomes. However, it is important to note that follow-up studies can be subject to various biases and limitations, such as loss to follow-up, recall bias, and changes in clinical practice over time, which must be carefully considered when interpreting the results.

Drug screening assays for antitumor agents are laboratory tests used to identify and evaluate the effectiveness of potential drugs or compounds that can inhibit the growth of tumor cells or induce their death. These assays are typically performed in vitro (in a test tube or petri dish) using cell cultures of various types of cancer cells.

The assays measure different parameters such as cell viability, proliferation, apoptosis (programmed cell death), and cytotoxicity to determine the ability of the drug to kill or inhibit the growth of tumor cells. The results of these assays can help researchers identify promising antitumor agents that can be further developed for clinical use in cancer treatment.

There are different types of drug screening assays for antitumor agents, including high-throughput screening (HTS) assays, which allow for the rapid and automated testing of a large number of compounds against various cancer cell lines. Other types of assays include phenotypic screening assays, target-based screening assays, and functional screening assays, each with its own advantages and limitations.

Overall, drug screening assays for antitumor agents play a critical role in the development of new cancer therapies by providing valuable information on the activity and safety of potential drugs, helping to identify effective treatments and reduce the time and cost associated with bringing new drugs to market.

'Tumor cells, cultured' refers to the process of removing cancerous cells from a tumor and growing them in controlled laboratory conditions. This is typically done by isolating the tumor cells from a patient's tissue sample, then placing them in a nutrient-rich environment that promotes their growth and multiplication.

The resulting cultured tumor cells can be used for various research purposes, including the study of cancer biology, drug development, and toxicity testing. They provide a valuable tool for researchers to better understand the behavior and characteristics of cancer cells outside of the human body, which can lead to the development of more effective cancer treatments.

It is important to note that cultured tumor cells may not always behave exactly the same way as they do in the human body, so findings from cell culture studies must be validated through further research, such as animal models or clinical trials.

Radiotherapy dosage refers to the total amount of radiation energy that is absorbed by tissues or organs, typically measured in units of Gray (Gy), during a course of radiotherapy treatment. It is the product of the dose rate (the amount of radiation delivered per unit time) and the duration of treatment. The prescribed dosage for cancer treatments can range from a few Gray to more than 70 Gy, depending on the type and location of the tumor, the patient's overall health, and other factors. The goal of radiotherapy is to deliver a sufficient dosage to destroy the cancer cells while minimizing damage to surrounding healthy tissues.

Leukemia L1210 is not a medical definition itself, but it refers to a specific mouse leukemia cell line that was established in 1948. These cells are a type of acute myeloid leukemia (AML) and have been widely used in cancer research as a model for studying the disease, testing new therapies, and understanding the biology of leukemia. The L1210 cell line has contributed significantly to the development of various chemotherapeutic agents and treatment strategies for leukemia and other cancers.

Vinblastine is an alkaloid derived from the Madagascar periwinkle plant (Catharanthus roseus) and is primarily used in cancer chemotherapy. It is classified as a vinca alkaloid, along with vincristine, vinorelbine, and others.

Medically, vinblastine is an antimicrotubule agent that binds to tubulin, a protein involved in the formation of microtubules during cell division. By binding to tubulin, vinblastine prevents the assembly of microtubules, which are essential for mitosis (cell division). This leads to the inhibition of cell division and ultimately results in the death of rapidly dividing cells, such as cancer cells.

Vinblastine is used to treat various types of cancers, including Hodgkin's lymphoma, non-Hodgkin's lymphoma, testicular cancer, breast cancer, and others. It is often administered intravenously in a healthcare setting and may be given as part of a combination chemotherapy regimen with other anticancer drugs.

As with any medication, vinblastine can have side effects, including bone marrow suppression (leading to an increased risk of infection, anemia, and bleeding), neurotoxicity (resulting in peripheral neuropathy, constipation, and jaw pain), nausea, vomiting, hair loss, and mouth sores. Regular monitoring by a healthcare professional is necessary during vinblastine treatment to manage side effects and ensure the safe and effective use of this medication.

Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.

The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.

In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.

A drug combination refers to the use of two or more drugs in combination for the treatment of a single medical condition or disease. The rationale behind using drug combinations is to achieve a therapeutic effect that is superior to that obtained with any single agent alone, through various mechanisms such as:

* Complementary modes of action: When different drugs target different aspects of the disease process, their combined effects may be greater than either drug used alone.
* Synergistic interactions: In some cases, the combination of two or more drugs can result in a greater-than-additive effect, where the total response is greater than the sum of the individual responses to each drug.
* Antagonism of adverse effects: Sometimes, the use of one drug can mitigate the side effects of another, allowing for higher doses or longer durations of therapy.

Examples of drug combinations include:

* Highly active antiretroviral therapy (HAART) for HIV infection, which typically involves a combination of three or more antiretroviral drugs to suppress viral replication and prevent the development of drug resistance.
* Chemotherapy regimens for cancer treatment, where combinations of cytotoxic agents are used to target different stages of the cell cycle and increase the likelihood of tumor cell death.
* Fixed-dose combination products, such as those used in the treatment of hypertension or type 2 diabetes, which combine two or more active ingredients into a single formulation for ease of administration and improved adherence to therapy.

However, it's important to note that drug combinations can also increase the risk of adverse effects, drug-drug interactions, and medication errors. Therefore, careful consideration should be given to the selection of appropriate drugs, dosing regimens, and monitoring parameters when using drug combinations in clinical practice.

Chemoradiotherapy is a medical treatment that combines chemotherapy and radiotherapy. Chemotherapy involves the use of drugs to kill or damage cancer cells, while radiotherapy uses ionizing radiation to achieve the same goal. In chemoradiotherapy, these two modalities are used simultaneously or sequentially to treat a malignancy.

The aim of chemoradiotherapy is to increase the effectiveness of treatment by targeting cancer cells with both chemotherapy and radiation therapy. This approach can be particularly effective in treating certain types of cancer, such as head and neck cancer, lung cancer, esophageal cancer, cervical cancer, anal cancer, and rectal cancer.

The specific drugs used in chemoradiotherapy and the doses and schedules of both chemotherapy and radiotherapy vary depending on the type and stage of cancer being treated. The side effects of chemoradiotherapy can be significant and may include fatigue, skin reactions, mucositis, nausea, vomiting, diarrhea, and myelosuppression. However, these side effects are usually manageable with appropriate supportive care.

The esophagogastric junction (EGJ) is the region of the gastrointestinal tract where the esophagus (the tube that carries food from the mouth to the stomach) meets the stomach. It serves as a physiological sphincter, which helps control the direction of flow and prevent reflux of gastric contents back into the esophagus. The EGJ is also known as the gastroesophageal junction or cardia.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

Remission induction is a treatment approach in medicine, particularly in the field of oncology and hematology. It refers to the initial phase of therapy aimed at reducing or eliminating the signs and symptoms of active disease, such as cancer or autoimmune disorders. The primary goal of remission induction is to achieve a complete response (disappearance of all detectable signs of the disease) or a partial response (a decrease in the measurable extent of the disease). This phase of treatment is often intensive and may involve the use of multiple drugs or therapies, including chemotherapy, immunotherapy, or targeted therapy. After remission induction, patients may receive additional treatments to maintain the remission and prevent relapse, known as consolidation or maintenance therapy.

A trabeculectomy is a surgical procedure performed on the eye to treat glaucoma, an eye condition characterized by increased pressure within the eye that can lead to optic nerve damage and vision loss. The main goal of this operation is to create a new channel for the aqueous humor (the clear fluid inside the eye) to drain out, thus reducing the intraocular pressure (IOP).

During the trabeculectomy procedure, a small flap is made in the sclera (the white part of the eye), and a piece of the trabecular meshwork (a structure inside the eye that helps regulate the flow of aqueous humor) is removed. This opening allows the aqueous humor to bypass the obstructed drainage system and form a bleb, a small blister-like sac on the surface of the eye, which absorbs the fluid and reduces IOP.

The success of trabeculectomy depends on various factors, including the patient's age, type and severity of glaucoma, previous treatments, and overall health. Potential complications may include infection, bleeding, cataract formation, hypotony (abnormally low IOP), or failure to control IOP. Regular follow-up appointments with an ophthalmologist are necessary to monitor the eye's response to the surgery and manage any potential issues that may arise.

Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.

Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.

Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.

Vomiting is defined in medical terms as the forceful expulsion of stomach contents through the mouth. It is a violent, involuntary act that is usually accompanied by strong contractions of the abdominal muscles and retching. The body's vomiting reflex is typically triggered when the brain receives signals from the digestive system that something is amiss.

There are many potential causes of vomiting, including gastrointestinal infections, food poisoning, motion sickness, pregnancy, alcohol consumption, and certain medications or medical conditions. In some cases, vomiting can be a symptom of a more serious underlying condition, such as a brain injury, concussion, or chemical imbalance in the body.

Vomiting is generally not considered a serious medical emergency on its own, but it can lead to dehydration and other complications if left untreated. If vomiting persists for an extended period of time, or if it is accompanied by other concerning symptoms such as severe abdominal pain, fever, or difficulty breathing, it is important to seek medical attention promptly.

Thrombocytopenia is a medical condition characterized by an abnormally low platelet count (thrombocytes) in the blood. Platelets are small cell fragments that play a crucial role in blood clotting, helping to stop bleeding when a blood vessel is damaged. A healthy adult typically has a platelet count between 150,000 and 450,000 platelets per microliter of blood. Thrombocytopenia is usually diagnosed when the platelet count falls below 150,000 platelets/µL.

Thrombocytopenia can be classified into three main categories based on its underlying cause:

1. Immune thrombocytopenia (ITP): An autoimmune disorder where the immune system mistakenly attacks and destroys its own platelets, leading to a decreased platelet count. ITP can be further divided into primary or secondary forms, depending on whether it occurs alone or as a result of another medical condition or medication.
2. Decreased production: Thrombocytopenia can occur when there is insufficient production of platelets in the bone marrow due to various causes, such as viral infections, chemotherapy, radiation therapy, leukemia, aplastic anemia, or vitamin B12 or folate deficiency.
3. Increased destruction or consumption: Thrombocytopenia can also result from increased platelet destruction or consumption due to conditions like disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or severe bacterial infections.

Symptoms of thrombocytopenia may include easy bruising, prolonged bleeding from cuts, spontaneous nosebleeds, bleeding gums, blood in urine or stools, and skin rashes like petechiae (small red or purple spots) or purpura (larger patches). The severity of symptoms can vary depending on the degree of thrombocytopenia and the presence of any underlying conditions. Treatment for thrombocytopenia depends on the cause and may include medications, transfusions, or addressing the underlying condition.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Parenteral infusions refer to the administration of fluids or medications directly into a patient's vein or subcutaneous tissue using a needle or catheter. This route bypasses the gastrointestinal tract and allows for rapid absorption and onset of action. Parenteral infusions can be used to correct fluid and electrolyte imbalances, administer medications that cannot be given orally, provide nutritional support, and deliver blood products. Common types of parenteral infusions include intravenous (IV) drips, IV push, and subcutaneous infusions. It is important that parenteral infusions are administered using aseptic technique to reduce the risk of infection.

Nucleoside deaminases are a group of enzymes that catalyze the removal of an amino group (-NH2) from nucleosides, converting them to nucleosides with a modified base. This modification process is called deamination. Specifically, these enzymes convert cytidine and adenosine to uridine and inosine, respectively. Nucleoside deaminases play crucial roles in various biological processes, including the regulation of gene expression, immune response, and nucleic acid metabolism. Some nucleoside deaminases are also involved in the development of certain diseases and are considered as targets for drug design and discovery.

Beta-alanine is a non-essential amino acid, which means that it is not required in the diet because the body can produce it from other amino acids. It is produced in the liver and is also found in some foods such as meat, poultry, and fish.

Beta-alanine plays a role in the production of carnosine, a dipeptide molecule that helps to regulate muscle pH and improve muscle function during high-intensity exercise. When muscles contract during intense exercise, they produce hydrogen ions, which can cause the muscle pH to decrease (become more acidic), leading to fatigue and reduced muscle function. Carnosine acts as a buffer against this acidity, helping to maintain optimal muscle pH levels and improve performance during high-intensity exercise.

Beta-alanine supplements have been shown to increase carnosine levels in muscles, which may lead to improved athletic performance, particularly in activities that require short bursts of intense effort, such as weightlifting or sprinting. However, more research is needed to fully understand the effects and potential benefits of beta-alanine supplementation.

It's important to note that while beta-alanine supplements are generally considered safe for most people, they can cause a tingling sensation in the skin (paresthesia) when taken in high doses. This is a harmless side effect and typically subsides within an hour or so of taking the supplement.

Oxidoreductases are a class of enzymes that catalyze oxidation-reduction reactions, which involve the transfer of electrons from one molecule (the reductant) to another (the oxidant). These enzymes play a crucial role in various biological processes, including energy production, metabolism, and detoxification.

The oxidoreductase-catalyzed reaction typically involves the donation of electrons from a reducing agent (donor) to an oxidizing agent (acceptor), often through the transfer of hydrogen atoms or hydride ions. The enzyme itself does not undergo any permanent chemical change during this process, but rather acts as a catalyst to lower the activation energy required for the reaction to occur.

Oxidoreductases are classified and named based on the type of electron donor or acceptor involved in the reaction. For example, oxidoreductases that act on the CH-OH group of donors are called dehydrogenases, while those that act on the aldehyde or ketone groups are called oxidases. Other examples include reductases, peroxidases, and catalases.

Understanding the function and regulation of oxidoreductases is important for understanding various physiological processes and developing therapeutic strategies for diseases associated with impaired redox homeostasis, such as cancer, neurodegenerative disorders, and cardiovascular disease.

Clinical trials are research studies that involve human participants and are designed to evaluate the safety and efficacy of new medical treatments, drugs, devices, or behavioral interventions. The purpose of clinical trials is to determine whether a new intervention is safe, effective, and beneficial for patients, as well as to compare it with currently available treatments. Clinical trials follow a series of phases, each with specific goals and criteria, before a new intervention can be approved by regulatory authorities for widespread use.

Clinical trials are conducted according to a protocol, which is a detailed plan that outlines the study's objectives, design, methodology, statistical analysis, and ethical considerations. The protocol is developed and reviewed by a team of medical experts, statisticians, and ethicists, and it must be approved by an institutional review board (IRB) before the trial can begin.

Participation in clinical trials is voluntary, and participants must provide informed consent before enrolling in the study. Informed consent involves providing potential participants with detailed information about the study's purpose, procedures, risks, benefits, and alternatives, as well as their rights as research subjects. Participants can withdraw from the study at any time without penalty or loss of benefits to which they are entitled.

Clinical trials are essential for advancing medical knowledge and improving patient care. They help researchers identify new treatments, diagnostic tools, and prevention strategies that can benefit patients and improve public health. However, clinical trials also pose potential risks to participants, including adverse effects from experimental interventions, time commitment, and inconvenience. Therefore, it is important for researchers to carefully design and conduct clinical trials to minimize risks and ensure that the benefits outweigh the risks.

Anus neoplasms refer to abnormal growths or tumors in the anus, which is the opening at the end of the digestive tract where solid waste leaves the body. These growths can be benign (non-cancerous) or malignant (cancerous). Common types of anus neoplasms include squamous cell carcinoma, adenocarcinoma, and melanoma.

Squamous cell carcinoma is the most common type of anus cancer, accounting for about 80% of all cases. It begins in the squamous cells that line the anal canal and can spread to other parts of the body if left untreated.

Adenocarcinoma is a less common type of anus cancer that arises from glandular cells in the anus. This type of cancer is often associated with long-standing inflammatory conditions, such as anal fistulas or ulcerative colitis.

Melanoma is a rare form of skin cancer that can also occur in the anus. It develops from pigment-producing cells called melanocytes and tends to be aggressive with a high risk of spreading to other parts of the body.

Other less common types of anus neoplasms include basal cell carcinoma, sarcoma, and lymphoma. Treatment options for anus neoplasms depend on the type, stage, and location of the tumor, as well as the patient's overall health.

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults. It originates from the hepatocytes, which are the main functional cells of the liver. This type of cancer is often associated with chronic liver diseases such as cirrhosis caused by hepatitis B or C virus infection, alcohol abuse, non-alcoholic fatty liver disease (NAFLD), and aflatoxin exposure.

The symptoms of HCC can vary but may include unexplained weight loss, lack of appetite, abdominal pain or swelling, jaundice, and fatigue. The diagnosis of HCC typically involves imaging tests such as ultrasound, CT scan, or MRI, as well as blood tests to measure alpha-fetoprotein (AFP) levels. Treatment options for Hepatocellular carcinoma depend on the stage and extent of the cancer, as well as the patient's overall health and liver function. Treatment options may include surgery, radiation therapy, chemotherapy, targeted therapy, or liver transplantation.

HT-29 is a human colon adenocarcinoma cell line that is commonly used in research. These cells are derived from a colorectal cancer tumor and have the ability to differentiate into various cell types found in the intestinal mucosa, such as absorptive enterocytes and mucus-secreting goblet cells. HT-29 cells are often used to study the biology of colon cancer, including the effects of drugs on cancer cell growth and survival, as well as the role of various genes and signaling pathways in colorectal tumorigenesis.

It is important to note that when working with cell lines like HT-29, it is essential to use proper laboratory techniques and follow established protocols to ensure the integrity and reproducibility of experimental results. Additionally, researchers should regularly authenticate their cell lines to confirm their identity and verify that they are free from contamination with other cell types.

Neoplasm transplantation is not a recognized or established medical procedure in the field of oncology. The term "neoplasm" refers to an abnormal growth of cells, which can be benign or malignant (cancerous). "Transplantation" typically refers to the surgical transfer of living cells, tissues, or organs from one part of the body to another or between individuals.

The concept of neoplasm transplantation may imply the transfer of cancerous cells or tissues from a donor to a recipient, which is not a standard practice due to ethical considerations and the potential harm it could cause to the recipient. In some rare instances, researchers might use laboratory animals to study the transmission and growth of human cancer cells, but this is done for scientific research purposes only and under strict regulatory guidelines.

In summary, there is no medical definition for 'Neoplasm Transplantation' as it does not represent a standard or ethical medical practice.

Apoptosis is a programmed and controlled cell death process that occurs in multicellular organisms. It is a natural process that helps maintain tissue homeostasis by eliminating damaged, infected, or unwanted cells. During apoptosis, the cell undergoes a series of morphological changes, including cell shrinkage, chromatin condensation, and fragmentation into membrane-bound vesicles called apoptotic bodies. These bodies are then recognized and engulfed by neighboring cells or phagocytic cells, preventing an inflammatory response. Apoptosis is regulated by a complex network of intracellular signaling pathways that involve proteins such as caspases, Bcl-2 family members, and inhibitors of apoptosis (IAPs).

Fluoroacetates are organic compounds that contain a fluorine atom and an acetic acid group. The most well-known and notorious compound in this family is sodium fluoroacetate, also known as 1080 or compound 1080, which is a potent metabolic poison. It works by interfering with the citric acid cycle, a critical process that generates energy in cells. Specifically, fluoroacetates are converted into fluorocitrate, which inhibits an enzyme called aconitase, leading to disruption of cellular metabolism and ultimately cell death.

Fluoroacetates have been used as rodenticides and pesticides, but their use is highly regulated due to their high toxicity to non-target species, including humans. Exposure to fluoroacetates can cause a range of symptoms, including nausea, vomiting, seizures, and cardiac arrest, and can be fatal if not treated promptly.

"Random allocation," also known as "random assignment" or "randomization," is a process used in clinical trials and other research studies to distribute participants into different intervention groups (such as experimental group vs. control group) in a way that minimizes selection bias and ensures the groups are comparable at the start of the study.

In random allocation, each participant has an equal chance of being assigned to any group, and the assignment is typically made using a computer-generated randomization schedule or other objective methods. This process helps to ensure that any differences between the groups are due to the intervention being tested rather than pre-existing differences in the participants' characteristics.

Hematologic diseases, also known as hematological disorders, refer to a group of conditions that affect the production, function, or destruction of blood cells or blood-related components, such as plasma. These diseases can affect erythrocytes (red blood cells), leukocytes (white blood cells), and platelets (thrombocytes), as well as clotting factors and hemoglobin.

Hematologic diseases can be broadly categorized into three main types:

1. Anemia: A condition characterized by a decrease in the total red blood cell count, hemoglobin, or hematocrit, leading to insufficient oxygen transport to tissues and organs. Examples include iron deficiency anemia, sickle cell anemia, and aplastic anemia.
2. Leukemia and other disorders of white blood cells: These conditions involve the abnormal production or function of leukocytes, which can lead to impaired immunity and increased susceptibility to infections. Examples include leukemias (acute lymphoblastic leukemia, chronic myeloid leukemia), lymphomas, and myelodysplastic syndromes.
3. Platelet and clotting disorders: These diseases affect the production or function of platelets and clotting factors, leading to abnormal bleeding or clotting tendencies. Examples include hemophilia, von Willebrand disease, thrombocytopenia, and disseminated intravascular coagulation (DIC).

Hematologic diseases can have various causes, including genetic defects, infections, autoimmune processes, environmental factors, or malignancies. Proper diagnosis and management of these conditions often require the expertise of hematologists, who specialize in diagnosing and treating disorders related to blood and its components.

Hydroxyurea is an antimetabolite drug that is primarily used in the treatment of myeloproliferative disorders such as chronic myelogenous leukemia (CML), essential thrombocythemia, and polycythemia vera. It works by interfering with the synthesis of DNA, which inhibits the growth of cancer cells.

In addition to its use in cancer therapy, hydroxyurea is also used off-label for the management of sickle cell disease. In this context, it helps to reduce the frequency and severity of painful vaso-occlusive crises by increasing the production of fetal hemoglobin (HbF), which decreases the formation of sickled red blood cells.

The medical definition of hydroxyurea is:

A hydantoin derivative and antimetabolite that inhibits ribonucleoside diphosphate reductase, thereby interfering with DNA synthesis. It has been used as an antineoplastic agent, particularly in the treatment of myeloproliferative disorders, and more recently for the management of sickle cell disease to reduce the frequency and severity of painful vaso-occlusive crises by increasing fetal hemoglobin production.

Pentosyltransferases are a group of enzymes that catalyze the transfer of a pentose (a sugar containing five carbon atoms) molecule from one compound to another. These enzymes play important roles in various biochemical pathways, including the biosynthesis of nucleotides, glycoproteins, and other complex carbohydrates.

One example of a pentosyltransferase is the enzyme that catalyzes the addition of a ribose sugar to form a glycosidic bond with a purine or pyrimidine base during the biosynthesis of nucleotides, which are the building blocks of DNA and RNA.

Another example is the enzyme that adds xylose residues to proteins during the formation of glycoproteins, which are proteins that contain covalently attached carbohydrate chains. These enzymes are essential for many biological processes and have been implicated in various diseases, including cancer and neurodegenerative disorders.

"TOLAK : Fluorouracil Cream : 4% (w/w) fluorouracil (as fluorouracil sodium)" (PDF). Pdf.hres.ca. Archived (PDF) from the ... Fluorouracil (5-FU, 5-fluorouracil), sold under the brand name Adrucil among others, is a cytotoxic chemotherapy medication ... Fluorouracil's efficacy is decreased when used alongside allopurinol, which can be used to decrease fluorouracil induced ... "fluorouracil" is the INN, USAN, USP name, and BAN. The form "5-fluorouracil" is often used; it shows that there is a fluorine ...
"Fluorouracil". The American Society of Health-System Pharmacists. Archived from the original on 20 December 2016. Retrieved 8 ...
DHH 5-fluorouracil toxicity; 274270; DPYD 6-mercaptopurine sensitivity; 610460; TPMT Aarskog-Scott syndrome; 305400; FGD1 ABCD ...
Freeman, Nancy J.; Costanza, Mary E. (1988-01-01). "5-Fluorouracil-associated cardiotoxicity". Cancer. 61 (1): 36-45. doi: ...
There are several Combination therapies: 1. FEC: fluorouracil + cyclophosphamide + epirubicin; 2. FAC: fluorouracil + ... methotrexate and fluorouracil (CMF). In comparison to this the Epirubicin therapy contains fluorouracil/epirubicin/ ... cyclophosphamide (FEC). Three large randomized studies have directly compared the epirubicin-containing regimen fluorouracil/ ...
The fluoropyrimidines include fluorouracil and capecitabine. Fluorouracil is a nucleobase analogue that is metabolised in cells ... Kaldate RR, Haregewoin A, Grier CE, Hamilton SA, McLeod HL (2012). "Modeling the 5-fluorouracil area under the curve versus ... Capitain O, Asevoaia A, Boisdron-Celle M, Poirier AL, Morel A, Gamelin E (December 2012). "Individual fluorouracil dose ... such as 5-fluorouracil, are used to treat some cases of non-melanoma skin cancer. If the cancer has central nervous system ...
5-fluorouracil has received FDA approval. Removing the residual superficial tumor with surgery alone can result in large and ... The use of a chemotherapeutic agent such as 5-Fluorouracil or imiquimod can prevent the development of skin cancer. It is ... Some superficial cancers respond to local therapy with 5-fluorouracil, a chemotherapy agent. One can expect a great deal of ... This tumor is generally responsive to topic chemotherapy, such as imiquimod, or fluorouracil, although surgical treatment is ...
Ansfield proposed that dosages of a new drug, 5-Fluorouracil, be increased in the treatment of incurable cancer to find if it ... He was a leader in applying 5-FU (5-Fluorouracil) to humans, demonstrating its effectiveness as a chemotherapy drug. Ansfield ... His first faculty assignment was testing 5-FU (5-Fluorouracil), a new drug conceptualized and developed by Professor Charles ... ANSFIELD, FJ; SCHROEDER, JM; CURRERI, AR (July 28, 1962). "Five Years Clinical Experience with 5-Fluorouracil". JAMA. 181 (4): ...
... and 5-fluorouracil. FAC (or CAF): 5-fluorouracil, doxorubicin, cyclophosphamide. AC (or CA): Adriamycin (doxorubicin) and ... FEC: 5-fluorouracil, epirubicin and cyclophosphamide. AT: Adriamycin (doxorubicin) and Taxotere (docetaxel). Since chemotherapy ... "Breakthrough - CMF (cyclophosphamide, methotrexate and 5-fluorouracil)". 2009-01-06. Archived from the original on 2009-01-06. ...
Cyclophosphamide Methotrexate Fluorouracil (CMF) is a commonly used regimen of breast cancer chemotherapy that combines three ... 2002). "The feasibility of classical cyclophosphamide, methotrexate, 5-fluorouracil (CMF) for pre- and post-menopausal node- ... "CMF (cyclophosphamide, methotrexate and 5-fluorouracil)". UK: Breakthrough Breast Cancer. Archived from the original on 2009-01 ... and fluorouracil (CMF) followed by radiation for stage III breast cancer: a phase II trial (CALGB 8944)". Breast Cancer Res. ...
Topical 5-fluorouracil (5-FU, Efudex, Carac) has been shown to be an effective therapy for diffuse, but minor actinic cheilitis ... 5-fluorouracil works by blocking DNA synthesis. Cells that are rapidly growing need more DNA, so they accumulate more 5- ... Treatment options include 5-fluorouracil, imiquimod, scalpel vermillionectomy, chemical peel, electrosurgery, and carbon ... fluorouracil, resulting in their death. Normal skin is much less affected. The treatment usually takes 2-4 weeks depending on ...
Bhadra D, Bhadra S, Jain S, Jain NK (May 2003). "A PEGylated dendritic nanoparticulate carrier of fluorouracil". International ...
5-fluorouracil, capecitabine); high consumption of energy drinks have been associated with variant angina[citation needed]. ...
Chu, Edward (September 2007). "Clinical Colorectal Cancer: "Ode to 5-Fluorouracil"". Clinical Colorectal Cancer. 6 (9): 609. ... and a world-renowned cancer researcher who developed the medication Fluorouracil. In 1951 the Heidelbergers hired Herb Fritz Jr ...
... and fluorouracil Cyclophosphamide, methotrexate, and fluorouracil. Docetaxel and cyclophosphamide. Docetaxel, doxorubicin, and ... A series of studies has established that 6 months of chemotherapy with either gemcitabine or fluorouracil, as compared with ... Studies have shown that fluorouracil is an effective adjuvant chemotherapy among patients with microsatellite stability or low- ... July 2003). "Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy ...
Longley, D. B.; Harkin, D. P.; Johnston, P. G. (2003). "5-Fluorouracil: Mechanisms of action and clinical strategies". Nature ... methotrexate and fluorouracil. The phenomenon was first reported in 1954 by Hazel D. Barner and Seymour S. Cohen in Escherichia ... "The Mode of Action of 5-Fluorouracil and Its Derivatives". Proceedings of the National Academy of Sciences of the United States ...
Longley, DB; Harkin DP; Johnston PG (May 2003). "5-fluorouracil: mechanisms of action and clinical strategies". Nat. Rev. ...
August 2009). "Identification of genes conferring resistance to 5-fluorouracil". Proceedings of the National Academy of ...
Treatment with a laser and topical 5-fluorouracil". J Reprod Med. 37 (5): 453-6. PMID 1324311. "Michael Brodman, M.D. = Female ...
"Identification of genes conferring resistance to 5-fluorouracil". Proceedings of the National Academy of Sciences of the United ...
The Fluorouracil Filtering Surgery Study Group (1989-12-01). "Fluorouracil Filtering Surgery Study One-Year Follow-up". ... Fluorouracil Filtering Surgery Study: This study investigated the safety and effectiveness of 5-fluorouracil after ... It showed that using 5-fluorouracil after glaucoma surgery improved patients' results and reduced the need for additional ...
Weiss, E; Amini, S (2007). "A Novel Treatment for Knuckle Pads With Intralesional Fluorouracil". Arch Dermatol. 143 (11): 1447- ... there has been some effectiveness with intralesional fluorouracil. Skin lesion List of cutaneous conditions Garrod's pad Mackey ...
Topical fluorouracil (5-FU) destroys AKs by blocking methylation of thymidylate synthetase, thereby interrupting DNA and RNA ... Topical creams, such as 5-fluorouracil or imiquimod, may require daily application to affected skin areas over a typical time ... Robins P, Gupta AK (August 2002). "The use of topical fluorouracil to treat actinic keratosis". Cutis. 70 (2 Suppl): 4-7. PMID ... Gupta AK, Davey V, Mcphail H (October 2005). "Evaluation of the effectiveness of imiquimod and 5-fluorouracil for the treatment ...
COVID-19 misinformation Fluorouracil Merck Index, 11th Edition, 2886. Wick, AN; Drury, DR; Nakada, HI; Wolfe, JB (1957). " ...
... fluorouracil and ingenol mebutate; radiation therapy; and surgical excision, including Mohs surgery (microscopically controlled ...
Keratosis can also be treated by using cryotherapy or fluorouracil. In more severe cases of XP, even minuscule amounts of UV ...
When elemental fluorine reacts with uracil, they produce 5-fluorouracil. 5-Fluorouracil is an anticancer drug (antimetabolite) ... Because 5-fluorouracil is similar in shape to, but does not undergo the same chemistry as, uracil, the drug inhibits RNA ...
... and fluorouracil (or "CMF"). Most chemotherapy medications work by destroying fast-growing and/or fast-replicating cancer cells ...
Upon entering the cell, 5-fluorouracil (5-FU) is converted to a variety of active metabolites, intracellularly. One such ... The most widely used inhibitor is 5-fluorouracil (5-FU) and its metabolized form 5-fluorodeoxyuridine monophosphate (5-FdUMP), ... 2002). "Induction of thymidylate synthase as a 5-fluorouracil resistance mechanism". Biochim. Biophys. Acta. 1587 (2-3): 194- ... Fluorouracil (5-FU) Activity edit]] The interactive pathway map can be edited at WikiPathways: "FluoropyrimidineActivity_WP1601 ...
Individuals with this condition may develop life-threatening toxicity following exposure to 5-fluorouracil (5-FU), a ... biochemical basis for familial pyrimidinemia and severe 5-fluorouracil-induced toxicity". J Clin Invest. 81 (1): 47-51. doi: ... impact of pharmacogenetics on 5-fluorouracil therapy". Clinical Advances in Hematology & Oncology. 2 (8): 527-532. ISSN 1543- ... "Profiling dihydropyrimidine dehydrogenase deficiency in patients with cancer undergoing 5-fluorouracil/capecitabine therapy". ...
"TOLAK : Fluorouracil Cream : 4% (w/w) fluorouracil (as fluorouracil sodium)" (PDF). Pdf.hres.ca. Archived (PDF) from the ... Fluorouracil (5-FU, 5-fluorouracil), sold under the brand name Adrucil among others, is a cytotoxic chemotherapy medication ... Fluorouracils efficacy is decreased when used alongside allopurinol, which can be used to decrease fluorouracil induced ... "fluorouracil" is the INN, USAN, USP name, and BAN. The form "5-fluorouracil" is often used; it shows that there is a fluorine ...
Fluorouracil Topical: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Apply fluorouracil cream with a nonmetal applicator, a glove, or your finger. If you apply fluorouracil cream with your finger ... Before using fluorouracil,. *tell your doctor and pharmacist if you are allergic to fluorouracil or any other medications. ... This is a sign that fluorouracil is working. Do not stop using fluorouracil unless your doctor has told you to do so. ...
Fluorouracil definition, a pyrimidine analog, C4H3FN2O2, used in the treatment of certain cancers. See more. ...
Fluorouracil, including Fluorouracil cream may be fatal if ingested by pets. Avoid allowing pets to contact the Fluorouracil ... FLUOROURACIL (UNII: U3P01618RT) (FLUOROURACIL - UNII:U3P01618RT) FLUOROURACIL. 50 mg in 1 g. ... One gram of fluorouracil is soluble in 100 mL of propylene glycol. The molecular weight of 5-fluorouracil is 130.08 and the ... Store Fluorouracil cream out of reach of pets. Safely discard or clean any cloth or applicator that may retain Fluorouracil ...
Compare Fluorouracil Topical head-to-head with other drugs for uses, ratings, cost, side effects and interactions. ... More about Fluorouracil topical More about Efudex (fluorouracil) More about Picato (ingenol) ... Fluorouracil topical Alternatives Compared. View side-by-side comparisons of medication uses, ratings, cost, side effects and ... Fluorouracil topical has an average rating of 7.5 out of 10 from a total of 287 ratings on Drugs.com. 67% of reviewers reported ...
fluorouracil (as fluorouracil sodium) 50 MG/ML Injectable Solution. SY. 7. 1791701. fluorouracil 500 MG in 10 ML Injection. PSN ... Withhold fluorouracil for neurologic toxicity. (5.4). * Diarrhea: Fluorouracil can cause severe diarrhea. Withhold fluorouracil ... FLUOROURACIL (UNII: U3P01618RT) (FLUOROURACIL - UNII:U3P01618RT) FLUOROURACIL. 50 mg in 1 mL. ... Withhold fluorouracil for Grade 3 or 4 diarrhea until resolved or decreased in intensity to Grade 1, then resume fluorouracil ...
Treatment of cells with 5-Fluorouracil leads to an accumulation of cells in S-phase and has been shown to induce p53 dependent ... 5-Fluorouracil is a potent antitumor agent that affects pyrimidine synthesis by inhibiting thymidylate synthetase thus ... 5-Fluorouracil is a potent antitumor agent that affects pyrimidine synthesis by inhibiting thymidylate synthetase thus ... IC50 value:;Target: Nucleoside antimetabolite/analog5-Fluorouracil is metabolized to ribonucleotides and deoxyribonucleotides, ...
The identification of genetic factors associated with either responsiveness or resistance to 5-fluorouracil (5-FU) chemotherapy ... Dihydropyrimidine dehydrogenase and the efficacy and toxicity of 5-fluorouracil Eur J Cancer. 2004 May;40(7):939-50. doi: ... Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). ... The identification of genetic factors associated with either responsiveness or resistance to 5-fluorouracil (5-FU) chemotherapy ...
CanMED: NDC. The Cancer Medications Enquiry Database (CanMED) is a two-part resource for cancer drug treatment related studies.
Fluorouracil. Medicine Status PIL SPC XPIL Legal Category Active Ingredient(s) Company Efudix 5% Cream ...
Bioaccumulation. Fluorouracil has low potential for bioaccumulation.. Toxicity. It cannot be excluded that fluorouracil is ... Risk. Risk of environmental impact of fluorouracil cannot be excluded, due to the lack of environmental toxicity data. ... Risk of environmental impact of fluorouracil cannot be excluded, due to the lack of environmental toxicity data. ... Persistence. It cannot be excluded that fluorouracil is persistent, due to the lack of data. ...
Store Fluorouracil away from direct sunlight and keep away from children. Avoid prolonged exposure to sunlight and use a ... 5-Fluorouracil can cause side effects such as mild nausea, vomiting, or appetite loss. ... 5-Fluorouracil - Handling. How should I handle 5-Fluorouracil safely?. 5-Fluorouracil - Storage. How should I store 5- ... 5-Fluorouracil - What is it for. ​5-Fluorouracil is an intravenous chemotherapy used alone or in combination with other agents ...
Shop 5-Fluorouracil, ∽99%, MP Biomedicals™ at Fishersci.ca ...
Low-dose continuous 5-fluorouracil infusion stimulates VEGF-A-mediated angiogenesis. Download Prime PubMed App to iPhone, iPad ... Low-dose continuous 5-fluorouracil infusion stimulates VEGF-A-mediated angiogenesis.. Acta Oncol. 2009; 48(3):418-25.AO ... AnimalsAntimetabolites, AntineoplasticCell ProliferationDose-Response Relationship, DrugEndothelium, VascularFluorouracil ... "Low-dose Continuous 5-fluorouracil Infusion Stimulates VEGF-A-mediated Angiogenesis." Acta Oncologica (Stockholm, Sweden), vol ...
Fluorouracil is a chemotherapy drug that works by slowing or stopping the growth of cancer cells. Salicylic acid works by ... Before using this medication, tell your doctor or pharmacist if you are allergic to fluorouracil or salicylic acid; or to ... softening the top layer of skin which helps fluorouracil work better. Salicylic acid belongs to the same class of drugs as ...
Sensitization to Low Dose 5-Fluorouracil: SUBSEQUENT ENHANCEMENT OF ITS SYSTEMIC ANTITUMOR EFFECT IN THE RAT. ... Sensitization to Low Dose 5-Fluorouracil: SUBSEQUENT ENHANCEMENT OF ITS SYSTEMIC ANTITUMOR EFFECT IN THE RAT. ... This report describes a novel method of immunochemotherapy; the active immunization to the drug 5-fluorouracil (5-FU) with ...
... with gemcitabine plus cisplatin experienced a longer overall survival and improved progression-free survival vs fluorouracil ... Patients in the fluorouracil plus cisplatin arm who received a first subsequent therapy had a partial response of 17.0%, 52.0% ... The OS was significantly longer in the gemcitabine plus cisplatin arm than the fluorouracil plus cisplatin (HR, 0.72; 95% CI, ... The PFS probabilities in the gemcitabine plus cisplatin and fluorouracil plus cisplatin arms was 21.2% (15.5%-27.6%) vs 6.0% ( ...
Objectives: To evaluate the benefit of cetuximab (Cx) addition to platinum-based and 5-fluorouracil chemotherapy (PFU) in ... Benefit of cetuximab addition to a platinum-fluorouracil-based chemotherapy according to KRAS-LCS6 variant in an unselected ...
Comprehensive suppliers list with E-mail/RFQ form for 5-Fluorouracil Toxicity Tests ... 5-Fluorouracil Toxicity Tests Suppliers. EMAIL INQUIRY to 1 suppliers Entrogen , Address: 18750 Oxnard St, No. 409, Tarzana, ... 5-Fluorouracil Toxicity Tests, ... Entrogen is a bio-technology company that deals with genotyping assays in the areas of ...
5-Fluorouracil (5-FU) is a widely used chemotherapeutic agent for breast cancer. However, acquired chemoresistance leads to a ... Pyrotinib Sensitizes 5-Fluorouracil-Resistant HER2+ Breast Cancer Cells to 5-Fluorouracil. Jianing Yi*, Shuai Chen*, Pingyong ... 2020). Pyrotinib Sensitizes 5-Fluorouracil-Resistant HER2+ Breast Cancer Cells to 5-Fluorouracil. Oncology Research, 28(5), 519 ... Pyrotinib; 5-Fluorouracil (5-FU); HER2; Breast cancer; Chemoresistance Cite This Article. Yi, J., Chen, S., Yi, P., Luo, J., ...
Topical 1% 5-fluorouracil in ocular surface squamous neoplasia: a long-term safety study ... Topical 1% 5-fluorouracil in ocular surface squamous neoplasia: a long-term safety study ... 5-fluorouracil (5-FU) as a sole or adjuvant treatment of ocular surface squamous neoplasia (OSSN). ...
... patients receiving fluorouracil-based chemotherapy is still unclear. MATERIAL AND METHODS:A total of 207 patients (Study Group ... DOSE OF FLUOROURACIL AND DOSE ADJUSTMENT FOR FLUOROURACIL: The initial dose of fluorouracil in the mFOLFOX6 and FOLFIRI ... The relationship between fluorouracil concentration in blood and serious adverse reactions, as well as between fluorouracil ... In other countries, monitoring of fluorouracil plasma concentration has resulted in improved individual fluorouracil dosing. ...
Irinotecan/Cetuximab or Infusional 5-Fluorouracil (5-FU)/Folinic Acid (FA)/Irinotecan (FOLFIRI)/Cetuximab With a Safety Lead-in ...
5-Fluorouracil is being increasing replaced in clinical trials with 3rd generation 5-FU drugs such as capecitabine. ... The anti-metabolite - 5-Fluorouracil (5-FU) - is the most widely used chemotherapeutic drug. It exerts its anti cancer effect ... Bryan, William (2006) Phenotypic and proteomic analysis of 5-Fluorouracil treated normal and carcinoma cells. PhD thesis, ... Phenotypic and proteomic analysis of 5-Fluorouracil treated normal and carcinoma cells ...
Tegafur, a prodrug of 5-fluorouracil (5-FU), is an oral fluorouracil antitumor drug used for the management of adenocarcinomas ... Determination of 5-fluorouracil and its prodrug tegafur in plasma and tissue by high-performance liquid chromatography in a ... Determination of 5-fluorouracil and its prodrug tegafur in plasma and tissue by high-performance liquid chromatography in a ...
Combination 5-fluorouracil, folinic acid and cisplatin (LV5FU2-CDDP) followed by gemcitabine or the reverse sequence in ... Combination 5-fluorouracil, folinic acid and cisplatin (LV5FU2-CDDP) followed by gemcitabine or the reverse sequence in ... Combination 5-fluorouracil, folinic acid and cisplatin (LV5FU2-CDDP) followed by gemcitabine or the reverse sequence in ...
... at concentrations of 5 x 10-6-5 x 10-4 M 5-fluorouracil. Translation of 5-fluorouracil-substituted poly(A)RNA in vitro in ... Analysis of the Effect of 5-Fluorouracil on the Synthesis and Translation of Polysomal Poly(A)RNA from Ehrlich Ascites Cells. ... Analysis of the Effect of 5-Fluorouracil on the Synthesis and Translation of Polysomal Poly(A)RNA from Ehrlich Ascites Cells. ... Analysis of the Effect of 5-Fluorouracil on the Synthesis and Translation of Polysomal Poly(A)RNA from Ehrlich Ascites Cells. ...
... an enzyme involved in the DNA synthesis process and metabolism of fluorouracil. This study included patients with a primary ... with oxaliplatin and 5-fluorouracil was effective in unresectable hepatocellular carcinoma (HCC). The program of FOLFOX-HAIC in ... From: One day versus two days of hepatic arterial infusion with oxaliplatin and fluorouracil for patients with unresectable ...
Strategy Treatment of cT4b Esophageal Squamous Cell Carcinoma Using Docetaxel, Cisplatin, and 5-Fluorouracil. MASANOBU NAKAJIMA ... Background/Aim: This study analyzed the outcomes of docetaxel, cisplatin, and 5-fluorouracil (DCF) therapy and DCF plus ... Strategy Treatment of cT4b Esophageal Squamous Cell Carcinoma Using Docetaxel, Cisplatin, and 5-Fluorouracil ... Strategy Treatment of cT4b Esophageal Squamous Cell Carcinoma Using Docetaxel, Cisplatin, and 5-Fluorouracil ...
  • 1% frequency): Local pain Itchiness Burning Stinging Crusting Weeping Dermatitis Photosensitivity Uncommon (0.1-1% frequency): Hyper- or hypopigmentation Scarring The United States package insert warns that acute cerebellar syndrome has been observed following injection of fluorouracil and may persist after cessation of treatment. (wikipedia.org)
  • These highlights do not include all the information needed to use FLUOROURACIL INJECTION safely and effectively. (nih.gov)
  • See full prescribing information for FLUOROURACIL INJECTION. (nih.gov)
  • How does the Fluorouracil Injection by Hospira medication work? (rxhealthmed.ca)
  • What form(s) does the Fluorouracil Injection by Hospira medication come in? (rxhealthmed.ca)
  • How should I use the Fluorouracil Injection by Hospira medication? (rxhealthmed.ca)
  • Fluorouracil is available as an intravenous (into the vein) injection. (rxhealthmed.ca)
  • Who should NOT take the Fluorouracil Injection by Hospira medication? (rxhealthmed.ca)
  • What side effects are possible with the Fluorouracil Injection by Hospira medication? (rxhealthmed.ca)
  • FLURACIL 250MG INJECTION contains 'Fluorouracil' that works by interfering with the growth of genetic material (DNA and RNA) of the cancer cells. (genericbucket.com)
  • Fluorouracil Kocak I.V. Injection is a powerful medication used in the treatment of various types of cancer, including colon, rectal, breast, stomach, and pancreatic cancer. (wikikenko.com)
  • Fluorouracil Kocak I.V. Injection is a powerful solution for patients battling colon, rectal, breast, stomach, or pancreatic cancer. (wikikenko.com)
  • Fluorouracil is available either as a solution for injection or as a topical cream or topical solution that's applied on the skin. (healthcareforpets.com)
  • Please note, this OEL/ADE monograph also applies to Fluorouracil sodium (CAS RN 14787-18-9) and Fluorouracil Fluorouracil tromethamine (CAS RN 78144-69-1) is indicated for the treatment of patients with adenocarcinoma of the colon and rectum, adenocarcinoma of the breast, gastric adenocarcinoma and pancreatic adenocarcinoma. (affygility.com)
  • For patients with pancreatic adenocarcinoma, Fluorouracil is administered either as an infusional regimen in combination with leucovorin or as part of a multidrug chemotherapy regimen that includes leucovorin. (wikikenko.com)
  • Fluorouracil cream and topical solution are used to treat actinic or solar keratoses (scaly or crusted lesions [skin areas] caused by years of too much exposure to sunlight). (medlineplus.gov)
  • Fluorouracil cream and topical solution are also used to treat a type of skin cancer called superficial basal cell carcinoma if usual types of treatment cannot be used. (medlineplus.gov)
  • Do not apply fluorouracil cream or topical solution to the eyelids or the eyes, nose, or mouth. (medlineplus.gov)
  • Fluorouracil Cream USP is topical preparations containing the fluorinated pyrimidine 5-fluorouracil, an antineoplastic antimetabolite. (nih.gov)
  • If applied twice daily, this would indicate systemic absorption of topical fluorouracil to be in the range of 5 to 6 mg per daily dose of 100 mg. (nih.gov)
  • Fluorouracil Cream USP is recommended for the topical treatment of multiple actinic or solar keratoses. (nih.gov)
  • There are no adequate and well-controlled studies in pregnant women with either the topical or the parenteral forms of fluorouracil. (nih.gov)
  • fluorouracil topical may also be used for purposes not listed in this medication guide. (drugs.com)
  • Fluorouracil topical has an average rating of 7.5 out of 10 from a total of 287 ratings on Drugs.com. (drugs.com)
  • fluorouracil topical side effects in more detail. (drugs.com)
  • Background/aims The aim of this study was to evaluate the long-term corneal toxicity of topical chemotherapy with 1% 5-fluorouracil (5-FU) as a sole or adjuvant treatment of ocular surface squamous neoplasia (OSSN). (bmj.com)
  • Efudex Cream or generic Fluorouracil is a topical anti-neoplastic medication your doctor can prescribe to treat low-risk types of skin cancer early, such as basil cell carcinoma (BCC) or squamous cell carcinoma (SCC), and for actinic keratosis (AK) as it is considered a precancerous skin condition. (discountdrugsfromcanada.com)
  • The containers of topical cream or topical solution may include the brand names Efudex, Carac, Tolak, and Fluoroplex or state "Fluorouracil. (healthcareforpets.com)
  • Pets can be exposed to fluorouracil by chewing on containers, usually tubes, of topical fluorouracil or by licking the area of your skin where you applied the medicine. (healthcareforpets.com)
  • Because of this, FDA asked makers of fluorouracil topical products to add new wording to the product labels that warn users about the danger to pets. (healthcareforpets.com)
  • Safely storing your fluorouracil topical products can save your pet's life. (healthcareforpets.com)
  • Patients with advanced nasopharyngeal carcinoma and who were treated with gemcitabine plus cisplatin experienced a longer overall survival and improved progression-free survival vs fluorouracil plus cisplatin. (cancernetwork.com)
  • Patients with recurrent or metastatic nasopharyngeal carcinoma who received first-line gemcitabine plus cisplatin had longer overall survival (OS) compared with fluorouracil plus cisplatin, according to the results of the phase 3 GEM20110714 study (NCT01528618) published in the Journal of Clinical Oncology . (cancernetwork.com)
  • Investigators determined that gemcitabine plus cisplatin yielded a median OS of 22.1 months (95% CI, 19.2-25.0) compared with 18.6 months (95% CI, 15.4-21.7) for fluorouracil plus cisplatin. (cancernetwork.com)
  • The probability of OS was 79.9 at 1 year %, 31.0% at 3 years, and 19.2% at 5 years for gemcitabine plus cisplatin and at 71.8% at 1 year, 20.4% at 3 years, and 7.8% at 5 years for fluorouracil plus cisplatin. (cancernetwork.com)
  • A total of 362 patients were enrolled on the trial and were randomized 1:1 to receive either gemcitabine plus cisplatin (n = 181) or the fluorouracil plus cisplatin (n = 181). (cancernetwork.com)
  • In the control arm, patients were treated with 4 g/m2 of continuous intravenous fluorouracil starting from day 1 and 80 mg/m2 of cisplatin on day 1. (cancernetwork.com)
  • In December of 2020, the duration of follow-up was comparable between the 2 cohorts, including 69.5 months (95% CI, 63.3-75.6) with gemcitabine plus cisplatin and 69.7 months (95% CI, 56.4-83.0) for fluorouracil plus cisplatin. (cancernetwork.com)
  • Of this population, 86.7% died (n = 314), including 81.8% (n = 148) of the gemcitabine plus cisplatin arm and 91.7% (n = 166) of the fluorouracil plus cisplatin arm. (cancernetwork.com)
  • The restricted mean value time for OS was 33.0 months (95% CI, 29.3-37.2) in the gemcitabine plus cisplatin group and 25.4 months (95% CI, 22.4-28.6) in the fluorouracil plus cisplatin group ( P = .003). (cancernetwork.com)
  • After discontinuing treatment, 51.9% (n = 94) of patients in the gemcitabine plus cisplatin group and 55.2% (n = 100) of patients in the fluorouracil plus cisplatin group started a first subsequent systemic therapy. (cancernetwork.com)
  • Within this population, 68.1% (n = 64) and 83.0% (n = 83) received a platinum-based combination therapy in both the gemcitabine plus cisplatin and fluorouracil plus cisplatin groups, respectively. (cancernetwork.com)
  • Patients in the fluorouracil plus cisplatin arm who received a first subsequent therapy had a partial response of 17.0%, 52.0% had stable disease, and 20% developed progressive disease. (cancernetwork.com)
  • Additionally, a second subsequent therapy was administered to 37.2% (n = 35) of patients in the gemcitabine plus cisplatin arm and 47.0% (n = 47) of patients in the fluorouracil plus cisplatin arm. (cancernetwork.com)
  • Background/Aim: This study analyzed the outcomes of docetaxel, cisplatin, and 5-fluorouracil (DCF) therapy and DCF plus concurrent radiotherapy (DCF-RT), both followed by conversion surgery, if possible, in patients with cT4b esophageal cancer. (iiarjournals.org)
  • Withhold or permanently discontinue fluorouracil in patients with evidence of acute early-onset or unusually severe toxicity, which may indicate near complete or total absence of dipyrimidine dehydrogenase (DPD) activity. (nih.gov)
  • Withhold fluorouracil for cardiac toxicity. (nih.gov)
  • The identification of genetic factors associated with either responsiveness or resistance to 5-fluorouracil (5-FU) chemotherapy, as well as genetic factors predisposing patients to the development of severe 5-FU-associated toxicity, is increasingly being recognised as an important field of study. (nih.gov)
  • Risk of environmental impact of fluorouracil cannot be excluded, due to the lack of environmental toxicity data. (janusinfo.se)
  • The impact of therapeutic drug management (TDM) on reducing toxicity and improving efficacy in colorectal cancer (CRC) patients receiving fluorouracil-based chemotherapy is still unclear. (medscimonit.com)
  • For fluorouracil: Patients with dihydropyrimidine dehydrogenase (DPD) deficiency are unable to metabolize fluorouracil normally and may have severe unexpected toxicity to fluorouracil. (medscape.com)
  • Fluorouracil is in a class of medications called antimetabolites. (medlineplus.gov)
  • Irinotecan liposomal is used in combination with fluorouracil and leucovorin for metastatic adenocarcinoma of the pancreas after disease progression following gemcitabine-based therapy. (medscape.com)
  • Multiple birth defects have been reported in a fetus of a patient treated with intravenous fluorouracil. (nih.gov)
  • Fluorouracil is recommended for administration either as an intravenous bolus or as an intravenous infusion. (nih.gov)
  • 5-Fluorouracil is an intravenous chemotherapy used alone or in combination with other agents for the treatment of certain types of cancer. (singhealth.com.sg)
  • During the same period, she received intravenous chemotherapy, in the form of 790 mg (500 mg/m 2 ) fluorouracil (5-FU) and 32 mg (20 mg/m 2 ) calcium folinate, for 5 consecutive days at 3-week intervals. (psychiatryinvestigation.org)
  • Tegafur, a prodrug of 5-fluorouracil (5-FU), is an oral fluorouracil antitumor drug used for the management of adenocarcinomas. (cun.es)
  • Capecitabine is a prodrug of fluorouracil that undergoes hydrolysis in liver and tissues to form the active moiety (fluorouracil), inhibiting thymidylate synthetase, which in turn blocks methylation of deoxyuridylic acid to thymidylic acid. (medscape.com)
  • Chemotherapy-naïve patients with mCRC, received bevacizumab (5 mg/kg every 2 weeks d 1 ), oxaliplatin (85 mg/m 2 on d 1 ), leucovorin (200 mg/m 2 ) on days 1 and 2 and 5-Fluorouracil (400 mg/m 2 as i.v. bolus and 600 mg/m 2 as 22 h i.v. continuous infusion on days 1 and 2) every 2 weeks. (biomedcentral.com)
  • In this manner, fluorouracil interferes with the synthesis of deoxyribonucleic acid (DNA) and to a lesser extent inhibits the formation of ribonucleic acid (RNA). (nih.gov)
  • The effects of 5-fluorouracil on the synthesis and translation in vitro of polyadenylic acid-containing polysomal RNA [poly(A)RNA] were studied in Ehrlich ascites cells incubated in vitro . (aspetjournals.org)
  • These results suggest that impairment in the synthesis of messenger RNA occurs only at high concentrations of 5-fluorouracil, but that the integrity of the translational activity of the RNA is not significantly impaired. (aspetjournals.org)
  • Fluorouracil is contraindicated in patients who are severely debilitated and in patients with bone marrow suppression due to either radiotherapy or chemotherapy. (wikipedia.org)
  • Systemic absorption studies of topically applied fluorouracil have been performed on patients with actinic keratoses using tracer amounts of 14 C-labeled fluorouracil added to a 5% preparation. (nih.gov)
  • All patients had been receiving nonlabeled fluorouracil until the peak of the inflammatory reaction occurred (2 to 3 weeks), ensuring that the time of maximum absorption was used for measurement. (nih.gov)
  • The success rate with Fluorouracil Cream USP is approximately 93%, based on 113 lesions in 54 patients. (nih.gov)
  • No fluorouracil dose has been proven safe in patients with absent DPD activity. (nih.gov)
  • A total of 42 patients who were assigned to the gemcitabine poststudy treatment arm received fluorouracil, capecitabine, tegafur, or S-1. (cancernetwork.com)
  • To evaluate the benefit of cetuximab (Cx) addition to platinum-based and 5-fluorouracil chemotherapy (PFU) in unselected recurrent and/or metastatic head and neck cancer patients (R/MHNC) according to KRAS-LCS6 variant status. (nih.gov)
  • Bethlehem, PA - September 19, 2018 - Saladax Biomedical Inc., a diagnostics company providing kits to test drug blood levels for personalized dose management and adherence, announced today that it welcomes new guidelines from the International Association of Therapeutic Drug Monitoring and Clinical Toxicology (IATDMCT) that "strongly recommend" monitoring levels of 5-Fluorouracil (5-FU) in patients on treatment. (saladax.com)
  • Fluorouracil has some effect on DNA and is useful in symptom palliation for patients with progressive disease. (medscape.com)
  • For patients with adenocarcinoma of the colon and rectum, Fluorouracil is typically administered as part of a combination therapy. (wikikenko.com)
  • Gastric adenocarcinoma patients can benefit from Fluorouracil as part of a platinum-containing multidrug chemotherapy regimen. (wikikenko.com)
  • Fluorouracil provides patients in Turkey with an effective tool in their fight against cancer, bringing them one step closer to recovery and a brighter future. (wikikenko.com)
  • At 12 months after the end of treatment in patients with multiple actinic keratosis lesions on the head, 5% fluorouracil cream was the most effective of four field-directed treatments," the study authors conclude. (uspharmacist.com)
  • p53, mdm-2, p21, and mib-1 expression were assessed by immunohistochemical methods in primary tumors derived from 134 patients who took part in a randomized multicenter trial comparing docetaxel to sequential methotrexate and 5-fluorouracil (MF) in advanced breast cancer. (lu.se)
  • Adjuvant polychemotherapy (e.g. with 58% to 68%) for patients under the age of 50.1 Besides an cyclophosphamide, methotrexate and 5-fluorouracil (CMF)) or improvement in clinical outcome, these figures indicate that anthracycline-containing regimes, produce substantial reduc- a large proportion of the patients will never recur after the tion in recurrence and mortality. (lu.se)
  • 5-Fluorouracil (5-FU) is a widely used chemotherapeutic agent for breast cancer. (techscience.com)
  • The anti-metabolite - 5-Fluorouracil (5-FU) - is the most widely used chemotherapeutic drug. (dcu.ie)
  • This study investigated changes in mTOR pathway and telomerase activity in hepatocarcinoma cell line SMMC-7721 treated with chemotherapeutic agent 5-fluorouracil (5-Fu). (biomedcentral.com)
  • Introduced in 1958, 5-Fluorouracil (5-FU) is one of the most common chemotherapeutic agents. (psychiatryinvestigation.org)
  • 5-Fluorouracil ( 5-FU ) is one of the most widely applied chemotherapeutic agents with a broad spectrum of activity. (bvsalud.org)
  • In the case of adenocarcinoma of the breast, Fluorouracil is administered as part of a multidrug regimen with cyclophosphamide. (wikikenko.com)
  • Fluorouracil interferes with genetic material (DNA and RNA), which is necessary for the growth and reproduction of cancer cells. (rxhealthmed.ca)
  • 5-Fluorouracil (5-FU) is widely applied in the treatment of various cancers, including colorectal cancer (CRC) [1,2]. (medscimonit.com)
  • Fluorouracil, also called "5-FU" or "5-fluorouracil," is an FDA-approved chemotherapy drug commonly used to treat a wide variety of cancers in people, including some types of skin cancers and a condition called solar or actinic keratosis, which can lead to skin cancer. (healthcareforpets.com)
  • Fluorouracil (5-FU, 5-fluorouracil), sold under the brand name Adrucil among others, is a cytotoxic chemotherapy medication used to treat cancer. (wikipedia.org)
  • Fluorouracil is a chemotherapy drug that works by slowing or stopping the growth of cancer cells. (alberta.ca)
  • Once it has been absorbed into your skin cells the active ingredient, Fluorouracil, is incorporated into the cancer cell's DNA or RNA. (discountdrugsfromcanada.com)
  • As well as interfering with the genetic material DNA and RNA of cancer cells, fluorouracil can interfere with some of your normal cells. (rxhealthmed.ca)
  • The most active agents for pancreatic cancer have been 5-fluorouracil (5-FU) and gemcitabine. (medscape.com)
  • While Fluorouracil can be highly beneficial in combating cancer, it is essential to be aware of potential side effects. (wikikenko.com)
  • If severe, discontinue fluorouracil until resolved or decreased to Grade 1, then resume at a reduced dose. (nih.gov)
  • Withhold fluorouracil until severe myelosuppression resolves, then resume at a reduced dose. (nih.gov)
  • Discontinue fluorouracil until resolved or decreased to Grade 1, then resume at a reduced dose. (nih.gov)
  • Albertsson P, Lennernäs B, Norrby K. Low-dose continuous 5-fluorouracil infusion stimulates VEGF-A-mediated angiogenesis. (unboundmedicine.com)
  • TY - JOUR T1 - Low-dose continuous 5-fluorouracil infusion stimulates VEGF-A-mediated angiogenesis. (unboundmedicine.com)
  • The recommended dose of fluorouracil varies widely according to the specific condition being treated, the response to therapy, and the other medications being used. (rxhealthmed.ca)
  • The dose of fluorouracil is based on body size. (rxhealthmed.ca)
  • For fluorouracil: Liver function should be assessed prior to each cycle for potential dose evaluation. (medscape.com)
  • Withhold fluorouracil and initiate ammonia-lowering therapy. (nih.gov)
  • Case report: A male patient aged 60 under treatment with PHT and PB in which serum concentrations of PHT (32.8 μg/ml) and PB (26.7 μg/ml) increased ∼2-fold after the start of postoperative adjuvant therapy with calcium levofolinate (l-LV) and fluorouracil (5-FU). (elsevierpure.com)
  • Therapy with 5-fluorouracil cream has not been evaluated in controlled studies, frequently causes local irritation, and is not recommended for the treatment of genital warts. (cdc.gov)
  • 2023. https://emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51321/all/fluorouracil. (unboundmedicine.com)
  • Hand-foot skin reactions with continuous infusion of fluorouracil may occur after 8 to 9 weeks or earlier. (singhealth.com.sg)
  • If you are using fluorouracil to treat basal cell carcinoma, you should continue using it until the lesions are gone. (medlineplus.gov)
  • Fluorouracil comes as a solution and a cream to apply to the skin. (medlineplus.gov)
  • Apply fluorouracil cream with a nonmetal applicator, a glove, or your finger. (medlineplus.gov)
  • If you apply fluorouracil cream with your finger, be sure to wash your hands well immediately afterwards. (medlineplus.gov)
  • Fluorouracil Cream USP contains 5% fluorouracil in a vanishing cream base consisting of methylparaben, polysorbate 60, propylene glycol, propylparaben, purified water, stearyl alcohol, and white petrolatum. (nih.gov)
  • Fluorouracil cream may cause fetal harm when administered to a pregnant woman. (nih.gov)
  • One birth defect (cleft lip and palate) has been reported in the newborn of a patient using fluorouracil cream as recommended. (nih.gov)
  • One birth defect (ventricular septal defect) and cases of miscarriage have been reported when fluorouracil cream was applied to mucous membrane areas. (nih.gov)
  • Information is also available online at https: Continue typing to refine, 5 fluorouracil cream. (shopwestcomb.com)
  • If you have concerns about the fluorouracil of your reaction to 5-FU cream, get in touch with your doctor. (shopwestcomb.com)
  • The total area of skin being treated with Efudix at any one time should not exceed cm 2 approximately 23 x 23 cm, 5 fluorouracil cream. (shopwestcomb.com)
  • Sadly, the FDA has received reports involving dogs that were exposed to one type of medicated cream called fluorouracil. (healthcareforpets.com)
  • abstract = "Objective: We report a case of sequential interaction of phenytoin (PHT) and phenobarbital (PB) with fluorouracil (5-FU). (elsevierpure.com)
  • Fluorouracil is in the antimetabolite and pyrimidine analog families of medications. (wikipedia.org)
  • the active immunization to the drug 5-fluorouracil (5-FU) with enhanced antitumor activity resulting from its subsequent systemic administration. (jci.org)
  • Experiments in various species revealed an impairment of fluorouracil fertility and reproductive performance of systemic 5-fluorouracil. (shopwestcomb.com)
  • 5-Fluorouracil is being increasing replaced in clinical trials with 3rd generation 5-FU drugs such as capecitabine. (dcu.ie)
  • In an additional study, negligible amounts of labeled material were found in plasma, urine, and expired CO 2 after 3 days of treatment with topically applied 14 C-labeled fluorouracil. (nih.gov)
  • Furthermore, Fluorouracil may impact fertility in both genders, making it important to avoid breastfeeding while undergoing treatment. (wikikenko.com)
  • Optimal treatment of AK lesions in the elderly depends on several factors, including adherence to treatment regimens fluorouracil modification of regimens to adjust to pharmacokinetic and pharmacodynamic changes that occur. (shopwestcomb.com)
  • Compared with fluorouracil, the hazard ratio for treatment failure was 2.03 (95% CI, 1.36-3.04) with imiquimod, 2.73 (95% CI, 1.87-3.99) with MAL-PDT, and 3.33 (95% CI, 2.29-4.85) with ingenol mebutate ( P ≤.001 for all comparisons), report the researchers, who also add that no unexpected toxic effects were documented. (uspharmacist.com)
  • Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). (nih.gov)
  • There is evidence that the metabolism of fluorouracil in the anabolic pathway blocks the methylation reaction of deoxyuridylic acid to thymidylic acid. (nih.gov)
  • The catabolic metabolism of fluorouracil results in degradation products (e.g. (nih.gov)
  • The effects of DNA and RNA deprivation are most marked on those cells which grow more rapidly and take up fluorouracil at a more rapid rate. (nih.gov)
  • Exposure of cells for 2 hr to concentrations of 5 x 10 -6 -5 x 10 -4 M 5-fluorouracil did not significantly alter the size distribution of poly(A)RNA labeled with either [ 3 H]adenosine or [ 3 H]5-fluorouracil. (aspetjournals.org)
  • Fluorouracil can cause severe diarrhea. (nih.gov)
  • Withhold fluorouracil for severe diarrhea until resolved. (nih.gov)
  • Fluorouracil can cause severe and fatal myelosuppression. (nih.gov)
  • For brands that may still be available, search under fluorouracil. (rxhealthmed.ca)