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.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
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.
Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae".
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
Tumors or cancer of the LUNG.
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.
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.
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.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
The products of chemical reactions that result in the addition of extraneous chemical groups to DNA.
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.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
A cell line derived from cultured tumor cells.
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)
An organoplatinum compound that possesses antineoplastic activity.
Positional isomer of CYCLOPHOSPHAMIDE which is active as an alkylating agent and an immunosuppressive agent.
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.
The forcible expulsion of the contents of the STOMACH through the MOUTH.
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)
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.
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.
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.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
The action of a drug in promoting or enhancing the effectiveness of another drug.
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.
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.
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.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
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.
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
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.
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.
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.
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.
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).
A malignant epithelial tumor with a glandular organization.
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.
Antagonist of urate oxidase.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)
A decrease in the number of NEUTROPHILS found in the blood.
A complex of related glycopeptide antibiotics from Streptomyces verticillus consisting of bleomycin A2 and B2. It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors.
Congener of FLUOROURACIL with comparable antineoplastic action. It has been suggested especially for the treatment of breast neoplasms.
Tumors or cancer of the STOMACH.
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
A malignant neoplasm of the germinal tissue of the GONADS; MEDIASTINUM; or pineal region. Germinomas are uniform in appearance, consisting of large, round cells with vesicular nuclei and clear or finely granular eosinophilic-staining cytoplasm. (Stedman, 265th ed; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1642-3)
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.
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.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Tumors or cancer of the ESOPHAGUS.
A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)
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.
Drugs used to prevent NAUSEA or VOMITING.
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 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)
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.
Neoplasms of the thin serous membrane that envelopes the lungs and lines the thoracic cavity. Pleural neoplasms are exceedingly rare and are usually not diagnosed until they are advanced because in the early stages they produce no symptoms.
Tumors or cancer of the URINARY TRACT in either the male or the female.
A subnormal level of BLOOD PLATELETS.
A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.
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)
Antimetabolites that are useful in cancer chemotherapy.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Guanine is a purine nucleobase, one of the four nucleobases in the nucleic acid of DNA and RNA, involved in forming hydrogen bonds between complementary base pairs in double-stranded DNA molecules.
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.
Inorganic compounds which contain platinum as the central atom.
Drugs used to potentiate the effectiveness of radiation therapy in destroying unwanted cells.
Initial drug treatment designed to bring about REMISSION INDUCTION. It is typically a short-term and high-dose drug treatment that is followed by CONSOLIDATION CHEMOTHERAPY and then MAINTENANCE CHEMOTHERAPY.
Preliminary cancer therapy (chemotherapy, radiation therapy, hormone/endocrine therapy, immunotherapy, hyperthermia, etc.) that precedes a necessary second modality of treatment.
Disorders of the blood and blood forming tissues.
Tumors or cancer of the UTERINE CERVIX.
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)
Therapeutic act or process that initiates a response to a complete or partial remission level.
Inorganic salts of thiosulfuric acid possessing the general formula R2S2O3.
Administration of the total dose of radiation (RADIATION DOSAGE) in parts, at timed intervals.

Tumour ablation and hepatic decompensation rates in multi-agent chemoembolization of hepatocellular carcinoma. (1/7975)

Thirty-seven cirrhotic patients with 62 hepatocellular carcinoma (HCC) foci--most Child-Pugh class B or C and/or with large, inoperable tumours--underwent 148 sessions of transcatheter arterial chemoembolization (TACE) using lipiodol, doxorubicin and cisplatin. Treatment efficacy was assessed by serial hepatic arteriography in 34/37 (91.9%) patients and abdominal CT scanning in 3/37 (8.1%) patients. Child-Pugh status was determined prior to each treatment session. Varying degrees of control of tumour neovascularity occurred for a median 390 days (range 90 to > 1680 days) in 33/34 (97.1%) patients in whom progress hepatic arteriography was performed. Ablation of tumour neovascularity occurred in 6/6 (100%), 4/12 (33.3%) and 6/16 (37.5%) patients with HCC diameters < 4 cm, 4-7 cm and > 8 cm, respectively (p < 0.02). Significantly more sessions were required for ablation of larger tumours (p < 0.05). Recurrent HCC was detected in 50% of patients after a median 240 days (range 60-1120 days). Deterioration in Child-Pugh status followed a session of TACE on 19/148 (12.8%) occasions but resulted in unscheduled hospitalization on only 4/148 (2.7%) occasions, the highest incidence (8.3%) in Child-Pugh C patients. Actuarial survival was 27/36 (75.0%) at 6 months, 17/34 (50.0%) at 12 months, 14/34 (41.2%) at 18 months, 9/31 (29.0%) at 24 months and 4/27 (14.8%) at 36 months. Multi-agent TACE with lipiodol, doxorubicin and cisplatin provides a useful anti-tumour effect, even in cirrhotic patients with large HCCs. The incidence of clinically significant deterioration in hepatic function due to ischaemia of non-tumorous liver is acceptably low, even in Child-Pugh C patients.  (+info)

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). (2/7975)

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)

Role of dexamethasone dosage in combination with 5-HT3 antagonists for prophylaxis of acute chemotherapy-induced nausea and vomiting. (3/7975)

Dexamethasone (20 mg) or its equivalent in combination with 5-HT3 antagonists appears to be the gold-standard dose for antiemetic prophylaxis. Additional to concerns about the use of corticosteroids with respect to enhanced tumour growth or impaired killing of the tumour cells, there is evidence that high-dosage dexamethasone impairs the control of delayed nausea and emesis, whereas lower doses appear more beneficial. To come closer to the most adequate dose, we started a prospective, single-blind, randomized trial investigating additional dosage of 8 or 20 mg dexamethasone to tropisetron (Navoban), a 5-HT3 receptor antagonist, in cis-platinum-containing chemotherapy. After an interim analysis of 121 courses of chemotherapy in 69 patients, we have been unable to detect major differences between both treatment alternatives. High-dose dexamethasone (20 mg) had no advantage over medium-dose dexamethasone with respect to objective and subjective parameters of acute and delayed nausea and vomiting. In relation to concerns about the use of corticosteroids in non-haematological cancer chemotherapy, we suggest that 8 mg or its equivalent should be used in combination with 5-HT3 antagonists until further research proves otherwise.  (+info)

MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (4/7975)

Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited.  (+info)

A novel trinuclear platinum complex overcomes cisplatin resistance in an osteosarcoma cell system. (5/7975)

Multinuclear platinum compounds have been designed to circumvent the cellular resistance to conventional platinum-based drugs. In an attempt to examine the cellular basis of the preclinical antitumor efficacy of a novel multinuclear platinum compound (BBR 3464) in the treatment of cisplatin-resistant tumors, we have performed a comparative study of cisplatin and BBR 3464 in a human osteosarcoma cell line (U2-OS) and in an in vitro selected cisplatin-resistant subline (U2-OS/Pt). A marked increase of cytotoxic potency of BBR 3464 in comparison with cisplatin in U2-OS cells and a complete lack of cross-resistance in U2-OS/Pt cells were found. A detailed analysis of the cisplatin-resistant phenotype indicated that it was associated with reduced cisplatin accumulation, reduced interstrand cross-link (ICL) formation and DNA platination, microsatellite instability, and reduced expression of the DNA mismatch repair protein PMS2. Despite BBR 3464 charge and molecular size, in U2-OS and U2-OS/Pt cells, BBR 3464 accumulation and DNA-bound platinum were much higher than those observed for cisplatin. In contrast, the frequency of ICLs after exposure to BBR 3464 was very low. The time course of ICL formation after drug removal revealed a low persistence of these types of DNA lesions induced by BBR 3464, in contrast to an increase of DNA lesions induced by cisplatin, suggesting that components of the DNA repair pathway handle the two types of DNA lesions differently. The cellular response of HCT116 mismatch repair-deficient cells was consistent with a lack of influence of mismatch repair status on BBR 3464 cytotoxicity. Because BBR 3464 produces high levels of lesions different from ICLs, likely including intra-strand cross-links and monoadducts, the ability of the triplatinum complex to overcome cisplatin resistance appears to be related to a different mechanism of DNA interaction (formation of different types of drug-induced DNA lesions) as compared with conventional mononuclear complexes rather than the ability to overcome specific cellular alterations.  (+info)

Testicular cancer: an oncological success story. (6/7975)

Testicular cancer has become a model for a curable neoplasm. Our studies with cisplatin combination chemotherapy allow us to conclude that: (a) short-duration intensive induction therapy with the most active agents in optimal dosage is more important than maintenance therapy; (b) modest dose escalation increases toxicity without improving therapeutic efficacy; (c) it is possible to develop curative salvage therapy for refractory germ cell tumors; and (d) preclinical models predicting synergism, such as vinblastine + bleomycin or cisplatin + etoposide have clinical relevance. Finally, testicular cancer has also become a model for new drug development. Cisplatin was approved by the Food and Drug Administration for testis and ovarian cancer, and etoposide and ifosfamide were approved for refractory germ cell tumors. The success of these studies confirms the importance of the continued search for new investigational drugs in all solid tumors.  (+info)

Multimodality therapy for locally advanced and limited stage IV breast cancer: the impact of effective non-cross-resistance late-consolidation chemotherapy. (7/7975)

To determine the effectiveness of non-cross-resistant late-consolidation chemotherapy in locally advanced breast cancer (LABC) and stage IV breast cancer, we review our experience with two regimens. Between 1985 and 1991, we enrolled 56 patients with LABC, who were treated with a doxorubicin-based adjuvant regimen, followed by a late-consolidation non-cross-resistant regimen containing methotrexate, 5-fluorouracil, cisplatin, and cyclophosphamide. Between 1985 and 1996, a total of 45 patients with limited stage IV breast cancer underwent surgical excision of all evaluable disease, making them metastatic (stage IV) with no evaluable disease. Surgery was followed by a doxorubicin-containing regimen and then a late-consolidation non-cross-resistant regimen, which was either methotrexate, 5-fluorouracil, cisplatinum, and cyclophosphamide or 5-fluorouracil, mitomycin, etoposide, and cisplatin. Twenty-four patients with limited bone metastases that were unresectable were treated with a doxorubicin-containing regimen, radiation therapy to all sites of disease, and then one of the two late non-cross-resistant regimens. With a median follow-up of 84 months, 78% of patients with LABC are alive, and 68% are free of disease. After a median follow-up of 44 months, 53% of patients with stage IV with no evaluable disease are alive and free of disease. The use of non-cross-resistant late-consolidation chemotherapy is an effective strategy in the treatment of patients with LABC and selected patients with limited stage IV breast cancer.  (+info)

Modification of non-conservative double-strand break (DSB) rejoining activity after the induction of cisplatin resistance in human tumour cells. (8/7975)

The induction of collateral radioresistance after the development of cisplatin resistance is a well-documented phenomenon; however, the exact processes that are responsible for the cisplatin-induced radioresistance remain to be elucidated. There was no obvious difference in the level of radiation-induced DNA double strand breaks (DSBs), in DSB rejoining rates, or the level of the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) in the cisplatin- and radiation-sensitive 2780/WT and cisplatin-resistant 2780/CP cell lines. However, there was a significantly (P < 0.01) lower level of DSB misrejoining activity within nuclear protein extracts derived from the cisplatin- and radiation-sensitive 2780/WT and OAW42/WT tumour cell lines than in similar extracts from their cisplatin- (and radiation-) resistant 2780/CP and OAW42/CP counterparts. All of the DSB misrejoining events involved deletions of between 134 and 444 bp that arose through illegitimate recombination at short repetitive sequences, such as those that arise through non-homologous repair (NHR). These data further support the notion that the radiosensitivity of DSB repair proficient human tumour cell lines may be partly determined by the predisposition of these cell lines to activate non-conservative DSB rejoining pathways. Furthermore, our data suggest that the induction of acquired cisplatin resistance is associated with a two- to threefold decrease in the activity of a non-conservative DSB rejoining mechanism that appears to be a manifestation of NHR.  (+info)

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.

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.

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.

I'm sorry for any confusion, but "Platinum" is not a medical term. Platinum is a chemical element with the symbol Pt and atomic number 78. It is a dense, malleable, ductile, highly unreactive, precious, silverish-white transition metal.

However, in the field of oncology, platinum-based compounds are used as chemotherapeutic drugs. These include:

1. Cisplatin: This is a platinum-containing drug that is used to treat various types of cancers such as testicular cancer, ovarian cancer, bladder cancer, and others. It works by forming crosslinks with the DNA of cancer cells, which disrupts their function and leads to cell death.

2. Carboplatin: This is another platinum-based chemotherapy drug that is used to treat various types of cancers such as ovarian cancer, lung cancer, and others. It is less toxic than cisplatin but has similar mechanisms of action.

3. Oxaliplatin: This is a third platinum-based chemotherapy drug that is used to treat colon cancer and rectal cancer. Like the other two drugs, it forms crosslinks with DNA and disrupts cell function leading to cell death.

These drugs are not made of pure platinum but contain platinum compounds that have been synthesized for medical use.

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.

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.

Etoposide is a chemotherapy medication used to treat various types of cancer, including lung cancer, testicular cancer, and certain types of leukemia. It works by inhibiting the activity of an enzyme called topoisomerase II, which is involved in DNA replication and transcription. By doing so, etoposide can interfere with the growth and multiplication of cancer cells.

Etoposide is often administered intravenously in a hospital or clinic setting, although it may also be given orally in some cases. The medication can cause a range of side effects, including nausea, vomiting, hair loss, and an increased risk of infection. It can also have more serious side effects, such as bone marrow suppression, which can lead to anemia, bleeding, and a weakened immune system.

Like all chemotherapy drugs, etoposide is not without risks and should only be used under the close supervision of a qualified healthcare provider. It is important for patients to discuss the potential benefits and risks of this medication with their doctor before starting treatment.

Lung neoplasms refer to abnormal growths or tumors in the lung tissue. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant lung neoplasms are further classified into two main types: small cell lung carcinoma and non-small cell lung carcinoma. Lung neoplasms can cause symptoms such as cough, chest pain, shortness of breath, and weight loss. They are often caused by smoking or exposure to secondhand smoke, but can also occur due to genetic factors, radiation exposure, and other environmental carcinogens. Early detection and treatment of lung neoplasms is crucial for improving outcomes and survival rates.

Ovarian neoplasms refer to abnormal growths or tumors in the ovary, which can be benign (non-cancerous) or malignant (cancerous). These growths can originate from various cell types within the ovary, including epithelial cells, germ cells, and stromal cells. Ovarian neoplasms are often classified based on their cell type of origin, histological features, and potential for invasive or metastatic behavior.

Epithelial ovarian neoplasms are the most common type and can be further categorized into several subtypes, such as serous, mucinous, endometrioid, clear cell, and Brenner tumors. Some of these epithelial tumors have a higher risk of becoming malignant and spreading to other parts of the body.

Germ cell ovarian neoplasms arise from the cells that give rise to eggs (oocytes) and can include teratomas, dysgerminomas, yolk sac tumors, and embryonal carcinomas. Stromal ovarian neoplasms develop from the connective tissue cells supporting the ovary and can include granulosa cell tumors, thecomas, and fibromas.

It is essential to diagnose and treat ovarian neoplasms promptly, as some malignant forms can be aggressive and potentially life-threatening if not managed appropriately. Regular gynecological exams, imaging studies, and tumor marker tests are often used for early detection and monitoring of ovarian neoplasms. Treatment options may include surgery, chemotherapy, or radiation therapy, depending on the type, stage, and patient's overall health condition.

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.

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.

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.

DNA adducts are chemical modifications or alterations that occur when DNA molecules become attached to or bound with certain harmful substances, such as toxic chemicals or carcinogens. These attachments can disrupt the normal structure and function of the DNA, potentially leading to mutations, genetic damage, and an increased risk of cancer and other diseases.

DNA adducts are formed when a reactive molecule from a chemical agent binds covalently to a base in the DNA molecule. This process can occur either spontaneously or as a result of exposure to environmental toxins, such as those found in tobacco smoke, certain industrial chemicals, and some medications.

The formation of DNA adducts is often used as a biomarker for exposure to harmful substances, as well as an indicator of potential health risks associated with that exposure. Researchers can measure the levels of specific DNA adducts in biological samples, such as blood or urine, to assess the extent and duration of exposure to certain chemicals or toxins.

It's important to note that not all DNA adducts are necessarily harmful, and some may even play a role in normal cellular processes. However, high levels of certain DNA adducts have been linked to an increased risk of cancer and other diseases, making them a focus of ongoing research and investigation.

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.

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.

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.

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.

Carboplatin is a chemotherapeutic agent used to treat various types of cancers, including ovarian, lung, and head and neck cancer. It is a platinum-containing compound that works by forming crosslinks in DNA, which leads to the death of rapidly dividing cells, such as cancer cells. Carboplatin is often used in combination with other chemotherapy drugs and is administered intravenously.

The medical definition of Carboplatin is:

"A platinum-containing antineoplastic agent that forms crosslinks with DNA, inducing cell cycle arrest and apoptosis. It is used to treat a variety of cancers, including ovarian, lung, and head and neck cancer."

Ifosfamide 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. Ifosfamide is used to treat various types of cancers, such as testicular cancer, small cell lung cancer, ovarian cancer, cervical cancer, and certain types of sarcomas.

The medical definition of Ifosfamide is:

Ifosfamide is a synthetic antineoplastic agent, an oxazaphosphorine derivative, with the chemical formula C6H15Cl2N2O2P. It is used in the treatment of various malignancies, including germ cell tumors, sarcomas, lymphomas, and testicular cancer. The drug is administered intravenously and exerts its cytotoxic effects through the alkylation and cross-linking of DNA, leading to the inhibition of DNA replication and transcription. Ifosfamide can cause significant myelosuppression and has been associated with urotoxicity, neurotoxicity, and secondary malignancies. Therefore, it is essential to monitor patients closely during treatment and manage any adverse effects promptly.

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.

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.

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.

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.

Carcinoma, non-small-cell lung (NSCLC) is a type of lung cancer that includes several subtypes of malignant tumors arising from the epithelial cells of the lung. These subtypes are classified based on the appearance of the cancer cells under a microscope and include adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. NSCLC accounts for about 85% of all lung cancers and tends to grow and spread more slowly than small-cell lung cancer (SCLC).

NSCLC is often asymptomatic in its early stages, but as the tumor grows, symptoms such as coughing, chest pain, shortness of breath, hoarseness, and weight loss may develop. Treatment options for NSCLC depend on the stage and location of the cancer, as well as the patient's overall health and lung function. Common treatments include surgery, radiation therapy, chemotherapy, targeted therapy, or a combination of these approaches.

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.

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.

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.

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.

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.

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).

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.

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.

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.

'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.

Testicular neoplasms are abnormal growths or tumors in the testicle that can be benign (non-cancerous) or malignant (cancerous). They are a type of genitourinary cancer, which affects the reproductive and urinary systems. Testicular neoplasms can occur in men of any age but are most commonly found in young adults between the ages of 15 and 40.

Testicular neoplasms can be classified into two main categories: germ cell tumors and non-germ cell tumors. Germ cell tumors, which arise from the cells that give rise to sperm, are further divided into seminomas and non-seminomas. Seminomas are typically slow-growing and have a good prognosis, while non-seminomas tend to grow more quickly and can spread to other parts of the body.

Non-germ cell tumors are less common than germ cell tumors and include Leydig cell tumors, Sertoli cell tumors, and lymphomas. These tumors can have a variety of clinical behaviors, ranging from benign to malignant.

Testicular neoplasms often present as a painless mass or swelling in the testicle. Other symptoms may include a feeling of heaviness or discomfort in the scrotum, a dull ache in the lower abdomen or groin, and breast enlargement (gynecomastia).

Diagnosis typically involves a physical examination, imaging studies such as ultrasound or CT scan, and blood tests to detect tumor markers. Treatment options depend on the type and stage of the neoplasm but may include surgery, radiation therapy, chemotherapy, or a combination of these modalities. Regular self-examinations of the testicles are recommended for early detection and improved outcomes.

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.

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.

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.

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.

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.

Vindesine is a type of chemotherapy medication known as a vinca alkaloid. It is derived from the Madagascar periwinkle plant and works by interfering with the formation of microtubules, which are necessary for cell division. This causes the cancer cells to stop growing and dividing, ultimately leading to their death.

Vindesine is used to treat several types of cancer, including lung cancer, Kaposi's sarcoma, and certain types of leukemia. It may be given alone or in combination with other chemotherapy drugs. The medication is typically administered intravenously (through an IV) in a healthcare setting.

Like all chemotherapy drugs, vindesine can cause side effects, including nausea, vomiting, hair loss, and increased risk of infection. It may also cause peripheral neuropathy, which is damage to the nerves that can result in numbness, tingling, or pain in the hands and feet. Vindesine can also affect blood cell production, leading to anemia, bleeding, or bruising.

It's important for patients receiving vindesine to be closely monitored by their healthcare team to manage any side effects and adjust the dosage as needed.

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.

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.

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!

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

Carcinoma, small cell is a type of lung cancer that typically starts in the bronchi (the airways that lead to the lungs). It is called "small cell" because the cancer cells are small and appear round or oval in shape. This type of lung cancer is also sometimes referred to as "oat cell carcinoma" due to the distinctive appearance of the cells, which can resemble oats when viewed under a microscope.

Small cell carcinoma is a particularly aggressive form of lung cancer that tends to spread quickly to other parts of the body. It is strongly associated with smoking and is less common than non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers.

Like other types of lung cancer, small cell carcinoma may not cause any symptoms in its early stages. However, as the tumor grows and spreads, it can cause a variety of symptoms, including coughing, chest pain, shortness of breath, hoarseness, and weight loss. Treatment for small cell carcinoma typically involves a combination of chemotherapy, radiation therapy, and sometimes surgery.

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.

Bleomycin is a type of chemotherapeutic agent used to treat various types of cancer, including squamous cell carcinoma, testicular cancer, and lymphomas. It works by causing DNA damage in rapidly dividing cells, which can inhibit the growth and proliferation of cancer cells.

Bleomycin is an antibiotic derived from Streptomyces verticillus and is often administered intravenously or intramuscularly. While it can be effective in treating certain types of cancer, it can also have serious side effects, including lung toxicity, which can lead to pulmonary fibrosis and respiratory failure. Therefore, bleomycin should only be used under the close supervision of a healthcare professional who is experienced in administering chemotherapy drugs.

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.

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.

Neoplasms, germ cell and embryonal are types of tumors that originate from the abnormal growth of cells. Here's a brief medical definition for each:

1. Neoplasms: Neoplasms refer to abnormal tissue growths or masses, which can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled cell division and may invade surrounding tissues or spread to other parts of the body through a process called metastasis.
2. Germ Cell Tumors: These are rare tumors that develop from the germ cells, which give rise to sperm and eggs in the reproductive organs (ovaries and testes). They can be benign or malignant and may occur in both children and adults. Germ cell tumors can also arise outside of the reproductive organs, a condition known as extragonadal germ cell tumors.
3. Embryonal Tumors: These are a type of malignant neoplasm that primarily affects infants and young children. They develop from embryonic cells, which are immature cells present during fetal development. Embryonal tumors can occur in various organs, including the brain (medulloblastomas), nervous system (primitive neuroectodermal tumors or PNETs), and other areas like the kidneys and liver.

It is essential to note that these conditions require professional medical evaluation and treatment by healthcare professionals with expertise in oncology and related fields.

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.

DNA repair is the process by which cells identify and correct damage to the DNA molecules that encode their genome. DNA can be damaged by a variety of internal and external factors, such as radiation, chemicals, and metabolic byproducts. If left unrepaired, this damage can lead to mutations, which may in turn lead to cancer and other diseases.

There are several different mechanisms for repairing DNA damage, including:

1. Base excision repair (BER): This process repairs damage to a single base in the DNA molecule. An enzyme called a glycosylase removes the damaged base, leaving a gap that is then filled in by other enzymes.
2. Nucleotide excision repair (NER): This process repairs more severe damage, such as bulky adducts or crosslinks between the two strands of the DNA molecule. An enzyme cuts out a section of the damaged DNA, and the gap is then filled in by other enzymes.
3. Mismatch repair (MMR): This process repairs errors that occur during DNA replication, such as mismatched bases or small insertions or deletions. Specialized enzymes recognize the error and remove a section of the newly synthesized strand, which is then replaced by new nucleotides.
4. Double-strand break repair (DSBR): This process repairs breaks in both strands of the DNA molecule. There are two main pathways for DSBR: non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ directly rejoins the broken ends, while HR uses a template from a sister chromatid to repair the break.

Overall, DNA repair is a crucial process that helps maintain genome stability and prevent the development of diseases caused by genetic mutations.

A germinoma is a type of tumor that develops in the brain or the spine, primarily in the pituitary gland or pineal gland. It is a rare form of primary central nervous system (CNS) cancer and is classified as a type of germ cell tumor. These tumors arise from cells that normally develop into sperm or eggs, which can migrate to unusual locations during embryonic development.

Germinomas are highly sensitive to radiation therapy and chemotherapy, making them generally treatable and curable with appropriate medical intervention. Symptoms of a germinoma may include headaches, nausea, vomiting, visual disturbances, hormonal imbalances, and neurological deficits, depending on the location and size of the tumor. Diagnosis typically involves imaging studies like MRI or CT scans, followed by a biopsy to confirm the presence of malignant cells.

"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.

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.

Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.

Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.

The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.

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.

Mesothelioma is a rare and aggressive form of cancer that develops in the mesothelial cells, which are the thin layers of tissue that cover many of the internal organs. The most common site for mesothelioma to occur is in the pleura, the membrane that surrounds the lungs. This type is called pleural mesothelioma. Other types include peritoneal mesothelioma (which occurs in the lining of the abdominal cavity) and pericardial mesothelioma (which occurs in the lining around the heart).

Mesothelioma is almost always caused by exposure to asbestos, a group of naturally occurring minerals that were widely used in construction, insulation, and other industries because of their heat resistance and insulating properties. When asbestos fibers are inhaled or ingested, they can become lodged in the mesothelium, leading to inflammation, scarring, and eventually cancerous changes in the cells.

The symptoms of mesothelioma can take many years to develop after exposure to asbestos, and they may include chest pain, coughing, shortness of breath, fatigue, and weight loss. Treatment options for mesothelioma depend on the stage and location of the cancer, but may include surgery, radiation therapy, chemotherapy, or a combination of these approaches. Unfortunately, the prognosis for mesothelioma is often poor, with a median survival time of around 12-18 months after diagnosis.

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.

Antiemetics are a class of medications that are used to prevent and treat nausea and vomiting. They work by blocking or reducing the activity of dopamine, serotonin, and other neurotransmitters in the brain that can trigger these symptoms. Antiemetics can be prescribed for a variety of conditions, including motion sickness, chemotherapy-induced nausea and vomiting, postoperative nausea and vomiting, and pregnancy-related morning sickness. Some common examples of antiemetic medications include ondansetron (Zofran), promethazine (Phenergan), and metoclopramide (Reglan).

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.

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.

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.

Pleural neoplasms refer to abnormal growths or tumors that develop in the pleura, which is the thin, double layered membrane that surrounds the lungs and lines the inside of the chest wall. These neoplasms can be benign (non-cancerous) or malignant (cancerous).

Malignant pleural neoplasms are often associated with lung cancer, mesothelioma, or metastasis from other types of cancer. They can cause symptoms such as chest pain, cough, shortness of breath, and weight loss. Diagnosis typically involves imaging tests like X-rays or CT scans, followed by biopsy to confirm the type of tumor. Treatment options may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.

Urologic neoplasms refer to abnormal growths or tumors in the urinary system, which includes the kidneys, ureters, bladder, prostate, and urethra. These growths can be benign (non-cancerous) or malignant (cancerous). Common types of urologic neoplasms include renal cell carcinoma, transitional cell carcinoma, bladder cancer, prostate cancer, and testicular cancer. It is important to note that early detection and treatment can significantly improve outcomes for patients with urologic neoplasms.

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.

Ondansetron is a medication that is primarily used to prevent nausea and vomiting caused by chemotherapy, radiation therapy, or surgery. It is a selective antagonist of 5-HT3 receptors, which are found in the brain and gut and play a role in triggering the vomiting reflex. By blocking these receptors, ondansetron helps to reduce the frequency and severity of nausea and vomiting.

The drug is available in various forms, including tablets, oral solution, and injection, and is typically administered 30 minutes before chemotherapy or surgery, and then every 8 to 12 hours as needed. Common side effects of ondansetron include headache, constipation, and diarrhea.

It's important to note that ondansetron should be used under the supervision of a healthcare provider, and its use may be contraindicated in certain individuals, such as those with a history of allergic reactions to the drug or who have certain heart conditions.

"Nude mice" is a term used in the field of laboratory research to describe a strain of mice that have been genetically engineered to lack a functional immune system. Specifically, nude mice lack a thymus gland and have a mutation in the FOXN1 gene, which results in a failure to develop a mature T-cell population. This means that they are unable to mount an effective immune response against foreign substances or organisms.

The name "nude" refers to the fact that these mice also have a lack of functional hair follicles, resulting in a hairless or partially hairless phenotype. This feature is actually a secondary consequence of the same genetic mutation that causes their immune deficiency.

Nude mice are commonly used in research because their weakened immune system makes them an ideal host for transplanted tumors, tissues, and cells from other species, including humans. This allows researchers to study the behavior of these foreign substances in a living organism without the complication of an immune response. However, it's important to note that because nude mice lack a functional immune system, they must be kept in sterile conditions and are more susceptible to infection than normal mice.

Amifostine is a medication that is used to protect tissues from the harmful effects of radiation therapy and certain chemotherapy drugs. It is an organic thiophosphate compound, chemically known as (3-Aminopropyl)amidophosphoric acid, and is administered intravenously.

Amifostine works by scavenging free radicals and converting them into non-reactive substances, which helps to prevent damage to normal cells during cancer treatment. It is particularly useful in protecting the kidneys from cisplatin-induced nephrotoxicity and reducing xerostomia (dry mouth) caused by radiation therapy in head and neck cancers.

The medication is typically given as a slow intravenous infusion over 15 minutes before cancer treatment, and its use should be monitored carefully due to potential side effects such as nausea, vomiting, hypotension, and allergic reactions. Healthcare professionals must consider the benefits and risks of amifostine therapy on a case-by-case basis, taking into account the patient's overall health status, cancer type, and treatment plan.

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.

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).

Tumor suppressor protein p53, also known as p53 or tumor protein p53, is a nuclear phosphoprotein that plays a crucial role in preventing cancer development and maintaining genomic stability. It does so by regulating the cell cycle and acting as a transcription factor for various genes involved in apoptosis (programmed cell death), DNA repair, and cell senescence (permanent cell growth arrest).

In response to cellular stress, such as DNA damage or oncogene activation, p53 becomes activated and accumulates in the nucleus. Activated p53 can then bind to specific DNA sequences and promote the transcription of target genes that help prevent the proliferation of potentially cancerous cells. These targets include genes involved in cell cycle arrest (e.g., CDKN1A/p21), apoptosis (e.g., BAX, PUMA), and DNA repair (e.g., GADD45).

Mutations in the TP53 gene, which encodes p53, are among the most common genetic alterations found in human cancers. These mutations often lead to a loss or reduction of p53's tumor suppressive functions, allowing cancer cells to proliferate uncontrollably and evade apoptosis. As a result, p53 has been referred to as "the guardian of the genome" due to its essential role in preventing tumorigenesis.

Guanine is not a medical term per se, but it is a biological molecule that plays a crucial role in the body. Guanine is one of the four nucleobases found in the nucleic acids DNA and RNA, along with adenine, cytosine, and thymine (in DNA) or uracil (in RNA). Specifically, guanine pairs with cytosine via hydrogen bonds to form a base pair.

Guanine is a purine derivative, which means it has a double-ring structure. It is formed through the synthesis of simpler molecules in the body and is an essential component of genetic material. Guanine's chemical formula is C5H5N5O.

While guanine itself is not a medical term, abnormalities or mutations in genes that contain guanine nucleotides can lead to various medical conditions, including genetic disorders and cancer.

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.

Platinum compounds refer to chemical substances that contain platinum in its positive valence state combined with other negatively charged ions or molecules. They are commonly used in medicine, particularly in the treatment of cancer. The most well-known platinum compound is cisplatin, which is a platinum-containing drug used to treat various types of tumors, including testicular, ovarian, and bladder cancers.

Cisplatin works by binding to the DNA of cancer cells, causing cross-linking of the DNA strands and preventing DNA replication and transcription. This leads to cell cycle arrest and apoptosis (programmed cell death) of the cancer cells. Other platinum compounds used in cancer therapy include carboplatin and oxaliplatin, which have similar mechanisms of action but differ in their chemical structures and toxicity profiles.

It is important to note that while platinum compounds can be effective in treating certain types of cancer, they can also cause significant side effects, including kidney damage, nerve damage, and hearing loss. Therefore, careful monitoring and management of these side effects are necessary during treatment with platinum compounds.

Radiation-sensitizing agents are drugs that make cancer cells more sensitive to radiation therapy. These agents work by increasing the ability of radiation to damage the DNA of cancer cells, which can lead to more effective tumor cell death. This means that lower doses of radiation may be required to achieve the same therapeutic effect, reducing the potential for damage to normal tissues surrounding the tumor.

Radiation-sensitizing agents are often used in conjunction with radiation therapy to improve treatment outcomes for patients with various types of cancer. They can be given either systemically (through the bloodstream) or locally (directly to the tumor site). The choice of agent and the timing of administration depend on several factors, including the type and stage of cancer, the patient's overall health, and the specific radiation therapy protocol being used.

It is important to note that while radiation-sensitizing agents can enhance the effectiveness of radiation therapy, they may also increase the risk of side effects. Therefore, careful monitoring and management of potential toxicities are essential during treatment.

Induction chemotherapy is a type of cancer treatment that involves the use of cytotoxic drugs to reduce the size of tumors prior to administering other forms of therapy, such as radiation therapy or surgery. The goal of induction chemotherapy is to eliminate as many cancer cells as possible and shrink the tumor to improve the chances of a successful outcome with subsequent treatments.

This approach is often used in the treatment of certain types of cancer, including lymphoma, leukemia, and testicular cancer, among others. The specific drugs used and the duration of treatment may vary depending on the type and stage of cancer being treated.

It's important to note that induction chemotherapy is a complex medical procedure that should be administered under the close supervision of an experienced oncologist. Patients undergoing this treatment may experience side effects, such as nausea, vomiting, fatigue, and hair loss, among others. However, these side effects can often be managed with supportive care and medications.

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.

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.

Uterine cervical neoplasms, also known as cervical cancer or cervical dysplasia, refer to abnormal growths or lesions on the lining of the cervix that have the potential to become cancerous. These growths are usually caused by human papillomavirus (HPV) infection and can be detected through routine Pap smears.

Cervical neoplasms are classified into different grades based on their level of severity, ranging from mild dysplasia (CIN I) to severe dysplasia or carcinoma in situ (CIN III). In some cases, cervical neoplasms may progress to invasive cancer if left untreated.

Risk factors for developing cervical neoplasms include early sexual activity, multiple sexual partners, smoking, and a weakened immune system. Regular Pap smears and HPV testing are recommended for early detection and prevention of cervical cancer.

Osteosarcoma is defined as a type of cancerous tumor that arises from the cells that form bones (osteoblasts). It's the most common primary bone cancer, and it typically develops in the long bones of the body, such as the arms or legs, near the growth plates. Osteosarcoma can metastasize (spread) to other parts of the body, including the lungs, making it a highly malignant form of cancer. Symptoms may include bone pain, swelling, and fractures. Treatment usually involves a combination of surgery, chemotherapy, and/or radiation therapy.

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.

Thiosulfates are salts or esters of thiosulfuric acid (H2S2O3). In medicine, sodium thiosulfate is used as an antidote for cyanide poisoning and as a topical treatment for wounds, skin irritations, and certain types of burns. It works by converting toxic substances into less harmful forms that can be eliminated from the body. Sodium thiosulfate is also used in some solutions for irrigation of the bladder or kidneys to help prevent the formation of calcium oxalate stones.

Dose fractionation is a medical term that refers to the practice of dividing the total dose of radiation therapy or chemotherapy into smaller doses, which are given over a longer period. This approach allows for the delivery of a higher total dose of treatment while minimizing damage to healthy tissues and reducing side effects.

In radiation therapy, fractionation is used to target cancer cells while sparing surrounding normal tissues. By delivering smaller doses of radiation over several treatments, healthy tissue has time to recover between treatments, reducing the risk of complications. The number and size of fractions can vary depending on the type and location of the tumor, as well as other factors such as the patient's overall health.

Similarly, in chemotherapy, dose fractionation is used to maximize the effectiveness of the treatment while minimizing toxicity. By administering smaller doses of chemotherapy over time, the body has a chance to recover between treatments, reducing side effects and allowing for higher total doses to be given. The schedule and duration of chemotherapy fractionation may vary depending on the type of drug used, the type and stage of cancer, and other factors.

Overall, dose fractionation is an important technique in both radiation therapy and chemotherapy that allows for more effective treatment while minimizing harm to healthy tissues.

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When cisplatin forms interstrand crosslinks (5'-GC), there is a severe distortion to the DNA helix due to a shortened distance ... "Cisplatin". National Cancer Institute. 2007-03-02. Retrieved 2017-10-09. Cimino, G. D.; Gamper, H. B.; Isaacs, S. T.; Hearst, J ... When cisplatin generates DNA crosslinks, it more frequently forms 1,2-intrastrand crosslinks (5'-GG), but also forms 1,3- ... Cisplatin (cis-diamminedichloroplatinum(II)) and its derivatives mostly act on adjacent guanines at their N7 positions. The ...
"Cisplatin". Science & Research (Drugs). United States Food and Drug Administration. Reuther LO, Vainer B, Sonne J, Larsen NE ( ... Genetic variants of TPMT have also been associated with cisplatin-induced ototoxicity in children. TPMT is now listed as a ... "Genetic variants in TPMT and COMT are associated with hearing loss in children receiving cisplatin chemotherapy". Nat. Genet. ... pharmacogenomic biomarker for adverse drug reactions to cisplatin by the FDA. Cancer pharmacogenomics GRCh38: Ensembl release ...
Several chemotherapeutic agents, for example Cisplatin, are associated with acute and chronic kidney injuries. Newer agents ... Cisplatin nephrotoxicity. In: UpToDate, Palevsky PM (Ed), UpToDate, Waltham, MA, 2013. http://www.uptodate.com/contents/ ... cisplatin-nephrotoxicity Robinson, Emily S.; Khankin, Eliyahu V.; Karumanchi, S. Ananth; Humphreys, Benjamin D. (1 November ...
... and cisplatin. These treatment regimens have been reported to lower local recurrence rates, prolong disease-free survival rates ... plus dacarbazine or cisplatin; cyclophosphamide, doxorubicin, plus dacarbazine; high dose methotrexate; or etoposide, ...
TMEM205 has been shown to be involved in Cisplatin resistance. Cisplatin is a chemotherapeutic drug that is commonly used to ... In addition to being involved in Cisplatin resistance there is growing evidence that the protein is also involved in the ... Shen DW, Gottesman MM (March 2012). "RAB8 enhances TMEM205-mediated cisplatin resistance". Pharmaceutical Research. 29 (3): 643 ... is associated with cisplatin resistance". Journal of Cellular Physiology. 225 (3): 822-8. doi:10.1002/jcp.22287. PMC 2971691. ...
The test is still used to assay samples of the drug cisplatin, but it is mainly of pedagogical interest, as it illustrates the ... The Kurnakov test is sometimes used to detect transplatin in samples of the drug cisplatin. In hot aqueous solution, the cis- ... "The Discovery and Development of Cisplatin". Journal of Chemical Education. 83 (5): 728-773. Bibcode:2006JChEd..83..728A. doi: ...
Alderden, Rebecca A.; Hall, Matthew D.; Hambley, Trevor W. (1 May 2006). "The Discovery and Development of Cisplatin". J. Chem ... An illustrative example is the preparation of the anti-cancer drug cisplatin from potassium tetrachloroplatinate. Beilstein ...
Cisplatin, or cis-diamminedichloroplatinum(II) is the first of a series of square planar platinum(II)-containing chemotherapy ... Side effects of cisplatin include nausea and vomiting, hair loss, tinnitus, hearing loss, and nephrotoxicity.) Organoplatinum ... The hexachloroplatinate ion The anion of Zeise's salt Dichloro(cycloocta-1,5-diene)platinum(II) Cisplatin Archaeologists have ... Riddell, Imogen A.; Lippard, Stephen J. (2018). "Cisplatin and Oxaliplatin:Our Current Understanding of Their Actions". In ...
Cisplatin and etoposide, Carboplatin and etoposide. The drug paclitaxel may be useful in the treatment of cisplatin-resistant ... About 68.1% of cisplatin-resistant cells appear to be sensitive to paclitaxel and 66.7% of paclitaxel-resistant cells to ... In Japan, first-line treatment is shifting to irinotecan and cisplatin. When the primary site is in the skin, it is referred to ... In cases of LS-SCLC, combination chemotherapy (usually cisplatin or carboplatin plus etoposide) is administered together with ...
Such agents include cisplatin and bleomycin. Cisplatin is known as a platinum coordination complex. Carboplatin and oxaliplatin ... Cisplatin and other platinum coordination complexes work by reacting with various sites on DNA in mainly cancer cells in order ... The mechanism of cisplatin in inducing ototoxicity is believed to involve the accumulation of reactive oxygen species, which ... The use of D-methionine to protect against hearing loss induced by drugs like cisplatin and aminoglycosides is preliminarily ...
Cleft lip and palate transmembrane protein 1-like protein (CLPTM1-like protein), also known as cisplatin resistance-related ... CRR9p is associated with cisplatin-induced apoptosis. CLPTM1L, which lies within a cancer susceptibility locus on chromosome 5 ...
Barnett Rosenberg, 82, American chemist, discovered cisplatin. Raul Solnado, 79, Portuguese actor and comedian, cardiovascular ...
Zamble, Deborah B.; Mu, David; Reardon, Joyce T.; Sancar, Aziz; Lippard, Stephen J. (1996-01-01). "Repair of Cisplatin−DNA ... Lippard on cisplatin, an anti-cancer drug. Her research considered the role of p53 in the cellular response to the drug. Zamble ... "Cisplatin and DNA repair in cancer chemotherapy". Trends in Biochemical Sciences. 20 (10): 435-439. doi:10.1016/S0968-0004(00) ... "HMG-domain proteins specifically inhibit the repair of the major DNA adduct of the anticancer drug cisplatin by human excision ...
... and cisplatin, which is used in chemotherapy. Amikacin should not be used with neuromuscular blocking agents, as they can ...
"Partial reversibility of cisplatin nephrotoxicity in children". The Journal of Pediatrics. 118 (4): 531-534. doi:10.1016/S0022- ...
Cisplatin was the first to be developed. Cisplatin is particularly effective against testicular cancer; the cure rate was ... Poklar N, Pilch DS, Lippard SJ, Redding EA, Dunham SU, Breslauer KJ (July 1996). "Influence of cisplatin intrastrand ... In this form of chemotherapy, commonly used drugs include cisplatin, oxaliplatin, and carboplatin, but several have been ... As studied mainly on cisplatin, but presumably for other members as well, platinum-based antineoplastic agents cause ...
Basu A, Krishnamurthy S (August 2010). "Cellular responses to Cisplatin-induced DNA damage". Journal of Nucleic Acids. 2010: 1- ...
2003). "Effect of cisplatin treatment on speckled distribution of a serine/arginine-rich nuclear protein CROP/Luc7A". Biochem. ... "Entrez Gene: CROP cisplatin resistance-associated overexpressed protein". Human LUC7L3 genome location and LUC7L3 gene details ... LUC7 like 3 pre-mRNA splicing factor (LUC7L3), also known as Cisplatin resistance-associated overexpressed protein, or CROP, is ... This gene encodes a cisplatin resistance-associated overexpressed protein (CROP). The N-terminal half of the CROP contains ...
Aziridines include thiotepa, mytomycin and diaziquone (AZQ). Cisplatin and derivatives include cisplatin, carboplatin and ... Drugs with medium risk include doxorubicin and platinum analogs such as cisplatin and carboplatin. On the other hand, therapies ... October 2014). "Strategic targeting of the PI3K-NFκB axis in cisplatin-resistant NSCLC". Cancer Biology & Therapy. 15 (10): ... Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ...
Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ... and platinum based chemotherapeutics such as cisplatin and carboplatin. In addition to medications, hearing loss can also ...
Cisplatin resistance occurs when cancer cells develop an enhanced ability to reverse such damage by removing the cisplatin from ... The cisplatin-resistant cells upregulate expression of the excision repair cross-complementing (ERCC1) gene and protein. Some ... In ovarian cancer, the ATP7B gene encodes for a copper efflux transporter, found to be upregulated in cisplatin-resistant cell ... Platinum-based chemotherapies, such as cisplatin, target tumour cells by cross-linking their DNA strands, causing mutation and ...
The major elements are cisplatin, carboplatin, and oxaliplatin. It has been reported with full recovery among early-stage ... It is known as the hyperthermic intraperitoneal chemotherapy (HIPEC), containing docetaxel, and cisplatin. Given the drug is ... and cisplatin, also known as the BEP treatment. Patients should be issued with 3-4 cycles of BEP to ensure full salvage. ... which consists of cisplatin, ifosfamide and paclitaxel. Yet, it is likely that OGCT survivors after BEP therapy will have ...
Commonly used drugs include cisplatin, vincristine, and methotrexate.[clarification needed] Side effects include anemia ( ...
July 2003). "Phase III study of pemetrexed in combination with cisplatin versus cisplatin alone in patients with malignant ... Cisplatin and pemetrexed together give patients a median survival of 12.1 months. Cisplatin in combination with raltitrexed has ... albeit with similar survival figures to patients receiving cisplatin. Cisplatin in combination with premetrexed disodium, folic ... For patients in whom cisplatin cannot be used, carboplatin can be substituted but non-randomised data have shown lower response ...
Rybak LP, Mukherjea D, Jajoo S, Ramkumar V (November 2009). "Cisplatin ototoxicity and protection: clinical and experimental ... and platinum based chemotherapeutics such as cisplatin and carboplatin. In 2007, the U.S. Food and Drug Administration (FDA) ...
"Investigation into ubiquitin signalling in response to cisplatin". Discovery Research Portal. University of Dundee. Retrieved 2 ... predicted to be a part of the ubiquitin ligase family and involved with DNA repair mechanisms after treatment with cisplatin, a ...
Cisplatin ("Platinol") was given instead of carboplatin ("Paraplatin"). He resided in Rome, New York with his second wife, ...
... to better understand how cisplatin invades tumor cells and interferes with their activity. The interaction of Cisplatin and DNA ... Cisplatin is one of the most frequently used chemotherapy medications for many forms of cancer. It was discovered in the 1960s ... Its proprietary drug candidates included BTP-114, a cisplatin prodrug, and BTP-277, a targeting ligand designed to bond ... As well as the intrastrand cross links created by cisplatin, monofunctional metal complexes may suggest possible cancer ...
Cisplatin was the first to be developed. In 1983 pediatric oncologist Roger Packer began incorporating cisplatin into adjuvant ... Cisplatin has been studied with Auger therapy to increase the therapeutic effects of cisplatin, without increasing normal ... "Cisplatin Use During Pregnancy". Drugs.com. 12 September 2019. Retrieved 25 February 2020. "Cisplatin". The American Society of ... It is suggested that an antibody reacting with a cisplatin-red-cell membrane is responsible for hemolysis. Cisplatin interferes ...
Cisplatin was found to break up the binding of p63 to p73 and reactivate the cell-death process. ... NewsAnatomyAnti cancer drugsBreast cancerCancersCisplatinDrugsEndocrine systemHormonesMedicine, Diagnosis, and Therapeutics ... Based on previous reports, the current study was designed to see if triple-negative tumors might be sensitive to cisplatin and ... Based on the research, a clinical trial to investigate the role of p63/p73 expression in determining cisplatin sensitivity will ...
More than half of patients treated with cisplatin-based chemotherapy develop hearing loss or tinnitus, which can be devastating ... Cisplatin is known to be highly ototoxic, the authors point out, but it achieves a very high cure rate when used for testicular ... The message is not that cisplatin should be avoided, but that "attention must be turned to survivorship, including an awareness ... More than half of patients with testicular cancer treated with first-line cisplatin-based chemotherapy in a recent study ...
p,Many testicular cancer survivors experience hearing loss after cisplatin-based chemotherapy, according to researchers at ... Platinum-based cisplatin is one of the most commonly used drugs in medical oncology that also has toxic effects on the inner ... Einhorn tested cisplatin with two additional drugs that were effective in killing testis cancer cells. The combination became ... IU study finds testicular cancer survivors may have hearing loss after cisplatin therapy IU School of Medicine Jun 27, 2016 ...
Epoxyeicosatrienoic Acids and Cisplatin-Induced Apoptosis. Yingmei Liu, Xiaodan Lu, Sinh Nguyen, Jean L. Olson, Heather K. Webb ... Epoxyeicosatrienoic Acids and Cisplatin-Induced Apoptosis. Yingmei Liu, Xiaodan Lu, Sinh Nguyen, Jean L. Olson, Heather K. Webb ... Epoxyeicosatrienoic Acids Prevent Cisplatin-Induced Renal Apoptosis through a p38 Mitogen-Activated Protein Kinase-Regulated ... Epoxyeicosatrienoic Acids Prevent Cisplatin-Induced Renal Apoptosis through a p38 Mitogen-Activated Protein Kinase-Regulated ...
CoAcS Ltd, Kimbolton House, Mount Beacon, Lansdown, Bath BA1 5QP Phone: +44 1225 312992. Fax: +44 1225 315339. Email: Click here to email. ...
Pemextred and Cisplatin will be given in conjunction with TRC102 on the first day of each cycle for 6 cycles. A treatment cycle ... Posted in mesothelioma clinical trials , Tagged cisplatin, mesothelioma clinical trials, methoxyamine, pemetrexed , Leave a ... Mesothelioma Clinical Trial Review- Methoxyamine, Cisplatin And Pemetrexed. Posted on April 6, 2016. by Ellie and Lisa ... The study drug TRC102 will be given in addition to Pemetrexed and Cisplatin. This group will be patients who would have been ...
Heres how to manage a malignant growth patient A guardian ought to give his/her entire being for the patients prosperity, particularly if its a disease patient. As a guardian, you can help in the recuperation. ...
We report, for the first time, cisplatin-sensitive human UKF-NB-4 cells remodelled into cisplatin-resistant cells via high and ... up-regulation in neuroblastoma cells and the mechanisms underlying the cisplatin-resistance. We confirmed the cisplatin- ... Cisplatin-based chemotherapy is a major regimen to treat neuroblastoma, but its clinical efficacy is limited by chemoresistance ... Overall, our data confirmed that up-regulation of hMT3 positively correlated with increased cisplatin-chemoresistance in ...
Inhibition of CHK1, a cell cycle G2/M checkpoint kinase has previously been shown to have a synergistic effect with cisplatin ... Our data demonstrates both CHK1 and WEE1 play a role in mediating resistance of A2780 cells to cisplatin and paclitaxel and ... Inhibition of CHK1, a cell cycle G2/M checkpoint kinase has previously been shown to have a synergistic effect with cisplatin ... Our data demonstrates both CHK1 and WEE1 play a role in mediating resistance of A2780 cells to cisplatin and paclitaxel and ...
This is a powerful anti-oxidant which has been demonstrated to protect the inner ear from damage caused by cisplatin. My mum ... This is a powerful anti-oxidant which has been demonstrated to protect the inner ear from damage caused by cisplatin. My mum ...
... studies have focused on the regimen etoposide and cisplatin and on etoposide, doxorubicin, and cisplatin. ... Cisplatin inhibits DNA synthesis and, therefore, cell proliferation, by causing DNA cross-linking and denaturation of the ... Adjuvant or palliative treatment for adrenocortical carcinoma (AC) has been studied by using mitotane, cisplatin, etoposide, ... Chemotherapy has focused on 3 antineoplastics-cisplatin, etoposide, and doxorubicin-given alone or in combination; ...
Detailed drug Information for Jantoven. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Cisplatin Injection April 23, 2024. Clindamycin Phosphate Injection April 22, 2024. Clonazepam Oral Tablets March 22, 2024. ...
We examined the anti-cancer, anti-proliferative and synergistic effects of Sambucus nigra extract with cisplatin chemotherapy ( ... Keywords: Apoptosis, Breast cancer, Cisplatin, Drug resistance, Sambucus nigra Full-Text [PDF 2339 kb] (449 Downloads) , , Full ... Sambucus Nigra Synergizes Cisplatin to Improve Apoptosis and Metabolic Disorders, and Reduce Drug Resistance in Two Human ... Roshankhah S, Ghanbari A, Salahshoor M R, Esmaeli M. Sambucus Nigra Synergizes Cisplatin to Improve Apoptosis and Metabolic ...
The Effecct of cisplatin on male white mice testicular tissue ... The Effecct of cisplatin on male white mice testicular tissue. ... Some studies reported the negative effect of cisplatin on male reproductive system.. Objective: To know the effect of cisplatin ... Cisplatin was given to the treatment group intravenously in the dose of 3 mg/kgBW for 7 days. At the end of the experiment, the ... Background: Cisplatin is a potent anticancer drug. In the therapy of various kinds of tumours. such as testicular, ovarian, ...
Primary treatment consisted of two blocks of high-dose ifosfamide (15 g/m(2)), methotrexate (12 g/m(2)), cisplatin (120 mg/m(2 ... Primary treatment consisted of two blocks of high-dose ifosfamide (15 g/m(2)), methotrexate (12 g/m(2)), cisplatin (120 mg/m(2 ... Primary treatment consisted of two blocks of high-dose ifosfamide (15 g/m(2)), methotrexate (12 g/m(2)), cisplatin (120 mg/m(2 ... Primary treatment consisted of two blocks of high-dose ifosfamide (15 g/m(2)), methotrexate (12 g/m(2)), cisplatin (120 mg/m(2 ...
Chemotherapy with gemcitabine, cisplatin, and docetaxel in the treatment for patients with muscle-invasive bladder cancer: a ... PURPOSE: To assess the antitumor activity and toxicity of gemcitabine, cisplatin, and docetaxel (GCD) regimen in patients with ... of 0-2 were treated with sequential cisplatin 80 mg/m(2) (d1), gemcitabine 1,100 mg/m(2) (d1 and d14), and docetaxel 80 mg/m(2 ...
The reversal of cisplatin-protein interactions by the modulating agent WR2721 and its metabolites WR1065 and WR33278. Cancer ... The reversal of cisplatin-protein interactions by the modulating agent WR2721 and its metabolites WR1065 and WR33278. In: ... The reversal of cisplatin-protein interactions by the modulating agent WR2721 and its metabolites WR1065 and WR33278. / Treskes ... The reversal of cisplatin-protein interactions by the modulating agent WR2721 and its metabolites WR1065 and WR33278. ...
P - cisplatin (sis-pla-tin). It is a treatment for lymphoma and myeloma. It is usually used before having a stem cell ... Etoposide, cisplatin and cytarabine are chemotherapy drugs. These drugs destroy quickly dividing cells, such as cancer cells. ... You start cisplatin as a continuous drip into your bloodstream that lasts for 4 days. ...
Crocetin combined with cisplatin exerts a synergistic anticancer effect by up-regulating the p53/p21 pathway.Dec 31, 2016. ... Encapsulation of crocetin into nanoparticles overcomes drug resistance in human ovarian cisplatin-resistant carcinoma cell line ...
... cisplatin; colistin (Coly-Mycin S); cyclosporine (Gengraf, Neoral, Restasis, Sandimmune); diuretics (water pills) such as ...
Cisplatin in Liver Cancer Therapy. Hamaya, Sae; Oura, Kyoko; Morishita, Asahiro; Masaki, Tsutomu. Afiliação *Hamaya S; ... Cisplatin is also used for the treatment of liver tumors other than HCC. This review summarizes the action and resistance ... Subsequently, for cisplatin-refractory cases due to drug resistance, a shift to systemic therapy with a different mechanism of ... cisplatin; drug resistance; hepatic arterial infusion chemotherapy; hepatocellular carcinoma; liver cancer; transarterial ...
Drugs: Cyclophosphamide, cisplatin, vincristine. Other: Aerobic training; neurocognitive remediation. For Strata S1: Standard ... Drugs: Cyclophosphamide, cisplatin, vincristine, vismodegib. Other: Aerobic training; neurocognitive remediation. For Strata N2 ... Drugs: Cyclophosphamide, cisplatin, vincristine, pemetrexed, gemcitabine. Other: Aerobic training; neurocognitive remediation. ... Six weeks after completion of radiotherapy, participants receive one cycle of chemotherapy (cisplatin, vincristine, and ...
Cisplatin for cancer therapy and overcoming chemoresistance. Ranasinghe R, Mathai ML, Zulli A. Ranasinghe R, et al. Among ...
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above. ...
Disruption of the gut microbiota confers cisplatin resistance in epithelial ovarian cancer ...
A CHLA clinical trial finds that N-acetylcysteine may be a promising next-generation therapy to reduce the risk of cisplatin- ... Will N-Acetylcysteine Be the Next Therapy to Prevent Cisplatin-Induced Hearing Loss? July 24, 2023 ...
FOXM1 confers acquired cisplatin resistance in breast cancer cells. Mol. Cancer Res. 2010, 8, 24-34. [Google Scholar] [CrossRef ...
  • Furthermore, the combination of a selective MATE inhibitor, pyrimethamine, with cisplatin also elevated creatinine and BUN levels compared to cisplatin alone. (nih.gov)
  • 5% compared to cisplatin alone) were vomiting, nausea, decreased hemoglobin, hypernatremia, and hypokalemia. (fda.gov)
  • Based on the research, a clinical trial to investigate the role of p63/p73 expression in determining cisplatin sensitivity will be led by MGH researchers through the Dana-Farber/Harvard Cancer Center in Boston in the coming weeks. (genengnews.com)
  • Platinum-based chemotherapeutic drugs such as cisplatin and carboplatin induce intra- and interstrand crosslinks, resulting in replication arrest, and cell death. (nuigalway.ie)
  • When S-phase XP30R0 cells were treated with cisplatin, a strong S-phase arrest was detected, however, when treated with carboplatin, arrest in S phase was less pronounced, and there was evidence for S-phase arrest in a second cell cycle. (nuigalway.ie)
  • They include certain antibiotics like gentamicin, cancer treatment drugs like cisplatin and carboplatin, and pain relievers that contain salicylate like aspirin, quinine, loop diuretics. (cdc.gov)
  • Ototoxicity and hearing loss associated with cisplatin can be severe and is considered to be a dose-limiting side effect. (wikipedia.org)
  • Other drugs (such as the aminoglycoside antibiotic class) may also cause ototoxicity, and the administration of this class of antibiotics in patients receiving cisplatin is generally avoided. (wikipedia.org)
  • The ototoxicity of both the aminoglycosides and cisplatin may be related to their ability to bind to melanin in the stria vascularis of the inner ear or the generation of reactive oxygen species. (wikipedia.org)
  • In September 2022, the U.S. Food and Drug Administration (FDA) approved sodium thiosulfate under the brand name Pedmark to lessen the risk of ototoxicity and hearing loss in people receiving cisplatin. (wikipedia.org)
  • The message is not that cisplatin should be avoided, but that "attention must be turned to survivorship, including an awareness of the functional impact of ototoxicity," the authors emphasize. (medscape.com)
  • Routine follow-up of adult-onset cisplatin-treated ototoxicity in cancer survivors should begin with prechemotherapy baseline measurements, resume shortly after treatment, and include annual query for hearing loss/tinnitus status and severity, especially as patients age, so that they are presented with available treatment strategies," the authors recommend. (medscape.com)
  • In the general population, HL begins in midlife, with two thirds of individuals age ≥ 70 years having bilateral HL, but for cancer survivors where treatment occurs earlier in life, cisplatin-related ototoxicity can exacerbate age-related HL," the authors explain. (medscape.com)
  • The potentially severe, negative impact of cisplatin-related ototoxicity on functional status warrants clinical intervention, survivorship support, and education," the researchers conclude. (medscape.com)
  • On September 20, 2022, the Food and Drug Administration approved sodium thiosulfate (Pedmark, Fennec Pharmaceuticals Inc.) to reduce the risk of ototoxicity associated with cisplatin in pediatric patients 1 month and older with localized, non-metastatic solid tumors. (fda.gov)
  • The researchers pointed out that because alterations in the highly successful testicular cancer regimens are unlikely for patients with advanced disease, their results underscore the importance of ongoing research aimed at the identification of genetic variants associated with cisplatin-related ototoxicity. (iu.edu)
  • Overexpression of hMT3 decreased the sensitivity of neuroblastoma UKF-NB-4 cells to cisplatin. (vut.cz)
  • Proadifen sensitizes resistant ovarian adenocarcinoma cells to cisplatin. (scilifelab.se)
  • Thus, the purpose of this study was to investigate the ability of proadifen to sensitize A2780 and A2780cis ovarian cancer cells to cisplatin (CDDP). (scilifelab.se)
  • Durvalumab plus gemcitabine and cisplatin is recommended, within its marketing authorisation, as an option for treating locally advanced, unresectable, or metastatic biliary tract cancer in adults. (nice.org.uk)
  • Standard treatment includes chemotherapy with gemcitabine and cisplatin. (nice.org.uk)
  • Clinical trial evidence shows that, compared with standard treatment, durvalumab plus gemcitabine and cisplatin increases how long people have before their condition gets worse and how long they live. (nice.org.uk)
  • So, durvalumab plus gemcitabine and cisplatin is recommended. (nice.org.uk)
  • To establish the maximally tolerated dose (MTD) of intraoperative Intrathoracic/Intraperitoneal hyperthermic gemcitabine and cisplatin combination modulated by amifostine and sodium thiosulfate in patients with malignant pleural mesothelioma. (mesotheliomacenter.org)
  • To study the pharmacokinetics of gemcitabine and cisplatin combination administered in this way. (mesotheliomacenter.org)
  • COG ACCL0431 enrolled 125 pediatric patients with solid tumors undergoing a chemotherapy regimen including cumulative cisplatin doses of 200 mg/m2 or higher, with individual cisplatin doses to be infused over 6 hours or less. (fda.gov)
  • Despite its use for more than 40 years, knowledge about the effects of cumulative cisplatin dose on hearing loss in survivors of adult-onset cancer has remained limited. (iu.edu)
  • They also discovered the molecular basis of this sensitivity, which may help identify patients most likely to benefit from cisplatin treatment. (genengnews.com)
  • p53 mutation and cyclin D1 amplification correlate with cisplatin sensitivity in xenografted human squamous cell carcinomas from head and neck. (lu.se)
  • For their study, Sanchez and colleagues enrolled cisplatin-treated testicular cancer survivors at eight cancer centers between 2012 and 2018. (medscape.com)
  • Many testicular cancer survivors experience hearing loss after cisplatin-based chemotherapy, according to researchers at Indiana University. (iu.edu)
  • The researchers, led by Lois B. Travis , M.D., Sc.D., the Lawrence H. Einhorn Professor of Cancer Research at the IU School of Medicine and a researcher at the Indiana University Melvin and Bren Simon Cancer Center , studied for the first time the cumulative effects of cisplatin-based chemotherapy on hearing levels in testicular cancer survivors through comprehensive audiometry measurements. (iu.edu)
  • Patients were randomized (1:1) to receive cisplatin-based chemotherapy with or without sodium thiosulfate administered at various doses of 10 g/m2, 15 g/m2, or 20 g/m2 based on actual body weight. (fda.gov)
  • Patients were randomized (1:1) to receive cisplatin-based chemotherapy with or without sodium thiosulfate. (fda.gov)
  • Sodium thiosulfate is administered as an intravenous infusion over 15 minutes following cisplatin infusions that are 1 to 6 hours in duration. (fda.gov)
  • Cells treated with Cisplatin alone or combined with Genipin, ROS negatively, while MMP positively correlated with cell viability. (medsci.org)
  • Overall, our data confirmed that up-regulation of hMT3 positively correlated with increased cisplatin-chemoresistance in neuroblastoma, and a high level of hMT3 could be one of the causes of frequent tumour relapses. (vut.cz)
  • Cisplatin interferes with DNA replication, which kills the fastest proliferating cells, which in theory are cancerous. (wikipedia.org)
  • Nausea and vomiting: cisplatin is one of the most emetogenic chemotherapy agents, but this symptom is managed with prophylactic antiemetics (ondansetron, granisetron, etc.) in combination with corticosteroids. (wikipedia.org)
  • Purpose- Clinical Trial TRC 102 in combination with 2 chemotherapy agents Cisplatin and Pemetrexed. (mesotheliomaquestions.com)
  • Based on previous reports, the current study was designed to see if triple-negative tumors might be sensitive to cisplatin and to investigate the underlying mechanism. (genengnews.com)
  • These results suggest that testing p63 and p73 levels in patients' tumors might help predict whether they would benefit from cisplatin therapy. (genengnews.com)
  • This trial is for advanced tumors with expansion to mesothelioma/ Phase II is TRC102 and Pemetrexed in patients with refractory to cisplatin and Pemetrexed. (mesotheliomaquestions.com)
  • Cisplatin is also used for the treatment of liver tumors other than HCC. (bvsalud.org)
  • Adjuvant or palliative treatment for adrenocortical carcinoma (AC) has been studied by using mitotane, cisplatin, etoposide, and doxorubicin. (medscape.com)
  • studies have focused on the regimen etoposide and cisplatin and on etoposide, doxorubicin, and cisplatin. (medscape.com)
  • In the treatment of unresectable advanced HCC, cisplatin is administered transhepatic arterially for local treatment . (bvsalud.org)
  • Cisplatin has a number of side effects that can limit its use: Nephrotoxicity (kidney damage) is the primary dose-limiting side effect and is of major clinical concern. (wikipedia.org)
  • In the present study, the role of MATE1 in the nephrotoxicity of cisplatin was investigated in vivo and in vitro. (nih.gov)
  • In conclusion, MATE1 mediates the efflux of cisplatin and is involved in cisplatin-induced nephrotoxicity. (nih.gov)
  • Based on previous observations that sEH inhibition attenuates cisplatin-induced nephrotoxicity by modulating nuclear factor- κ B signaling, we hypothesized that this strategy would also attenuate cisplatin-induced renal apoptosis. (aspetjournals.org)
  • Cisplatin selectively accumulates into the proximal tubule via basolateral-to-apical transport, where it disrupts mitochondrial energetics and endoplasmic reticulum Ca2+ homeostasis and stimulates reactive oxygen species and pro-inflammatory cytokines. (wikipedia.org)
  • Inhibition of sEH with AR9273 [1-adamantan-1-yl-3-(1-methylsulfonyl-piperidin-4-yl-urea)] reduced cisplatin-induced apoptosis through mechanisms involving mitochondrial apoptotic pathways and by reducing reactive oxygen species. (aspetjournals.org)
  • They found that increasing doses of cisplatin were associated with increased hearing loss at most of the tested frequencies, involving 4, 6, 8, 10, and 12 kHz. (iu.edu)
  • Different doses of the study drug will be distributed in conjunction with Pemetexed and Cisplatin in patients who have been previously treated. (mesotheliomaquestions.com)
  • Recent studies have shown that cisplatin noncompetitively inhibits an archetypal, membrane-bound mechanosensitive sodium-hydrogen ion transporter known as NHE-1. (wikipedia.org)
  • Cisplatin inhibits DNA synthesis and, therefore, cell proliferation, by causing DNA cross-linking and denaturation of the double helix. (medscape.com)
  • Cisplatin induced ROS was significantly decreased by detouring electrons to MFC, or increased by Genipin combined treatment. (medsci.org)
  • Renal mitochondrial Bax induction following cisplatin treatment was significantly decreased by treatment of mice with AR9273 and these antiapoptotic effects involved p38 mitogen-activated protein kinase signaling. (aspetjournals.org)
  • More than half of patients with testicular cancer treated with first-line cisplatin-based chemotherapy in a recent study developed hearing loss (HL) or tinnitus. (medscape.com)
  • Efficacy was evaluated in two multicenter open-label, randomized controlled trials in pediatric patients undergoing treatment with cisplatin-based chemotherapy for cancer: SIOPEL 6 (NCT00652132) and COG ACCL0431 (NCT00716976). (fda.gov)
  • SIOPEL 6 enrolled 114 patients with standard risk hepatoblastoma undergoing 6 cycles of perioperative cisplatin-based chemotherapy. (fda.gov)
  • Although this study was conducted in patients with testicular cancer, the authors point out that the general conclusions are likely applicable to patients with other types of adult-onset cancers that are commonly treated with cisplatin. (iu.edu)
  • They indicate that it will be important to follow patients given cisplatin-based chemotherapy long-term to better understand the extent to which the natural aging process may further add to hearing deficits, as it does in the general population. (iu.edu)
  • Our findings suggest that health care providers should, at a minimum, annually query patients who have received cisplatin-based chemotherapy about their hearing status, consulting with audiologists as indicated. (iu.edu)
  • The researchers also found high blood pressure was significantly related to hearing loss in these patients, even when cisplatin dose was taken into account. (iu.edu)
  • For patients treated with cisplatin-based regimens for other types of cancer, it might also influence a physician to offer an alternative to those patients found to be genetically susceptible to the ototoxic effects of cisplatin after carefully weighing the risks and benefits of alternative treatments. (iu.edu)
  • Patients were randomized (1:1) to capecitabine/cisplatin plus bevacizumab or capecitabine/cisplatin plus placebo. (knowcancer.com)
  • This group will be patients who would have been prescribed Pemetrexed and Cisplatin for regular treatment. (mesotheliomaquestions.com)
  • A pharmacokinetic analysis revealed the plasma concentration and renal accumulation of cisplatin to be higher in Mate1(-/-) mice than Mate1(+/+) mice 1h after a single intravenous administration of cisplatin (0.5mg/kg). (nih.gov)
  • Collectively, these in vivo and in vitro studies demonstrate a role for EETs in limiting cisplatin-induced renal apoptosis. (aspetjournals.org)
  • Inhibition of sEH represents a novel therapeutic strategy for protection against cisplatin-induced renal damage. (aspetjournals.org)
  • Cisplatin is administered intravenously as short-term infusion in normal saline for treatment of solid and haematological malignancies. (wikipedia.org)
  • Common neurological side effects of cisplatin include visual perception and hearing disorder, which can occur soon after treatment begins. (wikipedia.org)
  • However, because treatment involves cisplatin-based chemotherapy, these TC survivors are at risk for both short- and long-term adverse CBCT-related effects, including HL and tinnitus, with no preventive or protective measures available. (medscape.com)
  • Shorter the Genipin treatment before Cisplatin better promoted the Cisplatin induced ROS and subsequent cell death. (medsci.org)
  • Owing to the compensatory effects against Genipin, shorter Genipin treatment before Cisplatin was recommended in order to achieve better potentiation effect. (medsci.org)
  • This is for 14 study participants with previously untreated advanced, inoperable malignant mesothelioma for which Pemetrexed and Cisplatin is the regular treatment. (mesotheliomaquestions.com)
  • This review summarizes the action and resistance mechanism of cisplatin and describes the treatment of the major hepatobiliary cancers for which cisplatin is used as an anticancer agent , with a focus on HCC. (bvsalud.org)
  • KEMPINAS, W. G. Paternal treatment with cisplatin impairs reproduction of adult male offspring in rats. (bvsalud.org)
  • Moreover, in pig kidney proximal tubule cells, cisplatin-induced mitochondrial trafficking of Bax and cytochrome c , caspase-3 activation, and oxidative stress are significantly attenuated in the presence of epoxyeicosatrienoic acids (EETs). (aspetjournals.org)
  • Cisplatin is a chemotherapy medication used to treat a number of cancers. (wikipedia.org)
  • Researchers at the Massachusetts General Hospital Cancer Center (MGH) identified a subgroup of hard-to-treat breast cancers that may be sensitive to the drug cisplatin. (genengnews.com)
  • While triggering apoptosis through interfering with DNA replication remains the primary mechanism of cisplatin, this has not been found to contribute to neurological side effects. (wikipedia.org)
  • Similar mechanisms contributed to reduced apoptosis in Ephx2 −/− mice treated with cisplatin. (aspetjournals.org)
  • Comparative proteomic analysis demonstrated that several biological pathways related to apoptosis, transport, proteasome, and cellular stress were involved in cisplatin-resistance in hMT3 overexpressing UKF-NB-4 cells. (vut.cz)
  • Inhibition of UCP2-mediated proton leak with Genipin potentiated the cytotoxicity of Cisplatin. (medsci.org)
  • In experiments in vitro, the cellular uptake of cisplatin was stimulated by the expression of mouse MATE1 as well as organic cation transporters OCT1 and OCT2. (nih.gov)
  • Subsequently, for cisplatin -refractory cases due to drug resistance , a shift to systemic therapy with a different mechanism of action is expected to produce new antitumor effects. (bvsalud.org)
  • Cisplatin-based chemotherapy is a major regimen to treat neuroblastoma, but its clinical efficacy is limited by chemoresistance. (vut.cz)
  • IV infusion every 3 weeks with gemcitabine plus cisplatin up to 8 cycles followed by monotherapy every 4 weeks until disease progression or other discontinuation criteria. (astrazenecaclinicaltrials.com)
  • We investigated the impact of human metallothionein-3 (hMT3) up-regulation in neuroblastoma cells and the mechanisms underlying the cisplatin-resistance. (vut.cz)
  • Cisplatin (15mg/kg) was administered intraperitoneally to wild-type (Mate1(+/+)) and Mate1 knockout (Mate1(-/-)) mice. (nih.gov)
  • Three days after the administration of cisplatin, plasma creatinine and blood urea nitrogen (BUN) levels were increased in both Mate1(+/+) and Mate1(-/-) mice compared with vehicle-treated controls, and creatinine clearance was decreased. (nih.gov)
  • Moreover, a significant rise in creatinine and BUN levels was observed in cisplatin-treated Mate1(-/-) mice in comparison to Mate1(+/+) mice. (nih.gov)
  • The findings underscore the need for routine assessment for hearing loss and tinnitus during follow-up of cisplatin-treated survivors, the authors of the study emphasize. (medscape.com)
  • The biggest thing that we think when we hear cisplatin as oncologists are two things: kidney function, and the need to have a good kidney function, as well as the risk of hurting that kidney function depending on the dosing. (doctorpedia.com)
  • 2. The biggest thing that we think when we hear cisplatin as oncologists are two things: kidney function and dropping your bone marrow counts, specifically neutrophils, which are a part of your white blood cells that fight infection. (doctorpedia.com)
  • The researchers found that every 100 mg/m 2 increase in cumulative dose of cisplatin resulted in a 3.2 dB impairment in hearing. (iu.edu)
  • In 1974, Dr. Einhorn tested cisplatin with two additional drugs that were effective in killing testis cancer cells. (iu.edu)
  • Cisplatin is a platinum chemotherapy, which you've probably already heard the name of if you've been watching the videos on different cancer types. (doctorpedia.com)
  • The primary outcome was hearing loss according to American Speech-Language-Hearing Association (ASHA) criteria, assessed at baseline and 4-weeks after the final course of cisplatin. (fda.gov)
  • Platinum-based cisplatin is one of the most commonly used drugs in medical oncology that also has toxic effects on the inner ear. (iu.edu)
  • Cisplatin can increase levels of sphingosine-1-phosphate in the central nervous system, contributing to the development of post-chemotherapy cognitive impairment. (wikipedia.org)
  • This is a powerful anti-oxidant which has been demonstrated to protect the inner ear from damage caused by cisplatin. (lungevity.org)
  • An ultimate goal is to use the genetic results to develop effective agents that will protect the ear during the administration of cisplatin. (iu.edu)
  • In interfering with cell reproduction, some antineoplastic agents are specific to certain phases of the cell cycle, whereas others (eg, alkylating agents, anthracyclines, cisplatin) are not phase specific. (medscape.com)
  • Cisplatin was found to break up the binding of p63 to p73 and reactivate the cell-death process. (genengnews.com)
  • Genipin inhibited the UCP2 mediated anti-oxidative proton leak significantly promoted the Cisplatin induced ROS and subsequent cell death, which was similar to that of UCP2-siRNA. (medsci.org)
  • We report, for the first time, cisplatin-sensitive human UKF-NB-4 cells remodelled into cisplatin-resistant cells via high and constitutive hMT3 expression in an in vivo model using chick chorioallantoic membrane assay. (vut.cz)
  • Elevated expression of some ABC transporters may also determine the efficacy of cisplatin-based chemotherapy. (scilifelab.se)

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