Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)
Antimetabolites that are useful in cancer chemotherapy.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.
An inhibitor of nucleotide metabolism.
Any surgical procedure for treatment of glaucoma by means of puncture or reshaping of the trabecular meshwork. It includes goniotomy, trabeculectomy, and laser perforation.
Inosine 5'-Monophosphate. A purine nucleotide which has hypoxanthine as the base and one phosphate group esterified to the sugar moiety.
The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.
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.
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.
An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Inhibitors of the enzyme, dihydrofolate reductase (TETRAHYDROFOLATE DEHYDROGENASE), which converts dihydrofolate (FH2) to tetrahydrofolate (FH4). They are frequently used in cancer chemotherapy. (From AMA, Drug Evaluations Annual, 1994, p2033)
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
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.
The action of a drug in promoting or enhancing the effectiveness of another drug.
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 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.
Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
Established cell cultures that have the potential to propagate indefinitely.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
The rate dynamics in chemical or physical systems.
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.
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.
Phospholipids which have an alcohol moiety in ethereal linkage with a saturated or unsaturated aliphatic alcohol. They are usually derivatives of phosphoglycerols or phosphatidates. The other two alcohol groups of the glycerol backbone are usually in ester linkage. These compounds are widely distributed in animal tissues.
A cell line derived from cultured tumor cells.
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.
Pyrido-CARBAZOLES originally discovered in the bark of OCHROSIA ELLIPTICA. They inhibit DNA and RNA synthesis and have immunosuppressive properties.
A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72.
A group of 20-member macrolactones in which there are three remotely substituted pyran rings that are linked by a methylene bridge and an E-disubstituted alkene, and have geminal dimethyls at C8 and C18 carbons. Some interact with PROTEIN KINASE C.
Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.
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)
Tumors or cancer of the SKIN.
Plastic surgery performed, usually by excision of skin, for the elimination of wrinkles from the skin.
White or pink lesions on the arms, hands, face, or scalp that arise from sun-induced DNA DAMAGE to KERATINOCYTES in exposed areas. They are considered precursor lesions to superficial SQUAMOUS CELL CARCINOMA.
A genus of DNA viruses in the family PAPILLOMAVIRIDAE, causing cutaneous lesions in humans. Infections exist in latent form in the general population and are activated under conditions of IMMUNOSUPPRESSION.
A benign, non-neoplastic, usually self-limiting epithelial lesion closely resembling squamous cell carcinoma clinically and histopathologically. It occurs in solitary, multiple, and eruptive forms. The solitary and multiple forms occur on sunlight exposed areas and are identical histologically; they affect primarily white males. The eruptive form usually involves both sexes and appears as a generalized papular eruption.
Curved rows of HAIR located on the upper edges of the eye sockets.
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
A nucleoside antimetabolite antiviral agent that blocks nucleic acid synthesis and is used against both RNA and DNA viruses.
A genus of FLAVIVIRIDAE causing parenterally-transmitted HEPATITIS C which is associated with transfusions and drug abuse. Hepatitis C virus is the type species.
INFLAMMATION of the LIVER in humans that is caused by HEPATITIS C VIRUS lasting six months or more. Chronic hepatitis C can lead to LIVER CIRRHOSIS.
One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells. In addition to antiviral activity, it activates NATURAL KILLER CELLS and B-LYMPHOCYTES, and down-regulates VASCULAR ENDOTHELIAL GROWTH FACTOR expression through PI-3 KINASE and MAPK KINASES signaling pathways.
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.

Is early post-operative treatment with 5-fluorouracil possible without affecting anastomotic strength in the intestine? (1/3345)

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

Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (2/3345)

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

Dihydropyrimidine dehydrogenase deficiency and fluorouracil-related toxicity. (3/3345)

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

[3H]gemcitabine uptake by nucleoside transporters in a human head and neck squamous carcinoma cell line. (4/3345)

Cellular uptake of many chemotherapeutic nucleoside analogs is dependent on the activity of a family of nucleoside transport proteins located in the cell plasma membrane. In the present study, we examined the role of these transporters in the accumulation of gemcitabine by a human head and neck squamous carcinoma cell line. The uptake of [3H]gemcitibine was compared with that of [3H]uridine and [3H]formycin B in the parent cell line (HN-5a) and in a gemcitabine-resistant variant (GEM-8e). The HN-5a and GEM-8e cells were similar in their transport characteristics and expressed predominantly the es (equilibrative, inhibitor-sensitive) transporter subtype; less than 10% of the influx of [3H]formycin B or [3H]uridine was mediated by the ei (equilibrative inhibitor-resistant) system, and there was no evidence for Na+-dependent nucleoside transporters. [3H]Gemcitabine (10 microM) entered these cells via both the es and ei transporters with an initial rate of uptake similar to that seen with the use of [3H]formycin B or [3H]uridine. In addition, ATP-replete cells accumulated significantly less [3H]gemcitabine than did ATP-depleted cells, which is indicative of an active efflux mechanism for gemcitabine. These results show that gemcitabine is a substrate for both the es and ei nucleoside transporters of HN-5a and GEM-8e cells and that gemcitabine resistance of the GEM-8e cells cannot be attributed to changes in transporter activity. Further studies to define the characteristics of the putative efflux mechanism are clearly warranted because this system has the potential to significantly affect the clinical efficacy of gemcitabine.  (+info)

Modulation of the cytotoxicity of 3'-azido-3'-deoxythymidine and methotrexate after transduction of folate receptor cDNA into human cervical carcinoma: identification of a correlation between folate receptor expression and thymidine kinase activity. (5/3345)

Cervical carcinoma is an AIDS-defining illness. The expression of folate receptors (FRs) in cervical carcinoma (HeLa-IU1) cells was modulated by stable transduction of FR cDNA encapsidated in recombinant adeno-associated virus-2 in the sense and antisense orientation (sense and antisense cells, respectively). Although sense cells proliferated slower than antisense or untransduced cells in vivo and in vitro in 2% (but not 10%) FCS, [methyl-3H]thymidine incorporation into DNA was significantly increased in sense cells in 10% serum; therefore, the basis for this discrepancy was investigated. The activity of thymidine kinase (TK) was subsequently directly correlated with the extent of FR expression in single cell-derived clones of transduced cells. This elevated TK activity was not a result of recruitment of the salvage pathway based on the presence of adequate dTTP pools, normal thymidylate synthase (TS) activity, persistence of increased thymidine incorporation despite the exogenous provision of excess 5,10-methylene-tetrahydrofolate, and documentation of adequate folates in sense cells. The increase in TK activity conferred significant biological properties to sense cells (but not antisense or untransduced cells) as demonstrated by augmented phosphorylation of 3'-azido-3'-deoxythymidine (AZT) and concomitantly greater sensitivity to the cytotoxic effects of AZT. Conversely, sense cells were highly resistant to methotrexate, but this was reversed by the addition of AZT. The direct correlation of FR expression and TK activity indicates a previously unrecognized consequence of FR overexpression.  (+info)

Role of folylpolyglutamate synthetase and folylpolyglutamate hydrolase in methotrexate accumulation and polyglutamylation in childhood leukemia. (6/3345)

Inefficient polyglutamylation is a mechanism of resistance to methotrexate (MTX) in childhood T-lineage acute lymphoblastic leukemia (T-ALL) and in acute myeloid leukemia (AML) in comparison with childhood c/preB-ALL. We analyzed the profile of MTX polyglutamylation in childhood c/preB-ALL, T-ALL, and AML (n = 45, 15, and 14, respectively), the activity of the MTX-polyglutamate synthesizing enzyme folylpolyglutamate synthetase (FPGS) (n = 39, 11, and 19, respectively) and of the MTX-polyglutamate breakdown enzyme folylpolyglutamate hydrolase (FPGH) (n = 98, 25, and 34, respectively). MTX-Glu4-6 accumulation after 24 hours exposure to 1 micromol/L [3H]-MTX in vitro was lower in T-ALL (threefold) and AML (fourfold) compared with c/preB-ALL (P +info)

Phase I study of eniluracil, a dihydropyrimidine dehydrogenase inactivator, and oral 5-fluorouracil with radiation therapy in patients with recurrent or advanced head and neck cancer. (7/3345)

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

Colorectal liver metastasis thymidylate synthase staining correlates with response to hepatic arterial floxuridine. (8/3345)

We assessed whether intensity of colorectal liver metastasis staining with the thymidylate synthase (TS) antibody TS106 predicted response to hepatic arterial infusion (HAI) of floxuridine chemotherapy. Liver metastasis biopsies were taken during laparotomy for hepatic arterial cannulation and stained using the TS106 monoclonal antibody. Staining intensity was designated at histological examination by two independent assessors as either "high" or "low." Patients were treated by HAI, and liver metastasis response was assessed by comparison of computed tomography scan tumor volume before and after 4 months of treatment. A significant correlation (Fisher's exact test, P = 0.01) was noted between partial response to HAI and TS106 staining intensity in patients with colorectal liver metastases. Seventy-five percent of patients with evidence of a partial response had low TS staining compared with 29% of nonresponders. There was a significant difference (Fisher's exact test, P = 0.01) in the proportion of low (9 of 16) compared with high (3 of 20) TS staining tumors in which a partial response occurred. There was no significant difference (logrank test, P = 0.4) in survival from hepatic cannulation and HAI treatment of high (median, 322 days; interquartile range, 236-411) compared with low (median, 335 days; interquartile range, 301-547) TS staining patients. This study demonstrates an inverse correlation between TS immunohistochemical staining intensity in colorectal liver metastases and response to HAI. The results suggest that a prospective assessment of TS staining intensity in colorectal liver metastases would be useful to determine whether this method can be used to define patients who will benefit from HAI chemotherapy.  (+info)

5FU caused an increased S-phase arrest and a more sustained activation of the DNA damage repair pathway in the absence of p53 or p21. PD-L1 expression increased upon 5FU treatment which was more pronounced in p53-/- or p21-/- cells. By using FUdR, a metabolite of 5FU that acts through inhibition of thymidylate synthase (TS), we were able to reproduce the effect of 5FU on PD-L1 expression. Thymidine depletion can lead to stalled replication fork that in the absence of p53/p21 axis, cause elongated activation of ATR pathway. Inhibiting ATR/CHK1 by small molecule can reduce PD-L1 upregulation. Using siRNA we identified STAT3 as a key regulator of the 5FU-mediated PD-L1 upregulation.. ...
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Gemcitabine (Gemzar) chemotherapy side effects, how its given, how it works, precautions and self care tips for treatment of multiple cancers
Antimetabolites A new perspective ScienceDirect - Novel Developments in the Use of Antimetabolites. Novel Developments in the Use of Antimetabolites, Nucleosides, least partially, explain the efficacy of TFT
TH-302: 340 mg/m2 of TH-302 be administered IV over 30 minutes on Days 1, 8 and 15 of every 28-day cycle.. Gemcitabine: 1,000 mg/m2 administered IV over 30 minutes on Days 1, 8 and 15 of a 28-day cycle. Gemzar (Gemcitabine): 1,000 mg/m2 administered IV over 30 minutes on Days 1, 8 and 15 of a 28-day cycle.. TH-302: 340 mg/m2 of TH-302 will be administered IV over 30 minutes on Days 1, 8 and 15 of every 28-day cycle.. ...
Gemcitabine PCH Teva 2000mg/vial is a medicine available in a number of countries worldwide. A list of US medications equivalent to Gemcitabine PCH Teva 2000mg/vial is available on the Drugs.com website.
Gemcitabine Mylan is a medicine available in a number of countries worldwide. A list of US medications equivalent to Gemcitabine Mylan is available on the Drugs.com website.
TY - JOUR. T1 - Klinische en preklinische farmacologie van de combinatie cisplatine en gemcitabine. AU - Crul, M.. AU - Van Zandwijk, N.. AU - Beijnen, J. H.. AU - Schellens, J. H M. PY - 2005/3/18. Y1 - 2005/3/18. UR - http://www.scopus.com/inward/record.url?scp=16344393382&partnerID=8YFLogxK. M3 - Article. AN - SCOPUS:16344393382. VL - 140. SP - 369. EP - 371. JO - Pharmaceutisch Weekblad. JF - Pharmaceutisch Weekblad. SN - 0031-6911. IS - 11. ER - ...
Venetoclax + Decitabine combination chemo for AML. Learn important drug side-effects information by listening, watching videos, & reading | ChemoExperts
Our results demonstrate that inhibition of the PI3K-PKB/Akt cell survival pathway enhances gemcitabine-induced apoptosis in PK1 and PK8 human pancreatic cancer cells. Gemcitabine at 20 μm caused minimal apoptosis in these cells, indicative of their drug-resistant nature. However, flow cytometric analysis showed that gemcitabine is able to induce cell cycle perturbations with a decrease in the G2-M-phase peak and a build-up of cells in the G1/early S-phase, consistent with its mechanism of action as an inhibitor of DNA elongation. Gemcitabine treatment was also associated with increased reactive oxygen generation, indicative of oxidative stress. It is therefore apparent that gemcitabine accumulates at a sufficient concentration in the cells to inhibit its nuclear target and that drug resistance is not simply due to failure of drug uptake or metabolism. These findings suggest that the suppression of apoptosis after gemcitabine exposure may be a relevant resistance mechanism in these cell ...
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The current study highlights a novel glycosylation-dependent mechanism that confers gemcitabine resistance by preventing DNA damage. Experimental procedures Cell culture MiaPaCa-2 and BxPC-3 cell lines were obtained from ATCC. increased gemcitabine sensitivity ratio, an indication of gemcitabine toxicity. Gemcitabine-resistant MiaPaCa-2 cells display higher ST6Gal-I levels than treatment-na?ve WEHI-9625 cells along with a reduced gemcitabine sensitivity ratio, suggesting that WEHI-9625 chronic chemotherapy selects for clonal variants with more abundant ST6Gal-I. Finally, we examined Suit2 PDAC cells and Suit2 derivatives with enhanced metastatic potential. Intriguingly, three metastatic and chemoresistant subclones, S2-CP9, S2-LM7AA, and S2-013, exhibit up-regulated ST6Gal-I relative to parental Suit2 cells. ST6Gal-I KD in S2-013 cells increases gemcitabine-mediated DNA damage, indicating that suppressing ST6Gal-I activity sensitizes inherently resistant cells to gemcitabine. Together, these ...
This study will investigate the efficacy and tolerability of axitinib in patients with biliary tract cancer refractory to gemcitabine-based chemotherapy. The
See BOXED WARNINGS) There are clear dose-dependent toxic effects seen with fludarabine phosphate, USP. Dose levels approximately 4 times greater (96 mg/m2/day for 5 to 7 days) than that recommended for CLL (25 mg/m2/day for 5 days) were associated with a syndrome characterized by delayed blindness, coma and death. Symptoms appeared from 21 to 60 days following the last dose. Thirteen of 36 patients (36%) who received fludarabine phosphate, USP at high doses (96 mg/m2/day for 5 to 7 days) developed this severe neurotoxicity. Similar severe central nervous system toxicity, including coma, seizures, agitation and confusion, has been reported in patients treated at doses in the range of the dose recommended for chronic lymphocytic leukemia.. The effect of chronic administration of fludarabine phosphate, USP on the central nervous system is unknown; however, patients have received the recommended dose for up to 15 courses of therapy.. Severe bone marrow suppression, notably anemia, thrombocytopenia ...
Safety and efficacy of azacitidine in myelodysplastic syndromes Carlos E Vigil, Taida Martin-Santos, Guillermo Garcia-ManeroDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USAPurpose: The clinical efficacy, different dosages, treatment schedules, and safety of azacitidine are reviewed.Summary: Azacitidine is the first drug FDA-approved for the treatment of myelodysplastic syndromes that has demonstrated improvements in overall survival and delaying time to progression to acute myelogenous leukemia. The recommended dosage of azacitidine is 75 mg/m2 daily for 7 days, with different treatment schedules validated. It appears to be well tolerated, with the most common adverse effects being myelosuppression. Several other off-label recommendations were also analyzed.Conclusion: Azacitidine is the first DNA hypomethylating agent approved by FDA for the treatment of myelodysplastic syndromes with demonstrated efficacy.Keywords: Azacitidine, MDS, hypomethylating agents
PURPOSE: A randomized three-arm phase II study was undertaken to evaluate the optimum administration schedule of pemetrexed and gemcitabine in chemotherapy-naïve patients with non-small-cell lung cancer. PATIENTS AND METHODS: Patients were randomly assigned to three schedules of pemetrexed 500 mg/m2 plus gemcitabine 1,250 mg/m2, separated by a 90-minute interval, on a 21-day cycle as follows: schedule A, pemetrexed followed by gemcitabine on day 1 and gemcitabine on day 8; schedule B, gemcitabine followed by pemetrexed on day 1 and gemcitabine on day 8; and schedule C, gemcitabine on day 1 and pemetrexed followed by gemcitabine on day 8. RESULTS: One hundred fifty-two eligible patients (schedule A, n = 59; schedule B, n = 31, and schedule C, n = 62) received a median of five (schedule A), two (schedule B), and four (schedule C) treatment cycles. Overall, 66% of patients experienced grade 3 or 4 neutropenia. Common grade 3 and 4 nonhematologic toxicities were dyspnea (11%), fatigue (16%), and
GSK1120212 is a potent and highly selective inhibitor of MEK phosphorylation and kinase activity and has demonstrated potent anti-proliferative activity against human pancreatic cancer cell lines. This study is a Phase II, randomized placebo-controlled trial of the MEK inhibitor GSK1120212 plus gemcitabine vs. placebo plus gemcitabine in subjects with metastatic pancreatic cancer. Eligible subjects will receive intravenous gemcitabine with oral GSK1120212 or placebo. Therapy will continue until treatment discontinuation criteria are met. The primary objective will be to compare the overall survival of subjects in the GSK1120212 plus gemcitabine arm vs. subjects in the placebo plus gemcitabine arm. Secondary objectives include comparison of progression free survival, overall response rate, and duration of response between the two arms. Exploratory research objectives include the evaluation of population pharmacokinetics as well as blood and tissue based biomarkers. Safety will also be monitored ...
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The proportion of attributable deaths varied according to a patients MDS risk status. The proportion of deaths attributable to MDS increased from 31.5% among low-risk patients to 48.8% in the intermediate-risk category and 74.1% of patients with high-risk MDS. CAD/stroke as the cause of death decreased from a high of 26.3% of patients with low-risk disease to 20.6% of patients with intermediate risk-MDS to 9.3% of patients with high-risk MDS.. Treatment of Myelodysplastic Syndrome. Lower-risk myelodysplastic syndrome patients are treated initially for the specific complications of the disease, such as anemia and low blood counts. If more aggressive therapy is needed, strategies that are considered standard of care include chemotherapy using hypomethylating agents (5-azacitidine and decitabine) and lenalidomide.. Higher-risk myelodysplastic syndrome patients usually need more aggressive therapy, but much depends on the age and condition of the patient. Younger patients with high-risk disease are ...
Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic stem cell disorders that have a substantial impact on patients quality of life, in addition to causing significant morbidity and mortality. The hypomethylating agents (HMAs) azacitidine and decitabine are approved for use in the United States and in Europe for the treatment of MDS or acute myeloid leukemia (AML) and, in the case of azacitidine, prolong survival in higher-risk patients.
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E. Patel, I. Bjarnason, P. Smethurst, T.J. Peters; Intestinal Permeability and Transglutaminase Alterations in Methotrexate-Induced Enteropathy in the Rat. Clin Sci (Lond) 1 December 1984; 67 (s9): 65P. doi: https://doi.org/10.1042/cs067065Pa. Download citation file:. ...
E. Patel, I. Bjarnason, P. Smethurst, T.J. Peters; Intestinal Permeability and Transglutaminase Alterations in Methotrexate-Induced Enteropathy in the Rat. Clin Sci (Lond) 1 January 1984; 67 (s9): 65P. doi: https://doi.org/10.1042/cs067065Pa. Download citation file:. ...
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Data from the BAYPAN study presented at the American College of Clinical Oncologys 2011 Annual Meeting did not support the addition of sorafenib to gemcitabine therapy in the treatment of advanced pancreatic cancer (APC), in contrast to an earlier Phase I study that demonstrated that this combination was well tolerated and had activity in APC patients.
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Cellular Bcl-2 content was directly correlated with the cytotoxicity of gemcitabine in pancreatic carcinoma. Therefore, routine immunohistochemical analyses may be useful in predicting gemcitabine efficacy, and patients who would likely not benefit could be spared gemcitabine administration. Further …
BackgroundSmall series and retrospective studies have suggested that treatment with gemcitabine may be associated with pulmonary toxicity. However, a prospective evaluation of cancer patients treated with gemcitabine-based chemotherapy without neoplastic involvement of the thorax and without adminis
We describe a colorimetric and fluorescent probe 3a to detect cellular peroxynitrite with high selectivity and sensitivity. 3a was successfully applied in the bioimaging of exogenous and endogenous peroxynitrite in living cells. The up-regulation of peroxynitrite in cancer cells and normal cells during 5-fluorourac
Azacitidine For with NDC 69097-805 is a a human prescription drug product labeled by Cipla Usa Inc.. The generic name of Azacitidine For is azacitidine.
To be sure this medication is not causing harmful effects, your blood may need to be tested on a regular basis. Your kidney and liver function may also need to be tested. Do not miss any follow-up visits. You must remain under the care of a doctor while you are taking Xeloda.. DOSAGE Use xeloda as directed by your doctor.. If you missed a dose take it as soon as you remember. If it is almost time for your next dose, wait until then to take the medicine and skip the missed dose. Do not take extra medicine to make up the missed dose.. STORAGE Store Xeloda at room temperature away from moisture and heat. Keep it tightly closed when not in use.. MORE INFO: Active Ingredient: capecitabine ...
To be sure this medication is not causing harmful effects, your blood may need to be tested on a regular basis. Your kidney and liver function may also need to be tested. Do not miss any follow-up visits. You must remain under the care of a doctor while you are taking Xeloda.. DOSAGE Use xeloda as directed by your doctor.. If you missed a dose take it as soon as you remember. If it is almost time for your next dose, wait until then to take the medicine and skip the missed dose. Do not take extra medicine to make up the missed dose.. STORAGE Store Xeloda at room temperature away from moisture and heat. Keep it tightly closed when not in use.. MORE INFO: Active Ingredient: capecitabine ...
This observational study will evaluate the safety and efficacy of Avastin (bevacizumab) in combination with 5-Fluorouracil based chemotherapy as first-l
In this report, we highlight the remarkable clinical outcome of a patient with advanced, gemcitabine-resistant, pancreatic cancer who was treated with DNA damaging agents based on the observation of significant activity of this class of drugs against a personalized xenograft generated from the patients surgically resected tumor. Contrary to the expected median survival of 3 months for pancreatic cancer patients who progress on gemcitabine, this individual is virtually symptom-free for 3 years after progression to the first-line chemotherapy. Nearly complete sequencing of all of the coding genes in this patients cancer revealed biallelic inactivation of the PALB2 gene, a DNA repair gene, loss of which mechanistically explains the observed sensitivity of the patients cancer to DNA damaging agents (8). Of note, in a conventional protocol-based regimen, MMC would not have been used in a second-line setting for gemcitabine-refractory pancreatic cancer. Thus, this study highlights the ...
Gemcitabine for Injection by Accord Healthcare Inc.: Gemcitabine belongs to the group of cancer-fighting medications known as antineoplastics, and specifically to the group of antineoplastics known as antimetabolites. Gemcitabine fights cancer by preventing the growth of cancer cells, which eventually results in their destruction. It is used to treat certain types of lung cancer, bladder cancer, breast cancer, and cancer of the pancreas.
ORLANDO -- The addition of Avastin (bevacizumab) to Gemzar (gemcitabine) did not improve survival of advanced pancreatic cancer in a randomized trial, researchers here reported.
Author Summary There are few treatment options for advanced pancreatic cancer. The chemotherapeutic drug Gemcitabine is routinely used, yet 95% of patients die within 5 years of diagnosis. Surprisingly, Gemcitabine experiments with pancreatic tumor cells in the laboratory dish show that most cells will be killed by this drug. It is obvious that the dish does not adequately represent the more complex condition in real tumors. We apply mathematical modeling to simulate tumor growth to try to understand how results from the laboratory could be used to predict the treatment response in real tumors. The model simulates flow of substances such as oxygen within tumors and how this flow affects the response of cells to drug treatment. We set the inputs for the model with values obtained from the laboratory experiments. The model predicts the treatment to mostly fail in real tumors regardless of the characteristics of individual cells. We confirm these results by treating real tumors in mice, showing that our
This study is designed to establish the safety and efficacy of a combination of Erbitux (cetuximab)/Gemzar (gemcitabine)/radiation in patients with panc
Synonyms for 5-fluorouracil in Free Thesaurus. Antonyms for 5-fluorouracil. 1 word related to fluorouracil: antimetabolite. What are synonyms for 5-fluorouracil?
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Contact: Rebecca Wong (415) Questions and Answers Regarding Vidaza (azacitidine for injectable suspension) and Demethylating Agents The recent approval of a third drug for the treatment of MDS
By 2018, five new drugs will have been launched for the treatment of myelodysplastic syndromes (MDS), three of which are expected to offer much-needed second-line therapeutic options in the hypomethylating agent (HMA)-refractory higher-risk MDS population, according to a new study. - News - PharmaTimes
ABSTRACT 5-fluorouracil is an antineoplastic agent as an antimetabolite that used for treating breast, colorectal and gastric cancers. Several compound as a derivative 5 fluorouracil has been synthesis for increase its ...
Antimetabolite A substance bearing a close structural resemblance to one required for normal physiological functioning, and exerting its effect by interfering with the utilization of the essential metabolite. It competes with, replaces, or antagonizes a particular metabolite; for example, ethionine is an antimetabolite of methionine.methotrexatefolic acidcancerCancercancercancer
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ATLANTA -- Oral azacitidine (Vidaza) given for up to 21 days per 4-week cycle for myelodysplastic syndrome appeared safe and effective in patients with lower-risk disease, a researcher said here.
... an antimetabolite; (Ox)aliplatin - a platinum-based alkylating antineoplastic agent. GEMOX-R regimen is a highly effective ...
... an antimetabolite; (C)yclophosphamide - an alkylating antineoplastic agent from the oxazafosforine group; (M)itoxantrone - a ...
Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a ... which are divided into broad categories such as alkylating agents and antimetabolites. Traditional chemotherapeutic agents act ...
... a platinum-based antineoplastic agent, which inhibits DNA repair and/or DNA synthesis; IRI - irinotecan (Camptosar), a ... a pyrimidine analog and antimetabolite which incorporates into the DNA molecule and stops DNA synthesis; OX - oxaliplatin ( ...
... a platinum-based antineoplastic agent, which inhibits DNA repair and/or DNA synthesis. The regimen emerged in 2010 as a new ... a pyrimidine analog and antimetabolite which incorporates into the DNA molecule and stops DNA synthesis; IRIN - irinotecan ( ...
Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a similar structure to the ... Antineoplastic drugs may also increase the risk of learning disabilities among children of health care workers who are exposed ... Unlike alkylating agents, anti-metabolites are cell cycle dependent. This means that they only work during a specific part of ... In the 1970s, antineoplastic (chemotherapy) drugs were identified as hazardous, and the American Society of Health-System ...
Antimetabolites[edit]. Deoxycytidine (left) and two anti-metabolite drugs (center and right); gemcitabine and decitabine. The ... Main article: List of antineoplastic agents. There is an extensive list of antineoplastic agents. Several classification ... Main article: Antimetabolite. Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a ... Subtypes of the anti-metabolites are the anti-folates, fluoropyrimidines, deoxynucleoside analogues and thiopurines.[32][37] ...
... an antimetabolite; (P)latinol (cisplatin), a platinum-based antineoplastic, also an alkylating antineoplastic agent. Effective ...
... antimetabolites, antineoplastic MeSH D27.505.954.248.147 - antimitotic agents MeSH D27.505.954.248.150 - antineoplastic agents ... antimetabolites MeSH D27.888.569.042.030 - antimetabolites, antineoplastic MeSH D27.888.569.071 - antispermatogenic agents MeSH ... antimetabolites, antineoplastic MeSH D27.505.519.217 - antioxidants MeSH D27.505.519.217.500 - free radical scavengers MeSH ... antineoplastic agents MeSH D27.505.954.248.025 - angiogenesis inhibitors MeSH D27.505.954.248.106 - antibiotics, antineoplastic ...
... antimetabolite - antimicrotubule agent - antimitotic agent - antineoplastic - antineoplastic antibiotic - antioxidant - ...
Antineoplastic+Antimetabolites at the US National Library of Medicine Medical Subject Headings (MeSH) "How Chemotherapy Drugs ... An antimetabolite is a chemical that inhibits the use of a metabolite, which is another chemical that is part of normal ... Anti-metabolites also affect RNA synthesis. However, because thymidine is used in DNA but not in RNA (where uracil is used ... Antimetabolites can be used in cancer treatment, as they interfere with DNA production and therefore cell division and tumor ...
In the past, antimetabolites (e.g., cytarabine, hydroxyurea), alkylating agents, interferon alfa 2b, and steroids were used as ... Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes ...
Antineoplastic+Antimetabolites at the US National Library of Medicine Medical Subject Headings (MeSH) ... An antimetabolite is a chemical that inhibits the use of a metabolite, which is another chemical that is part of normal ... Antimetabolites can be used in cancer treatment,[3] as they interfere with DNA production and therefore cell division and tumor ... Anti-metabolites masquerade as a purine (azathioprine, mercaptopurine) or a pyrimidine, chemicals that become the building- ...
Anticancer agents (Antimetabolites, Alkylating, Spindle poisons, Antineoplastic, Topoisomerase inhibitors). Immune disease (L03 ...
G-CSF is still included, even though the "G" is taken out of the acronym.) Amsacrine is an alkylating antineoplastic agent that ... an antimetabolite that has been proven to be the most active toward AML among various cytotoxic drugs in single-drug trials; ... an antimetabolite that, while not active toward AML, increases formation of an active cytarabine metabolite, ara-CTP, in AML ...
Timmis, G.M.; Williams, Donald Charles (1967). "Chemotherapy of Cancer: the Antimetabolite Approach: The Antimetabolite ... It shows antineoplastic activity and has been used in the treatment of acute leukemia. The compound closely resembles guanine ...
Anticancer agents (Antimetabolites, Alkylating, Spindle poisons, Antineoplastic, Topoisomerase inhibitors). Immune disease (L03 ...
... is in the antimetabolite family of medications. It is a purine analogue of guanine and works by disrupting DNA and ... The second pathway is the methylation of thioguanine to 2-amino-6-methylthiopurine, which is minimally effective as an anti-neoplastic ... One route is through the deamination by the enzyme guanine deaminase to 6-thioxanthine, which has minimal anti-neoplastic ... as a result it is immunosuppressive at lower doses and anti-leukemic/anti-neoplastic at higher doses. Thioguanine is ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Flucytosine or 5-fluorocytosine - an antimetabolite pyrimidine analog [12]. *Griseofulvin - binds to polymerized microtubules ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites[edit]. Antimetabolites interfere with the synthesis of nucleic acids. These include: *folic acid analogues, ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. immune disease. (L03-L04). * ...
Antimetabolites. *Alkylating. *Spindle poisons. *Antineoplastic. *Topoisomerase inhibitors. Immune disease. (L03-L04). * ...
... have shown superior antiproliferative activity to rapalogs and in vivo models have confirmed these potent antineoplastic ... Antimetabolites. *purine synthesis inhibitors *Azathioprine. *Mycophenolic acid. *pyrimidine synthesis inhibitors *Leflunomide ...
Intracellular chemotherapeutic agents / antineoplastic agents (L01). SPs/MIs. (M phase). Block microtubule assembly. *Vinca ... antimetabolites. (S phase). Folic acid. *Dihydrofolate reductase inhibitor (Aminopterin. *Methotrexate#. *Pemetrexed. * ...
This antineoplastic or immunomodulatory drug article is a stub. You can help Wikipedia by expanding it.. *v ... antimetabolites. (S phase). Folic acid. *Dihydrofolate reductase inhibitor (Aminopterin. *Methotrexate#. *Pemetrexed. * ...
This antineoplastic or immunomodulatory drug article is a stub. You can help Wikipedia by expanding it.. *v ... Antimetabolites. *purine synthesis inhibitors *Azathioprine. *Mycophenolic acid. *pyrimidine synthesis inhibitors *Leflunomide ...
Chemotherapy is the treatment of cancer with one or more cytotoxic anti-neoplastic drugs (chemotherapeutic agents) as part of a ... which are divided into broad categories such as alkylating agents and antimetabolites.[144] Traditional chemotherapeutic agents ...
Antimetabolites. *purine synthesis inhibitors *Azathioprine. *Mycophenolic acid. *pyrimidine synthesis inhibitors *Leflunomide ... Intracellular chemotherapeutic agents / antineoplastic agents (L01). SPs/MIs. (M phase). Block microtubule assembly. *Vinca ...
Both in vitro and in vivo analysis show the anti-neoplastic activity of docetaxel to be effective against a wide range of known ... antimetabolites. (S phase). Folic acid. *Dihydrofolate reductase inhibitor (Aminopterin. *Methotrexate#. *Pemetrexed. * ... cancer cells, cooperate with other anti-neoplastic agents activity, and have greater cytotoxicity than paclitaxel, possibly due ...
Antifolates, such as pralatrexate, are part of a group of compounds known as antimetabolites with structural similarity to ... Intracellular chemotherapeutic agents / antineoplastic agents (L01). SPs/MIs. (M phase). Block microtubule assembly. *Vinca ... the antimetabolites are most effective against actively dividing cells and are largely cell-cycle phase specific.[5] ... naturally occurring molecules involved in DNA synthesis.[5] Cancer cells mistake antimetabolites for normal metabolites[5] ...
Another amino acid-like drug is the antineoplastic agent melphalan. Tumor cells spend less time in resting phases than normal ... antimetabolites. (S phase). Folic acid. *Dihydrofolate reductase inhibitor (Aminopterin. *Methotrexate#. *Pemetrexed. * ...
Pemetrexed Pemetrexed functions as an antimetabolite. Pemetrexed inhibits thymidylate synthase, dihydrofolate reductase and ... and approved pembrolizumab in combination with pemetrexed and platinum-based antineoplastic (carboplatin or cisplatin) as first ...
What is Antimetabolites, antineoplastic? Meaning of Antimetabolites, antineoplastic medical term. What does Antimetabolites, ... antineoplastic in the Medical Dictionary? Antimetabolites, antineoplastic explanation free. ... redirected from Antimetabolites, antineoplastic). Also found in: Dictionary, Thesaurus, Encyclopedia. antimetabolite. [an″te-, ... Antimetabolites, antineoplastic , definition of Antimetabolites, antineoplastic by Medical dictionary https://medical- ...
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Antimetabolite; DMARDs, ImmunomodulatorsAntimetabolite antineoplastic agents interfere with cell functions by competing for its ... Immunosuppressants; Antineoplastics, Antimetabolite; DMARDs, Immunomodulators. Antimetabolite antineoplastic agents interfere ... encoded search term (Which medications in the drug class Immunosuppressants; Antineoplastics%2C Antimetabolite; DMARDs%2C ... Which medications in the drug class Immunosuppressants; Antineoplastics, Antimetabolite; DMARDs, Immunomodulators are used in ...
Antineoplastics, Antimetabolite. Class Summary. Antimetabolite therapy may be used as part of combination therapy in patients ... Antineoplastics, Topical. Class Summary. Nonsurgical options for the treatment of cSCC include topical chemotherapy and topical ... Antineoplastics, EGFR Inhibitor. Class Summary. Multiple chemotherapeutic agents have been used to treat metastatic cSCC. ... Antineoplastics, Alkylating. Class Summary. Cisplatin is another chemotherapeutic drug of choice for metastatic cSCC. Although ...
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Azacitidine is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on ...
Drug Class: Immunosuppressants; Antineoplastics, Antimetabolite; DMARDs, Immunomodulators. What Is Methotrexate and How Does It ... Antineoplastic dosage range: 30-40 mg/m²/week to 100-12,000 mg/m² with leucovorin rescue ... Only for use by physicians experienced in antimetabolite therapy. *For intrathecal and high-dose methotrexate therapy, use ... Administer therapy under supervision of physician experienced in use of antimetabolite therapy ...
Antineoplastic drugs. Alkylating agents, antimetabolites, microtubule-damaging drugs, topoisomerase inhibitors. Last updated on ... Introduction to antineoplastic drugs. Antineoplastic agents can be divided into two subtypes:. *Cytotoxic compounds - drugs ... Antimetabolites. Antimetabolites are structurally similar to substrates of intermediary metabolism. Theyre typically prodrugs ... Antineoplastic drugs: cytokines, tyrosine kinase inhibitors, monoclonal antibodies, agents inducing differentiation. Leave a ...
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Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the ... A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the thymidylate ...
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antineoplastics. Pharm. Class.. antimetabolites. -- To view the remaining sections of this topic, please log in or purchase a ...
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Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic ... Drug Class: Antineoplastic Agents, Antimetabolites. PRODUCT INFORMATION. REPRESENTATIVE TRADE NAMES. Venetoclax - Venclexta® ... Venetoclax was found to have activity against refractory and relapsed CLL and was approved for use as an antineoplastic agent ... Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic ...
Pharmacotherapeutic group: Antineoplastic agents; Antimetabolites; Pyrimidine analogues. ATC code: L01BC02.. Mechanism of ... Bone marrow depression after radiotherapy or treatment with other antineoplastic agents.. • Management of non-malignant disease ... The drug is believed to function as an antimetabolite. After intracellular conversion to the active deoxynucleotide, it ... a qualified physician who is conversant with the use of potent antimetabolites and has the facilities for regular monitoring of ...
Segmentation by type of anti-neoplastic pharmaceutical agents,. Alkylating Agents. Antimetabolites. Antitumor Antibiotics. ... Anti-Neoplastic Pharmaceutical Agents Market: Key Players. Some of the key players in manufacturing of anti-neoplastic ... The global anti-neoplastic pharmaceutical agents market is segmented based on type of cancer, anti-neoplastic pharmaceutical ... Anti-neoplastic agents do not get stabilized in one part of the body, however they travel through body and help in destruction ...
Therapeutic Class: Antineoplastic Agent. Pharmacologic Class: Antimetabolite. Uses For mercaptopurine. Mercaptopurine (6-MP) ... belongs to the group of medicines known as antimetabolites. It is used in combination with other medicines as maintenance ...
  • Among the antimetabolites used as antineoplastic agents are the folic acid analog methotrexate and the pyrimidine analog fluorouracil. (thefreedictionary.com)
  • 5-Fluorouracil (5-FU) is a classic antimetabolite anticancer drug with a chemical structure similar to endogenous intermediates or building blocks of DNA or RNA synthesis. (medscape.com)
  • Fluorouracil is an antineoplastic anti-metabolite. (rcsb.org)
  • Fluorouracil is an antimetabolite antineoplastic agent. (ashp.org)
  • The most active cytotoxic drug against this malignancy, the antimetabolite 5-fluorouracil, was developed more than forty years ago, and as a single agent produces responses in only 10 to 15% of patients which in general last less than one year. (scielo.br)
  • FLUOROPLEX ® (fluorouracil) 1% Topical Cream is an antineoplastic/antimetabolite product for dermatological use. (nih.gov)
  • EFUDEX Solutions and Cream are topical preparations containing the fluorinated pyrimidine 5-fluorouracil, an antineoplastic antimetabolite. (nih.gov)
  • Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, which is necessary for conversion of folate to biologically active tetrahydrofolate. (medscape.com)
  • Antimetabolites like methotrexate are structurally similar to important metabolites and can be incorporated into DNA or damage DNA in other ways. (greek.doctor)
  • Methotrexate is an antimetabolite and antifolate agent with antineoplastic and immunosuppressant activities. (news-medical.net)
  • Methotrexate -- A toxic anticancer drug that is an analogue of folic acid and an antimetabolite. (inciid.org)
  • A pyrimidine analog that is an antineoplastic antimetabolite. (rcsb.org)
  • Antineoplastics (or "antitumor antibiotics", or "noncovalent DNA-binding drugs", or "cytotoxic antibiotics", see also neoplastics) are drugs that inhibit and combat the development of tumors . (bionity.com)
  • The adverse health effects associated with antineoplastic agents (cancer chemotherapy drugs, cytotoxic drugs) in cancer patients and some non-cancer patients treated with these drugs are well-documented. (bionity.com)
  • Pemetrexed is an anti-cancer ("antineoplastic" or "cytotoxic") chemotherapy drug. (chemocare.com)
  • Antimetabolites that are useful in cancer chemotherapy. (wakehealth.edu)
  • This medication is a form of antimetabolite chemotherapy, prescribed for leukemia in children and adolescents. (medindia.net)
  • The use of purine analogue antimetabolites in combination chemotherapy of solid tumors has been proposed. (aacrjournals.org)
  • Antimetabolite antineoplastic agents interfere with cell functions by competing for its receptors or enzymes involved in the synthesis of DNA. (medscape.com)
  • However, hereditary genetic variants may interfere with the pharmacokinetics of antimetabolites and other anti-cancer drugs, which may lead to severe adverse events. (cancerindex.org)
  • Antineoplastic agents interfere with cell reproduction. (medscape.com)
  • Antimetabolites are drugs that interfere with the function of enzymes involved in DNA synthesis. (tapi.com)
  • Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic leukemia (CLL). (nih.gov)
  • en] This review article describes the identification of the tyrosine kinase BCR/ABL as the hallmark of chronic myeloid leukemias (CML) as well as the development of a specific inhibitor of this tyrosine kinase, the STI571 (Glivec, imatinib mesylate). (ac.be)
  • Ox)aliplatin - a platinum-based alkylating antineoplastic agent. (wikipedia.org)
  • Alkylating agents, antimetabolites, and antibiotics have all been considered inhibitors of wound healing. (medscape.com)
  • However, the use of immunosuppressive or antineoplastic agents may predispose the patient to an even greater risk of infection, and physicians may consider the use of prophylactic antibiotics. (medscape.com)
  • Who might be exposed to antineoplastic agents in hospitals? (cdc.gov)
  • When are workers most likely to be exposed to antineoplastic agents in hospitals? (cdc.gov)
  • Statistically significant genotoxic effects and genetic damage (for example, increased micronuclei formation and increases in sister chromatid exchange and chromo- somal aberrations) have been reported in hospital phar- macists and nurses exposed to antineoplastic agents. (cdc.gov)
  • However, for the healthcare workers that are exposed to antineoplastic agents as part of their work practice, precautions should be taken to eliminate or reduce exposure as much as possible. (bionity.com)
  • What health effects can be caused by exposure to antineoplastic agents? (cdc.gov)
  • How can I protect myself from exposure to antineoplastic agents? (cdc.gov)
  • The purpose of this brochure is to -- make you aware of the adverse health effects of antineoplastic agents, -- describe how you can be exposed to these agents, and -- provide and identify control methods and work practices to prevent or reduce your exposure to antineoplastic agents. (cdc.gov)
  • Pharmacists that prepare these drugs or nurses that may prepare and/or administer them are the two occupational groups with the highest potential exposure to antineoplastic agents. (bionity.com)
  • If you experience any of these health problems when working with antineoplastic agents, report them to your supervisor or safety officer. (cdc.gov)
  • Antimetabolites, Antineoplastic" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
  • The antineoplastic mercaptopurine, an analog of the nucleotide adenine and the purine base hypoxanthine, is a metabolic antagonist of both compounds. (thefreedictionary.com)
  • An antimetabolite antineoplastic agent with immunosuppressant properties. (drugbank.ca)
  • 13. Antineoplastic drugs. (greek.doctor)
  • Most antineoplastic drugs target what activity? (brainscape.com)
  • The increased use of antineoplastic agents in veterinary oncology also puts these workers at risk for exposure to these drugs. (bionity.com)
  • Thioguanine is an anticancer (antineoplastic) agent belonging to the class of drugs called antimetabolites. (encyclopedia.com)
  • Alimta belongs to a class of drugs called Antineoplastics, Antimetabolite . (rxlist.com)
  • Changes in the nail unit are common during treatment with antineoplastic drugs. (eviq.org.au)
  • Venetoclax was found to have activity against refractory and relapsed CLL and was approved for use as an antineoplastic agent in the United States in 2016. (nih.gov)
  • This medication is an oral antineoplastic agent, prescribed for cutaneous T-cell lymphoma (CTCL, a type of skin cancer), lung cancer, breast cancer and Kaposi's sarcoma. (medindia.net)
  • This medication is an antineoplastic agent, prescribed for prostate cancer with prednisone. (medindia.net)
  • It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth. (ebi.ac.uk)
  • An orally administered hydrazine derivative antineoplastic agent. (cancer.gov)
  • An effective antineoplastic agent and is used for a variety of cancer s. (cancer.gov)
  • an antimetabolite antineoplastic agent that inhibits DNA polymerase and thus inhibits DNA synthesis during a specific phase of the cell cycle. (thefreedictionary.com)
  • Used as an antineoplastic agent (to attack abnormal tissue growth). (inciid.org)
  • It is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. (selleckchem.com)
  • Azacitidine belongs to the class of substances termed antimetabolites. (tapi.com)
  • Azauridine A triazine nucleoside used as an antineoplastic antimetabolite. (scitoys.com)
  • Mercaptopurine (6-MP) belongs to the group of medicines known as antimetabolites. (drugs.com)
  • A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites. (cancer.gov)
  • Antineoplastic agents can also be organized according to their chemical class, mechanism of action, therapeutic use or their toxicities. (umn.edu)
  • To be useful, antimetabolites must be significantly more toxic to cancer cells than to normal cells. (thefreedictionary.com)
  • Angiogenesis has been identified as an important target for antineoplastic therapy. (aacrjournals.org)