Antimetabolites: 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, Antineoplastic: Antimetabolites that are useful in cancer chemotherapy.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Floxuridine: 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.Tetrahydrouridine: An inhibitor of nucleotide metabolism.Trabeculectomy: 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 Monophosphate: Inosine 5'-Monophosphate. A purine nucleotide which has hypoxanthine as the base and one phosphate group esterified to the sugar moiety.Phosphoribosyl Pyrophosphate: The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.Fluorouracil: 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.Leukemia L1210Mitomycin: 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.6-Mercaptopurine: 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.Methotrexate: 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.Cytarabine: 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)Folic Acid Antagonists: 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)Purines: 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.Drug Screening Assays, Antitumor: 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.Drug Synergism: The action of a drug in promoting or enhancing the effectiveness of another drug.Neoplasms: 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.Cell Survival: 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.Drug Evaluation, Preclinical: Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.Tumor Cells, Cultured: 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.DeoxycytidineCell Cycle: 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.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Antibiotics, Antineoplastic: Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Antineoplastic Agents, Phytogenic: Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.Kinetics: The rate dynamics in chemical or physical systems.Antineoplastic Agents, Alkylating: 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)Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.Leukemia P388: An experimental lymphocytic leukemia originally induced in DBA/2 mice by painting with methylcholanthrene.Antineoplastic Combined Chemotherapy Protocols: 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.Phospholipid Ethers: 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Apoptosis: 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.Ellipticines: Pyrido-CARBAZOLES originally discovered in the bark of OCHROSIA ELLIPTICA. They inhibit DNA and RNA synthesis and have immunosuppressive properties.Gallium: A rare, metallic element designated by the symbol, Ga, atomic number 31, and atomic weight 69.72.Bryostatins: 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.Thiadiazines

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)

*Antimetabolite

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 ... The presence of antimetabolites can have toxic effects on cells, such as halting cell growth and cell division, so these ...

*List of MeSH codes (D16)

... antimetabolites, antineoplastic MeSH D27.505.954.248.147 --- antimitotic agents MeSH D27.505.954.248.150 --- antineoplastic ... antineoplastic agents, alkylating MeSH D27.888.569.042 --- antimetabolites MeSH D27.888.569.042.030 --- antimetabolites, ... antimetabolites, antineoplastic MeSH D27.505.519.217 --- antioxidants MeSH D27.505.519.217.500 --- free radical scavengers MeSH ... File "2006 MeSH Trees".) MeSH D27.505.519.124 --- alkylating agents MeSH D27.505.519.124.035 --- antineoplastic agents, ...

*ICD-10 Chapter XX: External causes of morbidity and mortality

Antineoplastic antimetabolites (Y43.2) Antineoplastic natural products (Y43.3) Other antineoplastic drugs (Y43.4) ...

*FCM (chemotherapy)

... an antimetabolite; (C)yclophosphamide - an alkylating antineoplastic agent from the oxazafosforine group; (M)itoxantrone - a ...

*GemOx

... an antimetabolite; (Ox)aliplatin - a platinum-based antineoplastic agent with alkylating mechanism of action. GEMOX-R regimen ...

*Index of oncology articles

... antimetabolite - antimicrotubule agent - antimitotic agent - antineoplastic - antineoplastic antibiotic - antioxidant - ...

*DHAP (chemotherapy)

... an antimetabolite; (P)latinol (cisplatin), a platinum-based antineoplastic agent with an alkylating mechanism; Effective ...

*FOLFOXIRI

... 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 ( ...

*Cancer

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 ...

*FOLFIRINOX

... 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 ( ...

*Chemotherapy

Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a similar structure to the ... Antineoplastic Agents in Encyclopedia of Molecular Pharmacology, 2nd Edition, Volume 1. Eds. Offermanns S and Rosenthal W. ... Unlike alkylating agents, anti-metabolites are cell cycle dependent. This means that they only work during a specific part of ... Pemetrexed is another anti-metabolite that affects purine and pyrimidine production, and therefore also inhibits DNA synthesis ...

*Chronic myelogenous leukemia

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 ...

*Hydroxycarbamide

2015). Hydroxyurea is a monohydroxyl-substituted urea (hydroxycarbamate) antimetabolite. Similar to other antimetabolite anti- ... Hydroxycarbamide is in the antineoplastic family of medications. It is believed to work by blocking the making of DNA. ... Hydroxyurea has many pharmacological applications under the Medical Subject Headings classification system: Antineoplastic ...

*8-Azaguanine

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 ...

*FLAG (chemotherapy)

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 is not active toward AML, but increases formation of an active cytarabine metabolite, ara-CTP, in AML ...

*Tioguanine

... 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 ...
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This phase I trial studies the side effects and best dose of ceritinib and combination chemotherapy in treating patients with advanced solid tumors or
Gemcitabine (Gemzar) chemotherapy side effects, how its given, how it works, precautions and self care tips for treatment of multiple cancers
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.. ...
Learn about azacitidine for cancer treatment. Injected under the skin or into a vein, azacitidine helps restore the production of healthy blood cells and destroy abnormal ones.
This trial is evaluating the anti-tumor activity, safety, and tolerability of MK-3475 in combination with azacitidine in subjects with chemo-refractory
Azacitidine Injection official prescribing information for healthcare professionals. Includes: indications, dosage, adverse reactions, pharmacology and more.
Venetoclax + Decitabine combination chemo for AML. Learn important drug side-effects information by listening, watching videos, & reading | ChemoExperts
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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 ...
Thirty-five trials (9,979 participants) were included in the review. Sample sizes ranged from 40 to 824. The reviewers did not publish the results of the quality assessment. Length of follow-up was unclear. Numbers of patients lost to follow-up were unclear.. Significant benefits were observed with gemcitabine combination therapy with cytotoxic agents (23 trials, 5,577 participants) compared to single-agent gemcitabine in overall survival (OR 1.15, 95% CI 1.03 to 1.28) and progression-free survival (OR 1.27, 95% CI 1.14 to 1.42).. Statistically significant benefits were observed for overall survival (OR 1.33, 95% CI 1.08 to 1.64) and progression-free survival (OR 1.53, 95% CI 1.24 to 1.88) when gemcitabine was combined with fluoropyrimidine and compared to gemcitabine monotherapy (six trials, n=1829). Both oral capecitabine and infused 5-fluorouracil were used in fluoropyrimidine treatment.. Analysis of gemcitabine-oxaliplatin combinations found significant benefits in overall survival (OR 1.33, ...
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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.
Fludarabine Phosphate Actavis is a medicine available in a number of countries worldwide. A list of US medications equivalent to Fludarabine Phosphate Actavis is available on the Drugs.com website.
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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 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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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
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.
Two New Antimetabolites of Biotin: α-Methyldethiobiotin and α-Methylbiotin: Two new antimetabolites of biotin were isolated from culture filtrates of Streptomyc
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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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 ...
Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells. Treatment with 5-FU increased the levels of cleaved caspase-3 and PARP in ACH2 cells compared with uninfected and latently infected p53 null J1.1 cells. The levels of expression and activation of p53 were higher in both latently infected ACH2 and NCHA2 cells than in uninfected cells. Furthermore, the activation levels of p53 in both cells were further increased upon 5-FU treatment. Consistent with p53 status, apoptosis was markedly increased in ACH2 and NCHA2 cells compared with uninfected and latently infected J1.1 cells upon treatment with other anticancer drugs such as doxorubicin and etoposide. Inhibition of p53 in cells with latent HIV-1 infection diminished apoptosis upon 5-FU treatment ...
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
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.
Using gemcitabine for pancreatic cancer is generally effective, as it works by interfering with the spread of cancer cells in the...
At ASH 2015, Dr. Yogenthiran Saunthararajah from Cleveland Clinic discussed his abstract titled Mechanisms of Resistance to 5-Azacytidine/Decitabine in MDS-AML and Pre-Clinical In Vivo Proof of Principle of Rational Solutions to Extend Response., MPNUniversity.tv Website
Gemcitabine HCl is an inhibitor of DNA synthesis with IC50 of 50 nM, 40 nM, 18 nM and 12 nM in PANC1, MIAPaCa2, BxPC3 and Capan2 cells, respectively.
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The global 5-fluorouracil market is valued at xx million US$ in 2018 is expected to reach xx million US$ by the end of 2025, growing at a CAGR of xx% during 2019-2025. This report focuses on 5-fluorouracil volume and value at global level, regional ...
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SOARES, Pedro M. G. et al. Methotrexate-induced intestinal mucositis delays gastric emptying and gastrointestinal transit of liquids in awake rats. Arq. Gastroenterol. [online]. 2011, vol.48, n.1, pp.80-85. ISSN 0004-2803. http://dx.doi.org/10.1590/S0004-28032011000100016.. CONTEXT: Methotrexate and other anticancer agents can induce intestinal mucositis, which is one of the most common limiting factor that prevent further dose escalation of the methotrexate. OBJECTIVES: To evaluate the gastric emptying and gastrointestinal transit of liquids in methotrexate-induced intestinal mucositis. METHODS: Wistar rats received methotrexate (2.5 mg/kg/day for 3 days, subcutaneously) or saline. After 1, 3 and 7 days, sections of duodenum, jejunum and ileum were removed for assessment of epithelial damage and myeloperoxidase activity (biochemical marker of granulocyte infiltration). Others rats were pre-treated with methotrexate or saline, gavage-fed after 3 or 7 days with a standard test liquid meal, and ...
5-Fluorouracil (5-FU) and its orally administered prodrug, capecitabine, are fluoropyrimidine-based chemotherapeutic agents that are widely used for the treatment of colorectal cancer and other solid tumors.. The dihydropyrimidine dehydrogenase (DPYD) gene encodes the rate-limiting enzyme for fluoropyrimidine catabolism and eliminates over 80% of administered 5-FU. Dihydropyrimidine dehydrogenase (DPYD) activity is subject to wide variability, mainly due to genetic variation. This results in a broad range of enzymatic deficiency from partial (3%-5% of population) to complete loss (0.2% of population) of enzyme activity.(2,3) Patients who are deficient in DPYD are at an increased risk for side effects and toxicity when undergoing 5-FU treatment.(4) In addition, pathogenic homozygous or compound heterozygous variants within DPYD are associated with dihydropyrimidine dehydrogenase (DPD) deficiency. DPD deficiency shows large phenotypic variability, ranging from no symptoms to a convulsive disorder ...
TY - JOUR. T1 - A phase i study of IMP321 and gemcitabine as the front-line therapy in patients with advanced pancreatic adenocarcinoma. AU - Wang-Gillam, Andrea. AU - Plambeck-Suess, Stacey. AU - Goedegebuure, Peter. AU - Simon, Peter O.. AU - Mitchem, Jonathan B.. AU - Hornick, John R.. AU - Sorscher, Steven. AU - Picus, Joel. AU - Suresh, Rama. AU - Lockhart, Albert. AU - Tan, Benjamin. AU - Hawkins, Williams G.. PY - 2013/6/1. Y1 - 2013/6/1. N2 - Purpose This phase I study was conducted to determine the safety profile and maximum tolerated dose (MTD) of IMP321, a soluble lymphocyte activation gene-3 (LAG-3) Ig fusion protein and MHC Class II agonist, combined with gemcitabine in patients with advanced pancreatic adenocarcinoma. Patients and methods Patients with advanced pancreatic adenocarcinoma were treated with gemcitabine (1,000 mg/m2)(level 1), gemcitabine (1,000 mg/m 2) plus IMP 321 at 0.5 mg (level 2) and 2.0 mg (level 3), respectively. Safety, toxicity, and immunological markers at ...
Histone deacetylase (HDAC) inhibitors either alone or in combination with hypomethylating agents have limited clinical effect in acute myeloid leukemia (AML). Previously, we demonstrated that AML patients with higher miR (microRNA)-29b expression had better response to the hypomethylating agent decitabine. Therefore, an increase in miR-29b expression preceding decitabine treatment may provide a therapeutic advantage. We previously showed that miR-29b expression is suppressed by a repressor complex that includes HDACs. Thus, HDAC inhibition may increase miR-29b expression. We hypothesized that priming AML cells with the novel HDAC inhibitor (HDACI) AR-42 would result in increased response to decitabine treatment via upregulation of miR-29b. Here, we show that AR-42 is a potent HDACI in AML, increasing miR-29b levels and leading to downregulation of known miR-29b targets (that is, SP1, DNMT1, DNMT3A and DNMT3B). We then demonstrated that the sequential administration of AR-42 followed by decitabine
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Treatment with hypomethylating agents (HMAs) improves overall survival (OS) in patients who achieve a response of stable disease (SD) or better (complete remission [CR], partial remission [PR], or hematologic improvement [HI]). It is not well established if patients who achieve SD at 4-6 months of therapy should be offered different therapies to optimize their response or continue with the same regimen. Clinical data were obtained from the MDS Clinical Research Consortium database. SD was defined as no evidence of progression and without achievement of any other responses.
MANHATTAN BEACH, Calif., Nov. 9, 2012 /PRNewswire/ -- The Pancreatic Cancer Action Network is pleased to announce Abraxane® extends survival for patients with advanced pancreatic cancer. According to Celgene Corporation, Abraxane in combination with gemcitabine when given to advanced pancreatic cancer patients who had not received previous treatment demonstrated a statistically significant improvement in overall survival compared to patients receiving gemcitabine alone. (Logo: http://photos.prnewswire.com/prnh/20111004/LA79914LOGO). The phase III study included 861 metastatic pancreatic cancer patients from around the world. Full results from the clinical trial will be presented at the American Society of Clinical Oncologys 2013 Gastrointestinal Cancers Symposium being held in January. "Historically, few effective treatment options for pancreatic cancer have existed. We are thrilled to have a new treatment option for patients with advanced pancreatic cancer. We look forward to learning more ...
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Purpose To assess the immunomodulatory and clinical effects of lenalidomide with standard treatment of gemcitabine in patients with advanced pancreatic cancer. Patients and Methods Patients with advanced pancreatic cancer were treated in first line with lenalidomide orally for 21 days of a 28 days cycle and the standard regimen for gemcitabine. In Part I, which we previously have reported, the dose of lenalidomide was defined (n = 12). In Part II, every other consecutive patient was treated with either lenalidomide (Group A, n = 11) or gemcitabine (Group B, n = 10) during cycle 1. From cycle 2 on, all Part II patients received the combination. Results A significant decrease in the proliferative response of peripheral blood mononuclear cells and the frequency of DCs were noted in patients at baseline compared to healthy control donors while the frequencies of CD4+ and CD8+ T cells, NK-cells and MDSCs were significantly higher in patients compared to controls. In Group A, a significant increase in ...
Radley, J M. and Scurfield, G, "Effects of 5-fluorouracil on mouse bone marrow." (1979). Subject Strain Bibliography 1979. 792 ...
Fludarabine Phosphate Injection is a cancer medication that interferes with the growth and spread of cancer cells in the body. It is used to treat B-cell
In this report, we have found that anti-DLL4 has broad spectrum activity in pancreatic xenografts based on testing a panel of patient-derived tumor models. In vivo studies showed that anti-DLL4 was efficacious, alone and in combination with gemcitabine, in reducing tumor growth in all pancreatic tumors tested, including both low- and high-grade tumors. Anti-DLL4 treatment had a potent effect in delaying tumor recurrence after gemcitabine treatment. Furthermore, anti-DLL4 was found to reduce tumor initiating cell frequency as a single agent and in combination with gemcitabine. Agents that reduce CSC frequency have the potential to provide significant clinical benefit by reducing tumor recurrence after therapy and by inhibiting the metastatic spread of the disease. In contrast to anti-DLL4, treatment with gemcitabine alone was ineffective at reducing CSC frequency. While gemcitabine is a standard agent for treatment of pancreatic cancer, the effect of gemcitabine on survival has been disappointing ...
Gemcitabine monotherapy has been the standard of care for patients with metastatic pancreatic cancer for several decades. Despite recent advances in various chemotherapeutic regimens and in the development of targeted therapies, metastatic pancreatic cancer remains highly resistant to chemotherapy. 1
We hypothesized that tumors exposed to high levels of IGF1R ligands are dependent on IGF1R for growth and survival. This would manifest as enhanced sensitivity to tumor inhibition of IGF1R in patients with high levels of ligands or of IGFBP-3, a binding protein that stabilizes circulating ligands and is cleaved by local proteases to release ligands at the tissue level. The functions of the other binding proteins are not well characterized but may sequester ligands in circulation and away from tissues; therefore, low levels of these binding proteins would promote IGF1R ligand availability and thus tumor dependence on IGF1R.. In this phase II study of ganitumab and gemcitabine in metastatic pancreatic adenocarcinoma, baseline levels of circulating factors of the IGF axis were evaluated for potential associations with survival. The treatment effect of ganitumab was enhanced in patients with higher baseline levels of total IGF-1, IGF-2, and IGFBP-3 and lower baseline levels of IGFBP-2 as compared ...
Schneider G, Schmid RM. Genetic alterations in pancreatic carcinoma. Mol Cancer. 2003; 2: 15. Altwegg R, Ychou M, Guillaumon V, Thezenas S, Senesse P, Flori N, et al. Second-line therapy for gemcitabine-pretreated advanced or metastatic pancreatic cancer. World J Gastroenterol. 2012; 18: 1357-64. Burris HA, Moore MJ, Andersen J, Green MR, Rothenberg ML, Modiano MR, et al. Improvements in survival and clinical benefit with gemcitabine as first-line therapy for patients with advanced pancreas cancer: a randomized trial. J Clin Oncol 1997; 15: 2403-2413. Moore MJ, Goldstein D, Hamm J, Figer A, Hecht JR, Gall¬inger S, et al. Erlotinib plus gemcitabine compared with gemcitabine alone in patients with advanced pancreatic cancer: a phase III trial of the National Cancer Institute of Canada Clinical Trials Group. J Clin Oncol 2007; 25: 1960-1966. Conroy T, Desseigne F, Ychou M, et al. FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. N Engl J Med 2011; 364: 1817-1825. Von Hoff DD, Ervin ...
BACKGROUND: Interfant-99 was an international collaborative treatment protocol for infants with acute lymphoblastic leukemia (ALL). PROCEDURE: We collected data on 103 infants at the time of their first treatment with high-dose methotrexate (HD MTX), 5 g/m(2). Children ,6 months of age received two-third of the calculated dose based on body surface area (BSA), children 6-12 months three-fourth of the calculated dose, and children ,12 months full dose. RESULTS: The median steady-state MTX concentration at the end of the 24-hr infusion was 57.8 microM (range 9.5-313). The median systemic clearance was 6.22 L/hr/m(2) BSA, and tended to increase with age (P = 0.099). Boys had higher clearance than girls, 6.77 and 5.28 L/hr/m(2) (P = 0.030), and tended to have lower median MTX concentration at 24 hr. Eight infants had MTX levels below 20 microM, a level judged to be sufficient in B-lineage ALL in children ,1 year of age. All infants tolerated the dose well enough to receive a second dose of HD MTX ...
The purpose of this study is to find out what effects (good and/or bad) chemotherapy combined with external radiation therapy and possible removal of your bladder has on you and your cancer. The chemotherapy drugs used in this study (5-Fluorouracil, cisplatin, and gemcitabine) are not experimental drugs. This research is being done because we do not know whether one combination of drugs with radiation is superior to another in the treatment of your disease. This study uses similar therapies to the standard treatment, but chemotherapy and radiation therapy are given before removal of the bladder is considered. In this study, bladder removal is advised if, after chemotherapy and radiation, your tumor has not completely disappeared, if your tumor comes back, or if it gets larger.. Patients who participate in this trial will be randomized into two groups. Patients will receive either cisplatin and 5-FU chemotherapy and radiation twice per day OR gemcitabine chemotherapy and radiation once per day. ...
Therapy for acute myeloid leukemia (AML) in elderly populations (,65 years) is still a challenge for scientists and hematologists worldwide, and represents an urgent medical need. Notably, the identification and the recognition of molecular and epigenetic mechanisms involved in the pathogenesis of such a heterogeneous disease, are providing new tools for a more successful and targeted approach. Azacitidine is a hypomethylating agent (HMA) with relevant activity in patients affected by myelodysplastic syndrome (MDS) and AML with low blast cells percentage (,30%), in terms of reduction of transfusion dependence, and improvement of quality of life ...
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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 ...
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Improvements in therapy in advanced pancreatic cancer have been very difficult to come by. As a molecularly targeted agent, erlotinib has been shown to add a survival benefit when combined with gemcitabine for patients facing pancreatic cancer," said Dr. Malcolm Moore, study chair and medical oncologist at Princess Margaret Hospital in Toronto, Canada, and Chair of the Gastrointestinal Disease Site, NCIC Clinical Trials Group. "Erlotinib represents a notable step forward for patients and healthcare providers in a disease with a very poor prognosis ...
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The effects of exposure of bone marrow to specific methotrexate (MTX) concentrations were studied by constant infusion of the drug into C57BL mice. The residual marrow nucleated cell count was determined in 168 mice at specific intervals. In vitro culture of colony-forming cells (CFU-C) was also performed in 69 of these mice. Duration of exposure varied from 12 to 72 hr. Plateau plasma MTX concentrations were studied in the range from 10-8 to 10-5 m. The total number of nucleated cells per femur fell to a nadir of 30% of control for all drug concentrations studied. The nadir was reached earliest with the highest drug concentrations. The percentage of CFU-C per 7.5 × 104 nucleated cells plated increased after 48-hr infusions compared to the percentage after 24-hr infusions. This increase was seen at all plasma concentrations studied. The total number of CFU-C per femur at plasma MTX concentrations above 10-6 m decreased in the first 24 hr to 40% of control, but then the number significantly ...
MILAN, Italy-A four-drug chemotherapy cocktail prolongs progression-free survival in patients with advanced pancreatic cancer, according to a study published online by The Lancet Oncology.
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Capecitabine is a cancer medicine that interferes with the growth of cancer cells and slows their spread in the body. Capecitabine is used to treat colon cancer, and breast or colorectal cancer that has spread to other parts of the body. Capecitabine is often used in combination with other cancer medications and/or...
In vitro induction of apoptosis by AZA was clearly evident and occurred predominantly via the intrinsic apoptotic pathway. This is consistent with the recognized cytotoxic activity of AZA and preceded the expected hypomethylating activity of AZA, which was first observed - using the hypermethylated p16 gene as a marker of global demethylation - 48 hours after exposure to AZA. The mechanisms by which AZA induces cytotoxicity are not fully elucidated and may well be cell-type dependent. Studies undertaken in the 1970s led to the hypothesis that the principle mechanism of cytotoxicity was incorporation of AZA into RNA.39 This, in turn, was thought to lead to inhibition of protein synthesis and cell death. Data also suggested that later incorporation into DNA could not only inhibit DNA synthesis but also sensitize cells to the effects of other DNA-damaging drugs.40 More recently it has been shown that 5-aza-2′-deoxycytidine (decitabine) cell killing is dependent on the p53 DNA-damage response ...
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Gemcitabine Hydrochloride and Docetaxel in Treating Patients with Relapsed or Refractory Colorectal Cancer That Is Metastatic or Cannot Be Removed by Surgery
used in combination with intravenous 5-fluorouracil-based chemotherapy, is indicated for first-line treatment of patients with metastatic carcinoma of the colon or rectum.
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Detail záznamu - Simultaneous delivery of doxorubicin and gemcitabine to tumors in vivo using prototypic polymeric drug carriers - Detail záznamu - Knihovna Akademie věd České republiky
Compared with conventional care regimens, VIDAZA doubled overall survival times in subsets of patients with poor-risk cytogenetics and in patients with morphologic dysplastic-related changes ...
Alimta infusion contains the active ingredient pemetrexed disodium, which is a type of chemotherapy medicine for cancer called a cytotoxic antimetabolite.
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In this article you will know all of the Main drugs used in cancer treatment. Know about Mitotic Inhibitors, Antibiotics, Antimetabolites and Alkylating
Methotrexate, sold under the trade names Rheumatrex and Trexall, is classified as an antimetabolite medication. This means that it effectively interferes...
Van Der Wilt, C.L.; Marinelli, A.; Pinedo, H.M.; Cloos, J.; Smid, K.; Van D.V.lde, C.J.H.; Peters, G.J., 1995: The effect of different routes of administration of 5-fluorouracil on thymidylate synthase inhibition in the rat
Background: Metastatic pancreatic adenocarcinoma has a short median overall survival (OS) of 5-6 months. However, a subgroup of patients survives more than 1 year. We analyzed the survival outcomes of this subgroup and evaluated clinical and pathological factors that might affect survival durations. Methods: We identified 20 patients with metastatic or recurrent pancreatic adenocarcinoma who received single-agent gemcitabine and had an OS longer than 1 year. Baseline data available after the diagnosis of metastatic or recurrent disease was categorized as: 1) clinical/demographic data (age, gender, ECOG PS, number and location of metastatic sites); 2) Laboratory data (Hematocrit, hemoglobin, glucose, LDH, renal and liver function and CA19-9); 3) Pathologic data (margins, nodal status and grade); 4) Outcomes data (OS, Time to Treatment Failure (TTF), and 2 year-OS). The lowest CA19-9 levels during treatment with gemcitabine were also recorded. We performed a univariate analysis with OS as the ...
Fludarabine Phosphate Tablets is a cancer medication that interferes with the growth and spread of cancer cells in the body. It is used to treat B-cell chronic
Most patients with pancreatic cancer are either unresectable at diagnosis or will suffer from a relapse after initial surgery, resulting in a 5-year OS of 6% (11). The median OS of patients with advanced or metastatic pancreatic cancer is 6 months with most chemotherapeutic options (4). Treatment with FOLFIRINOX has offered a new option for patients with advanced pancreatic cancer and a good performance status (8). However, it was reported that a considerable percentage of patients, up to 50%, treated with FOLFIRINOX experienced grade 3 and 4 toxicities (7,8). Understanding the features that determine response or resistance to this chemotherapy regimen could permit the selection of the most suitable patients for treatment with FOLFIRINOX. Thus, in our study, we evaluated clinical and histological markers and their associations with response to FOLFIRINOX.. The objective response rate, defined as the percentage of patients with CR and PR, was slightly higher (55.1%) in our overall study ...
Dihydropyrimidine dehydrogenase (DPD) is a major determinant of the efficacy and toxicity of 5-fluorouracil in various cancer therapies. Single nucleotide polymorphisms (SNPs) within DPYD have been studied extensively for years. However, known SNPs do not explain most cases of altered DPD activity and response to 5-FU. Furthermore, variations of DPYD expression in cancer patients have been reported; however, the underlying molecular mechanism is unclear. This suggests that regulation of DPYD expression may be an additional mechanism to control DPD activity. In this study, we focused on epigenetic regulation of DPD and specifically investigated the role of histone methylation on DPYD expression. Inhibition of the H3K27 methyl-transferase Ezh2 by either GSK-126 or a dominant-negative histone H3 mutant significantly increased DPYD expression in various cell lines. The expression of thymidylate synthetase, a major target of 5-fluorouracil toxicity, was not altered. Consistent with elevated DPYD ...
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Increasingly, the effectiveness of adjuvant chemotherapy agents for breast cancer has been related to changes in the genomic profile of tumors. We investigated correspondence between growth inhibitory concentrations of paclitaxel and gemcitabine (GI50) and gene copy number, mutation, and expression first in breast cancer cell lines and then in patients. Genes encoding direct targets of these drugs, metabolizing enzymes, transporters, and those previously associated with chemoresistance to paclitaxel (n = 31 genes) or gemcitabine (n = 18) were analyzed. A multi-factorial, principal component analysis (MFA) indicated expression was the strongest indicator of sensitivity for paclitaxel, and copy number and expression were informative for gemcitabine. The factors were combined using support vector machines (SVM). Expression of 15 genes (ABCC10, BCL2, BCL2L1, BIRC5, BMF, FGF2, FN1, MAP4, MAPT, NFKB2, SLCO1B3, TLR6, TMEM243, TWIST1, and CSAG2) predicted cell line sensitivity to paclitaxel with 82% accuracy.
Case Report: Gemcitabine therapy was initiated following tumor recurrence in a patient with ovarian cancer, who was previously treated twice with carboplatin and paclitaxel. Radiological findings waned and tumor marker concentrations decreased after gemcitabine treatment. However, edema and ascites development was observed on the fifth treatment cycle. Laboratory results revealed increased blood urea nitrogen and creatinine levels, decreased serum albumin concentrations, and increased 24-hour urinary protein excretion. Renal biopsy findings were compatible with membranous glomerulonephritis. Gemcitabine administration was stopped and the cyclophosphamide and steroid therapy were initiated. The symptoms and findings disappeared after the cessation of gemcitabine and immunosuppressive treatment ...
The U.S. Food and Drug Administration has approved irinotecan liposome injection (Onivyde), in combination with fluorouracil (5-FU) and leucovorin, to treat patients with metastatic pancreatic cancer who have been previously treated with gemcitabine-based chemotherapy.. The effectiveness of liposomal irinotecan was demonstrated in a three-arm, randomized, open-label study of 417 patients with metastatic pancreatic adenocarcinoma whose cancer had grown after receiving the chemotherapeutic drug gemcitabine or a gemcitabine-based therapy.1 The study was designed to determine whether patients receiving liposomal irinotecan plus 5-FU/leucovorin or liposomal irinotecan alone lived longer than those receiving 5-FU/leucovorin.. Patients treated with liposomal irinotecan plus 5-FU/leucovorin lived an average of 6.1 months, compared to 4.2 months for those treated with only 5-FU/leucovorin. There was no survival improvement for those who received only liposomal irinotecan compared to those who received ...
Use of the gemcitabine (Gemzar) plus docetaxel (Taxotere) combination in metastatic breast cancer is motivated by the different mechanisms of action of the drugs, partially nonoverlapping toxicity profiles, and good single-agent activities of both drugs in treatment-naive and anthracycline-pretreated patients. In phase II trials, combinations of gemcitabine at 900 or 1,000 mg/m2 on days 1 and 8 and docetaxel at 75 to 100 mg/m2 on either day 1 or day 8 every 3 weeks, or gemcitabine at 800 mg/m2 on days 1, 8, and 15 and docetaxel at 35 mg/m2 on days 1, 8, and 15 or 100 mg/m2 on day 1 every 4 weeks, have produced response rates of 36% to 79% in patients receiving primarily second-line treatment; response rates were greater than 50% in five of six studies. In phase II trials using every-2-week regimens of gemcitabine at 1,500 or 2,000 mg/m2 on day 1 and docetaxel at 50 or 65 mg/m2 on day 1 or 55 mg/m2 on day 8, response rates were 50% in pretreated patients and 66% in treatment-naive patients. Neutropenia
TY - JOUR. T1 - A multicenter phase II randomized trial of docetaxel/gemcitabine versus docetaxel/capecitabine as first-line treatment for advanced breast cancer. T2 - A gruppo oncologico italia meridionale study. AU - Vici, P.. AU - Giotta, F.. AU - Di Lauro, L.. AU - Sergi, D.. AU - Vizza, E.. AU - Mariani, L.. AU - Latorre, A.. AU - Pizzuti, L.. AU - DAmico, C.. AU - Giannarelli, D.. AU - Colucci, G.. PY - 2011/12. Y1 - 2011/12. N2 - Objective: To evaluate two docetaxel-based regimens as first-line treatment in advanced breast cancer patients. Methods: Patients were randomly assigned to docetaxel/gemcitabine (arm A: docetaxel 75 mg/m 2 on day 1, gemcitabine 1,000 mg/m 2 on days 1 and 8) or docetaxel/capecitabine (arm B: docetaxel 75 mg/m 2 on day 1, capecitabine 1,250 mg/m 2 twice daily on days 1-14); both chemotherapy regimens were repeated every 21 days. The primary objective of the study was to evaluate the response rate. Results: Seventy-two patients were enrolled (36 each in arms A and ...
Combined gemcitabine and cisplatin (GC) treatment is a first line chemotherapy for bladder cancer. However, acquired resistance to GC has been a major problem. To address the mechanism of gemcitabine resistance, and to identify potential biomarkers or target proteins for its therapy, we aimed to identify candidate proteins associated with gemcitabine resistance using proteomic analysis. We established gemcitabine‑resistant human bladder cancer cell lines (UMUC3GR and HT1376GR) from gemcitabine‑sensitive human bladder cancer cell lines (UMUC3 and HT1376). We compared the protein expression of parental and gemcitabine‑resistant cell lines using isobaric tags for relative and absolute quantification (iTRAQ) and liquid chromatography tandem mass spectrometry. Among the identified proteins, ethylmalonyl‑CoA decarboxylase (ECHDC1) expression was significantly increased in both of the gemcitabine‑resistant cell lines compared to the respective parental cell lines. Silencing of ECHDC1 reduced ...
Abstract. A phase III clinical trial showed gemcitabine chemotherapy combined with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib significantly improved overall survival in patients with advanced pancreatic cancer. Therefore, we studied whether addition of gemcitabine to erlotinib in cancer cells having intrinsic or acquired erlotinib resistance could restore chemosensitization in these cells. We studied the synergistic effect of erlotinib and gemcitabine in EGFR-overexpressing A-431 cells with acquired erlotinib resistance and in intrinsic erlotinib-resistant triple negative breast cancer (TNBC) BT-549, MDA-MB-231 and MDA-MB-468 cell lines. Erlotinib and gemcitabine were synergistic in both parental intrinsically erlotinib-sensitive A-431 cells (combination index = 0.69 at the effective dose [ED50]) and in two A-431 cell pools that had acquired erlotinib resistance (combination indices = 0.63 and 0.49 at ED50). The synergistic effect of erlotinib and gemcitabine on ...

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... is an antimetabolite indicated as an adjunct to ab externo glaucoma surgery.. Includes: indications, dosage, adverse reactions ... pharmacology and more.MITOMYCIN FOR INJECTION USP: Novopharm: Antineoplastic Action And Clinical Pharmacology: Mitomycin was ...
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Antimetabolites, antineoplastic | definition of Antimetabolites, antineoplastic by Medical dictionaryAntimetabolites, antineoplastic | definition of Antimetabolites, antineoplastic by Medical dictionary

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- ...
more infohttp://medical-dictionary.thefreedictionary.com/Antimetabolites%2C+antineoplastic

Cutaneous Squamous Cell Carcinoma Medication: Antineoplastics, Topical, Antineoplastics, EGFR Inhibitor, Topical Skin Products,...Cutaneous Squamous Cell Carcinoma Medication: Antineoplastics, Topical, Antineoplastics, EGFR Inhibitor, Topical Skin Products,...

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 ...
more infohttps://emedicine.medscape.com/article/1965430-medication

Which medications in the drug class Immunosuppressants; Antineoplastics, Antimetabolite; DMARDs, Immunomodulators are used in...Which medications in the drug class Immunosuppressants; Antineoplastics, Antimetabolite; DMARDs, Immunomodulators are used in...

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 ...
more infohttps://www.medscape.com/answers/201886-107763/which-medications-in-the-drug-class-immunosuppressants-antineoplastics-antimetabolite-dmards-immunomodulators-are-used-in-the-treatment-of-hodgkin-lymphoma

Vidaza
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        Antimetabolites, Antineoplastic,  Enzyme InhibitorsVidaza - Antimetabolites, Antineoplastic, Enzyme Inhibitors

Azacitidine is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on ...
more infohttps://pharmacycode.com/Vidaza.html

Azacitidina [INN-Spanish]
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        Antimetabolites, Antineoplastic,  Enzyme InhibitorsAzacitidina [INN-Spanish] - Antimetabolites, Antineoplastic, Enzyme Inhibitors

Azacitidine is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on ...
more infohttps://pharmacycode.com/Azacitidina_%5BINN-Spanish%5D.html

Fludarabine Phosphate Monograph for Professionals - Drugs.comFludarabine Phosphate Monograph for Professionals - Drugs.com

Antimetabolite antineoplastic agent; synthetic purine antagonist.1 2 3 4 5 6 7 9 21 95 ... Class: Antineoplastic Agents. VA Class: AN300. Chemical Name: 2-Fluoro-9-(5-O-phosphono-β-D-arabinofuranosyl)9H -purin-6-amine ... Cytarabine substantially decreases fludarabine metabolism7 67 74 and may inhibit the antineoplastic effect of fludarabine 67 ... Use under supervision of a qualified clinician experienced in therapy with antineoplastic agents.1 9 95 ...
more infohttps://www.drugs.com/monograph/fludarabine-phosphate.html

Methotrexate (Trexall): Side Effects, Dosages, Treatment, Interactions, WarningsMethotrexate (Trexall): Side Effects, Dosages, Treatment, Interactions, Warnings

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 ...
more infohttps://www.rxlist.com/consumer_methotrexate_trexall/drugs-condition.htm

Raltitrexed (CAS 112887-68-0) 99% purity (ab142974) |AbcamRaltitrexed (CAS 112887-68-0) 99% purity (ab142974) |Abcam

Potent antimetabolite antineoplastic agent. Selective thymidylate synthase inhibitor. Inhibits cell growth (IC50 = 9 nM, L1210 ...
more infohttps://www.abcam.com/raltitrexed-thymidylate-synthase-inhibitor-ab142974.html

Bevacizumab, Gemcitabine, and Oxaliplatin in Treating Patients With Metastatic Pancreatic Cancer - Full Text View -...Bevacizumab, Gemcitabine, and Oxaliplatin in Treating Patients With Metastatic Pancreatic Cancer - Full Text View -...

Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic Agents. ...
more infohttps://clinicaltrials.gov/ct2/show/study/NCT00112528?show_locs=Y

First Line Metastatic Colorectal Cancer Therapy in Combination With FOLFOX - Full Text View - ClinicalTrials.govFirst Line Metastatic Colorectal Cancer Therapy in Combination With FOLFOX - Full Text View - ClinicalTrials.gov

Antineoplastic Agents. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antimetabolites, Antineoplastic. ...
more infohttps://www.clinicaltrials.gov/ct2/show/NCT00384176

Detection and Enumeration of Circulating Tumor Cells in Rectal Cancer - Full Text View - ClinicalTrials.govDetection and Enumeration of Circulating Tumor Cells in Rectal Cancer - Full Text View - ClinicalTrials.gov

Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic Agents. To Top ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01671891?cond=rectal+cancer&rank=36

Standard Versus Continuous Capecitabine in Advanced Breast Cancer - Full Text View - ClinicalTrials.govStandard Versus Continuous Capecitabine in Advanced Breast Cancer - Full Text View - ClinicalTrials.gov

Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic Agents. To Top ... Capecitabine is a pro-drug of 5-FU and mimics an i.v. continuous infusion administration of this antimetabolite. On the other ...
more infohttps://clinicaltrials.gov/show/NCT00418028

RCSB PDB - URF Ligand Summary PageRCSB PDB - URF Ligand Summary Page

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 ...
more infohttps://www.rcsb.org/ligand/URF

5-azacytidine Valproic Acid and ATRA in AML and High Risk MDS - Full Text View - ClinicalTrials.gov5-azacytidine Valproic Acid and ATRA in AML and High Risk MDS - Full Text View - ClinicalTrials.gov

Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic Agents. Enzyme ...
more infohttps://clinicaltrials.gov/ct2/show/NCT00339196

RCSB PDB - MTX Ligand Summary PageRCSB PDB - MTX Ligand Summary Page

Methotrexate is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the ... An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of tetrahydrofolate dehydrogenase and ...
more infohttps://www.rcsb.org/ligand/MTX

DHFR | Cancer Genetics WebDHFR | Cancer Genetics Web

Antimetabolites, Antineoplastic. *Trimetrexate. *Acute Lymphocytic Leukaemia. *Messenger RNA. *Risk Factors. *Tumor Stem Cell ...
more infohttp://www.cancerindex.org/geneweb/DHFR.htm

TPMT | Cancer Genetics WebTPMT | Cancer Genetics Web

Antimetabolites, Antineoplastic. *Pharmacogenetics. *Case-Control Studies. Tag cloud generated 16 March, 2017 using data from ... However, hereditary genetic variants may interfere with the pharmacokinetics of antimetabolites and other anti-cancer drugs, ...
more infohttp://www.cancerindex.org/geneweb/TPMT.htm

Mercaptopurine - DrugBankMercaptopurine - DrugBank

An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by ... An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by ...
more infohttps://www.drugbank.ca/drugs/DB01033

Drug CategoriesBrowse DrugBank Categories - DrugBankDrug CategoriesBrowse DrugBank Categories - DrugBank

An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes... more. 1. 7. Details. ...
more infohttps://www.drugbank.ca/categories