1 edition of Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists found in the catalog.
Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists
1982 by U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, National Technical Information Service [distributor in [Bethesda, Md.?], Springfield, Va .
Written in English
|Statement||Joseph R. Bertino, consulting reviewer.|
|Contributions||Bertino, Joseph R., National Cancer Institute (U.S.), International Cancer Research Data Bank., Cancer Information Dissemination and Analysis Center on Virology, Immunology, and Biology.|
|The Physical Object|
|Pagination||viii, 66 p. ;|
|Number of Pages||66|
METHOTREXATE, the most widely used antimetabolite in cancer chemotherapy, has an essential role in the treatment of such diverse diseases as acute lymphocytic leukemia, non-Hodgkin's lymphoma, oste Cited by:
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Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists (OCoLC) Material Type: Government publication: Document Type: Book: All Authors / Contributors: Joseph R Bertino; International Cancer Research Data Bank.; Cancer Information Dissemination and Analysis Center for Virology, Immunology, and Biology.
In addition, other mechanisms of resistance that are present in most epithelial cancer cells are also operative in melanoma. This chapter reviews how melanoma orchestrates these mechanisms to become extremely resistant to methotrexate, where both E2F1 and Chk1, two molecules with dual roles in survival/apoptosis, play prominent by: 4.
Walter RD, Bergmann B, Kansy M, Wiese M, Seydel JK. Pyrimethamin-resistant Plasmodium falciparum lack cross-resistance to methotrexate and 2,4-diamino(substituted benzyl) pyrimidines.
Parasitol Res ; – PubMed CrossRef Google ScholarCited by: Both high-folate diets and supplemental folic acid may help reduce the toxic side-effects of low-dose methotrexate without decreasing its effectiveness. Anyone taking low-dose methotrexate for the health problems listed above should consult with a physician about the need for.
Methotrexate (MTX), formerly known as amethopterin, is a chemotherapy agent and immune system suppressant. It is used to treat cancer, autoimmune diseases, ectopic pregnancy, and for medical abortions. Types of cancers it is used for include breast cancer, leukemia, lung cancer, lymphoma, and osteosarcoma.
Types of autoimmune diseases it is used for include psoriasis, rheumatoid arthritis, and Metabolism: Hepatic and intracellular. Author(s): Bertino,Joseph R; International Cancer Research Data Bank.; Cancer Information Dissemination and Analysis Center for Virology, Immunology, and Biology.
Title(s): Selected abstracts on mechanisms of resistance to methotrexate and other folate. Mechanisms of antifolate resistance and methotrexate efficacy in leukemia cells. Fotoohi AK(1), Albertioni F. Author information: (1)Department of Oncology and Pathology, Cancer Center Karolinska, Karolinska Institute, Karolinska University Hospital, Stockholm, by: Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists / Joseph R.
Folic acid and lactobacillus casei [microform] Arthur Michael Streeter; Folic acid metabolism in health and disease / editors, Mary Frances Picciano, E.L. Robert Stokstad, Jess.
Methotrexate has been widely used for the treatment of rheumatoid arthritis (RA). The mechanisms of action of methotrexate are complex. Developed as a folic acid ana-logue, methotrexate inhibits purine and pyrimidine synthesis, which accounts for its efficacy in the therapy of cancer as well as for some of its toxicities.
Recently, many studiesCited by: Development of folates and folic acid antagonists in cancer chemotherapy: Innisbrook, Tarpon Springs, F Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists / Joseph Selected abstracts on mechanisms of resistance to methotrexate and other folate antagonists book.
Folate fortification: report of the Expert Panel on Folate Fortification /. Molecular Mechanisms of Methotrexate Resistance is responsible for the metabolism of natural folates and a broad range of folate antagonists to polyglutamate derivatives.
selected for. Abstract. Drug resistance limits the effectiveness of methotrexate (MTX) for the treatment of acute leukemia. An increased understanding of the pathways involved in folate metabolism has allowed investigations of the mechanisms of resistance observed in leukemic blasts obtained from by: Studies have shown no reduced efficacy of methotrexate with a folate:methotrexate dose ratio ofthat is, the dose of folate can be at least three times that of methotrexate before there is any effect on efficacy.
For a once-weekly dose of 15 mg methotrexate, up to 45 mg of Cited by: 1. Methotrexate, a folate antagonist, is a potent anti-inflammatory agent when used weekly in low concentrations, the anti-phlogistic action of which is due to increased adenosine release at inflamed sites.
Studies have demonstrated that methotrexate polyglutamates are active inhibitors of several enzymatic reactions, including dihydrofolate. Chan ESL, Cronstein BN.
Mechanisms of action of methotrexate. Bull Hosp Jt Dis. ;71(Suppl 1):S Abstract As one of the most utilized disease-modifying anti-rheumatic drugs, methotrexate (MTX) has revolutionized the treatment of rheumatoid arthritis as well as many other non-rheumatic chronic inflammatory diseases.
Far from a simple anti-File Size: KB. In the present study, we characterized the mechanisms underlying resistance of human CCRF-CEM leukemia cells that were selected for resistance to this panel of drugs using clinically relevant exposure schedules.
Moreover, we analyzed the impact of these antifolate resistance mechanisms on cellular folate homeostasis. Materials and methods Cited by: It is not entirely clear how methotrexate works to treat rheumatoid arthritis, although it is thought to work by affecting the immune system.
However, please for more info do talk to a doc/pharmacist, take care. hebatullah 6 Apr Thank you for your answer. Rajive Goel 6 Apr Further Information. Search for questions. Now widely regarded as a gold standard in the therapy of rheumatoid arthritis and many other inflammatory diseases, a yardstick against which the efficacy of newer disease-modifying antirheumatic drugs and biologic agents are judged, our understanding of the mechanisms of action of methotrexate (MTX) has also broadened over its many years in clinical use.
Methotrexate is a drug classified as an antimetabolite. It is used to treat some cancers as well as rheumatoid arthritis. t slows or stops the growth of cancer cells and suppresses the immune system. The effects of three folate antagonists were studied on these cell lines and also on CCRF-CEM/R3 cells, characterized by impaired methotrexate transport but normal levels of dihydrofolate reductase.
In a multivariate analysis, folic acid use was the major determinant of continuation of MTX over the period of retrospective study. Cumulative MTX ‘survival’ at 5 yr was 67% for those receiving supplementary folate vs 31% in those who were not (PAuthor: S.
Whittle, R. Hughes. folic acid antagonist: [ an-tag´o-nist ] antagonistic muscle. (see illustration.) 1. a substance that tends to nullify the action of another, as a drug that binds to a cellular receptor for a hormone, neurotransmitter, or another drug blocking the action of that substance without producing any.
Intrathecal methotrexate can lead to prolongedplasma levels of methotrexate through this egress and lead to potential systemic toxicity; 10 to 15 mg/m2 of methotrexate given intrathecally generates more than mol/L plasma levels two to three times longer than if the methotrexate were given intravenously Fifty percent to 70% of Cited by: Other mechanisms (perhaps mediated by inhibition of other folate-dependent enzymes) resulting in a clonal deletion of T cells by apoptosis, and decreased production of IL-1 and other inflammatory mediators may also contribute to its anti-inflammatory effects (Kremer, ).
We have analyzed the activities of the antifolates pyrimethamine (PM), chlorcycloguanil (CCG), WR, trimethoprim (TMP), methotrexate (MTX), and trimetrexate (TMX) against Kenyan Plasmodium falciparum isolates adapted in vitro for long-term culture.
We have also assessed the relationship between these drug activities and mutations in dihydrofolate reductase (dhfr), a domain of Cited by: Background/Purpose: Rheumatoid arthritis (RA) is one of the most prevalent systemic autoimmune disorders.
The folate antagonist methotrexate (MTX) is an anchor drug in the treatment of RA. Here, we aim to provide insight into the pharmacological effects of MTX by gene expression analysis Methods: Subanalysis of microarray data was performed for a set of 18 [ ]. First developed to treat malignancies, methotrexate is now commonly used to treat gynecological problems, inflammatory arthritis, skin disease and probably other ailments as well.
This work is designed to give a broad overview of the history of methotrexate's development, its prior use and its current therapeutic uses.5/5(1). Drug resistance limits the effectiveness of methotrexate (MTX) for the treatment of acute leukemia.
An increased understanding of the pathways involved in folate metabolism has allowed investigations of the mechanisms of resistance observed in leukemic blasts obtained from by: Methotrexate should be administered with great caution, if at all, to patients with significant current or previous liver disease, especially if due to alcohol (see sections and ).
Patients with renal impairment. Methotrexate should be used with caution in patients with impaired renal function (see sections and ). Read "Development of methotrexate proline prodrug to overcome resistance by MDA-MB cells, Bioorganic & Medicinal Chemistry Letters" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
There is reasonable evidence that folic acid 5–10 mg per week leads to reduction in methotrexate (MTX) toxicity in rheumatoid arthritis (RA). However, this is based on studies conducted with lower MTX dosage than used currently.
It is unclear whether higher doses of folic acid may be better in reducing toxicity. This was a double-blind randomized controlled trial of 24 weeks by: The enantiomer L-methotrexate is absorbed forty times more readily than D-methotrexate, by the reduced folate carrier and the folate receptor protein, the mechanisms used to absorb folic acid.
Inside the cell methotrexate is polyglutamated by folylpolyglutamate synthase (FPGS) by forming a peptide link between the carboxylic acid group of. Psoriasis is a chronic, inflammatory multisystem disease, which affects up to % of the U.S.
population. The guideline is based on current evidence, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients about benefits as well as risks that may be associated.
Reversal of Methotrexate Binding to Dihydrofolate Reductase by and other labora- tories (4, 8) have interpreted these observations on the basis of an interaction between methotrexate and a single high was preincubated with methotrexate and NADPH then. Methotrexate (MTX) eradicates leukemic cells by disrupting de novo nucleotide biosynthesis and DNA replication, resulting in cell death.
Since its introduction inMTX-containing chemotherapeutic regimens have proven instrumental in achieving curative effects in acute lymphoblastic leukemia (ALL). However, drug resistance phenomena pose major obstacles to efficacious ALL Cited by: Panel A: Uptake of MTX via the reduced folate carrier (1) and human folate receptor (2).
MTX within the cell (3) is polyglutamated with up to 5 glutamic acid moieties [MTX(Glu n)]. It is the polyglutamated form of MTX that is retained long-term and is a potent inhibitor of DHFR (4) and thymidylate synthase (5), as well as purine biosynthesis (6).
Methotrexate use results in a decreased supply of folates. Folic acid is co-administered to minimise the adverse effects of folate deficiency (stomatitis, bone marrow toxicity, abnormal liver function tests and gastrointestinal intolerance).
Total weekly doses of 5 – mg File Size: KB. Background/Purpose: Low-dose weekly methotrexate (MTX) is the first-choice second-line drug in the treatment of juvenile idiopathic arthritis (JIA). Folate (as either Folic acid (FA) or Folinic acid (FLA)) effectively ameliorates or prevents some of MTX’s adverse events (AE) in adults with RA.
Folate supplementation in JIA, therefore, has become the standard of care in many [ ]. Methotrexate was first developed in the s as a specific antagonist of folic acid. This drug inhibits the proliferation of malignant cells, primarily by inhibiting the de novo synthesis of purines and pyrimidines.
Because administration of high doses of reduced folic acid (folinic acid) or even folic acid itself can reverse the antiproliferative effects of methotrexate, it is clear that Cited by: Methotrexate Injection, USP Isotonic Liquid, Contains Preservative is available in 25 mg/mL, 2 mL (50 mg) vials.
Each 25 mg/mL, 2 mL vial contains methotrexate sodium equivalent to 50 mg methotrexate, % w/v of Benzyl Alcohol as a preservative, and the following inactive ingredients: Sodium Chloride % w/v and Water for Injection qs ad File Size: KB.
TNF inhibitors are more effective than DMARDs at improving fatigue and general well-being in RA patients, despite relatively modest effects on .Multiple conformers in active site of human dihydrofolate reductase F31R/Q35E double mutant suggest structural basis for methotrexate resistance.
Journal Biol. Chem.,↑ DIHYDROFOLATE REDUCTASE COMPLEXED WITH METHOTREXATE. (n.d.). Other mechanisms. Modification of drug target. Cells survival depends on a balanced assembly and disassembly of the highly conserved cytoskeletal filaments formed from actin and tubulin.
Microtubules are assembled from α-tubulin and β-tubulin heterodimers, along with other proteins such as microtubule-associated by: