Tumor resistance to antimetabolites.
1. The inherent or acquired resistance of certain tumors to cytotoxic drug therapy is a major clinical problem. 2. Resistance to the chemotherapeutic antimetabolites (e.g., methotrexate, 5-fluorouracil, tomudex and gemcitabine) is no exception. 3. Mechanisms of resistance include mutations, amplification of target genes, altered drug transport, differences in nucleoside and nucleobase salvage pathways, DNA damage-response pathways and cell cycle control pathways.
Kinsella
A R
AR
Department of Surgery, University of Liverpool, UK.
Smith
D
D
D000964:Antimetabolites, Antineoplastic / Q000627:therapeutic use*; D018797:Cell Cycle Proteins / Q000378:metabolism; D004249:DNA Damage; D004273:DNA, Neoplasm / Q000187:drug effects; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D019008:Drug Resistance, Neoplasm / Q000235:genetics; D005472:Fluorouracil / Q000627:therapeutic use; D005784:Gene Amplification; D006801:Humans; D008727:Methotrexate / Q000627:therapeutic use; D009154:Mutation; D009369:Neoplasms / Q000188:drug therapy* / Q000235:genetics*; D011799:Quinazolines / Q000627:therapeutic use; D013876:Thiophenes / Q000627:therapeutic use; D000093542:Gemcitabine
D000964:Antimetabolites, Antineoplastic; D018797:Cell Cycle Proteins; D004273:DNA, Neoplasm; D011799:Quinazolines; D013876:Thiophenes; D003841:Deoxycytidine; C068874:raltitrexed; D005472:Fluorouracil; D008727:Methotrexate; D000093542:Gemcitabine