Gene amplification and altered enzymes as mechanisms for the development of drug resistance

Cancer Treat Rep. 1983 Oct;67(10):901-4.

Abstract

Two known mechanisms by which neoplastic cells may become resistant to chemotherapeutic agents are reviewed, using methotrexate (MTX) resistance as a model. These mechanisms are an increased level of target enzyme, found in several instances to be a consequence of gene amplification, or an altered target enzyme or receptor, less capable of binding the drug. An example of MTX resistance due to low-level gene amplification in leukemia cells from an MTX-resistant patient is described. Strategies for selectively eradicating these resistant cell populations may be formulated based on the mechanism by which these cells became drug-resistant.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Drug Resistance
  • Gene Amplification*
  • Humans
  • Methotrexate / pharmacology*
  • Neoplasms / drug therapy*
  • Neoplasms / enzymology
  • Neoplasms / genetics
  • Tetrahydrofolate Dehydrogenase / genetics*

Substances

  • Tetrahydrofolate Dehydrogenase
  • Methotrexate