The role of O-6 methylguanine DNA methyltransferase (MGMT) in drug resistance and strategies for its inhibition

Semin Cancer Biol. 1991 Aug;2(4):257-65.

Abstract

The marginal level of clinical responses to the Chloroethylnitrosoureas (CENU, i.e. BCNU, CCNU, MeCCNU) suggests that there may exist an innate mechanism of resistance in tumors to these chemotherapeutic agents. A decade of research from many laboratories around the world has led to the identification of the mechanisms for tumor cell resistance to the CENU. The ability to prevent the formation of DNA interstrand crosslinks, thought to be the critical lethal lesion induced by these agents, is accomplished in a majority of human tumors by the unique DNA repair protein O-6 methylguanine DNA methyltransferase (MGMT). This review addresses the identification of this mechanism of resistance to therapy, and chemotherapeutic strategies to inhibit this DNA repair system, in an attempt to sensitize resistant tumors to the CENU.

Publication types

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

MeSH terms

  • Animals
  • DNA Repair
  • Drug Resistance / physiology*
  • Ethylnitrosourea / analogs & derivatives
  • Ethylnitrosourea / pharmacology*
  • Guanine / analogs & derivatives
  • Guanine / pharmacology
  • Humans
  • Methyl Methanesulfonate / pharmacology
  • Methylnitronitrosoguanidine / pharmacology
  • Methyltransferases / physiology*
  • Neoplasms / drug therapy*
  • O(6)-Methylguanine-DNA Methyltransferase
  • Rats
  • Streptozocin / pharmacology

Substances

  • Methylnitronitrosoguanidine
  • Streptozocin
  • Guanine
  • O-(6)-methylguanine
  • Methyl Methanesulfonate
  • Methyltransferases
  • O(6)-Methylguanine-DNA Methyltransferase
  • Ethylnitrosourea