Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft

Cancer Res. 1997 Jul 15;57(14):2933-6.

Abstract

A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2.

Publication types

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

MeSH terms

  • Animals
  • DNA Methylation*
  • DNA Repair*
  • Drug Resistance
  • Glioblastoma / drug therapy*
  • Glioblastoma / genetics
  • Humans
  • Melanocyte-Stimulating Hormones / analysis
  • Methyltransferases / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Microsatellite Repeats
  • Neoplasm Transplantation
  • O(6)-Methylguanine-DNA Methyltransferase
  • Transplantation, Heterologous
  • Tumor Cells, Cultured

Substances

  • Melanocyte-Stimulating Hormones
  • Methyltransferases
  • O(6)-Methylguanine-DNA Methyltransferase