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Loss of the mismatch repair protein MSH6 in human glioblastomas is associated with tumor progression during temozolomide treatment.

Authors
  • Cahill, Daniel P1
  • Levine, Kymberly K
  • Betensky, Rebecca A
  • Codd, Patrick J
  • Romany, Candice A
  • Reavie, Linsey B
  • Batchelor, Tracy T
  • Futreal, P Andrew
  • Stratton, Michael R
  • Curry, William T
  • Iafrate, A John
  • Louis, David N
  • 1 Molecular Pathology Unit, Neurosurgical Service, Brain Tumor Center, and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Type
Published Article
Journal
Clinical cancer research : an official journal of the American Association for Cancer Research
Publication Date
Apr 01, 2007
Volume
13
Issue
7
Pages
2038–2045
Identifiers
PMID: 17404084
Source
Medline
License
Unknown

Abstract

Loss of MSH6 occurs in a subset of post-XRT + temozolomide glioblastoma recurrences and is associated with tumor progression during temozolomide treatment, mirroring the alkylator resistance conferred by MSH6 inactivation in vitro. MSH6 deficiency may therefore contribute to the emergence of recurrent glioblastomas during temozolomide treatment.

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