Abstract
Defects in mismatch repair contribute to development of approximately 15% of colon cancers and to origination of endometrial, gastric and other cancers. Tumors with defects in mismatch repair exhibit marked resistance to alkylators and a variety of anticancer agents that modify DNA to create substrates for the mismatch repair system. These altered drug responses appear to derive from requirements for mismatch repair proteins in signalling apoptosis, altered cell cycle checkpoint behaviour and/or loss of mismatch repair dependent toxicity arising from futile repair cycling. Altered repair mechanisms for mismatched substrates in mismatch repair defective tumors provide both challenges for development of tumor-phenotype-screening methodologies to assure appropriate therapy is administered for these cancers and foci for development of new therapy approaches that capitalize on modified drug responses in mismatch repair- defective cells. Copyright 1999 Harcourt Publishers Ltd.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
