Journal
CANCER CELL
Volume 6, Issue 2, Pages 139-150Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2004.06.024
Keywords
-
Categories
Funding
- NCI NIH HHS [CA13330, CA76329, CA84301, CA93484] Funding Source: Medline
- NIEHS NIH HHS [ES11040] Funding Source: Medline
- NIGMS NIH HHS [R01 GM050006, GM50006] Funding Source: Medline
Ask authors/readers for more resources
Mutations in DNA mismatch repair (MMR) genes cause hereditary nonpolyposis colorectal cancer (HNPCC), and MMR defects are associated with a significant proportion of sporadic cancers. MMR maintains genome stability and suppresses tumor formation by preventing the accumulation of mutations and by mediating an apoptotic response to DNA damage. We describe the analysis of a dominant MSH6 missense mutation in yeast and mice that causes loss of DNA repair function while having no effect on the apoptotic response to DNA damaging agents. Our results demonstrate that MSH6 missense mutations can effectively separate the two functions, and that increased mutation rates associated with the loss of DNA repair are sufficient to drive tumorigenesis in MMR-defective tumors.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available