Abstract:
:Mice defective in the mismatch repair (MMR) gene Msh2 manifest an enhanced predisposition to skin cancer associated with exposure to UVB radiation. This predisposition is further heightened if the mice are additionally defective for the nucleotide excision repair gene Xpc. To test the hypothesis that the predisposition of Msh2 mutant mice to skin cancer reflects a mutator phenotype associated with increased proliferation of skin cells following exposure to UV radiation, Msh2 mutant mice were exposed to the tumor promoter TPA. Such mice showed a robust proliferative response in the skin, but did not manifest evidence of dysplasia or neoplasia. We conclude that the predisposition of Msh2 mice to UVB radiation-induced skin cancer reflects an interaction between the processes of mismatch repair and some other excision repair mode, the exact nature of which remains to be established.
journal_name
DNA Repair (Amst)journal_title
DNA repairauthors
Meira LB,Cheo DL,Reis AM,Claij N,Burns DK,te Riele H,Friedberg ECdoi
10.1016/s1568-7864(02)00143-xkeywords:
subject
Has Abstractpub_date
2002-11-03 00:00:00pages
929-34issue
11eissn
1568-7864issn
1568-7856pii
S156878640200143Xjournal_volume
1pub_type
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