Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 109, Issue 5, Pages 858-865Publisher
WILEY
DOI: 10.1002/jcb.22481
Keywords
COMMON FRAGILE SITES; PROMOTER METHYLATION; DNA DAMAGE CHECKPOINT; FHIT; DNA REPAIR
Categories
Funding
- NIH T32 [T32GM068412]
- National Cancer Institute [CA132453, CAl20516, CA115965]
- USPHS
- Ohio State University Comprehensive Cancer Center
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More than 12 years and >800 scientific publications after the discovery of the first gene at a chromosome fragile site, the FHIT gene at FRA3B, there are still questions to pursue concerning the selective advantage conferred to cells by loss of expression of FHIT, the most frequent target of allele deletion in precancerous lesions and cancers. These questions are considered in light of recent investigations of genetic and epigenetic alterations to the locus and in a retrospective consideration of biological roles of the Fhit protein discovered through functional studies. J. Cell. Biochem. 109: 858-865, 2010. (C) 2010 Wiley-Liss, Inc.
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