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By R. Ettarh

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Extra resources for Colorectal Cancer Biology - From Genes to Tumor

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AuroraA/STK15 T+91A is a general low penetrance cancer susceptibility gene: a metaanalysis of multiple cancer types. 8, pp1368-73, ISSN 1460-2180. M. ; Campbell, H. G. (2005). Germline susceptibility to colorectal cancer due to base-excision repair gene defects. 112-9, ISSN 0002-9297. E. (2007). Constitutive deficiency in DNA mismatch repair: is it time for Lynch III? 499-500, ISSN 1339-0004. ; Cravo, M. & Nobre Leitao, C. (2009). APC or MUTYH mutations account for the majority of clinically wellcharacterized families with FAP or AFAP phenotype and patients with more than 30 adenomas.

A meta-analysis of 32 studies correlating MSI status with clinical outcomes included patients with both germline LS mutations and sporadic MMR defects. 83) compared to individuals with MSI-high tumours. Polymorphisms in MMR genes are also associated with specific phenotypes. , 2009). , 2010). Together these data suggest that tumours that have deficits in DNA repair capabilities through germline or somatic mutations show better survival than tumours competent in DNA repair. 6. Conclusion In summary, just over a third of colorectal cancer risk is thought to be due to inherited genetic factors.

It is possible that some of these are real associations, but are population-specific or depend upon gene-environment interactions present only in certain individuals. Candidate genes for CRC case/control studies have been chosen in a variety of ways. Variants and genes studied include common variants in high-risk genes, genes in pathways believed to be important in CRC and genes in pathways linked to environmental factors associated with CRC. , 2008). A large number of cancer susceptibility and resistance loci for cancers of the lung, colon, skin, liver, and the hematopoetic system have been identified using mouse models.

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