By R. Ettarh

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Nakamura, Y. (1991). Screening guidelines and premorbid diagnosis of familial adenomatous polyposis using linkage. 6, pp. 1658-64, ISSN 0016-5085. A. M. (1999). Genetic testing and counseling for hereditary forms of colorectal cancer. 86, No. 2450-50, ISSN 1097-0142. ; Slimani, N. & Riboli, E. (2006). Body size and risk of colon and rectal cancer in the European Prospective Investigation into cancer and nutrition (EPIC). 320-31, ISSN 1460-2105. P. S. (2008). 1 variation to the risk of developing colorectal cancer.

2011 Houlston et al. , 2008 Tomlinson et al. 2007; Xiong et al. 2011 Table 2. Low-penetrance variants associated with CRC Risk OR, odds ratio; *The common allele is the risk allele. , 2011; He et al. 2011). However, rs3802842 on chromosome 11q23 is associated with no increased risk in Japanese populations. , 22 Colorectal Cancer Biology – From Genes to Tumor 2011). These examples illustrate that specific variants identified by GWAS are often markers for the causal, as yet unidentified variant, which may be absent or in different linkage disquilibrium patterns with the identified SNP in other populations.

Approximately 80% of all cases of CRC are associated with chromosomal instability [1] and are likely to have mutations in the Adenomatous Polyposis Coli (APC) gene whereas the remaining 20% with microsatellite instability appears to be due primarily to epigenetic inactivation of the DNA mismatch repair (MMR) gene MLH1 [2]. The disease HNPCC accounts for somewhere between 2% and 5% of all CRCs diagnosed and is associated with a younger age of disease onset compared to the general population [3,4].

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Colorectal Cancer Biology - From Genes to Tumor by R. Ettarh
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