By R. Ettarh
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From its advent, oncological chemotherapy has been weighted down through its terrible selectivity simply because such a lot antiproliferative medicinal drugs are poisonous not just to tumor cells but additionally to special populations of the body’s non-neoplastic cells. the ensuing issues of negative effects are compounded by means of problems in predicting the specified efficiency of chemotherapy in person sufferers.
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Additional resources for Colorectal Cancer Biology - From Genes to Tumor
4. Low-penetrance risk alleles The majority of genetic risk for CRC in the population is likely to be due to low-penetrance susceptibility alleles which act with other low-pentrance variants and the environment. A debate in the field is whether most of the genetic risk will be due to common variants with low effects and allele frequencies greater than 1% or rare or unique variants with low to moderate effects (Bodmer, 2006). Historically, variants conferring an increased risk of CRC in the general population have been identified through cohort or population-based case/control studies looking at candidate genes, but recent genome-wide association studies (GWAS) have been quite successful in identifying well-replicated variants conferring risk.
Additional variants on 8q24 including rs7014346, rs783728, and rs10505477 were also identified in subsequent screens (Tenesa et al. 2008; Poynter et al. 2007). Several groups have replicated these findings and show a consistent effect of the rs6983267 variant. This SNP falls into a genepoor region on 8q24 with the closest gene, cMYC, 335 kb away. One study showed that the rs6983267 variant falls within an enhancer element and alleles differentially bind a WNTrelated transcription-factor 7-like 2 (TCF7L2).
Smokijng and colorectal cancer: a meta-analysis. 2765-78, ISSN 0098-7484. ; Rozen, P. J. (1990). 655-65, ISSN 0042-9686. W. (2000). Colon cancer screening. 837-53, ISSN 0016-5085. P. & Pharoah, P. (2006). Relative and absolute risk of colorectal cancer for individuals with a family history: a meta-analysis. European Journal of Cancer. 216-27, ISSN 0959-8049. K. W. (2009). Germline bone morphogenesis protein receptor 1A mutation causes colorectal tumorigenesis in hereditary mixed polyposis syndrome.