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Houlston, R., Bevan, S., Williams, A., et al. (1998) Mutations in DPC4 (SMAD4) cause juvenile polyposis syndrome, but only account for a minority of cases. Human Molecular Genetics, 7, 1907-1912. doi:10.1093/hmg/7.12.1907

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• TITLE: Molecular biology of colorectal cancer: Review of the literature

  AUTHORS: Elrasheid A. H. Kheirelseid, Nicola Miller, Michael J. Kerin

  KEYWORDS: Genetics of Colorectal Cancer; Molecular Biology of Colorectal Cancer; Colorectal Cancer

  JOURNAL NAME: American Journal of Molecular Biology, Vol.3 No.2, April 30, 2013

  ABSTRACT: Colorectal cancer (CRC) results from the progressive accumulation of genetic and epigenetic alterations that lead to the transformation of normal colonic epithelium to colon adenocarcinoma. From the analysis of the molecular genesis of colon cancer, four central tenets concerning the pathogenesis of cancer have been established. The first is that the genetic and epigenetic alterations that underlie colon cancer formation promote the cancer formation process because they provide a clonal growth advantage to the cells that acquire them. The second tenet is that cancer emerges via a multi-step progression at both the molecular and the morphologic level. The third is that loss of genomic stability is a key molecular step in cancer formation. The fourth is that hereditary cancer syndromes frequently correspond to germ line forms of key genetic defects whose somatic occurrences drive the emergence of sporadic colon cancers.