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Molecular Biology of Colon Cancer

  • Chapter
Book cover Colorectal Cancer

Part of the book series: Current Clinical Oncology ((CCO))

Abstract

Colorectal cancer affects approx 140,000 people in the United States each year, resulting in more than 55,000 deaths. Colorectal cancer develops as the result of the progressive accumulation of genetic and epigenetic alterations that lead to the transformation of normal colonic epithelium to colon adenocarcinoma. The loss of genomic stability is a key molecular and pathophysiological step in this process and serves to create a permissive environment for the occurrence of alterations in tumor suppressor genes and oncogenes. Alterations in these genes, which include APC, CTNNB1, KRAS2, BRAF, MADH4/SMAD4, TP53, PIK3CA, and TGFBR2, appear to promote colon tumorigenesis by perturbing the function of signaling pathways, such as the transforming growth factor-β and PI3K signaling pathways, or by affecting genes that regulate genomic stability, such as the mutation mismatch repair genes.

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Grady, W.M. (2007). Molecular Biology of Colon Cancer. In: Markman, M., Saltz, L.B. (eds) Colorectal Cancer. Current Clinical Oncology. Humana Press. https://doi.org/10.1007/978-1-59745-215-1_1

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