Abstract
Colorectal cancer is one of the most intensively studied cancers with well-documented precursor lesions. The acquisition of genomic instability plays a central role in its development. In the majority of cases, tumor growth results from different combinations of sporadic genetic events and epigenetic alterations, resulting in increased cell proliferation and decreased cell death. Three main pathways have been identified: chromosomal instability (CIN) pathway, microsatellite instability (MSI) pathway, and CpG island hypermethylation phenotype (CIMP) pathway. Within these pathways, somatic BRAF and/or KRAS mutations have been identified as major players. Up to 5% of colorectal cancers develop in the setting of inherited syndromes, such as Lynch syndrome, familial adenomatous polyposis, MUTYH-associated polyposis, and certain hamartomatous polyposis conditions, including Peutz-Jeghers syndrome and juvenile polyposis syndrome. In this chapter, we describe the above-mentioned pathways and syndromes in detail, referring to different molecular events and different precursor lesions. In the last part, we address possible future perspectives in colorectal carcinogenesis.
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Brčić, I., Callé, C., Langner, C. (2017). Molecular and Cellular Mechanisms of Carcinogenesis in the Large Bowel. In: Haybaeck, J. (eds) Mechanisms of Molecular Carcinogenesis – Volume 2. Springer, Cham. https://doi.org/10.1007/978-3-319-53661-3_4
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