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Critical Reviews™ in Oncogenesis
SJR: 0.946 SNIP: 0.503 CiteScore™: 2

ISSN Print: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v12.i3-4.50
pages 273-287

Colorectal Cancer: A Multipathway Disease

Jeremy R. Jass
Department of Pathology, McGill University, Duff Medical Building, 3775 University Street, Montreal, Quebec H3A 2B4, Canada


The linear sequence of genetic alterations illustrated in the Vogelstein model provides a readily understandable illustration of the fundamental principles underlying colorectal tumorigenesis. However, it is now clear that colorectal cancer is a multi-pathway disease. In this review, the concept that inactivation of the tumor suppressor gene APC serves to initiate virtually all colorectal cancers is shown to be an oversimplification. APC inactivation may have important tumorigenic pathogenic effects beyond the mere initiation of precancerous adenomas. Furthermore, the early evolution of colorectal neoplasia must sometimes occur by mechanisms other than inactivation of APC or related alterations that would drive dysregulated Wnt pathway signaling. Oncogenic mutations implicating both BRAF and KRAS are highlighted as alternative initiating steps that synergize with DNA methylation and occur within the context of serrated polyps. CRC comprises subgroups with particular clinical, pathological, and molecular features.

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