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Critical Reviews™ in Oncogenesis

Erscheint 4 Ausgaben pro Jahr

ISSN Druckformat: 0893-9675

ISSN Online: 2162-6448

SJR: 0.395 SNIP: 0.322 CiteScore™:: 2.5 H-Index: 54

Indexed in

Colorectal Cancer: A Multipathway Disease

Volumen 12, Ausgabe 3-4, 2006, pp. 273-287
DOI: 10.1615/CritRevOncog.v12.i3-4.50
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ABSTRAKT

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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