Bashyam, M.D. and Raman, R. (2013) Molecular Origins of Colon and Rectal Cancer: Not a Wnt–Wnt Situation. Current Colorectal Cancer Reports, 9 (4). pp. 365-371. ISSN 1556-3790

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Abstract

Extensive studies have provided crucial molecular and epidemiological insights into disease progression of late-onset colon cancer, the predominant colorectal cancer (CRC) subtype in the West. Most colon cancer cases are driven by mutational inactivation of the adenomatous polyposis coli tumor suppressor gene, causing chromosomal instability owing to constitutive activation of the Wnt pathway. A minor proportion of cases are caused by inactivation of the mismatch repair pathway resulting in microsatellite instability. Distinct etiological and molecular characteristics are, however, beginning to be unraveled in CRC occurring in developing nations. A preponderance of rectal (over colon) and early-onset (over late-onset) cancers appears to be the hallmark of CRC in developing countries. More importantly, the possible occurrence of unique non-Wnt tumorigenesis pathways in early-onset rectal cancer has been suggested in several populations. Although CRC research has mainly focused on the canonical Wnt signaling pathway for over two decades, it is imperative now to study alternative oncogenesis pathways to combat the ever-increasing rectal cancer burden in developing countries.

Item Type:	Article
Uncontrolled Keywords:	Colorectal cancer; Early onset; Wnt signaling; Microsatellite instability
Depositing User:	Users 2 not found.
Date Deposited:	15 Sep 2015 08:45
Last Modified:	22 Sep 2017 08:37
URI:	http://cdfd.sciencecentral.in/id/eprint/518

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