Current Colorectal Cancer Reports

, Volume 9, Issue 4, pp 365–371 | Cite as

Molecular Origins of Colon and Rectal Cancer: Not a Wnt–Wnt Situation

Molecular Biology (S Anant, Section Editor)


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.


Colorectal cancer Early onset Wnt signaling Microsatellite instability Adenomatous Polyposis coli 


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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  1. 1.Laboratory of Molecular OncologyCentre for DNA Fingerprinting and DiagnosticsHyderabadIndia

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