COMMENTARY

Colorectal neoplasms

DNA alkylation and DNA methylation: cooperating mechanisms driving the formation of colorectal adenomas and adenocarcinomas?

William M Grady¹, Cornelia M Ulrich²

¹ Clinical Research Division, Fred Hutchinson Cancer Research Center, Department of Medicine, University of Washington Medical School, Seattle, Washington, USA, and R&D Service, VA Puget Sound Health Care System, USA
² Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Department of Epidemiology, University of Washington, Seattle, Washington, USA

Correspondence to:
Correspondence to:
Dr William M Grady
Fred Hutchinson Cancer Research Center 1100 Fairview Ave N, D4-100, Seattle, WA 98109, USA; wgrady@fhcrc.org

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Defining our understanding of the association between DNA alkylation and colon carcinogenesis

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The first 150 words of the full text of this article appear below.

Colorectal cancer has been called a disease of the somatic genome based on the fact that numerous somatic mutations have been identified in colorectal cancer, and these mutations have been shown to play a functional role in driving the formation of these cancers.^1,2 More recently, a wealth of studies have implicated alterations in the epigenome, particularly aberrant CpG island DNA methylation, as also being important in cancer formation.^3–5 Hence colorectal cancer is a disease that directly results from the serial accumulation of genetic alterations (for example, mutations in genes such as APC, KRAS and TP53) and epigenetic alterations (for example, aberrant methylation of MLH1 and CDKN2A, etc.) in an evolving clone of colon epithelial cells, which in aggregate leads to the initiation and progression of neoplasms along a polyp to cancer progression sequence.⁶

In order to appreciate the significance of the epigenetic alterations in colorectal . . . [Full text of this article]

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