© 2005 Oxford University Press
EDITORIAL |
DNA Methylation, Field Effects, and Colorectal Cancer
Affiliations of authors: Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA (EG); Department of Medicine, Channing Laboratory, Brigham and Women's Hospital/Harvard Medical School, Boston, MA (EG); Cancer Epidemiology Program, Dana-Farber/Harvard Cancer Center, Boston, MA (EG, SO); Department of Pathology, Brigham and Women's Hospital, Boston, MA (SO); Department of Medical Oncology, Dana-Farber Cancer Institute/Harvard Medical School, Boston, MA (SO)
Correspondence to: Edward Giovannucci, MD, ScD, Harvard School of Public Health, Bldg. II, Rm. 331A, 665 Huntington Ave., Boston, MA 02115 (e-mail: egiovann@hsph.harvard.edu).
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The concept of field effect was first introduced by Slaughter et al. (1) in 1953, when they studied the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma. This concept, also called field defect or field cancerization, was proposed to explain the development of multiple primary tumors in the same organ and locally recurrent cancer. Field effects are considered to underlie the multicentricity of cancer in many, if not all, patients who have multiple tumors in the same organ but no apparent familial predisposition to those tumors. In the multistep carcinogenesis model proposed by Fearon and Vogelstein (2), genetic alterations occur in a stepwise fashion such that a clone that has growth advantage proliferates, acquires more genetic alterations, and undergoes another selection for survival and growth, eventually resulting in cancer. According to this model, precancerous cells that are in proximity to cancer cells
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