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Annals of Clinical & Laboratory Science 39:331-337 (2009)
© 2009 Association of Clinical Scientists

Review

Field Effect in Cancer–An Update

Hong Chai and Robert E. Brown
Department of Pathology and Laboratory Medicine, University of Texas Health Science Center–Medical School at Houston, Houston, Texas

Address correspondence to Robert E. Brown, M.D., Department of Pathology and Laboratory Medicine, University of Texas Medical School-Houston, 6431 Fannin Street MSB 2.286; Houston, TX 77030, USA; tel 713 500 5332; fax 713,500 0695; e-mail: robert.brown{at}uth.tmc.edu.

The concept "field effect in cancer" originated in 1953 from the histopathological observations of Slaughter and colleagues [1] regarding the occurrence of multiple primary oral squamous cell carcinomas and their local recurrences. The development of modern molecular technologies has extended the field effect concept by exploring the molecular abnormalities in tissues that appear histologically normal. To date, such field effect biomarkers have been reported in several sites and organs, eg, head and neck, colon and rectum, prostate, breast, lung, esophagus, stomach, and skin. Two popular hypotheses have been proposed. One hypothesis implicates genetic alterations that occur in a stepwise fashion (initiation, promotion, and progression); a clone gains growth advantage and acquires more genetic alterations, which eventually result in cancer. A second hypothesis focuses on epigenetic alterations, which include hypermethylation of the DNA promoter of certain tumor suppressor genes, leading to down-regulation of these genes. In this update, we discuss in detail the evidence that supports these two hypotheses. In addition, we attempt to provide a comprehensive overview of the field effect in carcinogenesis and its possible mechanisms in various organs. Moreover, we discuss the potential utilization of field effect biomarkers in cancer prevention, surgical considerations, and clinical prognosis.

Keywords: field effect, carcinogenesis, field cancerization, multiple primary cancers, DNA methylation






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