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JNCI Journal of the National Cancer Institute 2001 93(9):664-665; doi:10.1093/jnci/93.9.664
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 9, 664-665, May 2, 2001
© 2001 Oxford University Press

EDITORIAL

Promoter Hypermethylation—Can This Change Alone Ever Designate True Tumor Suppressor Gene Function?

Stephen B. Baylin, James G. Herman

Affiliations of authors: The Johns Hopkins Comprehensive Cancer Center and The Johns Hopkins Medical Institutions, Baltimore, MD.

Correspondence to: Stephen B. Baylin, M.D., The Johns Hopkins Comprehensive Cancer Center and The Johns Hopkins Medical Institutions, Cancer Research Bldg., 1650 E. Orleans St., Rm. 540, Baltimore, MD 21231 (e-mail: sbaylin@jhmi.edu).

We recently commented on the burgeoning evidence that epigenetically mediated gene silencing can selectively produce loss of key gene functions in cancer (1). In this issue of the Journal, Burbee et al. (2) report that yet another gene, RASSF1A, is silenced in association with promoter hypermethylation in small-cell lung cancer (SCLC), in non-small-cell lung cancer (NSCLC), and in breast cancers. Dammann et al. (3) recently made a similar finding in lung tumors. Burbee et al. (2) demonstrate that the frequency of RASSF1A gene silencing virtually parallels that of the incidence of the loss of heterozygosity (LOH) for chromosome 3p21, the region that harbors the gene. Both groups (2,3) find that RASSF1A promoter hypermethylation is an extremely frequent occurrence in SCLC, a tumor in which chromosome . . . [Full Text of this Article]

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