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Oncology Center [S. J. N., J. G. H., N. E. D., J. R. G.] and Department of Pathology [E. G.], The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231; Department of Pathology, Vanderbilt University, Nashville, Tennessee 37232 [F. F. P.]; Lilly Research Labs, Eli Lilly and Company, Indianapolis, Indiana 46285 [J. R. G., P. W. I.]; and the Institute of Medicine, National Academy of Sciences, Washington, DC 20418 [S. J. N.]
Loss of expression for both the estrogen receptor-
and
E-cadherin genes has been linked to disease
progression in human ductal breast carcinomas and has been associated
with aberrant 5' CpG island methylation. To assess when, during
malignant progression, such methylation begins and whether such
methylation increases with advancing disease, we have surveyed 111
ductal carcinomas of the breast for aberrant methylation of the
estrogen receptor- and E-cadherin 5' CpG islands. Hypermethylation
of either CpG island was evident prior to invasion in 
30% of ductal
carcinoma in situ lesions and increased significantly to
nearly 60% in metastatic lesions. Coincident methylation of both CpG
islands also increased significantly from 20% in ductal carcinoma
in situ to nearly 50% in metastatic lesions.
Furthermore, in all cases, the pattern of methylation displayed
substantial heterogeneity, reflecting the well-established,
heterogeneous loss of expression for these genes in ductal carcinomas
of the breast.
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