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Allelic Loss on Chromosome 17 in Ductal Carcinoma in Situ of the Breast¹

Divisions of Human Molecular Genetics [D. M. R., K. F., M. H., T. S., S. A. W., H. R. D-K.], and General Surgery [D. M. R., S. A. W.]; Department of Pathology [J. H. R.], Washington University School of Medicine, St. Louis, Missouri 63110; Department of Surgery [A. M. T.], University of Edinburgh, Edinburgh, Scotland EH6 9YW; and MRC Human Genetics Unit [M. W.], Western General Hospital, Edinburgh, Scotland

Multiple tumor suppressor genes are implicated in the oncogenesis and progression of invasive carcinoma of the breast. To investigate the chronology of genetic changes we studied loss of heterozygosity on chromosome 17 in ductal carcinoma in situ, a preinvasive breast cancer. A micro-dissection technique was used to separate tumor from normal stromal cells prior to DNA extraction and loss of heterozygosity was assayed mainly using simple sequence repeat polymorphism markers and the polymerase chain reaction. Loss of heterozygosity on 17p was observed in 8 of 28 tumors (29%) when compared with normal control DNA, whereas no loss was seen on 17q, suggesting that at least one locus on 17p is involved early in the development of breast cancer.

¹ These studies were supported in part by a VA RAG Grant and ACS Grant #42048R (to D.M.R.), NIH Grant HG00304 (to H. D-K.).

² To whom requests for reprints should be addressed, at Suite 6104, Queeny Tower, One Barnes Hospital Plaza, St. Louis, MO 63110.

Received 3/31/93. Accepted 5/18/93.

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