This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bare, J. W. Articles by Epstein, E. H. Search for Related Content PubMed PubMed Citation Articles by Bare, J. W. Articles by Epstein, E. H., Jr.

Loss of Heterozygosity at Chromosome 1q22 in Basal Cell Carcinomas and Exclusion of the Basal Cell Nevus Syndrome Gene from This Site¹

Department of Dermatology, San Francisco General Hospital [J. W. B., E. H. E., Jr.], and Department of Obstetrics and Gynecology, and Pediatrics, University of California [R. V. L.], San Francisco, California 94143

Basal cell carcinomas, the most common human tumors, generally appear sporadically and in small numbers. Rarely, they may appear in great numbers and at an earlier age as a manifestation of the basal cell nevus syndrome, an autosomal dominant inherited disorder. Drawing on the retinoblastoma paradigm, we have begun a search for tumor suppressor genes important in the development of basal cell carcinomas by comparing DNA of tumors and normal cells. Loss of heterozygosity, a frequent marker of the site of tumor suppressor genes, was found at chromosome 1q in one-third of the tumors studied. However, comparison of the inheritance of DNA markers versus the inheritance of the basal cell nevus syndrome in one large kindred excluded this area of chromosome 1q as the site of the gene whose abnormality causes this hereditary disease. These data suggest that large deletions may accompany the development of cutaneous, low grade tumors just as they accompany the development of visceral, high grade cancers.

¹ This investigation was supported in part by NIH Grants AR39953 (to E. H. E., Jr.) and NS25541 (to R. V. L.) and a grant from the University of California Cancer Coordinating Committee (to E. H. E., Jr.). This work was published in part in abstract form (Clin. Res., 38: 221A, 1990).

² To whom requests for reprints should be addressed, at: Room 269, Building 100, San Francisco General Hospital, 1001 Potrero Street, San Francisco, CA 94110.

Received 8/19/91. Accepted 12/27/91.