ASSOCIATION OF ALLELIC LOSSES ON HUMAN CHROMOSOMAL ARMS 11Q AND 16Q IN SPORADIC BREAST-CANCER

Breast-carcinoma development presumably results from multiple mutation al events in tumor-associated genes. Certain results indicate that som e tumor-suppressor genes may combine their pathogenetic potential to s ynergistically promote tumor growth. In an effort to identify such mec hanisms in breast tumors, a series of 77 (group 1) paired blood tumor samples from patients with sporadic mammary carcinomas was analyzed fo r loss of heterozygosity with 15 polymorphic markers on the chromosoma l arms 7q, 11q, 13q, 16q, 17p and 17q. A significant association was o bserved for the combination of allelic losses on chromosomes 11q and 1 6q. In order to confirm these findings, we studied a second independen t series of 189 breast-tumor patients (group 2) with comparable histop athological tumor stages. Group 2 was examined for the same genetic al terations using the identical set of polymorphic markers. The data fro m this group confirmed the detected association of loss of heterozygos ity on chromosomes 11q and 16q and indicate the cooperation of putativ e tumor-suppressor genes on the chromosomal arms 11q and 16q in a sub- set of breast carcinomas. The regions involved harbor the candidate ge nes ATM (mutated in ataxiatelangiectasia) on chromosome 11q23 and UVO (uvomorulin, cadherin E) and BBC1 (breast basic conserved 1) on chromo some 16q22-q24. (C) 1996 Wiley-Liss, Inc.