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Comparative genomic hybridization of ductal carcinoma in situ of the breast—evidence of multiple genetic pathways
Author(s) -
Buerger Horst,
Otterbach Friedrich,
Simon Ronald,
Poremba Christopher,
Diallo Raihanatou,
Decker Thomas,
Riethdorf Lutz,
Brinkschmidt Christian,
DockhornDworniczak Barbara,
Boecker Werner
Publication year - 1999
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199903)187:4<396::aid-path286>3.0.co;2-l
Subject(s) - ductal carcinoma , comparative genomic hybridization , breast cancer , biology , in situ , pathology , in situ hybridization , genetic heterogeneity , lesion , cancer , cancer research , phenotype , chromosome , genetics , medicine , gene , chemistry , organic chemistry , gene expression
There is strong evidence that ductal carcinoma in situ (DCIS) represents a precursor lesion of invasive breast cancer. In order to analyse specific chromosomal alterations of DCIS, 38 paraffin‐embedded specimens of DCIS and six associated invasive carcinomas were examined by means of comparative genomic hybridization (CGH). Losses of 16q material were seen almost exclusively in well‐ and intermediately‐differentiated DCIS. These two subgroups differed in the average number of genetic imbalances, 2·5 and 5·5 respectively. Additionally, a higher frequency of gains of 1q and losses of 11q material was seen in intermediately‐differentiated in contrast to well‐differentiated DCIS. Poorly‐differentiated DCIS displayed a higher frequency of amplifications (17q12, 11q13) and a higher average rate of genetic imbalances (7·1). Analysis of adjacent invasive breast carcinoma revealed a genetic pattern almost identical to the one seen in the DCIS counterpart. These data characterize DCIS as a genetically far‐advanced, heterogeneous lesion and as a direct precursor of invasive breast cancer. Copyright © 1999 John Wiley & Sons, Ltd.