Comparative genomic hybridization analysis on male breast cancer

The spectrum of genetic alterations in primary male breast cancer is not well established. We analyzed chromosomal imbalances in 39 tumor samples from primary male breast cancer by comparative genomic hybridization (CGH) and correlated CGH findings with clinicopathological factors. Chromosomal gains...

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Published inInternational journal of cancer Vol. 118; no. 10; pp. 2455 - 2460
Main Authors Rudlowski, Christian, Schulten, Hans‐Jürgen, Golas, Mariola Monika, Sander, Bjoern, Barwing, Roland, Palandt, Jens‐Ekkehard, Schlehe, Bettina, Lindenfelser, Rüdiger, Moll, Roland, Liersch, Torsten, Schumpelick, Volker, Gunawan, Bastian, Füzesi, László
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 15.05.2006
Wiley-Liss
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Summary:The spectrum of genetic alterations in primary male breast cancer is not well established. We analyzed chromosomal imbalances in 39 tumor samples from primary male breast cancer by comparative genomic hybridization (CGH) and correlated CGH findings with clinicopathological factors. Chromosomal gains were most frequent at 1q (46%), 8q (46%), 16p (36%), 17q (36%), Xq (28%), 20q (26%) and Xp (18%). Losses were most commonly observed at 8p (36%), 16q (28%), 13q (28%), 6q (18%), 11q (18%) and 22q (18%). Gains at 16p, 20q and Xq and losses at 13q correlated significantly with higher degree of cytogenetic complexity. Significant associations with clinicopathological factors were observed for +8q and −16q with larger tumor size and −16q with lower proliferative activity and lower grade of malignancy. A comparison with reported CGH data from female breast cancer showed a similar pattern of chromosomal imbalances, including +1q, −8p, +8q, −13q, +16p, −16q, +17q and +20q. Our results indicate that male breast cancer shares a common pattern of imbalances with female breast cancer, suggesting that similar genetic events may underlie the development and progression of male and female breast cancer. © 2005 Wiley‐Liss, Inc.
Bibliography:The first 2 authors contributed equally to this work.
ObjectType-Article-1
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ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.21646