ORCID Profile
0000-0002-9101-9131
Current Organisations
University of Milan
,
European Institute of Oncology
,
IRCCS European Institute of Oncology (IEO)
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Publisher: Wiley
Date: 04-01-2016
DOI: 10.1111/HIS.12883
Publisher: Elsevier BV
Date: 11-2016
Publisher: Impact Journals, LLC
Date: 17-04-2018
Publisher: Wiley
Date: 28-12-2017
DOI: 10.1002/PATH.5006
Publisher: American Association for Cancer Research (AACR)
Date: 14-08-2016
DOI: 10.1158/1078-0432.CCR-15-2840
Abstract: Purpose: Male breast cancer is rare, and its genomic landscape has yet to be fully characterized. Lacking studies in men, treatment of males with breast cancer is extrapolated from results in females with breast cancer. We sought to define whether male breast cancers harbor somatic genetic alterations in genes frequently altered in female breast cancers. Experimental Design: All male breast cancers were estrogen receptor–positive, and all but two were HER2-negative. Fifty-nine male breast cancers were subtyped by immunohistochemistry, and tumor–normal pairs were microdissected and subjected to massively parallel sequencing targeting all exons of 241 genes frequently mutated in female breast cancers or DNA-repair related. The repertoires of somatic mutations and copy number alterations of male breast cancers were compared with that of subtype-matched female breast cancers. Results: Twenty-nine percent and 71% of male breast cancers were immunohistochemically classified as luminal A–like or luminal B–like, respectively. Male breast cancers displayed a heterogeneous repertoire of somatic genetic alterations that to some extent recapitulated that of estrogen receptor (ER)-positive/HER2-negative female breast cancers, including recurrent mutations affecting PIK3CA (20%) and GATA3 (15%). ER-positive/HER2-negative male breast cancers, however, less frequently harbored 16q losses, and PIK3CA and TP53 mutations than ER-positive/HER2-negative female breast cancers. In addition, male breast cancers were found to be significantly enriched for mutations affecting DNA repair–related genes. Conclusions: Male breast cancers less frequently harbor somatic genetic alterations typical of ER-positive/HER2-negative female breast cancers, such as PIK3CA and TP53 mutations and losses of 16q, suggesting that at least a subset of male breast cancers are driven by a distinct repertoire of somatic changes. Given the genomic differences, caution may be needed in the application of biologic and therapeutic findings from studies of female breast cancers to male breast cancers. Clin Cancer Res 22(16) 4045–56. ©2016 AACR.
Publisher: Wiley
Date: 29-07-2015
DOI: 10.1002/PATH.4566
Publisher: Wiley
Date: 17-03-2016
DOI: 10.1002/PATH.4691
Publisher: Wiley
Date: 29-06-2015
DOI: 10.1111/HIS.12735
Publisher: Wiley
Date: 24-05-2015
DOI: 10.1111/HIS.12712
Location: Italy
Location: Italy
Location: United States of America
No related grants have been discovered for Nicola Fusco.