| Literature DB >> 31340200 |
Cathy B Moelans1, Joep de Ligt2, Petra van der Groep1,3, Pjotr Prins2, Nicolle J M Besselink2,4, Marlous Hoogstraat2, Natalie D Ter Hoeve1, Miangela M Lacle1, Robert Kornegoor5, Carmen C van der Pol6, Wendy W J de Leng1, Ellis Barbé7, Bert van der Vegt8, John Martens9, Peter Bult10, Vincent T H B M Smit11, Marco J Koudijs2,4, Isaac J Nijman2,4, Emile E Voest4,12, Pier Selenica13, Britta Weigelt13, Jorge S Reis-Filho13, Elsken van der Wall6, Edwin Cuppen2,14, Paul J van Diest1.
Abstract
Male breast cancer (MBC) is extremely rare and accounts for less than 1% of all breast malignancies. Therefore, clinical management of MBC is currently guided by research on the disease in females. In this study, DNA obtained from 45 formalin-fixed paraffin-embedded (FFPE) MBCs with and 90 MBCs (52 FFPE and 38 fresh-frozen) without matched normal tissues was subjected to massively parallel sequencing targeting all exons of 1943 cancer-related genes. The landscape of mutations and copy number alterations was compared to that of publicly available estrogen receptor (ER)-positive female breast cancers (smFBCs) and correlated to prognosis. From the 135 MBCs, 90% showed ductal histology, 96% were ER-positive, 66% were progesterone receptor (PR)-positive, and 2% HER2-positive, resulting in 50, 46 and 4% luminal A-like, luminal B-like and basal-like cases, respectively. Five patients had Klinefelter syndrome (4%) and 11% of patients harbored pathogenic BRCA2 germline mutations. The genomic landscape of MBC to some extent recapitulated that of smFBC, with recurrent PIK3CA (36%) and GATA3 (15%) somatic mutations, and with 40% of the most frequently amplified genes overlapping between both sexes. TP53 (3%) somatic mutations were significantly less frequent in MBC compared to smFBC, whereas somatic mutations in genes regulating chromatin function and homologous recombination deficiency-related signatures were more prevalent. MDM2 amplifications were frequent (13%), correlated with protein overexpression (P = 0.001) and predicted poor outcome (P = 0.007). In conclusion, despite similarities in the genomic landscape between MBC and smFBC, MBC is a molecularly unique and heterogeneous disease requiring its own clinical trials and treatment guidelines.Entities:
Keywords: amplification; breast cancer; copy number; genomic; male; mutation
Year: 2019 PMID: 31340200 PMCID: PMC6938562 DOI: 10.1530/ERC-19-0278
Source DB: PubMed Journal: Endocr Relat Cancer ISSN: 1351-0088 Impact factor: 5.678