Some studies have attempted to determine specific genomic abnormalities present in MBC and relate these to prognosis and/or compare them to FBC. One of the first of these studies used comparative genomic hybridisation (CGH) of 39 MBC and showed gains of 1q, 8q, 16p, 17q, Xq, 20q and Xp and losses of 8p, 16q, 13q, 6q, 11q and 22q [9]. This pattern was common to genomic imbalances observed in FBC. Another study looked at a cohort of 106 MBCs analysed by multiplex ligation-dependent probe amplification analyses to determine relative gene copy numbers for specific breast cancer genes [10]. A distinctive group of cancers with a poor prognosis were identified, characterized by frequent copy number gains in 6 genes. Amplification of one of these genes, CCND1, was also found to be an independent prognostic factor. Interestingly, gains in some of these genes were not seen in FBC cases. Another study of 56 MBC cases found that compared to FBC, MBC was more likely to have genomic gains and less likely to have genomic losses [11]. Hierarchical clustering revealed two distinct genomic subgroups, termed male-simple and male-complex, one of which (male-simple) appeared distinct from the six subgroups identified in the FBC reference cohort. Finally, a recently published genome-wide association study (GWAS) of 823 MBC cases identified a single nucleotide polymorphism (SNP) at 14q24.1 in the RAD51B gene that was significantly associated with MBC risk as was TOX3 (16q12.1) [12].