MBC had worse OS than FBC in HR+/HER2- (Hazard ratio [HaR], 1.5; P=0.0005), HR+/HER2+ (HaR, 2.8; P<0.0001) and triple negative (HaR, 4.3; P<0.0001) (Pinteraction<0.02).
This study suggests that the Lys/Lys genotype confers susceptibility to BC risk among women of Asian ancestry, particularly for ER-positive, PR-positive, and HER2-negative tumor types.
Preoperative MBD was a strong independent prognostic factor in operable primary invasive female breast cancer, especially in patients with age >50 years and the HRc(+)/HER2(-) subtype.
The 21-gene recurrence score (RS) assay estimates the risk of distant recurrence and chemotherapy benefit in early-stage, ER+/HER2- female breast cancer.
A case-control series of 433 BRCA1/2 mutation-negative MBC and female breast cancer (FBC) cases and 849 male and female controls was included in the study.
BC subtype correlated with TIL density (p = 0.015), as we observed a higher density for human epidermal growth factor receptor type 2 (HER2) positive BC compared to luminal HER2-negative subtype.
Two classifications of Female Breast Cancer (FBC) subgroups (based in ER, PR, HER2, 2000 classification, and in ER, PR, HER2, ki67, 2013 classification) were used to achieve their prognostic value in MBC patients.
In male breast cancer (MBC) amplification of HER2, located on chromosome 17, occurs at a lower frequency than in FBC, where it is part of complex rearrangements.
The four most frequent BRCA1 mutation (2798 T > C, 3971 G > A, 3971 G > A and 624 C > T) found in female breast cancer cases in Guangxi are all located in exon 10.
This study seeks to quantify the risk of having BRCA1 mutation in female breast cancer patients with triple-negative phenotype compared with those with other phenotypes.
Therefore, the impact of anthracycline sensitivity linked to HER2/Topo II-α alterations as found in female breast cancer has low clinical significance for this specific male breast cancer phenotype.
There have been previous reports of increased PrCa risk in male BRCA1 mutation carriers in female breast cancer families, but there is a controversy as to whether this risk is substantiated.
In view of these similarities, we investigated whether the prevalence of PALB2 mutations was increased in breast cancer families with the occurrence of BRCA2 associated tumours other than female breast cancer.
However, the observed predominance of BRCA2 (0.12) over BRCA1 mutations (0.05) is in contrast with the higher proportion of BRCA1 mutations communicated for most previous studies, even those with a predominance of site-specific BC families.
However, the observed predominance of BRCA2 (0.12) over BRCA1 mutations (0.05) is in contrast with the higher proportion of BRCA1 mutations communicated for most previous studies, even those with a predominance of site-specific BC families.
Moreover, an analysis of genes correlated to steroid receptors and ERBB2 suggested a prominent role for the androgen receptor in MBC with a minor relevance for progesterone receptor and ERBB2, although, similarly to FBC, a genomic amplification could be observed.
64 families with a history of male breast cancer aged 60 or less or with a family history of male and female breast cancer were screened for the presence of BRCA1 and BRCA2 mutations.