Beyond mutations in established breast cancer predisposing genes, LoF mutations in PMS2 and FANCL among MBC patients are reported here for the first time.
We quantified adipocytes, crown-like structures (CLS) and the presence of CD8, α smooth muscle actin (αSMA) and CD68+ macrophages in both cohorts, and determined how these affected survival, in the contemporary MBC cohort.
Breast markers as NY-BR-1, GATA-3, mammaglobin, and BRST-2 are established tools for labelling primary and metastatic female breast cancer; however, none of them has been sufficiently studied in male breast cancer.
We investigated copy number status of 22 BC-related genes in 18 cases of pure ductal carcinoma <i>in situ</i> (DCIS) and in 49 cases of invasive carcinoma (IC) with adjacent DCIS (DCIS-AIC) in males using multiplex ligation-dependent probe amplification (MLPA).
Since overall prognosis and systemic therapy recommendations for MBC are similar to breast cancer in women, we describe the first case of MBC treated with BCS and IORT.
Since overall prognosis and systemic therapy recommendations for MBC are similar to breast cancer in women, we describe the first case of MBC treated with BCS and IORT.
Body mass index (P = .023) and DACH1 (P = .034) were correlated with MBC prognosis, whereas the expression of AR (P = .049), SIX1 (P = .048), surgery (P < .001), and chemotherapy (P = .001) were important for FBC in addition to already known factors: tumor size and location, TNM stage (lymph nodes and organ metastasis), radiotherapy, and ER and human epidermalgrowth factor receptor-2 (HER2) expression.
Treatments are wholly informed by clinical studies conducted in women, based on assumptions that underlying biology is similar.<b>Experimental Design:</b> A transcriptomic investigation of male and female breast cancer was performed, confirming transcriptomic data <i>in silico</i> Biomarkers were immunohistochemically assessed in 697 MBCs (<i>n</i> = 477, training; <i>n</i> = 220, validation set) and quantified in pre- and posttreatment samples from an MBC patient receiving everolimus and PI3K/mTOR inhibitor.<b>Results:</b> Gender-specific gene expression patterns were identified. eIF transcripts were upregulated in MBC. eIF4E and eIF5 were negatively prognostic for overall survival alone (log-rank <i>P</i> = 0.013; HR = 1.77, 1.12-2.8 and <i>P</i> = 0.035; HR = 1.68, 1.03-2.74, respectively), or when coexpressed (<i>P</i> = 0.01; HR = 2.66, 1.26-5.63), confirmed in the validation set.
Treatments are wholly informed by clinical studies conducted in women, based on assumptions that underlying biology is similar.<b>Experimental Design:</b> A transcriptomic investigation of male and female breast cancer was performed, confirming transcriptomic data <i>in silico</i> Biomarkers were immunohistochemically assessed in 697 MBCs (<i>n</i> = 477, training; <i>n</i> = 220, validation set) and quantified in pre- and posttreatment samples from an MBC patient receiving everolimus and PI3K/mTOR inhibitor.<b>Results:</b> Gender-specific gene expression patterns were identified. eIF transcripts were upregulated in MBC. eIF4E and eIF5 were negatively prognostic for overall survival alone (log-rank <i>P</i> = 0.013; HR = 1.77, 1.12-2.8 and <i>P</i> = 0.035; HR = 1.68, 1.03-2.74, respectively), or when coexpressed (<i>P</i> = 0.01; HR = 2.66, 1.26-5.63), confirmed in the validation set.
Treatments are wholly informed by clinical studies conducted in women, based on assumptions that underlying biology is similar.<b>Experimental Design:</b> A transcriptomic investigation of male and female breast cancer was performed, confirming transcriptomic data <i>in silico</i> Biomarkers were immunohistochemically assessed in 697 MBCs (<i>n</i> = 477, training; <i>n</i> = 220, validation set) and quantified in pre- and posttreatment samples from an MBC patient receiving everolimus and PI3K/mTOR inhibitor.<b>Results:</b> Gender-specific gene expression patterns were identified. eIF transcripts were upregulated in MBC. eIF4E and eIF5 were negatively prognostic for overall survival alone (log-rank <i>P</i> = 0.013; HR = 1.77, 1.12-2.8 and <i>P</i> = 0.035; HR = 1.68, 1.03-2.74, respectively), or when coexpressed (<i>P</i> = 0.01; HR = 2.66, 1.26-5.63), confirmed in the validation set.
Overexpression of FOXM1 was associated with well-established markers of poor prognosis; thus FOXM1 may represent a potential novel prognostic marker for MBC.
Treatments are wholly informed by clinical studies conducted in women, based on assumptions that underlying biology is similar.<b>Experimental Design:</b> A transcriptomic investigation of male and female breast cancer was performed, confirming transcriptomic data <i>in silico</i> Biomarkers were immunohistochemically assessed in 697 MBCs (<i>n</i> = 477, training; <i>n</i> = 220, validation set) and quantified in pre- and posttreatment samples from an MBC patient receiving everolimus and PI3K/mTOR inhibitor.<b>Results:</b> Gender-specific gene expression patterns were identified. eIF transcripts were upregulated in MBC. eIF4E and eIF5 were negatively prognostic for overall survival alone (log-rank <i>P</i> = 0.013; HR = 1.77, 1.12-2.8 and <i>P</i> = 0.035; HR = 1.68, 1.03-2.74, respectively), or when coexpressed (<i>P</i> = 0.01; HR = 2.66, 1.26-5.63), confirmed in the validation set.
Treatments are wholly informed by clinical studies conducted in women, based on assumptions that underlying biology is similar.<b>Experimental Design:</b> A transcriptomic investigation of male and female breast cancer was performed, confirming transcriptomic data <i>in silico</i> Biomarkers were immunohistochemically assessed in 697 MBCs (<i>n</i> = 477, training; <i>n</i> = 220, validation set) and quantified in pre- and posttreatment samples from an MBC patient receiving everolimus and PI3K/mTOR inhibitor.<b>Results:</b> Gender-specific gene expression patterns were identified. eIF transcripts were upregulated in MBC. eIF4E and eIF5 were negatively prognostic for overall survival alone (log-rank <i>P</i> = 0.013; HR = 1.77, 1.12-2.8 and <i>P</i> = 0.035; HR = 1.68, 1.03-2.74, respectively), or when coexpressed (<i>P</i> = 0.01; HR = 2.66, 1.26-5.63), confirmed in the validation set.
The expression of DDR kinases (pATR, pATM, pChk1, pChk2, and pWee1) and DNA damage markers (pRPA32 and γ-H2AX) was evaluated by immunohistochemistry in 289 MBC samples to assess their association.