Abstract
Male Breast Cancer (MBC) has a familial component thus identification of polymorphic risk alleles of candidate genes and/or cytogenetic anomalies may help to predict the risk for the offspring of MBC patients. The conventional metaphase cytogenetics can indicate loci that are hotspots while analysis by single nucleotide polymorphism arrays (SNP-A) can identify chromosomal defects which may play a role in the etiology of cancer. A cumulative genotype risk due to each allele of candidate genes of the signaling pathways regulating c-MYC, HIF1A, TP53 and BRCA1 may be a factor facilitating cancer development. Cancer risk was assessed in a 35-year-old healthy son of a 60-year-old MBC patient with a family history of cancer by metaphase cytogenetics, SNP-A and analysis of 25 polymorphisms in six genes TP53, MDM2, VEGF, VEGFR1, HIF1A, and BRCA1. The risk genotype GG-TT of MDM2 309T > G and VEGF-417C/T polymorphisms along with chromosomal instability shown by cytogenetic analysis and SNP-A, rare de novo duplication Yp, deletion in 7q pericentromeric region indicate an increased risk of cancer in the healthy son of an MBC patient.
Highlights
A family history of breast cancer confers a relative risk of 2.5 with 20% of men with breast cancer having a positive family history [1]
Cancer risk was assessed in a 35-year-old healthy son of a 60-year-old Male Breast Cancer (MBC) patient with a family history of cancer by metaphase cytogenetics, single nucleotide polymorphism arrays (SNP-A) and analysis of 25 polymorphisms in six genes TP53, MDM2, VEGF, VEGFR1, HIF1A, and BRCA1
The risk genotype GG-TT of MDM2 309T > G and VEGF417C/T polymorphisms along with chromosomal instability shown by cytogenetic analysis and SNP-A, rare de novo duplication Yp, deletion in 7q pericentromeric region indicate an increased risk of cancer in the healthy son of an MBC patient
Summary
A family history of breast cancer confers a relative risk of 2.5 with 20% of men with breast cancer having a positive family history [1]. Polymorphisms in both high and low penetrance genes contribute to breast tumorigenesis in combination with exogeneous (diet, pollution) and endogeneous (hormones) factors [3]. HIF1A up-regulates expression of VEGF during hypoxia in the majority of solid tumors [5]. HIF1A expression has been associated with male breast cancer [12]
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