Breast cancer, a highly penetrant hereditary disorder, is the most common cancer in women worldwide. Approximately 10% of breast cancer cases are hereditary and 15% of patients with invasive breast cancer have a first-degree relative with the same disorder. Genetic counseling has become an important tool of the health care system providing information and support to families at risk of a genetic disorder. Oncology research teams have designed breast cancer screening guidelines for highrisk patients. Along the past decade, several genes have been identified as genetically related to breast cancer inheritance. BRCA1 and BRCA2 are considered the most important genes related to inheritance predisposition of breast cancer, along with PTEN and TP53 [1]. The BRCA1 and BRCA2 structures are different but their functions are interconnected and related to DNA repair. The susceptibility of breast cancer for patients with the BRCA1 mutation is up to 87% for older women. Another gene, TP53, codes for a protein that acts as the guardian of the genome, binds to DNA in order to perform transcriptional regulatory functions, regulation of the cell cycle and apoptosis among other functions. According to genetic counseling and epidemiologic studies, the risk of developing cancer for patients with TP53 polymorphisms is 90%. Regarding the gene PTEN, germline mutations increases the risk of breast cancer and about 80% of patients with breast cancer carry germline mutations in the gene. PTEN is an oncogene and codes for a protein with phosphatase activity, related to the regulation of cell cycle, controlling cells growth and able to promote cell cycle arrest. Currently, genetic counseling endeavor to identify patients at risk of genetic anomalies, study family history and inheritance patterns, calculate risks of recurrence, and provide information regarding testing and treatment procedures. Therefore, breast cancer patients and their families are presented with possibilities of screening for BRCA1, BRCA2, TP53, and PTEN mutations, and preventive care such as chemoprevention and prophylactic surgery.

RAD51a is a highly conserved protein and its major role is the repair of DNA double strand breaks. Endogenous species are generated during normal cell metabolic activities and can cause damage to DNA, as well as several environmental factors. The interactions RAD51a perform with other proteins help the maintenance of oncogenetic metabolism within cells. RAD51a interacts with PCNA, FANCD2 and ABL1, among many other cancer-related proteins. PCNA acts as a DNA clamp and is related to the replication process, FANCD2 arrests DNA replication fork progression in response to DNA damage and ABL1 is a proto-oncogene related to cell differentiation. Protein-protein interactions (PPIs) are governed by the presence of hot spots within the interface of interaction. Identifying residues directly involved in PPIs enables the likelihood of modulating such complexes with biologically active small molecules such as synthetic peptides, which leads to a new era of diseases treatment. Here, we use an in silico approach to determine the best free-energy of interaction between RAD51a and the targeted cancer-related proteins PCNA, FANCD2 and two chains of ABL1. We propose an interaction interface between RA-D51a and those proteins and identified hot spots that could be useful to understand the molecular basis of their interaction. We believe that further studies may find small-targeted molecules with therapeutics properties that could modulate those interactions and increase our knowledge regarding the complex trait diseases such as cancer.