Relationship between B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) and homologous recombination regulatory genes in invasive ductal breast carcinomas.

摘要: B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1) is a Polycomb group protein that able to induce telomerase activity, enabling the immortalization of epithelial cells. Immortalized cells are more susceptible double-strand breaks (DSB), which subsequently repaired by homologous recombination (HR). BRCA1 among HR regulatory genes involved in response DNA damage associated with RAD51 protein, accumulates foci after signaling H2AX, another important marker damage. Topoisomerase IIIs (topoIIIs) removes intermediates before chromosomal segregation, preventing cellular structure. In breast carcinomas positive for BMI-1 role proteins remains be investigated. The aim this study was evaluate association between and proteins. Using tissue microarrays containing 239 cases primary tumors, expression Bmi-1, BRCA-1, Rad51, p53, Ki-67, topoIIIs, estrogen receptors (ER), progesterone (PR), HER-2 analyzed immunohistochemistry. We observed high Bmi-1 66 (27.6%). Immunohistochemical overexpression related ER (p=0.004), PR (p<0.001), Ki-67 p53 (p=0.003), BRCA-1 (p= 0.003), H2AX (p=0.024) topoIIIs (p<0,001). Our results show relationship genes, suggesting might an event regulation. However, further studies necessary understand mechanisms could regulate pathways invasive ductal