Non-steroidal aromatase inhibitor

BRCA2 gene is located on chromosome 13q12 and also classified as a tumour suppressor gene; though shares no homology with the BRCA1 gene. However, it can bind with BRCA1 to participate in DNA damage response pathway. BRCA2 protein functions as a mediator of the core mechanism of homologous recombination. Its mutations are linked to breast carcinomas that are ER and PR positive.  Though rarely associated with basal-like phenotype but still linked to a higher grade (II or III) when compared to age-matched sporadic cases

Tamoxifen has long been the standard for breast cancer treatment.  Studies are underway determining the effectiveness of aromatase inhibitors after or in place of Tamoxifen treatment.  Both types of aromatase inhibitors have shown superior performance to Tamoxifen in clinical trials, enabling women with advanced disease to live longer and stopping recurrences in women made cancer-free.  Large scale studies have shown switching from Tamoxifen to an aromatase inhibitor during the course of treatment will produce superior results to staying on Tamoxifen the whole way.

One hundred thirty patients were randomly assigned (EE group, n = 64; EP group, n = 66). Based on intent-to-treat analysis, treatment with EE improved median PFS to months versus months with EP (hazard ratio [HR], ; 95% CI, to ; one-sided P = .055; two-sided P = .11 [predefined significance level of .10, one-sided]). Median overall survival was an exploratory end point and improved to months with EE versus months with EP (HR, ; 95% CI, to ; P = .036). Fatigue and neutropenia were the most frequent grade 3/4 toxicities. Treatment discontinuation because of adverse events was higher in the EE group versus the EP group (11% v 2%). Protein lysine hyperacetylation in the EE biomarker subset was associated with prolonged PFS.

Non-steroidal aromatase inhibitor

non-steroidal aromatase inhibitor


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