Therapeutic Role of Tamoxifen for Triple-Negative Breast Cancer: Leveraging the Interaction Between ERβ and Mutant p53

The absence of effective therapeutic targets and aggressive nature of triple-negative breast cancer (TNBC) renders this disease subset difficult to treat. Although estrogen receptor beta (ER beta) is expressed in TNBC, studies on its functional role have yielded inconsistent results. However, recently, our preclinical studies, along with other observations, have shown the potential therapeutic utility of ER beta in the context of mutant p53 expression. The current case study examines the efficacy of the selective estrogen receptor modulator tamoxifen in p53-mutant TNBC with brain metastases. Significant increase in ER beta protein expression and anti-proliferative interaction between mutant p53 and ER beta were observed after cessation of tamoxifen therapy, with significant regression of brain metastases. This case study provides supporting evidence for the use of tamoxifen in p53-mutant, ER beta+TNBC, especially in the setting of brain metastasis.

Automated summary

The absence of effective therapeutic targets and aggressive nature of triple-negative breast cancer (TNBC) makes it difficult to treat. Studies on the functional role of estrogen receptor beta (ER beta) in TNBC have yielded inconsistent results. However, recent preclinical studies have shown the potential therapeutic utility of ER beta in the context of mutant p53 expression. This case study provides supporting evidence for the use of tamoxifen in p53-mutant, ER beta+TNBC, especially in the setting of brain metastasis.