“These findings suggest that ESR2-TP53 combination can be used to stratify TNBC into therapeutically actionable subgroups,” Dr. Das and coinvestigators proposed.
“Our data that treatment with tamoxifen can lead to sequestration of mutant TP53 away from TP73 and thereby reactivate tumor suppressor activities of TP73, provide for the first time, a strong rationale for suggesting that tamoxifen therapy could be beneficial to basal-type/TNBC patients expressing mutant TP53,” they concluded. “On the other hand, based on our data that ESR2 is proproliferative in the WT [wild-type] TP53 context, we predict that in TNBCs expressing WT TP53, tamoxifen or other agents that increase ESR2-WTP53 interaction may not only be ineffective as antitumor agents, but also may contribute to adverse outcome.”
The authors disclosed that they had no conflicts of interest. The study was supported by the several sources including the National Cancer Institute and Susan G. Komen for the Cure.
SOURCE: Mukhopadhyay UK et al. J Natl Cancer Inst. 2019 Apr 16. doi: 10.1093/jnci/djz051.