What is it about?
In tumor cells, activating mutations of ESR1 gene serve DNA repair and a consequential apoptotic death instead of a proliferative activity. In tumors, estrogen receptor expression and its activation via liganded and unliganded pathways restores genomic functions. Inhibition of either estrogen or growth factor mediated regulatory pathways is a medical mistake.
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Why is it important?
Results of genetic studies on both estrogen- and antiestrogen-treated tumors were reanalyzed and associations among ER-blockade, compensatory restoration of ER-signaling and clinical behavior of cancers were investigated.
Perspectives
Upregulation of ER-signaling induced by natural estrogens is a beneficial process even in tumor cells promoting their domestication and elimination while in case of antiestrogen administration; increased ER-signaling is a compensatory action to strengthen residual genome stabilization.
professor Zsuzsanna Suba
National Institute of Oncology Budapest
Read the Original
This page is a summary of: Activating mutations of ESR1, BRCA1 and CYP19 aromatase genes confer tumor response in breast cancers treated with antiestrogens, Recent Patents on Anti-Cancer Drug Discovery, February 2017, Bentham Science Publishers,
DOI: 10.2174/1574892812666170227110842.
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