PPARs as determinants of the estrogen receptor lineage: Use of synthetic lethality for the treatment of estrogen receptornegative breast cancer

1Citations
Citations of this article
7Readers
Mendeley users who have this article in their library.

Abstract

The Dilemma: Estrogen receptora-negative (ER-) breast cancer lacks a specific critical target to control tumor progression. The Objective: To identify mechanisms that enable increased expression of the ER+ lineage in an otherwise ER- breast cancer. Preface: The nuclear receptor superfamily members PPARγ and PPARδ regulate gene expression associated with a multitude of pathways, including intermediary metabolism, angiogenesis, proliferation and inflammation (see reviews [1-3]). Recent developments using transgenic and knockout mice, as well as pharmacologic intervention with PPARγ and PPARδ agonists, have revealed a previously unknown relationship between PPARγ suppression and PPARδ activation that leads to the appearance of ER+ tumors, enabling a synthetic lethality approach by anti-ER therapy. The ability to selectively affect the ER+ lineage by modulating PPARγ and PPARδ activity represents a new clinical paradigm and opportunity to treat ER- cancer with PPARγ and PPARδ modulating agents, ultimately rendering them more responsive to adjuvant therapy.

Author supplied keywords

Cite

CITATION STYLE

APA

Glazer, R. I., & Kopelovich, L. (2017). PPARs as determinants of the estrogen receptor lineage: Use of synthetic lethality for the treatment of estrogen receptornegative breast cancer. Oncotarget, 8(31), 50337–50341. https://doi.org/10.18632/oncotarget.17302

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free