Indira Benakanakere

TL;DR: Women who ingest progestins for hormone therapy or oral contraception could be more at risk for developing breast cancer because of proliferation of existing latent tumor cells.

TL;DR: The flavonoid apigenin, which was previously found to inhibit progestin-dependent VEGF synthesis in human breast cancer cells in vitro, significantly delayed the development of, and decreased the incidence and multiplicity of, MPA-accelerated DMBA-induced mammary tumors in this animal model, suggesting that Apigenin has important chemopreventive properties for those breast cancers that develop in response to progestins.

TL;DR: It is proposed that progestins can accelerate the development of mammary tumors and that antiangiogenic agents and/or the use of antiprogestins that can reduce tumor incidence might be a viable therapeutic option for treatment of progestin-accelerated tumors.

TL;DR: It is concluded that the combined targeting of mtp53 and the tumor vasculature is a novel effective strategy for combating advanced breast tumors.

TL;DR: Apigenin blocks progestin-dependent induction of V EGF mRNA and protein and broadly inhibits the ability of progestins to alter the expression of other components of the angiogenesis pathway, including progesterone receptor and VEGF receptors, in human breast cancer cells.