this study states that progesterone promotes breast growth and has implications of breast cancer. However, this study looked at progestins not progesterone. Studies have shown a reduction of breast cancer risk with progesterone and an increase with progestins. It would have been nice to have looked at "progesterone" metabolites. This study shows the flaw that many have: the intermix progesterone and progestins as if they are one in the same and they are clearly not
Progestin is not a good synthetic progesterone anyways; but this study shows that progestin in obese women in the form of contraception, increases the risk of type II DM.
Finally, something that lowers the risk associated with synthetic progestins. Progestins are progesterone pretenders that increase breast cancer. Apigenin, a component of bioflavonoid, was shown to inhibit growth and intact cause cell death.
Study compared bioidentical progesterone (micronized progesterone) to a synthetic progestin in the inhibition of endometrial hyperplasia progression. The study found that the synthetic progestin worked best, but they both inhibited progression of the endometrial hyperplasia when followed out to 3 months therapy.
This study looked at relative risk, but estrogen plus progestin reduces the risk of colorectal cancer. Progestin is a poor sythetic progesterone analogue. One wonders what additional benefit progesterone may add as studies have shown with regards to breast cancer.
medroxyprogesterone acetate, synthetic progestin, shown to increase inflammation signaling in human breast cancer cells. This is a proposed mechamism by which growth stimulation occurs with prover and breast cancer.
The presence and activity of PR significantly affect the prognostic value of ER.
The observed loss of PR protein expression in a subset of ER+/PR+ breast cancers, because of hypermethylation or deletion of the PR gene locus, results in the loss of ER prognostic value
These findings emphasize the clinical value of assessing both PR and ER expression in breast cancer samples
PR is an essential modulator of ER-regulated genes but also that it significantly contributes to the prognostic value of ER in ER+/PR+ breast cancers
PR-regulated genes have independent prognostic value, and the presence of PR correlates with favorable clinicopathological outcomes
this study demonstrates that progestin-activated PR redirects ER chromatin binding and functions as a genomic estrogen agonist and as a phenotypic estrogen antagonist in ER+/PR+ breast cancer cells and human tumors
Approximately 80% of ER+ breast cancers are also positive for PR,
In isolation, both hormones activate or inhibit cellular processes in similar directions, although the magnitude of these effects is less for progestin alone than for estrogen alone
PR-mediated antagonism of estrogenic phenotypes is well documented
joint activation of ER and PR antagonized ER-regulated oncogenic processes
WOW!! study finds that progesterone through PR activity antagonizes ER protein expression by the cell. This has huge implications in breast cancer and possible prostate cancer. But then again, women don't need progesterone; only estrogen. The presence of PR correlates with improved clinicopathological outcomes. The authors do seem to get confused about progesterone and progestins. They are not one in the same.
Estrogen with progestin worsens cognitive decline in women >65. Little can be taken from this study other than, medroxyprogesterone acetate is a bad drug and should not be given to women for any purpose, especially in those >65. One wonders if bioidentical, physiologic hormone replacement would have the same effect? I doubt it. The likely negative impact of hormones on the brain in women >65 is due to the negative effects of MPA, the change in inflammatory cytokines, and the change in receptors.
There is absolutely no reason for women to take medroxyprogesterone acetate. Whether the author realizes it or not, he states a truth that progestin is a "trigger" in carcinogenesis of the breast. This study was designed to look at high dose apigenin, which the study found increased risk.