>A recent publication in Science ("Prevention of Brca1-mediated mammary tumorigenesis in mice by a progesterone antagonist," Poole, et al., Dec. 1, 2006), with associated press conferences, reported an experiment in which a special kind of mouse was prepared, which lacked two tumor-suppressing genes called BRCA and p53.
>One of the functions of the BRCA gene product is to repair genetic damage, and another function is to (like progesterone) suppress the estrogen receptor and its functions. Estrogen, and some environmental carcinogens, can suppress the BRCA gene product. Estrogen can also turn off the tumor suppressor protein, p53. So it is interesting that a group of experimenters chose to produce a mouse that lacked both the normal BRCA and p53 genes. They had a mouse that was designed to unleash estrogen's effects, and that modeled some of the features of estrogen toxicity and progesterone deficiency.
>This mouse, lacking an essential gene that would allow progesterone to function normally, probably affecting progesterone's ability to eliminate the estrogen receptor, also lacked the tumor suppressor gene p53, which is required for luteinization (Cherian-Shaw 2004); in its absence, progesterone synthesis is decreased, estrogen synthesis is increased.
>(Chen, Y, et al., 1999: BRCA represses the actions of estrogen and its receptor, and, like progesterone, activates the p21 promoter, which inhibits cell proliferation. Aspirin and vitamin D also act through p21.)
>The mutant BRCA gene prevents the cell, even in the presence of progesterone, from turning off estrogen's effects the way it should. The antiestrogenic RU486 (some articles below), which has some of progesterone's effects (including therapeutic actions against endometrial and breast cancer), appears to overcome some of the effects of that mutation.
>It might have been proper to describe the engineered mouse that lacked both the BRCA and the p53 genes as a mouse in which the effects of estrogen excess and progesterone deficiency would be especially pronounced and deadly. To speak of progesterone as contributing to the development of cancer in that specially designed mouse goes far beyond bad science. However, that study makes sense if it is seen as preparation for the promotion of a new drug similar in effect to RU486, to prevent breast cancer.
>The study's lead author, Eva Lee, quoted by a university publicist, said "We found that progesterone plays a role in the development of breast cancer by encouraging the proliferation of mammary cells that carry a breast cancer gene." But they didn't measure the amount of progesterone present in the animals. They didn't "find" anything at all about progesterone. The "anti-progesterone" drug they used has been used for many years to treat uterine, ovarian, and breast cancers, in some cases with progesterone, to intensify its effects, and its protective effects are very likely the result of its antiestrogenic and anti-cortisol effects, both of which are well established, and relevant. In some cases, it acts like progesterone, only more strongly.
…
>The recent report that the incidence of breast cancer in the United States fell drastically between 2002 and 2004, following the great decline in estrogen sales, shows the magnitude of the injury and death caused by the falsifications of the estrogen industry–a matter of millions of unnecessary deaths, just in the years that I have been working on the estrogen issue. The current campaign against progesterone can be expected to cause many unnecessary cancer deaths (e.g., Plu-Bureau, et al., Mauvais-Jarvis, et al.), while distracting the public from the culpability of the estrogen industry.
http://raypeat.com/articles/articles/ru486.shtml
>When any part of a living organism is injured, for example by x-rays or surgery, the
emitted substances affect the endocrine and nervous systems, activating processes that
change metabolism and behavior. The injured tissue takes on new functions, for
example by locally synthesizing estrogen, cortisol (Vukelic, et al., 2011), and other
hormones, as well as stimulating the normal endocrine glands to secrete them.
…
>The drug industry is now looking for chemicals that will
specifically inhibit the carbonic anhydrase enzymes that are active in tumors. Existing
carbonic anhydrase inhibitors, such as acetazolamide, will inhibit those enzymes,
without harming other tissues. Aspirin has some effect as an inhibitor of carbonic
anhydrase (Bayram, et al., 2008). Since histamine, serotonin (Vullo, et al., 2007), and
estrogen (Barnett, et al., 2008; Garg, 1975) are carbonic anhydrase activators, their
antagonists would help to acidify the hypoxic cells. Testosterone (Suzuki, et al., 1996)
and progesterone are estrogen antagonists that inhibit carbonic anhydrase.
http://raypeat.com/articles/articles/cancer-disorder-energy.shtml