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  1. #1
    D00fy's Avatar
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    Nolvadex will help with progestin induced/prolactin gyno... (GOOD READ)

    I was doing searchs on "Deca " and i found a really old thread and i Bumped it for more studies,

    Mister X from EF...... Has posted some good info



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    Multihormonal regulation of the progesterone receptor in MCF-7 human breast cancer cells: interrelationships among insulin /insulin-like growth factor-I, serum, and estrogen.
    Endocrinology 1990 Feb;126(2):891-8 (ISSN: 0013-7227)
    Katzenellenbogen BS; Norman MJ [Find other articles with these Authors]
    Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
    Estrogen (E) is well known to be an important stimulator of progesterone receptor (PR) synthesis in target cells. We have observed that E stimulation of PR in MCF-7 human breast cancer cells (as monitored by progestin binding or Western blotting with anti-PR antibodies) increases as a function of serum concentration in the cell culture medium; PR stimulation by E is greatest in high serum medium (5% or 10% charcoal dextran-treated calf serum) and is not observed when cells are in medium containing serum concentrations below 1%, although estrogen receptor levels are well maintained. This suggests that some serum factor(s) may be essential for E to be able to stimulate PR. To better understand such factors, we have grown cells in serum-free medium and in serum-free medium supplemented with insulin (6.25 micrograms/ml) [corrected], transferrin (6.25 micrograms/ml), selenium (6.25 ng/ml), albumin (1.25 mg/ml) [corrected], and linoleic acid (5.35 micrograms/ml; ITS+). Unexpectedly, we found that addition of ITS+ (without E) increases PR levels in these cells, especially in the absence of serum and under low serum conditions where E stimulation of PR is poor. Analyses of the individual components in ITS+ reveal that insulin is the major active component. Dose-response studies indicate that high superphysiological (greater than 1 microgram/ml) concentrations of insulin are required. In contrast, low physiological levels of insulin-like growth factor-I (IGF-I; 10 or 40 ng/ml) are active, suggesting mediation by the IGF type I receptor system. At all serum concentrations (0-10%), the effects of ITS+ and E in increasing PR are synergistic. The fact that anti-E are able to suppress the insulin/IGF-I stimulation as well as the E stimulation of PR suggests that the anti-E can actively interfere with the action of the growth factor as well as the action of E. These results indicate that regulation of PR is multifactor and raise the possibility that PR may be regulated in vivo by both E and growth factors such as IGF-I that are known to be increased in these breast cancer cells by E.
    : Endocrinology 1990 Jan; 126(6):3217
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    Hormones as cancer growth factors.
    Lancet 1984 Oct 13;2(8407):843-4 (ISSN: 0140-6736)
    Israel L; Band P [Find other articles with these Authors]
    It is postulated that some hormones may regulate proliferation of cancer cells in the same way as growth factors produced by cellular oncogenes. The gene coding for the hormone's specific receptor would also act as a cellular oncogene. Normal adult breast cells show few if any oestrogen receptors. In the model put forward the oestrogen receptors in breast cancer cells should not be regarded as a marker of differentiation but as a survival advantage for the tumour when oestrogens are present. Prolactin and somatomedin may also behave as growth factors. In relation to the antitumour effects of hormone antagonists such as tamoxifen , it is postulated that cancer cells are immortalised and prevented from full differentiation by the presence of growth factors and their receptors. If receptor genes are re-expressed through the process of neoplastic transformation, their presence in cancers from unresponsive normal tissues should be regarded as a common event
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    Insulin-like growth factor 1 receptors in human breast cancer and their relation to estradiol and progesterone receptors.
    Cancer Res 1988 Nov 15;48(22):6429-33 (ISSN: 0008-5472)
    Peyrat JP; Bonneterre J; Beuscart R; Djiane J; Demaille A [Find other articles with these Authors]
    Centre Oscar Lambret, Lille, France.
    Insulin-like growth factor 1 (IGF1) binding sites were characterized in breast cancer. We demonstrate the presence of one high affinity binding site. Chemical cross-linking of 125I-IGF1 to breast cancer membranes in reducing condition and sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed one band with an apparent molecular weight of 130,000. The specificity of the binding was studied. IGF2 was a good competitor whereas insulin competed with a potency lower than 1/100 that of IGF1. This IGF1 binding corresponded to the previously described type 1 IGF receptor (IGF1-R). IGF1-R was determined in 76 human breast cancer biopsies. Ninety-three % of the tumors were positive. The specific binding range was 0-16.4%; the geometric IGF1-R mean level was 3.9%. There was a relation (chi 2 test) between IGF1-R and progesterone receptor positivity rates (P = 0.002). The IGF1-R concentrations were correlated (Spearman test) with those of estradiol receptor (P = 0.0018) and progesterone receptor (P = 0.0011). A positive linear correlation existed between IGF1-R and estradiol receptor (P = 0.006) and between IGF1-R and progesterone receptor (P = 0.003). Our demonstration of the presence of IGF1-R in human breast cancer biopsies suggests that IGF1, acting either via the endocrine, paracrine, or autocrine pathways, could stimulate tumor growth.

    If you appreciate the studies, thank 'Ivan Drago' from Anabolic Fitness, he looked up the research, not I.

    The bottom line is that increased IGF-1 level is nessecery for gyno to develope, no matter what is it ER, or PR.
    Nolvadex lower IGF-1 level very effectively(by 24%)

  2. #2
    D00fy's Avatar
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    Winstrol will help with progestin receptor activity, but to what degree, that's the Q
    Ellis AJ, Cawston TE, Mackie EJ.

    Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.

    The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.


    I scrapped this off of one of H.FPlex's posts on winstrol as well. For whatever it's worth, it does show the PR antagonist activity with stanozolol.

  3. #3
    D00fy's Avatar
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    Here is the Link

    http://boards.elitefitness.com/forum...34#post1292106


    GIVE CREDIT TO THOSE WHO RESPONDED!!!!!!!!!!!!!!!!
    thanx Mister X and the rest of yall

  4. #4
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    iron4life79 is offline Retired Moderator
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    interesting..........i'd like to see some other bros take on this. dr evil, any thoughts?

    peace bb79

  5. #5
    NightOp is offline Member
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    bump

  6. #6
    Dr.Evil's Avatar
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    many things bind to PR including estrogen. just by eliminating estrogen won't do anything in a deca cycle because the steroid nandrolone binds to the PR itself. it doesn't aromatize into estrogen or anything before binding to the PR. the only effective way for preventing deca gyno would be to introduce something to compete for the PR such as ru-486 and to a very small extent, winny.

  7. #7
    Mike's Avatar
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    Flame me if you will but I firmly believe that the only two USED compounds to attack or prevent gyno from deca etc are RU-486 and ZK-89.299. You need to do more than just bind to the progesterone receptor to deter gyno. (For example - estrogen binds to the PR, so by this logic wouldn't adding lots of estrogen to your cycle prevent gyno?? Try it if you want to )

    The reason RU-486 and ZK 89.299 work is because when they bind to the receptor it prevents progesterone from occupying the PR, when you do that you block the gene transcription that progesterone normally turns on, and the proteins needed to start the process of gyno, are never synthesized. That's why I dont believe that proving that winny binds to the PR doesnt actualy prove that it acts as some level of deterrent. The progesterone must be prevented from occupying the PR, this doesnt happen with EVERY compound that just binds to the PR.

    (btw Dr. E - I lost the post we were talking bout this in)

    **BTW - for those wondering what ZK-89.299 is

    Onapristone (ZK 89.299) is another progesterone antagonist. The only difference between these two progestrogen antagonists (ru-486 and zk-89.299), is the difference in antiglucocorticoid activities for the glucocorticoid receptor (GR). RU-486 provokes this action while Onapristone does not. RU-486 actually blocks corticoid action

  8. #8
    Dr.Evil's Avatar
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    yeah, i can't find it either.

    anyway, anything that binds to the PR and does not activate it will be a deterrant for others that can bind the PR that do activate it. this is simple competitive binding. ru-486 binds to the PR and does not activate it, leaving things like deca unable to bind to the PR. the same goes for winny. however, the binding affinity of winny to the PR is not nearly as strong as ru-486 and thus would not nearly be as successful if at all.

  9. #9
    D00fy's Avatar
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    whoop ,so Dr.Evil since u said winny is not strong enough to bind to the PR as ru-486,wouldn't upping to dosage of winny help?

  10. #10
    PunkRawk is offline Member
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    i looked at those studies for like 2 secs and noted this....WE ARE NOT FUCKING WOMEN....i have never heard of a case of man coming down with breast cancer...these studies dealing with prgest and estrodial all have to do with women....and why would you want to lower igf-1??? igf cannot possibly have anything to do with gyno....otherwise we would all have it...

  11. #11
    vanjag is offline Junior Member
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    PunkRawk...

    There are cases of male breast cancer, so don't be so ultimative on this, since you are obviously not sufficiently informed. And the fact that you are not a fucking woman is just partially right, because both sexes have the same receptors, it just depends what kinds of hormones they are stimulated with.

    ......

    These studies are all fine, but as from I've read here the general conclusion would be that all kinds of molecules bind to the progesterone receptor, but that's not enough for us to conclude that we should eliminate those compounds from the system, since they have other uses that outcome their PR activation by far.

  12. #12
    Dr.Evil's Avatar
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    Originally posted by D00fy
    whoop ,so Dr.Evil since u said winny is not strong enough to bind to the PR as ru-486,wouldn't upping to dosage of winny help?
    competitive binding can be tricky to explain. let's say you have enough winny to occupy all the PR in your body (receptor saturation). this is unlikely, but for the sake of explanation, let's assume this scenario. when something else comes along like deca that can bind stronger to the PR then it will likely displace the winny from the PR. now, let's assume your body has enough deca to saturate the PR in addition to having enough winny to saturate the PR. in this scenario deca will not displace all of the winny, but just a larger percentage of them. the higher the binding affinity is the higher the percentage of PR it will occupy over its competitors. you want this percentage to be in your favor, but unfortunately because winny's binding affinity to the PR is not that strong, the percentage will strongly disfavor you. having more winny can certainly help, but it will not be very effective at displacing the large amount of deca you put into your body.

    even if winny can occupy half of your PR and deca the other half, you're still going to be at high risk for progestenic gyno because half of your PR have been activated by deca.

  13. #13
    PunkRawk is offline Member
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    maybe i should be more specific in my generalizations...The first study like the others have a female breast cancer operative behind the studies. The invitro study is about female type PR. IGF-1 receptors exist in most of our tissues hence why GH will work on a multiple of systemic effects. Unfornutely too, as the article mentioned, IGF-1 also will help cancer cells to proliferate. They study how the PR and E receptors work to understand how breast cancer occurs and develops. Since male breast cancer is extremely low the focus is generally on the female gender where the occurance is much higher




    Originally posted by vanjag
    PunkRawk...

    There are cases of male breast cancer, so don't be so ultimative on this, since you are obviously not sufficiently informed. And the fact that you are not a fucking woman is just partially right, because both sexes have the same receptors, it just depends what kinds of hormones they are stimulated with.

    ......

    These studies are all fine, but as from I've read here the general conclusion would be that all kinds of molecules bind to the progesterone receptor, but that's not enough for us to conclude that we should eliminate those compounds from the system, since they have other uses that outcome their PR activation by far.

  14. #14
    D00fy's Avatar
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    thx good info for me

  15. #15
    vanjag is offline Junior Member
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    PunkRawk...

    What you are saying about IGF-1 is true, but note that it only helps tumor cell proliferation once there is a tumor, and does not act as a trigger mechanism to produce tumor cells. Of course, the study is done on women because to produce a sufficient statistical specimen of men with breast cancer, one would have to do a multicentrical clinical study, but the bottom line is that male breast cancer is histologically the same as female, it's only that it is much more common in females.

    This being said, if I had to focus on one or two compounds which would pose danger for male bodybuilders to develop breast cancer, it wouldn't be IGF-1, but estrogen or progesterone, since this is the molecule that induces natural proliferation of lactiferous tubules that later have the ability to undergo anaplastic change and produce a tumor. These are what give you gyno, and then you have much better chances of growing a breast tumor, and in my opinion, this is when IGF-1 comes into play, once tumor is formed. My opinion is that IGF-1 shouldn't be looked upon with fear of developing a tumor.

    V

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