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%)
