Breast Growth For Genetic Males

(22-01-2016, 08:33 PM)Lotus Wrote: [ -> ]A hypothesis to bigger boobs:

COX expression results in higher levels of prostaglandin E2 (PGE2), which in turn increases CYP19 mRNA & protein expression through increases in intracellular cyclic AMP levels.

(22-01-2016, 08:27 PM)Lotus Wrote: [ -> ]If we really want to blow the doors off aromatase we'd turn our attention to EGFR(epiderrmal growth factor), which sits of the outside of cells, and is esstetial part Mammary Gland Development. So, the question is " how come we don't know about it? ", my guess?.....its to F**kin complicated lol. I'll take at stab at it though: note the highlighted areas, I believe EGFR combined and inhibiting histone deacetylation (HDAC) while upregulating PGE2, should make for the strongest aromatase.......say what?, broad strokes of course, I'm still working on the rough edges as to how it translates to NBE. over stimulus concerns are top priority. In other words, if we can find away around the trouble spots, it lessens proliferation.


function of the epidermal growth factor receptor and erbB-2 during mammary gland morphogenesis.
Sebastian J1, Richards RG, Walker MP, Wiesen JF, Werb Z, Derynck R, Hom YK, Cunha GR, DiAugustine RP.
Author information
Abstract
The hormonal stimulation of mammary gland morphogenesis is believed to occur through growth factor receptor signaling pathways. To determine the importance of the epidermal growth factor receptor (EGFR) pathway, we examined extracts of inguinal mammary glands from prepubertal and pubertal mice for tyrosine-phosphorylated EGFR and other erbB receptors. Tyrosine phosphorylation of both EGFR and erbB-2 was detected in normal female BALB/c mice at 5-6 weeks of age, but not during the prepubertal stage, e.g., 24 days of age. Treatment of mice with estradiol or epidermal growth factor also stimulated the formation of mammary EGFR/erbB-2 phosphotyrosine. Waved-2 mice, which have impaired EGFR kinase activity, exhibited less mammary development than did wild-type (wt) mice when both were evaluated at 36 days of age. Because EGFR knockout (KO) mice die shortly after birth, glands from the newborns were implanted under the renal capsules of female nude mice. Under these conditions, extensive ductal growth was observed in mammary glands from wt animals; in contrast, glands from EGFR KO mice failed to grow beyond rudimentary structures. Tissue recombinants revealed that the wt fat pad supported the morphogenesis of EGFR KO epithelium, whereas the EGFR KO fat pad did not. Taken together, these data suggest that EGFR is essential for morphogenesis of the mammary ducts and functions during this period of mammary development as a heterodimer with erbB-2 in the mammary stroma.






http://www.intechopen.com/books/malignan...esotheliom

(15-05-2016, 11:06 PM)Lotus Wrote: [ -> ]

(15-05-2016, 06:24 PM)Tanya Marie Squirrel Wrote: [ -> ]in keeping with the thread, there are ERa receptors and ERb receptors, is there anywhere that lists which herbs are which? I havnt researched that yet.. perhaps I should

got this so far.. (hopefully its not a copy elsewhere).
http://www.ncbi.nlm.nih.gov/gene/2100/

(29-04-2015, 06:57 PM)Lotus Wrote: [ -> ]

(24-02-2015, 04:05 AM)Lotus Wrote: [ -> ]

Estrogen receptor alpha ERa is the growth receptor
Estrogen receptor beta ERb protects against cancer

Breast growth requires supplements that are pro ERa, having a good ratio of ERa to ERa is a proactive step in achieving normal growth vs malignant growth.

Botanical Modulation of Menopausal Symptoms: Mechanisms of Action?
https://www.thieme-connect.com/products/...32-1328187

(06-03-2015, 03:19 AM)Lotus Wrote: [ -> ]present study we show that caveolin-1 binds directly to ERalpha. This is part of the first part, which is party of the second part, (is that how it goes?) anyways, subcellular localization of COX-2 and caveolin-1 was determined.

J Biol Chem. 2001 Sep 14;276(37):34975-82. Epub 2001 Jun 29.

Colocalization and interaction of cyclooxygenase-2 with caveolin-1 in human fibroblasts.

Abstract
Results from our previous study suggest that cyclooxygenase-2 (COX-2) induced by phorbol 12-myristate 13-acetate (PMA) may be localized to caveolae-like structures (Liou, J.-Y., Shyue, S.-K., Tsai, M.-J., Chung, C.-L., Chu, K.-Y., and Wu, K. K. (2000) J. Biol. Chem. 275, 15314-15320). In this study, we determined subcellular localization of COX-2 and caveolin-1 by confocal microscopy. COX-2 in human foreskin fibroblasts stimulated by PMA (100 nm) or interleukin-1beta (1 ng/ml) for 6 h was localized to plasma membrane in addition to endoplasmic reticulum and nuclear envelope. Caveolin-1 was localized to plasma membrane, and image overlay showed colocalization of COX-2 with caveolin-1. This was confirmed by the presence of COX-2 and caveolin-1 in the detergent-insoluble membrane fraction of cells stimulated by PMA. Immunoprecipitation showed complex formation of COX-2 with caveolin-1 in a time-dependent manner. A larger quantity of COX-2 was complexed with caveolin-1 in PMA-treated than in interleukin-1beta-treated cells. Purified COX-2 complexed with glutathione S-transferase-fused caveolin-1, which was not inhibited by the scaffolding domain peptide. Caveolin-1-bound COX-2 was catalytically active, and its activity was not inhibited by the scaffolding domain peptide. These results suggest that COX-2 induced by PMA and interleukin-1beta is colocalized with caveolin-1 in the segregated caveolae compartment. Because caveolae are rich in signaling molecules, this COX-2 compartment may play an important role in diverse pathophysiological processes.
PMID: 11432874 [PubMed - indexed for MEDLINE]

Quote:The phosphatidylinositol 3 kinase (PI3K) pathway is one of the major pathways modulating cell growth, proliferation, metabolism, survival, and angiogenesis.