Somebody with a science background please interpret this, cause it seems interesting but I have no clue WTF the conclusion is.
Oh and I realize that the subjects are women etc… but hopefully there is something good here.
Well, not a science guy, but from my reading it seems that starting an AI, rather than a SERM, while the tumour is still present, as opposed to post-op, actually changes the makeup of the tumour.
How it changes seems to be on the cellular level where the tumour “devolves”(perhaps not the right word) and becomes more fibrous. This is what I interpret by the “pathological response” mentioned. I assume the Ki67 they refer to is some kind of protein marker or antibody that they use to measure the development stage of a tumour. It points out that AI treatment also reduces it spreading which is why I used “devolve”. So it looks like that tumours that are further along, revert back somewhat. The implication, by my account, would be that this would make treatment afterwards that much easier. In other words, you would be removing or treating a tumour that was less advanced? Interesting if I have it even half right…
[quote]MrZsasz wrote:
Well, not a science guy, but from my reading it seems that starting an AI, rather than a SERM, while the tumour is still present, as opposed to post-op, actually changes the makeup of the tumour.
How it changes seems to be on the cellular level where the tumour “devolves”(perhaps not the right word) and becomes more fibrous. This is what I interpret by the “pathological response” mentioned. I assume the Ki67 they refer to is some kind of protein marker or antibody that they use to measure the development stage of a tumour. It points out that AI treatment also reduces it spreading which is why I used “devolve”. So it looks like that tumours that are further along, revert back somewhat. The implication, by my account, would be that this would make treatment afterwards that much easier. In other words, you would be removing or treating a tumour that was less advanced? Interesting if I have it even half right…[/quote]
Believe it or not, I found this article cited by a poster that claimed that nolvadex would inflame gyno that occurred with the use of a 19nor like tren. How he got that I haven’t the foggiest. Plus I don’t really trust any of the posters at that forum, so I thought I’d bring it here.
Hopefully we’ll clear this tren-gyno thing up as there seems to be some confusion. I have a good idea of how I would treat it on myself, but I am not 100% confident.
[quote]bushidobadboy wrote:
Well the article does state that tamoxifen increases the number of progesterone receptors:
“This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression”
So the poster could be right.
Bushy[/quote]
Yikes, that's certainly not very cozy.
ToneBone
Sapasion has suggested as much.
Say, have you guys received PM’s from me? I’ve sent out three PM’s lately and gotten no response, two were to you guys (bushy/ITZ). Cortes’ thread got me thinking my PM is jacked.
[quote]Diana Bolann wrote:
MrZsasz wrote:
Well, not a science guy, but from my reading it seems that starting an AI, rather than a SERM, while the tumour is still present, as opposed to post-op, actually changes the makeup of the tumour.
How it changes seems to be on the cellular level where the tumour “devolves”(perhaps not the right word) and becomes more fibrous. This is what I interpret by the “pathological response” mentioned. I assume the Ki67 they refer to is some kind of protein marker or antibody that they use to measure the development stage of a tumour. It points out that AI treatment also reduces it spreading which is why I used “devolve”. So it looks like that tumours that are further along, revert back somewhat. The implication, by my account, would be that this would make treatment afterwards that much easier. In other words, you would be removing or treating a tumour that was less advanced? Interesting if I have it even half right…
Believe it or not, I found this article cited by a poster that claimed that nolvadex would inflame gyno that occurred with the use of a 19nor like tren. How he got that I haven’t the foggiest. Plus I don’t really trust any of the posters at that forum, so I thought I’d bring it here.
Hopefully we’ll clear this tren-gyno thing up as there seems to be some confusion. I have a good idea of how I would treat it on myself, but I am not 100% confident.[/quote]
Nope
There is no analogizing between that study and male normal tissue.
In short, PR is a product of ER activation by estrogen. Tamoxifen is a weak estrogen, early on (especially first two weeks), and may cause a temporary expression of PR. (Of interest, there is different behavior of ER+/PR- tumors with tamoxifen vs AIs…or so say some of us). (Ki 67 is a nuclear antigen that is a marker of cell division, and is not relevant to the question of gynecomastia). An increase of PR, caused by tamoxifen, would cause increased gyno under progesterone stimulation?–gee, that is a reach!
In short, no connection. I would believe that tam aggravated gynecomastia (of whatever cause) in the intact male, only after showing it experimentally. (And, incidentally, this type of manipulation was tried, naively, in women with breast cancer, in the 1980s, and failed)
[quote]DrSkeptix wrote:
Diana Bolann wrote:
MrZsasz wrote:
Well, not a science guy, but from my reading it seems that starting an AI, rather than a SERM, while the tumour is still present, as opposed to post-op, actually changes the makeup of the tumour.
How it changes seems to be on the cellular level where the tumour “devolves”(perhaps not the right word) and becomes more fibrous. This is what I interpret by the “pathological response” mentioned. I assume the Ki67 they refer to is some kind of protein marker or antibody that they use to measure the development stage of a tumour. It points out that AI treatment also reduces it spreading which is why I used “devolve”. So it looks like that tumours that are further along, revert back somewhat. The implication, by my account, would be that this would make treatment afterwards that much easier. In other words, you would be removing or treating a tumour that was less advanced? Interesting if I have it even half right…
Believe it or not, I found this article cited by a poster that claimed that nolvadex would inflame gyno that occurred with the use of a 19nor like tren. How he got that I haven’t the foggiest. Plus I don’t really trust any of the posters at that forum, so I thought I’d bring it here.
Hopefully we’ll clear this tren-gyno thing up as there seems to be some confusion. I have a good idea of how I would treat it on myself, but I am not 100% confident.
Nope
There is no analogizing between that study and male normal tissue.
In short, PR is a product of ER activation by estrogen. Tamoxifen is a weak estrogen, early on (especially first two weeks), and may cause a temporary expression of PR. (Of interest, there is different behavior of ER+/PR- tumors with tamoxifen vs AIs…or so say some of us). (Ki 67 is a nuclear antigen that is a marker of cell division, and is not relevant to the question of gynecomastia). An increase of PR, caused by tamoxifen, would cause increased gyno under progesterone stimulation?–gee, that is a reach!
In short, no connection. I would believe that tam aggravated gynecomastia (of whatever cause) in the intact male, only after showing it experimentally. (And, incidentally, this type of manipulation was tried, naively, in women with breast cancer, in the 1980s, and failed)
[/quote]
Since you obviously have some clue about this issue, do you have any idea about why there is some difference between the supposed two types of gyno?
[quote]MasterfulStroke wrote:
DrSkeptix wrote:
Diana Bolann wrote:
MrZsasz wrote:
Since you obviously have some clue about this issue, do you have any idea about why there is some difference between the supposed two types of gyno?[/quote]
I am not an expert in the subject, but I am not able to find much regarding progesterone-like steroids and the induction of gyno.
But why do we need to propose 2 types of gynecomastia, when one will do?
Here is an answer to a different question:
Measurement of androgen and estrogen receptors in breast tissue from subjects with anabolic steroid-dependent gynecomastia.
[i]
Calzada L, Torres-Calleja J, Martinez JM, Pedrón N.
Unidad de Investigación Médica en Medicina Reproductiva, Instituto Mexicano del Seguro Social, México DF. leo_calzada@yahoo.com
In order to assess the relationship between anabolic steroid administration and gynecomastia, we studied the effects produced by administering nandrolone decanoate and a mixture of propionate, phenilpropionate, isocaproate and testosterone decanoate to bodybuilders during a six month period. The following significant changes occurred: a 53% reduction in serum testosterone; LH and FSH levels were suppressed to 77% and 87%, respectively, in comparison to control values; and although 45% of the subjects showed an increase in serum estradiol levels, no statistically significant differences were found compared with control estradiol levels. With regard to estradiol and androgen receptors, 85% of gynecomastia tissue contained estradiol or androgen receptors, while 40% contained both. The mean values of estradiol and androgen receptors in the cytosol were 65 +/- 10 and 52 +/- 5 fmol/mg protein, respectively. Nuclear androgen and estradiol receptor levels were 33 +/- 7 and 67.5 +/- 9 fmol/mg protein, respectively. The presence of hormone receptors in gynecomastia receptive cells provides support for the hypothesis that gynecomastia is steroid-dependent.
[/i]
With such receptors (induced by either T or nandrolone), perhaps we do not need to think about progesterone receptors–i.e., there are no good selective PR antagonists (and nobody here really should want to take RU486).