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I understand that several scientific articles show that tamoxifen and other SERMS such as clomifene and raloxifen are effective in reducing gynecomastia for humans in different age groups and different modes (developing painful gynecomastia and/or lipomastia) respectively:

Two articles about tamoxifen, for example:

Note: I don't have full access to these articles.

Gynecomastic tissue composition

Gynecomastic tissue can be made of at least one tissue:

My problem

It was unclear to me when trying to read any article a non chemist (let alone biochemist), what is the mechanism of action of tamoxifen and other SERMs on gynecomastia.

My question

What is the mechanism of action of tamoxifen and other SERMs on gynecomastia?

Derivative questions

  • In the first article I linked to, what is the difference between "lump" type gynecomastia and "fatty" type gynecomastia (aren't both subtypes of lipomastia?)
  • Does it destroy "estrogen-dependent" fat cells up to necrosis? (if such cells at all exist)
  • Does it destroy "estrogen-dependent" mammary-gland cells up to necrosis? (if such cells at all exist)?
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According to this review article:

Estradiol and, to lesser degree, other estrogens, increase proliferation of breast epithelium and stroma and, consequently, increase the chances of mutation in rapidly proliferating epithelium

Tamoxifen and other SERMs generally act as competitive antagonist on breast estrogen receptor, which decreases estrogen's ability to induce breast tissue proliferation, hence its possible effect on gynecomastia.

As for your other questions, the first article you linked doesn't mention subtypes of gynecomastia in the abstract, and I can't find anything online about it. Necrosis is a cellular reaction to a pathological state such as infections. In general, drugs do not cause necrosis as an intended effect.

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