The mechanisms leading to the occurrence and progression of endometriosis are far from being completely understood. After implantation or differentiation of ectopic endometrium, further proliferation of the endometriosis implants will depend either on the endocrine status or on the local production of endocrine, immunological, growth and angiogenic factors. GnRH receptors as well as GnRH analogues binding to cell membranes have been detected on human breast, ovarian and endometrial cancer cells. Thus, along with an indirect effect due to hypoestrogenism, a direct effect of GnRH analogues on both breast, ovarian and endometrial cancer cells has been suggested as a possible mechanism of action. Likewise, we speculate whether GnRH analogues may also exert a direct modulatory effect on endometriosis cell growth.
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Mario Vignali (1998) studied this question.
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