A possible role of estrogens in carcinogenesis of non-target tissues.

Abstract:

:The mitogenic action of the estrogen-receptor complex is supposedly similar in both normal and malignant target tissues. As receptors are present in several types of non-target tissues, in the case of lesions at the nuclear acceptor sites, the complex in those might be able to cause successive mitoses. Estrogen-dependent tumors of non-target tissues have been reported by several investigators. In normal and malignant cells of the breast and some other types of non-endocrine cells, the ability to produce their own estrogens (from circulating precursors) has been shown. The locally formed estrogens might have a role in the initiation of some malignant transformations. Indications of this process are the switching to estrogen production of some neoplastic endocrine or undifferentiated cells, certain ectopic effects displayed by some cancerous tissues, and the possible roles of GH, PRL and cholesterol in the development of some malignancies. The present endocrine system for the synthesis of the sexual hormones might be a specialization of a system at the cellular level. Polypeptide hormones might evolve from regulatory parts of cyclases or phosphodiesterases. Traces of the original biological processes might still be maintained by several cell-types. :An hypothesis is presented which states that the endocrine systems for the synthesis of sex hormones as we know it presently might be a specialization of a system operating at the cellular level in multicellular organisms. If this were true, then a possible role of estrogens in the carcinogenesis of nontarget tissues may be postulated. Evidence for this hypothesis is highly theoretical, but is based on extrapolations from existing experimental data. The mitogenic effect of the estrogen-receptor complex is thought to be similar in both normal and malignant target tissues. Since receptors are present in several types of nontarget tissues, especially in the case of lesions at the nuclear acceptor sites, the complex might be able to cause successive mitoses in these regions, hence carcinogenesis. Several experimental approaches to test this hypothesis are presented as suggestions; these include using malignant tissues which are most likely to divide through the action of their own estrogen, such as feminizing hepatoma, and studying the mitogenic effect of locally formed estrogens through experimentation with the anti-estrogen CI-628.

journal_name

Med Hypotheses

journal_title

Medical hypotheses

authors

Litvay M

doi

10.1016/0306-9877(79)90044-6

subject

Has Abstract

pub_date

1979-09-01 00:00:00

pages

953-68

issue

9

eissn

0306-9877

issn

1532-2777

pii

0306-9877(79)90044-6

journal_volume

5

pub_type

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