IMR Press / CEOG / Volume 20 / Issue 4 / pii/1993041

Clinical and Experimental Obstetrics & Gynecology (CEOG) is published by IMR Press from Volume 47 Issue 1 (2020). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Original Research

Hypothesis for endometrial carcinoma carcinogenesis

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1 Obstetrics and Gynecology Hospital Brasov, Romania
Clin. Exp. Obstet. Gynecol. 1993, 20(4), 254–258;
Published: 10 December 1993
Abstract

Considering endometrial carcinoma as a natural experimental model for in vivo study of carcinogenesis, a hypothesis of endometrial type A carcinogenesis and some preventive prospects are advanced. Under the name of endometrial carcinoma two different types are considered: A) hormone dependent type, and B) autonomous type. Aging, obesity, hypertension and/or diabetes, persistent exposure to unopposed exogenous or endogenous estrogens are recognized epidemiological factors for endometrial carcinoma. Experimental and clinical studies have shown that in pregnancy associated with clinical conditions characterized by a compromised maternal circulation in the intervillous space, a state of true or relative hypoxia stimulates syncytial hyperplasia, as adaptive process, in order to increase the exchange area of the placenta. Vaginosonographic studies have shown in patients with endometrial thickness greater than or equal to 4 mm complex and atypical hyperplasia than endometrial carcinoma in a higher percentage than in patients with endometrial thickness less than 3 mm. It seems that hypoxia in endometrial thickness, greater than 3 mm promoted by estrogens, would be a supplementary proliferating factor. Immunological studies have shown, in patients with complex or atypical hyperplasia of the endometrium and/or endometrial carcinoma, a host immunological reaction (DTHS-reactivity test) to a pharmaceutical placental suspension, when injected intradermally. An extract prepared from placental suspension is also recognized in vitro, by patients' serum (Ouchterlony’s technique). To conclude, hypoxic insult, as common pathophysiological factor in most predisposing diseases for endometrial cancer, leads to a persistent multicellular hyperplasia of the endometrium. Sometimes populations with an altered growth pattern develop. Their occurrence marks a specific change from reactive hyperplasia into a genuine preneoplastic stage that in some cases, when not disturbed in their natural evolution, will become tumor after a given time. Genetic phenoplastic instability, in the presence of hypoxic selective pressure and sequential selection of preneoplastic cells for increased growth autonomy, are essential elements for the neoplastic development. Prevention and treatment of diseases predisposing to endometrial carcinoma and/or boosting of host immunological response against enxyme-altered cell proliferation in patients at risk, by a vacccine prepared from modified placental glycoproteins and an adjuvant, would be preventive measures.

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