Hypothesis for endometrial carcinoma carcinogenesis. Preventive prospects.
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.(ABSTRACT TRUNCATED AT 250 WORDS)
Corocleanu
M
M
Obstetrics and Gynecology Hospital, Brasov, Romania.
D000328:Adult; D002455:Cell Division; D015687:Cell Hypoxia / Q000502:physiology; D002471:Cell Transformation, Neoplastic; D004714:Endometrial Hyperplasia / Q000209:etiology; D016889:Endometrial Neoplasms / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D004717:Endometrium / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008875:Middle Aged; D009376:Neoplasms, Hormone-Dependent / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D011230:Precancerous Conditions / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D011247:Pregnancy; D012307:Risk Factors