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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrone (E1), a principal estrogen in postmenopausal women, may have profound consequences in the maintenance and progression of hormone-sensitive endometrial carcinoma. This study was designed to investigate the specific binding sites for E1 in the tumor and in the normal endometrium. The binding of [3H]E1 to the cytosolic fraction and KCl-soluble nuclear fraction from 3 endometrial carcinomas showed saturation kinetics with an apparent equilibrium dissociation constant of approximately 37 and 50 nM, respectively. The specific binding site of E1 was also found in 3 normal endometria. However, the binding capacity in the endometrial carcinoma increased to 1.5-fold of that in the normal endometrium. E2 did not affect [3H]E1 binding to any subcellular fraction from endometrial carcinoma specimens. These findings demonstrate the presence of specific binding sites for E1 in human endometrial carcinoma. The endometrial carcinoma growth may be mediated, at least in part, by E1 and its binding site interaction.
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PMID:Possible evidence for estrone-specific binding sites in human uterine endometrial carcinoma. 805 Jul 35

Despite evidence that estrogens and insulin are related to type 1 endometrial carcinoma (EC), their synergistic role has not been analyzed. Here, we investigated how estrogens cooperate with insulin to promote type 1 EC progression. We examined the clinical significance of serum estrogen and insulin levels using type 1 EC patients and control subjects. Univariate and multivariate logistic regression analyses for total, premenopausal, and postmenopausal subjects were performed. Type 1 EC risk was evaluated with respect to estrone, estradiol, and insulin levels based on odds ratios (ORs) using stratified data. Cell growth in vitro and in vivo, effects of insulin and estradiol on apoptosis and cell cycle distribution were measured after estradiol and insulin stimulation. Estrone and insulin concentrations were significantly high in type 1 EC patients and retained positive associations with type 1 EC after adjustment for BMI, WHR, diabetes, and hypertension. The odds ratio was significantly high for type 1 EC patients with higher levels of estrone/estradiol and insulin than for patients with higher levels of either estrone/estradiol or insulin, suggesting that estrogen and insulin play a synergistic role in type 1 EC carcinogenesis and progression. Compared to EC cells and cell-based xenografts treated with estradiol or insulin alone, those treated with estradiol and insulin exhibited stronger stimulation. Estrogen and insulin play synergistic roles in type 1 EC carcinogenesis and progression, extending our understanding of EC risks.
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PMID:Estrogen and insulin synergistically promote type 1 endometrial cancer progression. 2917 56


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