endometrial hyperplasia/hypoxia

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Hypoxia is involved in the reduction of HtrA3 in patients with endometrial hyperplasia and cancer.

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Endometrial cancer (EC) has recently become a major gynecological cancer and endometrial hyperplasia increases the risk for developing EC. Previous studies have reported that human high temperature requirement factor A3 (HtrA3), a member of ATP independent serine proteases family, is involved in

PTEN/PI3K/VEGF signaling pathway involved in the protective effect of xanthine oxidase inhibitor febuxostat against endometrial hyperplasia in rats.

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Endometrial hyperplasia (EH) is a medical condition that affects many females as it increases their uterine carcinogenic potential. EH results from entangling hormonal imbalance and inflammatory response. The study examined the role of a xanthine oxidase inhibitor, febuxostat, in a rat model of EH.

Silencing of hypoxia‑inducible adrenomedullin using RNA interference attenuates hepatocellular carcinoma cell growth in vivo.

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Adrenomedullin (ADM) is an angiogenic peptide that has been shown to increase the risk of endometrial hyperplasia and to promote tumor cell survival following hypoxia. ADM may induce microvessel proliferation and partially decrease hypoxia in solid tumors, thus contributing to the proliferation of

Downregulation of Proline Hydroxylase 2 and Upregulation of Hypoxia-Inducible Factor 1α are Associated with Endometrial Cancer Aggressiveness.

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Proline hydroxylase 2 (PHD2) is involved in tumorigenesis. This study aimed to examine PHD2 and hypoxia-inducible factor 1α (HIF-1α) expression in different endometrial tissues and explore the correlations between PHD2 and HIF-1α expression with clinicopathological characteristics of

HIF-1α and GLUT-1 Expression in Atypical Endometrial Hyperplasia, Type I and II Endometrial Carcinoma: A Potential Role in Pathogenesis.

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BACKGROUND Hypoxia-Inducible Factor 1α (HIF-1α) is one of the major adaptive responses to hypoxia, regulating the activity of glucose transporter -1 (GLUT-1), responsible for glucose uptake. OBJECTIVE To evaluate the immunohistochemical expression of both HIF-1α and GLUT-1 in type I and II

Autophagy in the physiological endometrium and cancer.

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Autophagy is a highly conserved catabolic process and a major cellular pathway for the degradation of long-lived proteins and cytoplasmic organelles. An increasing body of evidence has unveiled autophagy as an indispensable biological function that helps to maintain normal tissue

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