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Endometrial Atypical Hyperplasia and Risk of Endometrial Cancer - MDPI Hormonal Imbalances: Unopposed estrogen exposure is a key factor in the development of EAH and its progression to cancer [24, 25] Estrogen stimulates the proliferation of endometrial cells, while progesterone acts by counterbalancing through promotion of cellular differentiation and apoptosis [26]
Estrogen Signaling in Endometrial Cancer: a Key Oncogenic Pathway with . . . Consistent with the fundamental role of estrogens and progestogens in growth of the endometrium, many of the endometrial cancer risk factors involve excess estrogens or estrogen signaling unopposed by progesterone signaling (Fig 1)
Endometrial hyperplasia as a risk factor of endometrial cancer The most important risk factor for the development of EH is chronic exposure to unopposed estrogen Histopathologically, EH can be classified into EH without atypia (benign EH) and atypical EH endometrial intraepithelial neoplasia (EIN)
Endometrial Hyperplasia as an Endometrial Cancer Risk Factor: Review . . . Chronic exposure to unopposed estrogen is the leading risk factor for the development of EH Clinical management can range from monitoring to progestin therapy to a hysterectomy, depending on the risk of EC progression or concomitant EC and the patient's desire to maintain fertility
CEBPB promotes transformation of endometrial complex atypical . . . Chronic unopposed estrogen exposure is the most common risk factor for the development of CAH [4] Specific conditions include obesity, early menarche, late menopause, chronic anovulation, estrogen-secreting tumors and estrogen treatment regimens without counterbalanced progestin [2]
Exogenous Hormones and their Effects on the Endometrium With continued, longer term, unopposed estrogen exposure, a high proportion of patients will ultimately develop non-atypical endometrial hyperplasia A small number will also go on to develop endometrial intraepithelial neoplasia (EIN) (also called ‘atypical hyperplasia’) or even adenocarcinoma (see Chapters 17 and 18 )
The dose-effect relationship between unopposed oestrogens and . . . The 'unopposed oestrogen hypothesis' for endometrial cancer maintains that risk is increased by exposure to endogenous or exogenous oestrogen that is not opposed simultaneously by a progestagen, and that this increased risk is due to the induced mitotic activity of the endometrial cells
The Molecular Changes and Genetic Pathways of the Endometrial Precancers Risk factors of endometrial hyperplasia: Hormonal Imbalance: One of the most critical drivers of EH and its progression to EC is unopposed estrogen exposure, where the endometrium is subjected to prolonged estrogenic stimulation without the protective effects of progesterone [5] Many factors cause these hormonal imbalances