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gestational trophoblastic disease/hypoxia

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The aim of this study was to investigate the relationship between the expression of vascular endothelial growth factor (VEGF), transforming growth factor beta (TGF-beta1 and TGF-beta3), and hypoxia inducible factor 1 alpha (HIF-1alpha) in gestational trophoblastic diseases to highlight the possible

Two rare cases of methotrexate-induced pneumonitis and pleurisy in patients with gestational trophoblastic neoplasms.

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BACKGROUND Pneumonitis is a serious and unpredictable side-effect of treatment with methotrexate (MTX) that may result in a life-threatening outcome. Pulmonary toxicity of methotrexate in patients with a gestational trophoblastic neoplasm (GTN) has rarely been reported before. METHODS For the first

Overexpression of hypoxia-inducible factor 1α induces migration and invasion through Notch signaling.

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Choriocarcinoma (CC) is the highest malignant gestational trophoblastic tumor which causes high mortality without timely treatment. HIF-1α is a very important molecule promoting neoplasm aggressiveness, metastasis through the induction of the epithelial to mesenchymal transition (EMT). Several

Trophoblastic vasculogenic mimicry in gestational choriocarcinoma.

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Angiogenesis is a characteristic feature of solid tumors, which depend on the newly formed vasculature to prevent hypoxia and to sustain uncontrolled tumor cell proliferation. In this study, we investigated the blood supply system in 10 gestational choriocarcinomas on the basis of histopathological

NLRP7 is increased in human idiopathic fetal growth restriction and plays a critical role in trophoblast differentiation.

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Fetal growth restriction (FGR) the leading cause of perinatal mortality and morbidity is highly related to abnormal placental development, and placentas from FGR pregnancies are often characterized by increased inflammation. However, the mechanisms of FGR-associated inflammation are far from being
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