Titlebook: Cell and Molecular Biology of Endometrial Carcinoma; Hiroyuki Kuramoto (Professor),Masato Nishida (Pres Book 2003 Springer Japan 2003 angi

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书目名称Cell and Molecular Biology of Endometrial Carcinoma影响因子(影响力)




书目名称Cell and Molecular Biology of Endometrial Carcinoma影响因子(影响力)学科排名




书目名称Cell and Molecular Biology of Endometrial Carcinoma网络公开度




书目名称Cell and Molecular Biology of Endometrial Carcinoma网络公开度学科排名




书目名称Cell and Molecular Biology of Endometrial Carcinoma被引频次




书目名称Cell and Molecular Biology of Endometrial Carcinoma被引频次学科排名




书目名称Cell and Molecular Biology of Endometrial Carcinoma年度引用




书目名称Cell and Molecular Biology of Endometrial Carcinoma年度引用学科排名




书目名称Cell and Molecular Biology of Endometrial Carcinoma读者反馈




书目名称Cell and Molecular Biology of Endometrial Carcinoma读者反馈学科排名

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Endometrial Stress Neuropeptides: Paracrine Effects on Cell Proliferation and Apoptosisration of tumoral endometrial cells. CRH stimulates the production of proapoptotic protein Fas ligand by endometrial stromal and decidual cells, inducing apoptosis of activated lymphocytes. Similarly, endometrial dynorphins may induce apoptosis of stromal cells through the induction of the proapopto

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Effect of Hepatocyte Growth Factor on the Expression of Matrix Metalloproteinases in the Invasion of three cancer cells in the presence of HGF was observed by Boyden’s chamber assay. HGF enhanced the activation of MMP-2 and -9 by zymography of MMPs. HGF strongly induced MMP-9 mRNA expression in stromal cells, but had little effect on MMP-2 mRNA. MT1-MMP mRNA was detected only in KLE and stromal ce

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Estrogen Receptor Signaling and Crosstalk with the Ah Receptor in Endometrial Cancer Cells(TCDD) induce CYP1A1-dependent activity or reporter gene activity in cells transfected with constructs containing dioxin-responsive elements as promoters. Estrogen responsiveness was also confirmed in these cells, as evidenced by gene/reporter gene assay and the induction of cell proliferation by 17

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Inhibition of AKT Oncogenic Pathway in Endometrial Cancer Cellsse-1/2, suggesting that API-59 inhibits the AKT pathway at the AKT kinase level..We next investigated whether API-59 induces apoptosis in these endometrial cancer cell lines. Exposure to API-59 induced significant apoptosis in both Ishikawa and RL95-2 cancer cell lines, which express elevated AKT ki

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A New Paradigm for Vascular Endothelial Cell Growth Factor Receptor Signaling in Adult Endotheliumts its cellular responses via two high-affinity tyrosine kinase receptors, namely VEGFR-1 and VEGFR-2. Until recently, it was presumed that the majority of cellular effects induced by VEGF were mediated by VEGFR-2, whereas VEGFR-1 acted as a decoy. However, results from our laboratory and others hav