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

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書目名稱Cell and Molecular Biology of Endometrial Carcinoma
編輯Hiroyuki Kuramoto (Professor),Masato Nishida (Pres
視頻videohttp://file.papertrans.cn/223/222907/222907.mp4
概述Provides the newest information on endometrial cancer in the field of molecular biology
圖書封面Titlebook: Cell and Molecular Biology of Endometrial Carcinoma;  Hiroyuki Kuramoto (Professor),Masato Nishida (Pres Book 2003 Springer Japan 2003 angi
描述.The 15th International Symposium of the Japan Human Cell Society on Cell and Molecular Biology of Endometrial Carcinoma brought together leading researchers from Japan and around the world. The papers collected here are the work of twenty-two leaders in their field and are organized in ten major categories. The first section, in vitro experimental systems, takes up the pioneering work by Kuramoto in 1968 and Nishida in 1980 in establishing, respectively, the HEC-1 and hormone-responsive endometrial carcinoma cell lines. Other topics include apoptosis, proliferation, and growth factors; cell cycle regulators; signaling pathways; angiogenesis; carcinogenesis; hormones and hormone receptors; genes and gene expression; endometrial receptivity; and chemo-resistance and -sensitivity. Presenting the latest work in the cell and molecular biology of endometrial carcinoma, this volume is a valuable resource for gynecologists, pathologists, and molecular biologists..
出版日期Book 2003
關(guān)鍵詞angiogenesis; apoptosis; biology; carcinogenesis; carcinoma; cell; cell lines; chemoresistance; gene express
版次1
doihttps://doi.org/10.1007/978-4-431-53981-0
isbn_softcover978-4-431-67977-6
isbn_ebook978-4-431-53981-0
copyrightSpringer Japan 2003
The information of publication is updating

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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
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