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Hiroaki Okuyama

Researcher at Kyoto University

Publications -  58
Citations -  5653

Hiroaki Okuyama is an academic researcher from Kyoto University. The author has contributed to research in topics: Cancer & Cancer cell. The author has an hindex of 27, co-authored 58 publications receiving 5235 citations. Previous affiliations of Hiroaki Okuyama include Johns Hopkins University & Johns Hopkins University School of Medicine.

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Antiangiogenic Therapy Elicits Malignant Progression of Tumors to Increased Local Invasion and Distant Metastasis

TL;DR: It is reported that angiogenesis inhibitors targeting the VEGF pathway demonstrate antitumor effects in mouse models of pancreatic neuroendocrine carcinoma and glioblastoma but concomitantly elicit tumor adaptation and progression to stages of greater malignancy, with heightened invasiveness and in some cases increased lymphatic and distant metastasis.
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Hypoxia-Inducible Factor-1-Dependent Repression of E-cadherin in von Hippel-Lindau Tumor Suppressor–Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B

TL;DR: HIF-1 contributes to the epithelial-mesenchymal transition in VHL-null RCC by indirect repression of E-cadherin, a critical event in the pathogenesis of invasive and metastatic cancer.
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Effects of Aging and Hypoxia-Inducible Factor-1 Activity on Angiogenic Cell Mobilization and Recovery of Perfusion After Limb Ischemia

TL;DR: It is demonstrated that aging and HIF-1 loss-of-function impair the expression of multiple angiogenic cytokines, mobilization ofAngiogenic cells, maintenance of tissue viability, and recovery of limb perfusion following femoral artery ligation and gene therapy can counteract the pathological effects of aging in a mouse model of limb ischemia.
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Retaining cell–cell contact enables preparation and culture of spheroids composed of pure primary cancer cells from colorectal cancer

TL;DR: An innovative culture method for primary colorectal cancer cells, based on the principle that cell–cell contact of cancer cells was maintained throughout the process, allowed evaluation of chemosensitivity and signal pathway activation in cancer cells from individual patients.
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Stromal Cell–Derived Factor-1α and CXCR4 Expression in Hemangioblastoma and Clear Cell-Renal Cell Carcinoma: von Hippel-Lindau Loss-of-Function Induces Expression of a Ligand and Its Receptor

TL;DR: Results suggest that loss-of-function of a single tumor suppressor gene can up-regulate the expression of both a ligand and its receptor, which may establish an autocrine signaling pathway with important roles in the pathogenesis of hemangioblastoma and CC-RCC.