Y
Yuho Hayashi
Researcher at University of Texas MD Anderson Cancer Center
Publications - 9
Citations - 698
Yuho Hayashi is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Cell growth & Protein kinase B. The author has an hindex of 7, co-authored 8 publications receiving 656 citations.
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Journal ArticleDOI
Invasive glioblastoma cells acquire stemness and increased Akt activation.
TL;DR: An in vivo model of human invasive GBM in mouse brain from a GBM cell line with moderate tumorigenicity that allowed simultaneous primary tumor growth and dispersal of tumor cells in the brain parenchyma is developed and underscores complementary roles of the Erk and Akt pathways for GBM proliferation and disperseal.
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PTEN, NHERF1 and PHLPP form a tumor suppressor network that is disabled in glioblastoma.
Jennifer R. Molina,Nitin Agarwal,Fabiana C. Morales,Yuho Hayashi,Kenneth Aldape,Gilbert J. Cote,Maria-Magdalena Georgescu,Maria-Magdalena Georgescu +7 more
TL;DR: It is shown here that PTEN modulates the PI3K-Akt pathway in glioblastoma within a tumor suppressor network that includes Na+/H+ exchanger regulatory factor 1 (NHERF1) and pleckstrin-homology domain leucine-rich repeat protein phosphatases 1 (PHLPP1).
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Vitamin K2 induces autophagy and apoptosis simultaneously in leukemia cells.
Tomohisa Yokoyama,Keisuke Miyazawa,Munekazu Naito,Juri Toyotake,T Tauchi,Masahiro Itoh,Akira Yuo,Yuho Hayashi,Maria-Magdalena Georgescu,Yasuko Kondo,Seiji Kondo,Kazuma Ohyashiki +11 more
TL;DR: Autophagy becomes prominent when the cells are protected from rapid apoptotic death by a high expression level of Bcl-2, demonstrating that autophagy and apoptosis can be simultaneously induced by VK2.
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Roles of NHERF1/EBP50 in cancer.
TL;DR: An overview of the mechanisms by which this adaptor protein controls cell transformation is provided, and a model suggesting a dual role of NHERF1/EBP50 in cancer is proposed.
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NHERF1/EBP50 is a new marker in colorectal cancer.
TL;DR: This study identifies NHERF1 as a new player in CRC progression and supports the notion that the expression or subcellular distribution of NherF1 may be used as diagnostic marker for CRC, and concludes that alterations in the apical membrane localization of NHERFs contribute to CRC through the disruption of epithelial morphology.