Y
Yoshiaki Yura
Researcher at Osaka University
Publications - 105
Citations - 1726
Yoshiaki Yura is an academic researcher from Osaka University. The author has contributed to research in topics: Oncolytic virus & Apoptosis. The author has an hindex of 21, co-authored 103 publications receiving 1488 citations. Previous affiliations of Yoshiaki Yura include University of Tokushima.
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Effectiveness of BNCT for recurrent head and neck malignancies.
Itsuro Kato,Koji Ono,Yoshinori Sakurai,Masatoshi Ohmae,Akira Maruhashi,Yoshio Imahori,Mitsunori Kirihata,Mitsuhiro Nakazawa,Yoshiaki Yura +8 more
TL;DR: First in the world, six patients with a recurrent HNM who have been treated with BNCT are reported, indicating that BN CT represents a new and promising treatment approach even for a huge or far advanced HNM.
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Involvement of the Wnt-β-catenin pathway in invasion and migration of oral squamous carcinoma cells
Soichi Iwai,Atsuko Yonekawa,Chie Harada,Masakazu Hamada,Wataru Katagiri,Mituhiro Nakazawa,Yoshiaki Yura +6 more
TL;DR: It is suggested that aberrant cytoplasmic accumulation of β-catenin can induce Tcf/Lef-mediated transcriptional activity, up-regulate MMP-7, and induce epithelial and mesenchymal transition (EMT) to enhance the invasion and migration of oral SCC cells.
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Mutations of the APC, beta-catenin, and axin 1 genes and cytoplasmic accumulation of beta-catenin in oral squamous cell carcinoma.
TL;DR: The Axin1 gene may be one of the mutational target in oral SCC, and the cytoplasmic accumulation of beta-catenin is a common characteristic of oral S CC, but is not closely associated with mutational alterations in the APC, beta- catenin and Axin 1 genes.
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The effects of trichostatin A on the oncolytic ability of herpes simplex virus for oral squamous cell carcinoma cells
TL;DR: Results indicate that TSA enhanced the replication of the HSV-1 mutant through the activation of NF-κB and induced cell cycle arrest at G1 to inhibit cell growth.
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Immunogenic cell death by oncolytic herpes simplex virus type 1 in squamous cell carcinoma cells.
TL;DR: Results indicate that oncolytic HSV-1 RH2 produces damage-associated molecular patterns from SCC cells to induce cell death, which may contribute to the enhancement of tumor immunity by oncoleytic HSv-1.