H
Hitoshi Ohmori
Researcher at Nara Medical University
Publications - 75
Citations - 2183
Hitoshi Ohmori is an academic researcher from Nara Medical University. The author has contributed to research in topics: Metastasis & Cancer. The author has an hindex of 26, co-authored 75 publications receiving 1822 citations. Previous affiliations of Hitoshi Ohmori include Fukuoka University & Okayama Gakuin University.
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Journal ArticleDOI
Inhibition of heme oxygenase-1 by zinc protoporphyrin IX reduces tumor growth of LL/2 lung cancer in C57BL mice.
TL;DR: In contrast, CoPPIX treatment increased HO‐1 expression, enhanced tumorigenicity and MVD and reduced apoptosis, whereas cobalt PPIX (CoPPIX), an HO‐ 1 activator, increased both.
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Colon Cancer Cell-Derived High Mobility Group 1/Amphoterin Induces Growth Inhibition and Apoptosis in Macrophages
TL;DR: The results suggest that HMGB1/amphoterin induces growth inhibition and apoptosis in macrophages through RAGE intracellular signaling pathway.
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High mobility group box 1 released from necrotic cells enhances regrowth and metastasis of cancer cells that have survived chemotherapy.
Yi Luo,Yoshitomo Chihara,Kiyohide Fujimoto,Tomonori Sasahira,Masaomi Kuwada,Rina Fujiwara,Kiyomu Fujii,Hitoshi Ohmori,Hiroki Kuniyasu +8 more
TL;DR: It is suggested that HMGB1 released from necrotic cancer cells treated with a necrosis inducer enhances regrowth and metastasis of remnant cancer cells via RAGE activation.
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Cancer Usurps Skeletal Muscle as an Energy Repository
Yi Luo,Junya Yoneda,Hitoshi Ohmori,Takamitsu Sasaki,Kazutaka Shimbo,Sachise Eto,Yumiko Kato,Hiroshi Miyano,Tsuyoshi Kobayashi,Tomonori Sasahira,Yoshitomo Chihara,Hiroki Kuniyasu +11 more
TL;DR: HMGB1 released during tumorigenesis recruits muscle to supply glutamine to cancer cells as an energy source, suggesting that cancer energy production and host muscle are linked.
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High mobility group box-1-inducible melanoma inhibitory activity is associated with nodal metastasis and lymphangiogenesis in oral squamous cell carcinoma.
Tomonori Sasahira,Tadaaki Kirita,Naohide Oue,Ujjal K. Bhawal,Kazuhiko Yamamoto,Kiyomu Fujii,Hitoshi Ohmori,Yi Luo,Wataru Yasui,Anja-Katrin Bosserhoff,Hiroki Kuniyasu +10 more
TL;DR: Examination of MIA expression in 62 oral squamous cell carcinomas suggests that MIA expression is enhanced by the interaction of intracellular HMGB1 and NFkBp65 and MIA is closely involved in tumor progression and nodal metastasis by the increments of VEGF‐C and V EGF‐D in OSCC.