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Hiroki Takahashi

Researcher at Nagoya City University

Publications -  123
Citations -  3544

Hiroki Takahashi is an academic researcher from Nagoya City University. The author has contributed to research in topics: Cancer & Internal medicine. The author has an hindex of 28, co-authored 100 publications receiving 2994 citations. Previous affiliations of Hiroki Takahashi include Nagoya University & University of California, Los Angeles.

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Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth.

TL;DR: It is shown that CAFs are an important IL-6 source and that anti-IL-6 receptor antibody suppressed angiogenesis and inhibited tumor-stroma interactions, and CAFs contribute to drug-resistance acquisition in cancer cells.
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Interleukin-6 released by colon cancer-associated fibroblasts is critical for tumour angiogenesis: anti-interleukin-6 receptor antibody suppressed angiogenesis and inhibited tumour–stroma interaction

TL;DR: It is demonstrated that stromal fibroblasts isolated from colon cancer produced significant amounts of IL-6 and that colon cancer cells enhanced IL- 6 production by stromals, thereby inducing angiogenesis and offering new approaches to cancer therapy.
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CXCL8/IL‐8 and CXCL12/SDF‐1α co‐operatively promote invasiveness and angiogenesis in pancreatic cancer

TL;DR: It was shown that PaCa‐derived CXCL8 and fibroblast‐derivedCXCL12 cooperatively induced angiogenesis in vitro by promoting HUVEC proliferation, invasion, and tube formation.
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PTEN regulate angiogenesis through PI3K/Akt/VEGF signaling pathway in human pancreatic cancer cells

TL;DR: SiRNA-mediated inhibition of PTEN gene expression in pancreatic cancer cells increase their VEGF secretion, up-modulated the proliferation, and migration of co-cultured vascular endothelial cell and enhanced tubule formation by HUVEC.
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Activation of focal adhesion kinase enhances the adhesion and invasion of pancreatic cancer cells via extracellular signal-regulated kinase-1/2 signaling pathway activation

TL;DR: Investigation of the mechanism of activation of FAK and its downstream extracellular signal-regulated kinase (ERK)-1/2 signaling following stimulation by interleukin (IL)-1α and adhesion to ECM with subsequent enhancement of pancreatic cancer cell adhesion and invasion demonstrated that activation ofFAK is involved with the aggressive capability in Pancic cancer through Ras/ERK signaling pathway.