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Hideki Watanabe

Researcher at Jichi Medical University

Publications -  43
Citations -  5926

Hideki Watanabe is an academic researcher from Jichi Medical University. The author has contributed to research in topics: Medicine & Cancer. The author has an hindex of 13, co-authored 36 publications receiving 5406 citations. Previous affiliations of Hideki Watanabe include Nagoya University & Eisai.

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Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer

TL;DR: It is shown that a small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene in non-small-cell lung cancer (NSCLC) cells.
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Identification of Novel Isoforms of the EML4-ALK Transforming Gene in Non–Small Cell Lung Cancer

TL;DR: Two slightly different fusion cDNAs in which exon 6 of EML4 was joined to exon 20 of ALK were each identified in two individuals of the cohort and exhibited marked transforming activity in vitro as well as oncogenic activity in vivo.
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Eribulin mesylate reduces tumor microenvironment abnormality by vascular remodeling in preclinical human breast cancer models.

TL;DR: It is shown that eribulin induces remodeling of tumor vasculature through a novel antivascular activity in MX‐1 and MDA‐MB‐231 human breast cancer xenograft models, suggesting that Eribulin‐induced remodelling of abnormal tumor vasculation leads to a more functional microenvironment that may reduce the aggressiveness of tumors due to elimination of inner tumor hypoxia.
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Mouse microRNA profiles determined with a new and sensitive cloning method

TL;DR: The data indicate that the total number of miRNAs in vertebrates is larger than previously appreciated and that the expression of these molecules is tightly controlled in a tissue- and developmental stage-specific manner.
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Lenvatinib induces death of human hepatocellular carcinoma cells harboring an activated FGF signaling pathway through inhibition of FGFR–MAPK cascades

TL;DR: Results reveal that the F GF signaling pathway through MAPK cascades plays an important role in survival of HCC cell lines with an activated FGF signaling pathway under limited nutrients, and FGFR-MAPK cascade likely contribute to survival ofHCC cells with anactivated FGF signaled pathway under tumor microenvironments with limited nutrients.