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Naohiko Seki

Researcher at Chiba University

Publications -  391
Citations -  20245

Naohiko Seki is an academic researcher from Chiba University. The author has contributed to research in topics: microRNA & Cancer. The author has an hindex of 74, co-authored 381 publications receiving 18648 citations. Previous affiliations of Naohiko Seki include Toho University & National Institute of Radiological Sciences.

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Gene expression pattern in oral cancer cervical lymph node metastasis.

TL;DR: The hypothesis that the lymph node metastasis status can be predicted using the gene expression patterns of the primary OSCC, and may be a powerful tool in identifying patients at high risk of lymph nodes metastasis, is supported.
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Silencing Ku80 using small interfering RNA enhanced radiation sensitivity in vitro and in vivo.

TL;DR: It is indicated that combined therapy consisting of Ku80 siRNA and irradiation contributes to inhibition of tumor growth and may be a novel strategy for cancer treatment.
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RNA sequencing-based microRNA expression signature in esophageal squamous cell carcinoma: oncogenic targets by antitumor miR-143-5p and miR-143-3p regulation.

TL;DR: This study focused on both strands of pre-miR-143, and investigated their antitumor roles and target oncogenes in ESCC, and provided important insights into the molecular pathogenesis of ESCC.
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Gene Regulation by Antitumor miR-204-5p in Pancreatic Ductal Adenocarcinoma: The Clinical Significance of Direct RACGAP1 Regulation

TL;DR: This study focused on RACGAP1 (Rac guanosine triphosphatase-activating protein 1) because its expression was most significantly predictive of PDAC pathogenesis and the strategy to identify antitumor miRNAs and their target genes will help elucidate the molecular pathogenesis ofPDAC.
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Identification of methylation-silenced genes in colorectal cancer cell lines: genomic screening using oligonucleotide arrays.

TL;DR: The results suggest that aberrant promoter methylation is the primary mechanism of transcriptional silencing of the UCHL1 gene and that methylation of the UWG1 gene promoter increases during the development and progression of CRC.