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Tsuyoshi Takashima

Researcher at Hiroshima University

Publications -  11
Citations -  95

Tsuyoshi Takashima is an academic researcher from Hiroshima University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 4, co-authored 5 publications receiving 31 citations. Previous affiliations of Tsuyoshi Takashima include Osaka University.

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Molecular biological analysis of 5-FU-resistant gastric cancer organoids; KHDRBS3 contributes to the attainment of features of cancer stem cell

TL;DR: GC organoids are established and KHDRBS3, which is thought to play an important role in the acquisition of characteristics of CSCs in GC, is found to be a promising candidate marker for predicting therapeutic effect and prognosis in GC patients.
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Immunohistochemical analysis of SLFN11 expression uncovers potential non-responders to DNA-damaging agents overlooked by tissue RNA-seq.

TL;DR: It is found that the SLFN11 expression is tissue specific and varies during tumorigenesis, and the significance of immunohistochemical procedures for evaluating expression of SLFN 11 in patient samples is revealed and provides a robust resource of SL FN11 expression across adult human organs.
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Schlafen 11 predicts response to platinum-based chemotherapy in gastric cancers.

TL;DR: In this paper, the potential clinical utility of SLFN11 in the treatment of gastric cancer was investigated and the correlation between SLFN 11 expression and overall survival in 169 GC patients by an established immunohistochemical approach.
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Epigenetic suppression of SLFN11 in germinal center B-cells during B-cell development.

TL;DR: In this article, the effects of two epigenetic modifiers, an EZH2 inhibitor, tazemetostat (EPZ6438), and a histone deacetylase inhibitor, panobinostat, LBH589, on SLFN11 expression in Germinal center B-cells (GCBs) during B-cell development were investigated.
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Uc.63+ contributes to gastric cancer progression through regulation of NF-kB signaling

TL;DR: The results suggest that Uc.63+.63+ could be involved in GC progression by regulating GC cell growth and migration via NF-κB signaling through T-UCRs.