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Han W. Tun

Researcher at Mayo Clinic

Publications -  118
Citations -  2061

Han W. Tun is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Medicine & Lymphoma. The author has an hindex of 19, co-authored 88 publications receiving 1610 citations. Previous affiliations of Han W. Tun include University of Texas MD Anderson Cancer Center & Osaka University.

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Stearoyl-CoA Desaturase 1 Is a Novel Molecular Therapeutic Target for Clear Cell Renal Cell Carcinoma

TL;DR: Increased SCD1 expression supports ccRCC viability and therefore it is proposed as a novel molecular target for therapy either independently or in combination with an mTOR inhibitor for patients whose disease cannot be remedied with surgical intervention, such as in cases of advanced or metastatic disease.
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Surface modification of nanoparticles enables selective evasion of phagocytic clearance by distinct macrophage phenotypes.

TL;DR: The results suggest that bio-inspired nanoparticle surface design may enable evasion of specific components of the immune system and provide a rational approach for developing immune tolerant nanomedicines.
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Pathway Signature and Cellular Differentiation in Clear Cell Renal Cell Carcinoma

TL;DR: A model in which normal renal epithelial cells undergo dedifferentiation, EMT, and adipogenic transdifferentiation is proposed, resulting in ccRCC, characterized by a lack of epithelial differentiation, mesenchymal/adipogenic trans Differentiation, and pluripotent meschymal stem cell-like differentiation capacity in vitro.
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Pathway analysis of primary central nervous system lymphoma

TL;DR: The gene expression signature discovered in this study may represent a true "CNS signature" because it contrasted PCNSL with wide-spectrum non-CNS DLBCL on a genomic scale and performed an in-depth bioinformatic analysis.
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Neuronal pentraxin 2 supports clear cell renal cell carcinoma by activating the AMPA-selective glutamate receptor-4.

TL;DR: It is shown that neuronal pentraxin 2 (NPTX2) is overexpressed specifically in ccRCC primary tumors and metastases, and that it contributes to tumor cell viability and promotes cell migration through its interaction with the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluR4.