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Jen-Tsan Chi

Researcher at Duke University

Publications -  131
Citations -  10324

Jen-Tsan Chi is an academic researcher from Duke University. The author has contributed to research in topics: Gene expression profiling & Cancer. The author has an hindex of 43, co-authored 121 publications receiving 8651 citations. Previous affiliations of Jen-Tsan Chi include Durham University & Stanford University.

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Diversity, topographic differentiation, and positional memory in human fibroblasts

TL;DR: Cultured fetal and adult human fibroblasts maintained key features of HOX gene expression patterns established during embryogenesis, suggesting that HOX genes may direct topographic differentiation and underlie the detailed positional memory in fibro Blasts.
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Endothelial cell diversity revealed by global expression profiling

TL;DR: Tissue-specific expression patterns in different tissue microvascular ECs suggest they are distinct differentiated cell types that play roles in the local physiology of their respective organs and tissues.
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Gene Expression Programs in Response to Hypoxia: Cell Type Specificity and Prognostic Significance in Human Cancers

TL;DR: A gene-expression signature of the hypoxia response, derived from studies of cultured mammary and renal tubular epithelial cells, showed coordinated variation in several human cancers, and was a strong predictor of clinical outcomes in breast and ovarian cancers.
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A viral microRNA functions as an orthologue of cellular miR-155

TL;DR: It is reported that the miR-K12-11 miRNA encoded by Kaposi’s-sarcoma-associated herpes virus shows significant homology to cellular mi-155, including the entire miRNA ‘seed’ region.
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Targeting GLUT1 and the Warburg Effect in Renal Cell Carcinoma by Chemical Synthetic Lethality

TL;DR: A screen identifies a drug that specifically kills glycolysis-dependent cancer cells by inhibiting glucose uptake and identifies a class of compounds, the 3-series, exemplified by STF-31, which selectively kills RCCs by specifically targeting glucose uptake through GLUT1 and exploiting the unique dependence of these cells onGLUT1 for survival.