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Yves Pommier

Researcher at National Institutes of Health

Publications -  847
Citations -  65543

Yves Pommier is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Topoisomerase & DNA. The author has an hindex of 123, co-authored 789 publications receiving 58898 citations. Previous affiliations of Yves Pommier include Purdue University & Kyushu University.

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Phosphorylated fraction of H2AX as a measurement for DNA damage in cancer cells and potential applications of a novel assay.

TL;DR: The γ-H2AX ELISA represents a novel approach to quantifying DNA damage, which may lead to a better understanding of mutagenic pathways in cancer and provide a useful biomarker for monitoring the effectiveness of DNA-damaging anticancer agents.
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Cellular Topoisomerase I Inhibition and Antiproliferative Activity by MJ-III-65 (NSC 706744), an Indenoisoquinoline Topoisomerase I Poison

TL;DR: One of the idenoisoquinoline derivatives, MJ-III-65 (NSC 706744), is identified with both similarities and differences from CPT, which exhibits antitumor activity in mouse tumor xenografts and limited cross-resistance was observed in camptothecin-resistant cell lines.
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Batracylin (NSC 320846), a dual inhibitor of DNA topoisomerases I and II induces histone gamma-H2AX as a biomarker of DNA damage.

TL;DR: Batracylin is a dual Top1 and Top2 inhibitor and gamma-H2AX could be considered a biomarker in the ongoing clinical trials.
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Sister Chromatid Exchanges, Chromosomal Aberrations, and Cytotoxicity Produced by Antitumor Topoisomerase II Inhibitors in Sensitive (DC3F) and Resistant (DC3F/9-OHE) Chinese Hamster Cells

TL;DR: Short treatments of mammalian cells with topo II inhibitors produce reversibleTopo II-mediated DNA breaks which are associated with chromosomal aberrations and SCEs whose number correlates with cytotoxicity.
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ONC201 kills breast cancer cells in vitro by targeting mitochondria.

TL;DR: The data demonstrate that ONC201 kills cancer cells by disrupting mitochondrial function and further suggests that cancer cells that are dependent on glycolysis will be resistant to ONC200, and indicates that cells not dependent on mitochondrial respiration are ONC 201-resistant.