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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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The complexity of phosphorylated H2AX foci formation and DNA repair assembly at DNA double-strand breaks

TL;DR: It is reported here that γ-H2AX foci change composition during the cell cycle, with proteins 53BP1, NBS1 and MRE11 dissociating from foci in G2 and mitosis to return at the beginning of the following G1.
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Effects of morpholinyl doxorubicins, doxorubicin, and actinomycin D on mammalian DNA topoisomerases I and II.

TL;DR: The data indicate that some DNA intercalators are not only inhibitors of DNA topoisomerase II but act also on DNA top Loisomerase I, and the stabilization of cleavage intermediates by intercalator may have a common mechanism for DNA topISomersase I and DNA topisomersase II.
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ATR Inhibitors VE-821 and VX-970 Sensitize Cancer Cells to Topoisomerase I Inhibitors by Disabling DNA Replication Initiation and Fork Elongation Responses

TL;DR: The mechanistic rationale and proof of principle it provides to evaluate the combination of Top1 inhibitors with ATR inhibitors in clinical trials and the clinical derivative of VE-821 enhanced the in vivo tumor response to irinotecan without additional toxicity.
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Inhibition of histone deacetylase in cancer cells slows down replication forks, activates dormant origins, and induces DNA damage.

TL;DR: It is found that pharmacologic concentrations of SAHA induce replication-mediated DNA damage with activation of histone gammaH2AX, establishing a critical link between robust chromatin acetylation and DNA replication in human cancer cells.
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Synthesis of Cytotoxic Indenoisoquinoline Topoisomerase I Poisons

TL;DR: The potencies of the indenoisoquinolines as top1 inhibitors did not correlate with their potencies as cytotoxicity agents, as some of the most cytotoxic agents had little if any effect on top1.