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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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Concordance of gene expression and functional correlation patterns across the NCI-60 cell lines and the Cancer Genome Atlas glioblastoma samples

TL;DR: Many of the gene-gene correlations found in the NCI-60 do not reflect just the conditions of cell lines in culture; rather, they reflect processes and gene networks that also function in vivo.
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Mitochondrial tyrosyl-DNA phosphodiesterase 2 and its TDP2S short isoform.

TL;DR: A novel short isoform of TDP2 (TDP2S) expressed from an alternative transcription start site is identified and shown to protect human cells against mitochondrial‐targeted doxorubicin and reduce the mitochondria transcription levels in two different human cell lines.
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Replication-dependent cytotoxicity and Spartan-mediated repair of trapped PARP1-DNA complexes.

TL;DR: In this paper, the role of Spartan (SPRTN) is explored for DNA replication in human TK6 and chicken DT40 lymphoblastoid cells, and it is shown that SPRTN-deficient cells are hypersensitive to talazoparib and olaparib, but not to veliparib.
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TDP1 suppresses mis-joining of radiomimetic DNA double-strand breaks and cooperates with Artemis to promote optimal nonhomologous end joining.

TL;DR: It is suggested that TDP1 and Artemis perform different functions in the repair of terminally blocked DSBs by the C-NHEJ pathway, and that whereas an Artemis deficiency prevents end joining of some D SBs, a TDP2 deficiency tends to promote DSB mis-joining.
Journal Article

Differential GADD45, p21CIP1/WAF1, MCL-1 and topoisomerase II gene induction and secondary DNA fragmentation after camptothecin-induced DNA damage in two mutant p53 human colon cancer cell lines.

TL;DR: It is concluded that cellular response to CPT-induced DNA damage can involve p53-independent pathways leading to the induction of p 53-effector genes at the onset of apoptosis, associated with CPT sensitivity.