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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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Resistance to the CHK1 inhibitor prexasertib involves functionally distinct CHK1 activities in BRCA wild-type ovarian cancer.

TL;DR: It is reported that BRCAwt HGSOC develops resistance to prexasertib monotherapy via a prolonged G2 delay induced by lower CDK1/CyclinB1 activity, thus preventing cells from mitotic catastrophe and cell death, and highlighting a potential combination treatment approach to overcome CHK1i resistance.
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Bicyclic hydroxy-1H-pyrrolopyridine-trione containing HIV-1 integrase inhibitors.

TL;DR: Bicycleic hydroxy‐1H‐pyrrolopyridine‐triones are reported as a new family of HIV‐1 integrase inhibitors that were efficiently prepared using a key ‘Pummerer cyclization deprotonation cycloaddition’ cascade of imidosulfoxides.
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Adaptation of topoisomerase I paralogs to nuclear and mitochondrial DNA

TL;DR: It is proposed that adaptation of this domain to different chromatin environments in nuclei and mitochondria has driven evolutional development and conservation of organelle-restricted topoisomerase I paralogs in vertebrates.
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Lasonolide A, a potent and reversible inducer of chromosome condensation

TL;DR: It is revealed that LSA induces rapid and reversible premature chromosome condensation (PCC) associated with cell detachment, plasma membrane smoothening and actin reorganization, and the profound epigenetic alterations induced by LSA are demonstrated.
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TDP1 is Critical for the Repair of DNA Breaks Induced by Sapacitabine, a Nucleoside also Targeting ATM- and BRCA-Deficient Tumors.

TL;DR: The importance of TDP1 is identified as a novel determinant of response to CNDAC across various cancer types (especially non–small cell lung cancers), and the differential involvement of BRCA2, PARP1, and T DP1 in the cellular responses to C NDAC, AraC, and CPT is demonstrated.