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Elisabetta Leo
Researcher at AstraZeneca
Publications - 32
Citations - 2674
Elisabetta Leo is an academic researcher from AstraZeneca. The author has contributed to research in topics: Medicine & Olaparib. The author has an hindex of 11, co-authored 21 publications receiving 2131 citations. Previous affiliations of Elisabetta Leo include National Institutes of Health.
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Journal ArticleDOI
DNA topoisomerases and their poisoning by anticancer and antibacterial drugs.
TL;DR: This review focuses on the molecular and biochemical characteristics of topoisomerases and their inhibitors and discusses the common mechanism of action ofTopoisomerase poisons by interfacial inhibition and trapping of topisomerase cleavage complexes.
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Putative DNA/RNA helicase Schlafen-11 (SLFN11) sensitizes cancer cells to DNA-damaging agents
Gabriele Zoppoli,Marie Regairaz,Elisabetta Leo,William C. Reinhold,Sudhir Varma,Alberto Ballestrero,James H. Doroshow,Yves Pommier +7 more
TL;DR: It is concluded that SLFN11 expression is causally associated with the activity ofDDAs in cancer cells, has a broad expression range in colon and ovarian adenocarcinomas, and may behave as a biomarker for prediction of response to DDAs in the clinical setting.
Journal ArticleDOI
SLFN11 Blocks Stressed Replication Forks Independently of ATR
Junko Murai,Sai-Wen Tang,Elisabetta Leo,Simone A Baechler,Christophe E. Redon,Hongliang Zhang,Muthana Al Abo,Vinodh N. Rajapakse,Eijiro Nakamura,Lisa M. Miller Jenkins,Mirit I. Aladjem,Yves Pommier +11 more
TL;DR: It is concluded that SLFN11 is recruited to stressed replication forks carrying extended RPA filaments where it blocks replication by changing chromatin structure across replication sites.
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Inhibition of histone deacetylase in cancer cells slows down replication forks, activates dormant origins, and induces DNA damage.
Chiara Conti,Elisabetta Leo,Gabriel S. Eichler,Olivier Sordet,Melvenia M. Martin,Angela Fan,Mirit I. Aladjem,Yves Pommier +7 more
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.
Journal ArticleDOI
Rif1 provides a new DNA-binding interface for the Bloom syndrome complex to maintain normal replication
Dongyi Xu,Parameswary A. Muniandy,Elisabetta Leo,Jinhu Yin,Saravanabhavan Thangavel,Xi Shen,Miki,Keli Agama,Rong Guo,David A. Fox,Amom Ruhikanta Meetei,Lauren E. Wilson,Huy Nguyen,Nan Ping Weng,Steven J. Brill,Lei Li,Alessandro Vindigni,Yves Pommier,Michael M. Seidman,Weidong Wang +19 more
TL;DR: V vertebrate Rif1 contains a DNA‐binding domain that resembles the αCTD domain of bacterial RNA polymerase α; and this domain preferentially binds fork and Holliday junction (HJ) DNA in vitro and is required for R if1 to resist replication stress in vivo.