Yanfeng Liu
Yale University
56 Papers
106 Citations
Yanfeng Liu is an academic researcher from Yale University. The author has contributed to research in topics: Medicine & DNA repair. The author has an hindex of 20, co-authored 39 publications. Previous affiliations of Yanfeng Liu include Yale Cancer Center & Food and Drug Administration.
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Papers
2-Hydroxyglutarate produced by neomorphic IDH mutations suppresses homologous recombination and induces PARP inhibitor sensitivity.
Parker L. Sulkowski,Christopher D. Corso,Nathaniel D. Robinson,Susan E. Scanlon,Karin Purshouse,Hanwen Bai,Yanfeng Liu,Ranjini K. Sundaram,Denise C. Hegan,Nathan R. Fons,Gregory A. Breuer,Yuanbin Song,Ketu Mishra-Gorur,Henk M. De Feyter,Robin A. de Graaf,Yulia V. Surovtseva,Maureen Kachman,Stephanie Halene,Murat Gunel,Peter M. Glazer,Ranjit S. Bindra +20 more
TL;DR: It is reported that IDH1/2 mutations induce a homologous recombination defect that renders tumor cells exquisitely sensitive to poly(adenosine 5′-diphosphate–ribose) polymerase (PARP) inhibitors, and an unexpected link between oncometabolites, altered DNA repair, and genetic instability is uncovered.
Oncometabolites suppress DNA repair by disrupting local chromatin signalling
Parker L. Sulkowski,Sebastian Oeck,Sebastian Oeck,Jonathan Dow,Nicholas G Economos,Lily Mirfakhraie,Yanfeng Liu,Katelyn Noronha,Xun Bao,Jing Li,Brian Shuch,Megan C. King,Ranjit S. Bindra,Peter M. Glazer +13 more
TL;DR: It is shown that oncometabolite-induced inhibition of the lysine demethylase KDM4B results in aberrant hypermethylation of histone 3 lysines 9 and decreased homology-dependent DNA repair.
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Krebs-cycle-deficient hereditary cancer syndromes are defined by defects in homologous-recombination DNA repair
Parker L. Sulkowski,Ranjini K. Sundaram,Sebastian Oeck,Sebastian Oeck,Christopher D. Corso,Yanfeng Liu,Seth Noorbakhsh,Monica Niger,Monica Niger,Marta Boeke,Daiki Ueno,Aravind N. Kalathil,Xun Bao,Jing Li,Brian Shuch,Ranjit S. Bindra,Peter M. Glazer +16 more
TL;DR: It is reported that fumarate and succinate both suppress the homologous recombination DNA-repair pathway required for the resolution of DNA double-strand breaks (DSBs) and for the maintenance of genomic integrity, thus rendering tumor cells vulnerable to synthetic-lethal targeting with poly(ADP)-ribose polymerase (PARP) inhibitors.
In vivo correction of anaemia in β-thalassemic mice by γPNA-mediated gene editing with nanoparticle delivery
Raman Bahal,Nicole Ali McNeer,Elias Quijano,Yanfeng Liu,Parker L. Sulkowski,Audrey Turchick,Yi-Chien Lu,Dinesh Chandra Bhunia,Arunava Manna,Dale L. Greiner,Michael A. Brehm,Christopher J. Cheng,Francesc López-Giráldez,Adele S. Ricciardi,Jagadish Beloor,Diane S. Krause,Priti Kumar,Patrick G. Gallagher,Demetrios T. Braddock,W. Mark Saltzman,Danith H. Ly,Peter M. Glazer +21 more
TL;DR: Injection of thalassemic mice with SCF plus nanoparticles containing γPNAs and donor DNAs ameliorated the disease phenotype, with sustained elevation of blood haemoglobin levels into the normal range, reduced reticulocytosis, reversal of splenomegaly and up to 7% β-globin gene correction in HSCs, with extremely low off-target effects.
In utero nanoparticle delivery for site-specific genome editing
Adele S. Ricciardi,Raman Bahal,Raman Bahal,James S. Farrelly,Elias Quijano,Anthony H. Bianchi,Valerie L. Luks,Rachael Putman,Francesc López-Giráldez,Süleyman Coşkun,Eric Song,Yanfeng Liu,Wei-Che Hsieh,Danith H. Ly,David H. Stitelman,Peter M. Glazer,W. Mark Saltzman +16 more
TL;DR: Safe delivery of nanoparticles to fetal mouse tissues is demonstrated, and nanoparticles containing peptide nucleic acids to edit the beta-globin gene are effective in a mouse model of beta-thalassemia, and this work may provide the basis for a safe and versatile method of fetal gene editing for human monogenic disorders.