R
Ranjit S. Bindra
Researcher at Yale University
Publications - 140
Citations - 6646
Ranjit S. Bindra is an academic researcher from Yale University. The author has contributed to research in topics: DNA repair & DNA damage. The author has an hindex of 33, co-authored 115 publications receiving 5153 citations. Previous affiliations of Ranjit S. Bindra include Yale Cancer Center & Memorial Sloan Kettering Cancer Center.
Papers
More filters
Journal ArticleDOI
Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III
David B. Simon,Ranjit S. Bindra,T A Mansfield,Carol Nelson-Williams,E Mendonca,Richard Stone,S Schurman,Ahmet Nayir,Harika Alpay,Aysin Bakkaloglu,Juan Rodriguez-Soriano,JM Morales,Sami A. Sanjad,CM Taylor,Daniela T. Pilz,A Brem,Howard Trachtman,W Griswold,GA Richard,E John,Richard P. Lifton +20 more
TL;DR: The critical role of CLCNKB in renal salt reabsorption and blood–pressure homeostasis is demonstrated, and the potential role of specific C LCNKB antagonists as diuretic antihypertensive agents is demonstrated.
Journal ArticleDOI
Glioblastoma in adults: a Society for Neuro-Oncology (SNO) and European Society of Neuro-Oncology (EANO) consensus review on current management and future directions
Patrick Y. Wen,Michael Weller,Eudocia Q. Lee,Brian M. Alexander,Jill S. Barnholtz-Sloan,Floris P. Barthel,Tracy T. Batchelor,Ranjit S. Bindra,Susan M. Chang,E. Antonio Chiocca,Timothy F. Cloughesy,John DeGroot,Evanthia Galanis,Mark R. Gilbert,Monika E. Hegi,Craig Horbinski,Raymond Y. Huang,Andrew B. Lassman,Emilie Le Rhun,Michael Lim,Minesh P. Mehta,Ingo K. Mellinghoff,Giuseppe Minniti,David Nathanson,Michael Platten,Matthias Preusser,Patrick Roth,Marc Sanson,David Schiff,Susan C Short,Martin J B Taphoorn,Joerg C. Tonn,Jonathan Tsang,Roel G.W. Verhaak,Andreas von Deimling,Wolfgang Wick,Gelareh Zadeh,David A. Reardon,Kenneth Aldape,Martin J. van den Bent +39 more
TL;DR: Novel therapies such as targeted molecular therapies, agents targeting DNA damage response and metabolism, immunotherapies and viral therapies will be reviewed, as well as the current challenges and future directions for research.
Journal ArticleDOI
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.
Journal ArticleDOI
Down-Regulation of Rad51 and Decreased Homologous Recombination in Hypoxic Cancer Cells
Ranjit S. Bindra,Paul J. Schaffer,Alice Meng,Jennifer Woo,Kårstein Måseide,Matthew E. Roth,Paul M. Lizardi,David W. Hedley,Robert G. Bristow,Robert G. Bristow,Peter M. Glazer +10 more
TL;DR: It is reported that hypoxia specifically down-regulates the expression of RAD51, a key mediator of homologous recombination in mammalian cells, and a novel mechanism of genetic instability in the tumor microenvironment mediated by hypoxIA-induced suppression of the homologously recombination pathway in cancer cells is proposed.
Journal ArticleDOI
Hypoxia-induced down-regulation of BRCA1 expression by E2Fs.
Ranjit S. Bindra,Shannon L. Gibson,Alice Meng,Ulrica K. Westermark,Maria Jasin,Andrew J. Pierce,Robert G. Bristow,Marie Classon,Peter M. Glazer +8 more
TL;DR: It is proposed that hypoxia-induced decreases in BRCA1 expression and consequent suppression of homologous recombination may lead to genetic instability by shifting the balance between the high-fidelity homologously recombination pathway and the error-prone NHEJ pathway of DNA repair.