G
Gad Getz
Researcher at Broad Institute
Publications - 627
Citations - 309042
Gad Getz is an academic researcher from Broad Institute. The author has contributed to research in topics: Cancer & Biology. The author has an hindex of 189, co-authored 520 publications receiving 247560 citations. Previous affiliations of Gad Getz include University of Colorado Denver & University of California, San Diego.
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Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
Priscilla K. Brastianos,Scott L. Carter,Sandro Santagata,Daniel P. Cahill,Amaro Taylor-Weiner,Robert T. Jones,E.M. Van Allen,Michael S. Lawrence,Peleg M. Horowitz,Kristian Cibulskis,Keith L. Ligon,Josep Tabernero,Joan Seoane,Elena Martínez-Sáez,William T. Curry,Ian F. Dunn,Sun Ha Paek,Sung Hye Park,Aaron McKenna,Aaron Chevalier,Mara Rosenberg,Fred G. Barker,Corey M. Gill,P. Van Hummelen,Aaron R. Thorner,Bruce E. Johnson,Mai P. Hoang,Toni K. Choueiri,Sabina Signoretti,Carrie Sougnez,Michael S. Rabin,Nan Lin,Eric P. Winer,Anat Stemmer-Rachamimov,Matthew Meyerson,Levi A. Garraway,S. Gabriel,Eric S. Lander,Rameen Beroukhim,Tracy T. Batchelor,J. Baselga,David N. Louis,Gad Getz,William C. Hahn +43 more
TL;DR: Genomic analysis of brain metastases provides an opportunity to identify potentially clinically informative alterations not detected in clinically sampled primary tumors, regional lymph nodes, or extracranial metastases, suggesting that sequencing of primary biopsies alone may miss a substantial number of opportunities for targeted therapy.
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Nozzle: a report generation toolkit for data analysis pipelines
TL;DR: Nozzle is an R package that provides an Application Programming Interface to generate HTML reports with dynamic user interface elements to facilitate summarization and rapid browsing of complex results in data analysis pipelines where multiple analyses are performed frequently on big datasets.
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p190 RhoGAP promotes contact inhibition in epithelial cells by repressing YAP activity.
Scott R. Frank,Clemens P. Köllmann,Phi Luong,Giorgio G. Galli,Giorgio G. Galli,Lihua Zou,Andre Bernards,Andre Bernards,Gad Getz,Gad Getz,Raffaele A. Calogero,Morten Frödin,Steen H. Hansen +12 more
TL;DR: An essential role is revealed for p190A and p190B to promote contact inhibition of cell proliferation (CIP), a function that relies on RhoGAP activity, and a novel mechanism consistent with a tumor-suppressor function for ARHGAP35 is revealed.
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Longitudinal Single-Cell Dynamics of Chromatin Accessibility and Mitochondrial Mutations in Chronic Lymphocytic Leukemia Mirror Disease History
Livius Penter,Satyen H. Gohil,Caleb A. Lareau,Leif S. Ludwig,Erin M. Parry,Teddy Huang,Shuqiang Li,Wandi Zhang,Dimitri Livitz,Ignaty Leshchiner,Laxmi Parida,Gad Getz,Laura Z. Rassenti,Thomas J. Kipps,Jennifer R. Brown,Matthew S. Davids,Donna Neuberg,Kenneth J. Livak,Vijay G. Sankaran,Catherine J. Wu +19 more
TL;DR: In this paper, a single-cell mtDNA assay for transposase-accessible chromatin with sequencing to profile 163,279 cells from 9 patients with chronic lymphocytic leukemia (CLL) collected across disease course and utilize mitochondrial DNA (mtDNA) mutations as natural genetic markers of cancer clones.
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Distinct evolutionary paths in chronic lymphocytic leukemia during resistance to the graft-versus-leukemia effect.
Pavan Bachireddy,Christina Ennis,Vinhkhang N Nguyen,Satyen H. Gohil,Satyen H. Gohil,Satyen H. Gohil,Kendell Clement,Kendell Clement,Sachet A. Shukla,Sachet A. Shukla,Juliet Forman,Juliet Forman,Nikolaos Barkas,Samuel S. Freeman,Natalie Bavli,Liudmila Elagina,Ignaty Leshchiner,Arman W. Mohammad,Nathan Mathewson,Nathan Mathewson,Derin B. Keskin,Derin B. Keskin,Laura Z. Rassenti,Thomas J. Kipps,Jennifer R. Brown,Gad Getz,Vincent T. Ho,Vincent T. Ho,Andreas Gnirke,Donna Neuberg,Robert J. Soiffer,Robert J. Soiffer,Jerome Ritz,Jerome Ritz,Edwin P. Alyea,Edwin P. Alyea,Peter V. Kharchenko,Catherine J. Wu +37 more
TL;DR: Integrated genetic, transcriptomic, and epigenetic analyses of CLL cells from 10 patients revealed that the clinical kinetics of post-HSCT relapse are shaped by distinct molecular dynamics, which elucidate the biological pathways that underlie GvL resistance and posttransplant relapse.