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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Proceedings ArticleDOI
Abstract LB-231: Identifying cancer-related processes in normal tissues via RNA-seq
Keren Yizhak,Jaegil Kim,François Aguet,Julian M. Hess,Hailei Zhang,Eila Arich-Landkof,Noam Shoresh,Segrè Av,Chip Stewart,Dainel Rosebrock,Dimitri Livitz,Nicholas J. Haradhvala,Paz Polak,Timothy J. Sullivan,Xiao Li,Kristin G. Ardlie,Gad Getz +16 more
TL;DR: This study is the first to analyze a large number of samples across many tissues to explore the fundamental question of cancer initiation, and demonstrates that most of the known driver genes in this cohort can be discovered using the mutations detected based on the RNA data.
Journal ArticleDOI
Large-Scale CLL Genome Analysis Reveals Novel Cancer Genes, Including SF3B1
Youzhong Wan,Michael S. Lawrence,Lili Wang,Petar Stojanov,Carrie Sougnez,Kristen E. Stevenson,Lillian Werner,Wandi Zhang,Eric G. Folco,Bethany Tesar,Quinlan L. Sievers,Stacey Gabriel,Nir Hacohen,Robin Reed,Matthew Meyerson,Todd R. Golub,Eric S. Lander,Donna Neuberg,Jennifer R. Brown,Gad Getz,Catherine J. Wu +20 more
TL;DR: The discovery of striking associations between driver mutations and standard CLL prognostic markers (cytogenetic aberrations, IGVH mutational status) suggest synergistic interactions, and highlight pre-mRNA splicing as a critical but thus far unexplored cellular process contributing to CLL.
Supplementary Material 10
Rameen Beroukhim,Craig H. Mermel,Dale Porter,Guo Wei,Soumya Raychaudhuri,Jerry Donovan,Jordi Barretina,Jesse S. Boehm,Jennifer Dobson,Mitsuyoshi Urashima,Kevin T. Mc Henry,Reid M. Pinchback,Azra H. Ligon,Yoon Jae Cho,Leila Haery,Heidi Greulich,Michael R. Reich,Wendy Winckler,Michael S. Lawrence,Barbara A. Weir,Kumiko E. Tanaka,Derek Y. Chiang,Adam J. Bass,Alice Loo,Carter Hoffman,John R. Prensner,Ted Liefeld,Qing Gao,Derek Yecies,Sabina Signoretti,Elizabeth A. Maher,Frederic J. Kaye,Hidefumi Sasaki,Joel E. Tepper,Jonathan A. Fletcher,Josep Tabernero,José Baselga,Ming-Sound Tsao,Francesca Demichelis,Mark A. Rubin,Pasi A. Jänne,Mark J. Daly,Carmelo Nucera,Ross L. Levine,Benjamin L. Ebert,Stacey Gabriel,Anil K. Rustgi,Cristina R. Antonescu,Marc Ladanyi,Anthony Letai,Levi A. Garraway,Massimo Loda,David G. Beer,Lawrence D. True,Aikou Okamoto,Scott L. Pomeroy,Samuel Singer,Todd R. Golub,Eric S. Lander,Gad Getz,William R. Sellers,Matthew Meyerson +61 more
Journal ArticleDOI
Longitudinal circulating tumor DNA (ctDNA) whole-exome sequencing (WES) in the phase Ib/II trial of palbociclib and bazedoxifene reveals genomic dynamics and clonal evolution with the acquisition of treatment resistance in hormone receptor-positive, HER2-negative (HR+ HER2-), advanced breast cancer
Albert Grinshpun,Junko Tsuji,Tianyu Li,Douglas Russo,Leilani Anderson,Rebecca Rees,Carrie Cibulskis,Ignaty Leshchiner,Chip Stewart,Nadine Tung,Ian E. Krop,Eric P. Winer,Sara M. Tolaney,Gad Getz,Rinath Jeselsohn +14 more
TL;DR: Serial ctDNA WES and evolutionary studies enabled us to discover novel potential genomic mechanisms of tumor progression, and identified PIK3CA mutations as a candidate biomarker of resistance to the combination of palbociclib and bazedoxifene, which may apply to other next generation endocrine treatments.
Proceedings ArticleDOI
Abstract 2570: An integrated germline analysis platform for comprehensive clinical cancer genomics.
Eliezer M. Van Allen,Nikhil Wagle,Adam Keizun,Gregory V. Kryukov,Aaron McKenna,Franklin W. Huang,Elaine Hiller,Irene Rainville,Daniel Auclair,Lauren Ambrogio,Stacy W. Gray,Steven Joffe,Gad Getz,Judy Garber,Levi A. Garraway +14 more
TL;DR: The authors' germline analysis platform facilitates prospective clinical interpretation of germline genomic variants by prioritizing and representing alterations of potential clinical significance and integrates germline variants with clinically actionable somatic alterations for enhanced understanding of potential disease drivers at the individual patient level.