Austin M. Dulak
Harvard University
10 Papers
111 Citations
Austin M. Dulak is an academic researcher from Harvard University. The author has contributed to research in topics: Biology & Esophagus. The author has an hindex of 7, co-authored 7 publications. Previous affiliations of Austin M. Dulak include Broad Institute.
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Papers
Mutational heterogeneity in cancer and the search for new cancer-associated genes
Michael S. Lawrence,Petar Stojanov,Petar Stojanov,Paz Polak,Paz Polak,Paz Polak,Gregory V. Kryukov,Gregory V. Kryukov,Gregory V. Kryukov,Kristian Cibulskis,Andrey Sivachenko,Scott L. Carter,Chip Stewart,Craig H. Mermel,Craig H. Mermel,Steven A. Roberts,Adam Kiezun,Peter S. Hammerman,Peter S. Hammerman,Aaron McKenna,Aaron McKenna,Yotam Drier,Lihua Zou,Alex H. Ramos,Trevor J. Pugh,Trevor J. Pugh,Nicolas Stransky,Elena Helman,Elena Helman,Jaegil Kim,Carrie Sougnez,Lauren Ambrogio,Elizabeth Nickerson,Erica Shefler,Maria L. Cortes,Daniel Auclair,Gordon Saksena,Douglas Voet,Michael S. Noble,Daniel DiCara,Pei Lin,Lee Lichtenstein,David I. Heiman,Timothy Fennell,Marcin Imielinski,Marcin Imielinski,Bryan Hernandez,Eran Hodis,Eran Hodis,Sylvan C. Baca,Sylvan C. Baca,Austin M. Dulak,Austin M. Dulak,Jens G. Lohr,Jens G. Lohr,Dan A. Landau,Dan A. Landau,Dan A. Landau,Catherine J. Wu,Jorge Melendez-Zajgla,Alfredo Hidalgo-Miranda,Amnon Koren,Amnon Koren,Steven A. McCarroll,Steven A. McCarroll,Jaume Mora,Ryan S. Lee,Ryan S. Lee,Brian D. Crompton,Brian D. Crompton,Robert C. Onofrio,Melissa Parkin,Wendy Winckler,Kristin G. Ardlie,Stacey Gabriel,Charles W. M. Roberts,Charles W. M. Roberts,Jaclyn A. Biegel,Kimberly Stegmaier,Kimberly Stegmaier,Kimberly Stegmaier,Adam J. Bass,Adam J. Bass,Levi A. Garraway,Levi A. Garraway,Matthew Meyerson,Matthew Meyerson,Todd R. Golub,Dmitry A. Gordenin,Shamil R. Sunyaev,Shamil R. Sunyaev,Shamil R. Sunyaev,Eric S. Lander,Eric S. Lander,Eric S. Lander,Gad Getz,Gad Getz +96 more
TL;DR: A fundamental problem with cancer genome studies is described: as the sample size increases, the list of putatively significant genes produced by current analytical methods burgeons into the hundreds and the list includes many implausible genes, suggesting extensive false-positive findings that overshadow true driver events.
Mutational heterogeneity in cancer and the search for new cancer genes
Michael S. Lawrence,Petar Stojanov,Paz Polak,Gregory V. Kryukov,Kristian Cibulskis,Andrey Sivachenko,Scott L. Carter,Chip Stewart,Craig H. Mermel,Stephen A Roberts,Adam Kiezun,Peter S. Hammerman,Aaron McKenna,Yotam Drier,Lihua Zou,Alex H. Ramos,T. Pugh,Nico Stransky,Elena Helman,Jaegil Kim,C. Sougnez,L. Ambrogio,E. Nickerson,Erica Shefler,Maria L. Cortes,Daniel Auclair,Gordon Saksena,Doug Voet,Michael S. Noble,Daniel DiCara,Pei-Xuan Lin,Lee T Lichtenstein,David I. Heiman,T. Fennell,Marcin Imielinski,Bryan Hernandez,Eran Hodis,Sylvan C. Baca,Austin M. Dulak,Jens G. Lohr,Dan A. Landau,Catherine J. Wu,Jorge Melendez-Zajgla,Alfredo Hidalgo-Miranda,Amnon Koren,Steven A. McCarroll,Jaume Mora,Brian D. Crompton,Robert C. Onofrio,Melissa Parkin,W. Winckler,Kristin G. Ardlie,Stacey Gabriel,Charles Roberts,Jaclyn A. Biegel,Kimberly Stegmaier,Adam J. Bass,Levi A. Garraway,Matthew Meyerson,Todd R. Golub,Dmitry A. Gordenin,Shamil R. Sunyaev,Eric S. Lander,Gad Getz +63 more
TL;DR: A fundamental problem with cancer genome studies is described: as the sample size increases, the list of putatively significant genes produced by current analytical methods burgeons into the hundreds and the list includes many implausible genes, suggesting extensive false-positive findings that overshadow true driver events.
551
Gastrointestinal adenocarcinomas of the esophagus, stomach and colon exhibit distinct patterns of genome instability and oncogenesis
Austin M. Dulak,Steven E. Schumacher,Jasper van Lieshout,Yu Imamura,Cameron Fox,Byoungyong Shim,Alex H. Ramos,Gordon Saksena,Sylvan C. Baca,José Baselga,Josep Tabernero,Jordi Barretina,Peter C. Enzinger,Giovanni Corso,Franco Roviello,Lin Lin,Santhoshi Bandla,James D. Luketich,Arjun Pennathur,Matthew Meyerson,Shuji Ogino,Ramesh A. Shivdasani,David G. Beer,Tony E. Godfrey,Rameen Beroukhim,Adam J. Bass +25 more
TL;DR: Genomic features that were common and distinct to various gut-derived adenocarcinomas were defined, potentially informing novel opportunities for targeted therapeutic interventions and suggesting the potential use of genomic amplifications as biomarkers to guide therapy of gastric and esophageal cancers.
256
Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition
Gabrielle S. Wong,Gabrielle S. Wong,Jin Zhou,Jie Bin Liu,Zhong Wu,Xinsen Xu,Tianxia Li,David Xu,Steven E. Schumacher,Jens Puschhof,James M. McFarland,James M. McFarland,Charles Zou,Austin M. Dulak,Les Henderson,Peng Xu,Emily O'Day,Rachel Rendak,Wei-Li Liao,Fabiola Cecchi,Todd Hembrough,Sarit Schwartz,Christopher Szeto,Anil K. Rustgi,Kwok-Kin Wong,Kwok-Kin Wong,J. Alan Diehl,Karin Jensen,Francesco Graziano,Annamaria Ruzzo,Shaunt Fereshetian,Philipp Mertins,Philipp Mertins,Steven A. Carr,Rameen Beroukhim,Rameen Beroukhim,Kenichi Nakamura,Eiji Oki,Masayuki Watanabe,Masayuki Watanabe,Hideo Baba,Yu Imamura,Yu Imamura,Daniel V.T. Catenacci,Adam J. Bass,Adam J. Bass +45 more
TL;DR: It is demonstrated that inhibition of the guanine-exchange factors SOS1 and SOS2 or the protein tyrosine phosphatase SHP2 can attenuate this adaptive process and that targeting these factors can enhance the sensitivity of KRAS-amplified models to MEK inhibition in both in vitro and in vivo settings.
242
Comparison of cancer-associated genetic abnormalities in columnar-lined esophagus tissues with and without goblet cells.
Santhoshi Bandla,Jeffrey H. Peters,David Ruff,Shiaw Min Chen,Chieh Yuan Li,Kunchang Song,Kimberly Thoms,Virginia R. Litle,Thomas J. Watson,Nikita Chapurin,Michal J. Lada,Arjun Pennathur,James D. Luketich,Derick R. Peterson,Austin M. Dulak,Lin Lin,Adam J. Bass,David G. Beer,Tony E. Godfrey,Zhongren Zhou +19 more
TL;DR: This study reports the largest and most comprehensive comparison of DNA aberrations in IM and NGM genomes and shows that IM has a much higher frequency of cancer-associated mutations than NGM.