T
Todd R. Golub
Researcher at Harvard University
Publications - 454
Citations - 234100
Todd R. Golub is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Gene expression profiling. The author has an hindex of 164, co-authored 422 publications receiving 201457 citations. Previous affiliations of Todd R. Golub include Rush University Medical Center & Boston Children's Hospital.
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Journal ArticleDOI
MicroRNA Expression Signatures Accurately Discriminate Acute Lymphoblastic Leukemia from Acute Myeloid Leukemia.
Shuangli Mi,Jun Lu,Jun Lu,Miao Sun,Zejuan Li,Hao Zhang,Mary Beth Neilly,Yungui Wang,Zhijian Qian,Jie Jin,Yanming Zhang,Stefan K. Bohlander,Michelle M. Le,Richard A. Larson,Todd R. Golub,Todd R. Golub,Todd R. Golub,Janet D. Rowley,Jianjun Chen +18 more
TL;DR: It is found that overexpression of miR-128a and b in ALL was at least partly associated with hypomethylation, rather than amplification of DNA locus copy, which will enhance the understanding of the biological role of these miRNAs and their targets in leukemogenesis, and in determining the lineage fate of acute leukemia.
Journal ArticleDOI
Amplification of CRKL Induces Transformation and Epidermal Growth Factor Receptor Inhibitor Resistance in Human Non–Small Cell Lung Cancers
Hihu Wing Cheung,Jinyan Du,Jesse S. Boehm,Frank He,Barbara A. Weir,Xiaoxing Wang,Mohit Butaney,Lecia V. Sequist,Biao Luo,Jeffrey A. Engelman,David E. Root,Matthew Meyerson,Todd R. Golub,Pasi A. Jänne,William C. Hahn +14 more
TL;DR: It is shown that CRKL, encoding for an adaptor protein, is amplified and overexpressed in non-small cell lung cancer (NSCLC) cells that harbor 22q11.21 amplifications, andCRKL is credentialed as an oncogene in a subset of NSCLC and implicate CRKl as an additional mechanism of resistance to EGFR-directed therapy.
Journal ArticleDOI
Incidence of TEL/AML1 Fusion in Children With Relapsed Acute Lymphoblastic Leukemia
Mignon L. Loh,Lewis B. Silverman,M L Young,Donna Neuberg,Todd R. Golub,Stephen E. Sallan,D G Gilliland +6 more
TL;DR: The TEL/AML1 fusion was identified in only 1 of 32 analyzable relapsed ALL patients, in concordance with previous reports of improved disease-free survival in TEL or AML1-positive patients, and support the need for prospective analysis of prognosis in Tel/AMl1- positive patients.
Journal ArticleDOI
Genetic interrogation of circulating multiple myeloma cells at single-cell resolution.
Jens G. Lohr,Jens G. Lohr,Sora Kim,Joshua Gould,Birgit Knoechel,Birgit Knoechel,Yotam Drier,Yotam Drier,Matthew J. Cotton,Matthew J. Cotton,Matthew J. Cotton,Daniel Gray,Nicole Birrer,Bang Wong,Gavin Ha,Gavin Ha,Cheng-Zhong Zhang,Cheng-Zhong Zhang,Guangwu Guo,Guangwu Guo,Matthew Meyerson,Matthew Meyerson,Andrew Yee,Jesse S. Boehm,Noopur Raje,Todd R. Golub +25 more
TL;DR: It is demonstrated that circulating tumor cells in peripheral blood of multiple myeloma patients can provide the same genetic information as bone marrow samples, and sometimes more, and proposed that the genomic characterization of CTCs should be included in clinical trials to follow the emergence of resistant subclones after MM therapy.
Journal ArticleDOI
Re-programing Chromatin with a Bifunctional LSD1/HDAC Inhibitor Induces Therapeutic Differentiation in DIPG
Jamie N. Anastas,Barry M. Zee,Barry M. Zee,Jay H. Kalin,Mirhee Kim,Robyn Guo,Sanda Alexandrescu,Mario Andres Blanco,Stefanie Giera,Shawn M. Gillespie,Jayanta Das,Muzhou Wu,Sarah E. Nocco,Dennis M. Bonal,Quang-Dé Nguyen,Mario L. Suvà,Bradley E. Bernstein,Bradley E. Bernstein,Rhoda M. Alani,Todd R. Golub,Philip A. Cole,Philip A. Cole,Mariella G. Filbin,Mariella G. Filbin,Yang Shi,Yang Shi +25 more
TL;DR: A CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors is conducted, suggesting a strategy for treating DIPGs by simultaneously inhibiting LSD1 and HDACs.