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
The Six1 homeoprotein stimulates tumorigenesis by reactivation of cyclin A1
Ricardo D. Coletta,Kimberly L. Christensen,Kelly J. Reichenberger,Justin Lamb,Damian Micomonaco,Lili Huang,Douglas M. Wolf,Carsten Müller-Tidow,Todd R. Golub,Kiyoshi Kawakami,Heide L. Ford +10 more
TL;DR: The results demonstrate that cyclin A1 is required for the proliferative effect of Six1, and conclude that Six1 overexpression reinstates an embryonic pathway of proliferation in breast cancer by up-regulating cyclIn A1.
Journal ArticleDOI
Identification of Driver and Passenger Mutations of FLT3 by High-Throughput DNA Sequence Analysis and Functional Assessment of Candidate Alleles
Stefan Fröhling,Claudia Scholl,Ross L. Levine,Ross L. Levine,Marc M. Loriaux,Titus J. Boggon,Olivier Bernard,Roland Berger,Hartmut Döhner,Konstanze Döhner,Benjamin L. Ebert,Benjamin L. Ebert,Benjamin L. Ebert,Sewit Teckie,Todd R. Golub,Todd R. Golub,Todd R. Golub,Jingrui Jiang,Marcus M Schittenhelm,Benjamin H. Lee,James D. Griffin,Richard Stone,Michael Heinrich,Michael Heinrich,Michael W. Deininger,Brian J. Druker,Brian J. Druker,D. Gary Gilliland,D. Gary Gilliland +28 more
TL;DR: The concept that acquired mutations in cancer may not contribute to malignant transformation and underscore the importance of functional studies to distinguish "driver" mutations underlying tumorigenesis from biologically neutral "passenger" alterations are supported.
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Chronic cisplatin treatment promotes enhanced damage repair and tumor progression in a mouse model of lung cancer
Trudy G. Oliver,Kim L. Mercer,Leanne C. Sayles,James R. Burke,Diana Mendus,Katherine S. Lovejoy,Mei-Hsin Cheng,Aravind Subramanian,David Mu,Scott Powers,Denise G. Crowley,Roderick T. Bronson,Charles A. Whittaker,Arjun Bhutkar,Stephen J. Lippard,Todd R. Golub,Juergen Thomale,Tyler Jacks,E. Alejandro Sweet-Cordero +18 more
TL;DR: It is shown that lung tumors initially respond to cisplatin by sensing DNA damage, undergoing cell cycle arrest, and inducing apoptosis-leading to a significant reduction in tumor burden, and a novel role for PIDD as a regulator of chemotherapy response in human lung tumor cells is demonstrated.
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Chemical genetic strategy identifies histone deacetylase 1 (HDAC1) and HDAC2 as therapeutic targets in sickle cell disease
James E. Bradner,Raymond H. Mak,Shyam K. Tanguturi,Ralph Mazitschek,Stephen J. Haggarty,Kenneth N. Ross,Cindy Y. Chang,Jocelyn Bosco,Nathan West,Nathan West,Elizabeth M. Morse,Elizabeth M. Morse,Katherine Lin,John Paul Shen,Nicholas Kwiatkowski,Nele Gheldof,Job Dekker,Daniel J. DeAngelo,Steven A. Carr,Stuart L. Schreiber,Stuart L. Schreiber,Stuart L. Schreiber,Todd R. Golub,Todd R. Golub,Todd R. Golub,Benjamin L. Ebert,Benjamin L. Ebert +26 more
TL;DR: A unique bead-based strategy is developed for the identification of inducers of fetal hemoglobin transcripts in primary human erythroid cells and the potential of isoform-selective inhibitors of HDAC1 and HDAC2 for the treatment of sickle cell disease is suggested.
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Prognostic Gene Expression Signature for Patients With Hepatitis C–Related Early-Stage Cirrhosis
Yujin Hoshida,Augusto Villanueva,Angelo Sangiovanni,Manel Solé,Chin Hur,Karin L. Andersson,Raymond T. Chung,Joshua Gould,Kensuke Kojima,Supriya Gupta,Bradley Taylor,Andrew Crenshaw,Stacey Gabriel,Beatriz Minguez,Massimo Iavarone,Scott L. Friedman,Massimo Colombo,Josep M. Llovet,Josep M. Llovet,Todd R. Golub,Todd R. Golub,Todd R. Golub +21 more
TL;DR: This investigation investigated whether a liver-derived 186-gene signature previously associated with outcomes of patients with HCC is prognostic for patients with newly diagnosed cirrhosis but without HCC, and whether this signature might be used to identify patients with Cirrhosis in most need of surveillance and strategies to prevent the development of HCC.