Picture of Thomas Roberts

Thomas McCoy Roberts, Ph.D.

Professor of Biological Chemistry and Molecular Pharmacology

Research in the Roberts laboratory is centered on the molecular mechanisms of signal transduction in response to activated tyrosine kinases

Research:

Dr. Roberts is a Professor of Biological Chemistry and Molecular Pharmacology at Harvard Medical School and serves as Co-Chairman for the Department of Cancer Biology at Dana-Farber Cancer Institute. Dr. Roberts received his PhD from Harvard University where he also completed a postdoctoral fellowship. Dr Roberts’ laboratory has played a key role in the study of signal transduction and its translation into cancer therapy. The first definitive studies on phosphoinositide 3 (PI3) kinase were done by the Roberts lab in collaboration with the lab of Lewis Cantley.  In addition, the Roberts lab pioneered studies on the regulation of the serine/threonine kinase, Raf-1, and first characterized the interaction of 14-3-3 molecules with key signal transducers including Raf-1.   Due to the importance of PI3 kinase in human cancer, Roberts has studied it in detail, collaborating with Jean Zhao to generate conditional knockout mice for the commonly expressed catalytic subunits of PI3K.  The end goal of these studies, determining which isoforms to target in specific cancers, underlies the superior performance of isoform-specific inhibitors in the clinic.  Moreover, Zhao and Roberts gained a new understanding of a surprising functional specialization in the two enzymes (termed p110 and p110): p110 plays the major role in receptor tyrosine kinase and ras signaling, while p110 plays the major part in GPCR signaling and in tumors arising from PTEN loss.  Notably Dr Roberts’ basic research on tyrosine kinases carried out by Drs. Brian Druker and Helen Piwnica-Worms facilitated the kinase inhibitor program at Ciba Geigy, which led to the first successful tyrosine kinase cancer therapeutic, Gleevec.  Similarly, his research collaborations on PI3 kinase has facilitated the development of multiple classes of PI3Kinase inhibitors

Address: 

Dana-Farber Cancer Institute

Smith Building, Room 970A

450 Brookline Avenue

Boston, MA 02215

Publications View
Synthetic phosphopeptide immunogens yield activation-specific antibodies to the c-erbB-2 receptor.
Authors: Authors: Epstein RJ, Druker BJ, Roberts TM, Stiles CD.
Proc Natl Acad Sci U S A
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Regulation of the reverse transcriptase of human immunodeficiency virus type 1 by dNTPs.
Authors: Authors: West AB, Roberts TM, Kolodner RD.
Proc Natl Acad Sci U S A
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Polyomavirus middle T-antigen NPTY mutants.
Authors: Authors: Druker BJ, Sibert L, Roberts TM.
J Virol
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Tyrosine kinase triggering in thymocytes undergoing positive selection.
Authors: Authors: Carrera AC, Baker C, Roberts TM, Pardoll DM.
Eur J Immunol
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Both p21ras and pp60v-src are required, but neither alone is sufficient, to activate the Raf-1 kinase.
Authors: Authors: Williams NG, Roberts TM, Li P.
Proc Natl Acad Sci U S A
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ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.
Authors: Authors: Wood KW, Sarnecki C, Roberts TM, Blenis J.
Cell
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Extracellular calcium mimics the actions of platelet-derived growth factor on mouse fibroblasts.
Authors: Authors: Epstein RJ, Druker BJ, Irminger JC, Jones SD, Roberts TM, Stiles CD.
Cell Growth Differ
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Transformation-defective mutants of polyomavirus middle T antigen associate with phosphatidylinositol 3-kinase (PI 3-kinase) but are unable to maintain wild-type levels of PI 3-kinase products in intact cells.
Authors: Authors: Ling LE, Druker BJ, Cantley LC, Roberts TM.
J Virol
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The third subunit of protein phosphatase 2A (PP2A), a 55-kilodalton protein which is apparently substituted for by T antigens in complexes with the 36- and 63-kilodalton PP2A subunits, bears little resemblance to T antigens.
Authors: Authors: Pallas DC, Weller W, Jaspers S, Miller TB, Lane WS, Roberts TM.
J Virol
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Purification and initial characterization of the lymphoid-cell protein-tyrosine kinase p56lck from a baculovirus expression system.
Authors: Authors: Ramer SE, Winkler DG, Carrera A, Roberts TM, Walsh CT.
Proc Natl Acad Sci U S A
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