Thomas Force, M.D.

Contact Dr. Force

Center for Translational Medicine
1025 Walnut Street, Suite 316
Philadelphia, PA 19107

(215) 903-9520

Medical School
Harvard Medical School

Residency
Internal Medicine, University of Vermont, Burlington, VT

Fellowship
Clinical Fellow in Medicine, Brigham & Women's Hospital, West Roxbury VAMC, Boston, MA
Research Fellow in Medicine, Brigham and Women's Hospital, Boston, MA

Degree
M.D., Harvard Medical School 1978

University Appointment
James C. Wilson Professor of Medicine

Research and Clinical Interests
Dr. Force's focuses on the regulation of normal and stress-induced cardiomyocyte hypertrophy. Specifically, we study the signal transduction pathways that regulate growth responses, focusing on protein kinase cascades. Most recently, we have studied the role of glycogen synthase kinase-3beta, which is a potent negative regulator of growth, and its downstream targets, which include beta-catenin and its co-factors, the Tcf family of transcription factors, and the family of nuclear factors of activated T cells (NF-ATs), in hypertrophic growth. In addition, we study signaling mechanisms that regulate the response of the cell to ischemic injury. Making use of novel small molecule inhibitors, we have recently identified a novel mechanism by which the JNK family of stress-activated protein kinases regulate activity of the pro-survival kinase, Akt/PKB, and, via this mechanism, cardiomyocyte survival following ischemia/reperfusion.

Publications

Most Recent Peer-reviewed Publications

1. Serine 58 of 14-3-3ζ is a molecular switch regulating ASK1 and oxidant stress-induced cell death
2. Unique and overlapping functions of GSK-3 isoforms in cell differentiation and proliferation and cardiovascular development.
3. Deletion of GSK-3β in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation
4. Cardiotoxicity of the new cancer therapeutics - mechanisms of, and approaches to, the problem
5. Mechanisms of cardiac dysfunction associated with tyrosine kinase inhibitor cancer therapeutics.
6. SOK1 translocates from the Golgi to the nucleus upon chemical anoxia and induces apoptotic cell death.
7. Cardiotoxicity associated with sunitinib - Authors' reply
8. 17 Beta-Estradiol Differentially Affects Left Ventricular and Cardiomyocyte Hypertrophy Following Myocardial Infarction and Pressure Overload
9. The weakness of a big heart
10. Cardiotoxicity associated with tyrosine kinase inhibitor sunitinib
11. Not all hypertrophy is created equal
12. Molecular scaffolds regulate bidirectional crosstalk between Wnt and classical seven-transmembrane-domain receptor signaling pathways.
13. The GCK II and III subfamilies of the STE20 group kinases
14. Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition
15. Glycogen Synthase Kinase-3β-Actively Inhibiting Hypertrophy
16. Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease induction
17. Force et al. reply [5]
18. Activation of β-catenin signaling pathways by classical G-protein-coupled receptors: Mechanisms and consequences in cycling and non-cycling cells
19. p38 Mitogen-Activated Protein Kinase. A Future Target for Heart Failure Therapy?* * Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
20. Cardiotoxicity of the cancer therapeutic agent imatinib mesylate

View All Publications