Martin Carroll

Cancer Biology Program

Address

708 Biomedical Rsch Bldg II/III (Office)
732 Biomedical Rsch Bldg II/III (Lab)
421 Curie Boulevard
Philadelphia, PA 19104-6140

Office tel.: 215 573-5217
Lab tel.: 215 573-7617
Fax: 215 573-7049
E-mail: carroll2@mail.med.upenn.edu

Link(s)

Harvard College: AB (English and American Languages and Literature), 1982.

Dartmouth Medical School: MD, 1988.

Research Interests

• Molecular biology of leukemia

Key words: Leukemia, Src kinases, signal transduction, STAT5

Description of Research

My laboratory is focused on understanding the pathogenesis of myeloid leukemia's in order to develop new therapeutics. Models of acute myeloid leukemia suggest that a necessary step in transformation is the development of activated signal transduction pathways. However, the pathways activated and the mechanism of activation are unknown. We have pursued both candidate gene approaches and phospho-proteomic approaches to understanding the mechanism of disordered growth and survival signals in AML. All projects are based on use of primary AML cells from a large tissue bank. We have previously identified dysregulation of the PI3 kinase/mTOR signaling pathway in AML as well as dysregulation of the STAT5 signaling pathway. Projects in the lab currently focus on understanding mechanisms of rapamycin resistant mTOR signaling in AML and identification of targets of STAT5. In addition, we have recently characterized activation of Src kinases (particularly Lyn and Lck) in AML and shown that both Lyn and Lck contribute to AML cell survival in AML. We will be studying whether Src family kinases are necessary for AML stem cell survival and survival of AML cells in vivo. For the latter experiments, we have recently characterized a new model for studies of primary human AML cells using a NOG mouse. These mice engraft with AML cells and will form the basis for studies of signal transduction inhibitors as therapeutics for AML

Selected Publications

Xu Q., Thompson J.E., Carroll M. (2005). mTOR regulates Survival After Genotoxic Stress in Primary AML Cells. Blood, Dec 15;106(13), 4261-8.

Dierov J., Dierova R., Carroll, M. (2004) BCR/ABL Translocates to the Nucleus After DNA Damage and Disrupts an ATR Dependent Cell Cycle Checkpoint. Cancer Cell. Vol. 5, p. 275-285.

D.E. Tsai, S. Luger, A. Loren, A. Kemner, J. Thompson, S. Schuster, A. Perl, D. Porter, A. Bagg, M. Carroll. (2006). A phase I trial of bexarotene, a retinoid X receptor agonist, in relapsed or refractory non-M3 acute myeloid leukemia (AML). Cancer Biology & Therapy. 26;6(1).

*Ranuncolo S.M., Polo J.M., Dierov J., Shaknovich, R., Carroll M.and Melnick A.M. (2007). BCL6 Attenuates DNA Damage Sensing in Normal and Malignant B-Cells by Directly Repressing ATR. Nature Immunology, 8(7), 705-14. *(Co-last author)

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Lab

Rotation Projects

Personnel:

Jamil Dierov PhD, DS. - Staff Scientist
Sasha Perl, M.D. - Assistant Professor
Patty Sanchez, Ph.D. - Postdoctoral Fellow
Beth Burke - Graduate Student
Jamie Lynne Laird - Graduate Student
Robin Perry, M.D. - Clinical Fellow