Joseph Kissil, Ph.D.

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Wistar Institute Associate Professor of Cancer Biology
Department: Cancer Biology

Contact information
372 Wistar Institute (Office)
372 Wistar Institute (Lab)
3601 Spruce Street
Philadelphia, PA 19104
Office: 215 898-3874
BSc (Life Sciences)
Ben-Gurion University (Israel), 1993.
PhD (Molecular Genetics)
Weizmann Institute of Science (Israel), 1999.
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Description of Research Expertise

Research Interests
Genetic analysis of crosstalk between signaling pathways
Signal transduction and cancer
Molecular biology of neurofibromatosis type 2

Key words: Ras, Rac, Neurofibromatosis type 2, NF2, merlin.

Description of Research
The main interest of the lab is the understanding of signal transduction networks in vivo and their deregulation in cancer. We are studying the pathways regulated by the small G-proteins K-ras and Rac1 and dissecting the crosstalk between these pathways employing animal models. We are also focusing on the neurofibromatosis type 2 tumor suppressor gene (Nf2) and examining its role in the regulation of Ras/Rac crosstalk and how loss of Nf2 results in cancer. We approach these issues mainly in vivo, by developing animal models harboring specific knock-in mutations in genes of interest. These models are then used to examine the function of these mutations in development and cancer.

Currently, we are focusing on the crosstalk between Rac and Ras regulated pathways employing a conditional model of lung cancer. By combining conditional activation of K-ras with conditional deletion of Rac1, we demonstrated that Rac1 is required for tumorigenesis. We are examining what pathways downstream of Rac1 are required for K-ras-induced transformation. We have also recently found a possible link between the Rac-signaling pathways and cancer in the case of Neurofibromatosis type 2 (NF2), an inherited disorder that is characterized mainly by development of Schwann cell tumors of the eighth cranial nerve. The Nf2 gene is a tumor suppressor gene coding for a protein called merlin, which functions as a negative regulator of Rac signaling through its direct inhibitory function on p21-activated kinase 1. We are assessing whether this function is indeed the tumor suppressive function of merlin and whether targeting the p21-activated kinases would be beneficial as a treatment modality for neurofibromatosis type 2.

Rotation Projects for 2006-2007
- Crosstalk between small G-protein signaling networks in cancer.
- The role of the tumor microenvironment in tumorigenesis.
- Application of novel imaging technologies to the study of lung cancer.

Please contact Dr. Kissil directly about current rotation projects.

Lab personnel:
Scott Troutman - Lab manager
Chunling Yi - Postdoctoral fellow
Mi-young Cho - postdoctoral fellow
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Last updated: 09/14/2011
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