The laboratory of Joe Kissil focuses on the signaling networks that relay information from the outside of cells into the cell interior. These signaling pathways play a critical role in almost all forms of cellular communication, and their disruption frequently results in disease, including cancer. The Kissil lab’s intent is to determine how these pathways normally communicate with one another, and how their disruption leads to disease. In particular, the group studies how signaling pathways influence the development of neurofibromatosis type 2 (NF2), an inherited tumor disorder.

Kissil joined The Wistar Institute in 2004 after completing his postdoctoral fellowship at the Massachusetts Institute of Technology. He received his bachelor’s degree from Ben-Gurion University and his Ph.D. from the Weizmann Institute of Science. Kissil is a Wistar Associate Professor in the Department of Cancer Biology at the University of Pennsylvania. In 2010, he received an American Cancer Society Research Scholar award.

The Kissil laboratory seeks to expand the knowledge of various signal transduction pathways, and to help integrate this data into a comprehensive map of cellular signaling networks. Of particular interest are signaling pathways regulated by small G-proteins, such as Ras, Rac and Rho and how these pathways communicate with pathways that have been shown to play critical roles during development, such as the Notch and Wnt pathways. Following these and other leads, his laboratory is currently working on development of a potential treatments for NF2, a genetic disorder that produces benign tumors in the nervous system of young adults.

1 - Yi C, Troutman S, Fera D, Stemmer-Rachamimov A, Avila JL, Christian N, Luna Persson N, Shimono A, Speicher DW, Marmorstein R, Holmgren L, Kissil, JL., A tight junction-associated Merlin-angiomotin Complex mediates Merlin's regulation of mitogenic signaling and tumor suppressive functions., Cancer Cell. 2011 Apr 12;19(4):527-40., 21481793

2 - Jung Y, Kissil, JL, McCarty JH., B8 integrin and band 4.1B cooperatively regulate morphogenesis of the embryonic heart., Developmental Dynamics. 2011 Jan;240(1):271-17., 21181944

3 - Licciulli S, Kissil, JL., WT1: a weak spot in KRAS-induced transformation., Journal of Clinical Investigation. 2010 Nov 1;120(11):3804-7. doi: 10.1172/JCI144901. [Epub 2010 Oct 25], 20972324

4 - Yi C, Kissil, JL., Merlin in organ size control and tumorigenesis: Hippo versus EGFR?, Genes and Development. 2010 Aug 15:24(16):1673-9. [Comment], 20713513

5 - Mazumdar J, Hickey MM, Pant DK, Durham AC, Sweet-Cordero A, Vachani A, Jacks T, Chodosh LA, Kissil, JL, et al., HIF-2{alpha} deletion promotes Kras-driven lung tumor development., Proceedings of the National Academy of the Sciences of the U S A. 2010 Aug 10;107(32):14182-7. [Epub 2010 Jul 21], 20660313

6 - Hanlon L, Avila JL, Demarest RM, Troutman S, et al., Capobianco AJ, Kissil, JL., Notch1 functions as a tumor suppressor in a model of K-ras-induced pancreatic ductal adenocarcinoma., Cancer Research. 2010 Jun 1;70(11):4280-6. [Epub 2010 May 18] , 20484026

7 - Yi C, Maksimoska J, Marmorstein R, Kissil, JL., Development of small-molecule inhibitors of the group I p21-activated kinases, emerging therapeutic targets in cancer. [Review], Biochemical Pharmacology. 2010 Sep 1;80(5):683-689. [Epub 2010 Mar 17] , 20302846

8 - Horresh I, Bar V, Kissil, JL, Peles E., Organization of myelinated axons by Caspr and Caspr2 requires the cytoskeletal adapter protein 4.1B., Journal of Neuroscience. 2010 Feb 17;30(7):2480-9., 20164332

9 - Kissil, JL, Blakeley JO, Ferner RE, et al., What's new in neurofibromatosis? Proceedings from the 2009 NF Conference: New Frontiers., American Journal of Medical Genetics. 2010 Jan 15;152A(2): 269-83., 20082461

10 - Santos AM, Jung J, Aziz N, Kissil, JL, Pure E., Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice. , Journal of Clinical Invest. 2009 Dec;119(12):3613-25. doi: 10.1172/JCI38988. [Epub 2009 Nov 16] , 19920354