Adam B. Glick

Associate Professor of Veterinary & Biomedical Sciences
306C Life Sciences Building
Telephone: 814-865-7170
FAX: 814-863-1696
Email: abg11@psu.edu

Research Focus

My laboratory is focused on understanding the signaling pathways controlling squamous cancer formation in the skin in order to shed light on mechanisms of cancer development and to identify potential targets for new anti-cancer therapies.  Nonmelanoma skin cancer is increasing in the United States at alarming rates due to higher UV light exposure.  In addition the long term immunosuppression required for organ transplantation results in highly aggressive recurrent cutaneous squamous cell carcinoma.
We use the multistage mouse skin carcinogenesis model to understand mechanisms of cancer formation.  In this model cancers are generated in the skin of mice by topical application of carcinogens and repeated exposure to chemicals that cause outgrowth of benign tumors, some of which eventually progress to malignant squamous cell carcinomas.  The mouse epidermis serves as a useful model for human cancers since most solid tumors form in epithelial tissues, are frequently the result of some type of environmental or physical carcinogen exposure and progress though multiple stages.  Due to the superficial nature of the mouse skin tumors, the different stages can be easily quantitated and manipulated.  My lab is specifically focused on the TGF1 (transforming growth factor beta-1) signaling pathway and its role in skin cancer development. TGF1 is a growth factor secreted by normal and neoplastic cells that has multiple biological effects on epithelial, mesenchymal and immune cells.  It has a unique property of being a negative regulator of cell growth, and many human cancers are no longer responsive to TGF1 due to specific mutations in the signaling pathway.  However, many human cancers produce high levels of TGF1 which affect the immune system and the normal cells surrounding the tumor in a way that favors tumor growth.   Thus TGF1 can have both tumor suppressive and tumor promoting activities depending on tumor stage and tissue context.  We utilize several transgenic and knockout models to alter TGF1 signaling in vivo and in vitro and determine how this impacts cancer development.  We are particularly interested in what causes TGF1 action to switch from tumor suppressor to tumor promoter and have focused on how TGF1 production by normal and tumorigenic epithelial cells impacts the anti-tumor immune response, and how TGF1 signaling interacts with oncogenic pathways such as ras  and HPV E6/E7 to suppress or enhance the malignant phenotype.




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