Dr. Xiao-Jing Wang, M.D., Ph.D., is currently a John S. Gates endowed chair and Director of head & neck cancer research program at UCD, Professor in Department of Pathology, and has joint appointments in the departments of Otolaryngology, Dermatology, and Craniofacial Biology at UCD. Dr. Wang’s laboratory has developed the first genetically engineered mouse model that develops head& neck squamous cell carcinomas (HNSCC) with full penetrance. These lesions mimic human HNSCC at genetic and pathology levels. HNSCC represents the 6th most common cancer type worldwide and its prognosis has not been improved in the past 20 years. Dr. Wang has brought the best expertise to this campus to continuously develop various HNSCC mouse models, which will add an invaluable resource to this campus for evaluating the mechanisms and efficacy of the existing clinical trials for HNSCC prevention and treatments. Research in Wang laboratory uses both mouse models and human cancer samples for cross-species comparisons. The current activities in Wang laboratory include:
- Identification of biomarkers for diagnosis and therapy for human head and neck cancer;
- Molecular mechanisms of head & neck cancer including the properties of cancer stem cells, transcriptional machinery, microRNA functions;
- Experimental therapeutics of head and neck cancer with different genetic alterations;
- Tumor microenvironment including the role of inflammation, fibroblast activation and angiogenesis in cancer.
In addition to cancer biology, Dr. Wang’s laboratory studies molecular mechanisms of inflammatory skin diseases and normal stem cell fate determination during embryonic skin development.
- TGFb signaling in cancer – TGFb is a multifunctional cytokine. TGFb suppresses tumor formation. Paradoxically, it also promotes cancer metastasis. We are using conditional transgenic/knockout mouse models to alter individual TGFb1 signaling components in head and neck epithelia and skin epidermis, in order to determine the mechanisms of TGFb effects on cancer, including TGFb signaling through pathways of Smad, MAPK, Rho, etc.
- Smads in skin development – We have generated transgenic/knockout mice in which individual Smad genes are deleted or overexpressed. These mice exhibited developmental defects of the skin. We are interested in the analysis of the underlying signaling transduction mechanisms.
TGFb signaling in wound healing – TGFb1 has both positive and negative effects on wound healing. We will utilize gene-switch transgenic mice to study the stage specific effects of TGFb signaling on wound healing.
TGFb1 in skin diseases – Our transgenic mice overexpressing the latent TGFb1 in the skin mimic psoriasis and fibrosis. We will study the molecular basis of TGFb1-induced diseases.