Researcher’s Profile

Gloria H. Su, PhD


Dr. Gloria Su and her laboratory study the molecular genetics of head and neck squamous cell carcinoma (HNSCC) and pancreatic ductal adenocarcinoma, as well as mouse modeling needed for both cancer types. HNSCC and pancreatic ductal adenocarcinoma are both results of accumulated genetic alterations. Both cancer types share some common oncogenes and tumor-suppressor genes (e.g. p16 and p53), but each has its unique targeted mutations (e.g. Cyclin D1 for HNSCC and K-ras for pancreatic cancer). We continue to compare and contrast the molecular genetic profiles of these two cancer types using both broad genome-scanning approach and candidate-gene approach. By establishing the cancer genetic profiles, we hope to reveal new prognostic markers, discover tumor marker for early detection analysis, and develop chemopreventive and therapeutic treatments that target tumor-specific pathways.

Dr. Su’s laboratory has developed multiple genetically-engineered mouse models that recapitulate human pancreatic cancer at both genetic and histologic levels. Using these genetically-engineered mouse models, Dr. Su’s team is interrogating the biology of tumor development, progression, and metastasis. Notably, her team has reported that the loss of the wild-type KRAS is associated with pancreatic cancer metastasis in mice and in humans. They have also demonstrated that the inactivation of different tumor-suppressor genes following Kras activation may influence the dichotomy of PanIN and IPMN (pancreatic precancerous lesions) development and progression. Specifically, the inactivation of the activin signaling preferentially promotes the development of IPMN. In addition to mouse modeling, Dr. Su and her team have contributed to our understanding of the cancer genetics of human IPMN and recently shown that the dysregulation of the PI3K-PTEN signaling pathway is associated with poor prognosis among IPMN patients.

D. J. Lenshow, G. H. Su, L. A. Zuckerman, N. Nabavi, C. L. Jellis, G. S. Gray, J. Miller, J. A. Bluestone.  Expression and functional significance of an additional ligand for CTLA-4.  Proc. Natl. Acad. Sci. USA 1993; 90:11054-11058
G. H. Su, H. S. Ip, B. S. Cobb, M. Lu, H. Chen, M. C. Simon.  The Ets protein Spi-B is expressed exclusively in B cells and T cells during development. Journal of  Experimental Medicine 1996; 184:203-214
G. H. Su, H-M Chen, N. Muthusamy, L. A. Garrett-Sinha, D. Baunoch, D. G. Tenen, M. C. Simon.  Defective B cell receptor-mediated responses in mice lacking the Ets protein, Spi-B.  The EMBO Journal 1997; 16:7118-7129
G. H. Su, W. Hilgers, M. C. Sheker, D. J. Tang, C. J. Yeo, R. H. Hruban, S. E. Kern.  Alterations in pancreatic, biliary, and breast carcinomas support MKK4 as a genetically targeted tumor suppressor gene.  Cancer Research 1998; 58:2339-2342
G. H. Su, R. H. Hruban, R. K. Bansal, G. S. Bova, D. J. Tang, M. C. Sheker, A. M. Westerman, M. M. Entius, M. Goggins, C. J. Yeo, S. E. Kern.  Germline and somatic mutations of the STK11/LKB1 Peutz-Jeghers gene in pancreatic and biliary cancers.  American Journal of Pathology 1999; 154:1835-1840