Gloria H. Su, PhD
- Professor of Pathology and Cell Biology (in Otolaryngology/Head and Neck Surgery and in the Herbert Irving Comprehensive Cancer Center) at CUMC
Credentials & Experience
Education & Training
- BA, 1992 Biological Sciences, Northwestern University
- PhD, 1997 Immunology, University of Chicago
Honors & Awards
- 2015 Distinguished Achievement Award from Shanghai Tongji University East Hospital for exceptional contribution to pancreatic cancer research and clinical management
- 2014 Ruth Leff Siegel Award for Excellence in Pancreatic Cancer Research
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.
- Genetic profiling of human pancreatic cancer and head/neck cancer, and mouse modeling for both types
- Han Yan, Chih-Chieh Yu, Stuart A. Fine, Ayman Lee Youssof, Ye-Ran Yang, Jun Yan, Dillon C. Karg, Edwin C. Cheung, Richard A. Friedman, Haoqiang Ying, Emily I. Chen, Ji Luo, Yi Miao, Wanglong Qiu & Gloria H. Su. Loss of the wild-type KRAS allele promotes pancreatic cancer progression through functional activation of YAP1. Oncogene (2021). doi:10.1038/s41388-021-02040-9.
- D. Garcia-Carracedo, Y. Cai, W. Qiu, K. Saeki, R. A. Friedman, A. Lee, Y. Li, E. M. Goldberg, E. E. Stratikopoulos, R. Parsons, C. Lu, A. Efstratiadis, E. M. Philipone, A. J. Yoon, G. H. Su. PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice. Molecular Cancer Research 2020; 18(6):822-834 (Epub 2020 Mar 9).
- W. Qiu, H. E. Remotti, S. M. Tang, E. Wang, L. Dobberteen, A. L. Youssof , J. H. Lee, E. C. Cheung, and G. H. Su. Pancreatic DCLK1+ Cells Originate Distinctly from PDX1+ Progenitors and Contribute to the Initiation of Intraductal Papillary Mucinous Neoplasm in Mice. Cancer Letters 2018; 423:71-79 (Epub 2018, March 8).
- C. C. Yu, W. Qiu, C. S. Juang, M. M. Mansukhani, B. Halmos, G. H. Su. Mutant allele specific imbalance in oncogenes with copy number alterations: occurrence, mechanisms, and potential clinical implications. Cancer Letters 2017, January; 384:86-93 (Epub 2016 Oct 8).
- W. Qiu, S. M. Tang, S. Lee, A. T. Turk, A. N. Sireci, A. Qiu, C. Rose, C. Xie, J. Kitajewski, H.-J. Wen, H. C. Crawford, P. A. Sims, R. H. Hruban, H. E. Remotti, G. H. Su. Loss of Activin Receptor Type 1B Promotes Development of Intraductal Papillary Mucinous Neoplasms in Mice with Activated KRAS. Gastroenterology 2016; 150 (1)218-228 (Epub Sept 22, 2015).
- D. Garcia-Carracedo, C. C. Yu, N. Akhavan, S. A. Fine, F. SchÃ¶nleben, N. Maehara, D. C. Karg, C. Xie, W. Qiu, R. L. Fine, H. E. Remotti, G. H. Su. Smad4 loss synergizes with TGFalpha overexpression in promoting metaplasia, PanIN development, and fibrosis. PLoS One 2015, Mar 24;10(3):e0120851. PMCID: PMC4372593
- D. Garcia-Carracedo, A. T. Turk, S. A. Fine, N. Akhavan, B. C. Tweel, R. Parsons, J. A. Chabot, J. D. Allendorf, J. M. Genkinger, H. E. Remotti, G. H. Su. Loss of PTEN expression is associated with poor prognosis in patients with intraductal papillary mucinous neoplasms of the pancreas. Clin Cancer Research 2013, 19(24):6830-41. (Epub Nov 12, 2013). PMID: 24132918
- W. Qiu, F. Sahin, C.A. Iacobuzio-Donahue, Dario Garcia-Carracedo, W. M. Wang, Chia-Yu Kuo, Dan E. Arking, A. M. Lowy, R. H. Hruban, H. E. Remotti, G. H. Su. Disruption of p16 and Activation of Kras in Pancreas Increases Ductal Adenocarcinoma Formation and Metastasis in vivo. Oncotarget 2011, 2:862-73 (Epub Nov 23, 2011).
- W. Qiu, X. Li, H. Tang, A. S. Huang, A. A. Panteleyev, D. M. Owens, G. H. Su. Conditional activin reporter type IB (Acvr1b) knockout mice revealed hair loss abnormality. Journal of Investigative Dermatology 2011, 131:1067-76 (Epub Dec 2010).
- F. SchÃ¶nleben, W. Qiu, N. T. Ciau, D. J. Ho, X. Li, J. D. Allendorf, H. E. Remotti, G. H. Su.PIK3CA mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC) of the pancreas. Clinical Cancer Research 2006, 12:3851-5.
- W. Qiu, , X. Li, D. J. Ho, L. G. Close, S. Manolidis, B. P. Bennett, G. H. Su.PIK3CA mutations in head and neck squamous cell carcinoma. Clinical Cancer Research 2006, 12:1441-6.