Jin-Tang Dong, PhD

Professor, Hematology & Medical Oncology

Emory University School of Medicine

Office: Winship Cancer Institute of Emory University

Phone: (404) 712-2568

Fax: (404) 778-5530

Email: j.dong@emory.edu


Dr. Jin-Tang Dong received his PhD degree from the Peking Union Medical College and the Chinese Academy of Medical Sciences in 1989. After working as an Assistant Investigator at the same institution for a year, he completed postdoctoral training in Molecular Cancer Biology and Prostate Cancer at the National Institutes of Health (1990-1994) and the Johns Hopkins University School of Medicine (1994-1996). He started his faculty appointment as an Assistant Professor of Pathology, Biochemistry and Molecular Genetics at the University of Virginia in 1996, and joined the faculty of Emory University School of Medicine as an Associate Professor in 2002. He became a full professor in 2007. Dr. Dong received an NIH Director’s award, and is a Georgia Cancer Coalition Distinguished Cancer Scholar. His research interest has been in the molecular pathogenesis of human cancer, with a focus on the identification of novel tumor suppressors and the discovery of novel molecular pathways.


Dr. Dong's group has been studying the molecular pathogenesis of human cancer with a particular interest in prostate cancer. The group has devoted significant effort to the discovery of tumor suppressor genes using a combined genetic, biochemical and functional approach. They have found several potential tumor suppressor genes including KLF5 from 13q21, ATBF1 from 16q22, FOXO1A from 13q14, and U50 from 6q14. These genes are functionally inactivated in human cancers by chromosomal deletion, mutation, and/or excess protein degradation. Some of them, including KLF5 and ATBF1, are essential for normal development.

Dr. Dong's group currently focuses on whether and how functional interruption of the developmental transcription factors ATBF1 and KLF5 breaks the balance between cell proliferation and differentiation in epithelial homeostasis and thus causes the development and progression of cancer. Using tissue specific knockout/knockin mouse models as well as cultured epithelial cells, the team is examining the effect of gene deletion or mutation of KLF5 and ATBF1 on the balance between cell proliferation and differentiation as well as the structure and function of epithelia. They also determine whether interruption of these genes causes malignant transformation and/or tumor progression. Using genomic and biochemical approaches, they examine what molecular pathways mediate the function of KLF5 and ATBF1 in normal cells and the consequence of their functional interruption in carcinogenesis. The ultimate goal of Dr. Dong's research is to discover molecular pathways that can be useful for the development of biomarkers and therapeutic targets.