Molecular Oncology Program Research interests: The molecular and cellular bases of cancer development in selected model systems. 1120 15th Street CN 4132 Augusta, GA 30912 Office: (706) 721-4286 Laboratory: (706) 721-4285 E-mail: hding@georgiahealth.edu

Ding, Han-Fei, Ph.D.

Dr. Han-Fei DingGCC Distinguished Cancer Scholar
Member, Signaling and Angiogenesis Program
GRU Cancer Center
Professor of Pathology
Georgia Regents University

1410 Laney Walker Blvd., CN-2134
Augusta, GA  30912
Tel. 706-721-4286
Fax 706-721-1670
Email: hding@gru.edu

IFL Link | PubMed Link

 

Current Research

The research program of the Ding laboratory is to define the molecular and cellular basis of cancer development in select model systems. Ongoing projects include developmental biology of neuroblastoma and NF-kB2 signaling in the pathogenesis of lymphoma. For the neuroblastoma project, we are interested in the genes and signaling pathways that regulate neuroblastoma cell proliferation and differentiation. We are currently working on Bmi-1 and HOX genes. Bmi-1 normally controls the self-renewal of stem cells. We recently obtained evidence implicating a crucial role for Bmi-1 in the pathogenesis of neuroblastoma by regulating the degradation of cyclins, which function as positive regulators of cell cycle progression. HOX genes are master regulators of morphogenesis and cell differentiation. We recently uncovered a critical role of HOX genes in regulation of neuroblastoma cell differentiation, providing novel targets for the development of therapeutic drugs for neuroblastoma treatment. For the NF-kB2 project, we have recently generated the first, and so far the only, line of transgenic mice with targeted expression of a tumor-derived NF-kB2 mutant, p80HT, in lymphocyte. Using this animal model, we have demonstrated for the first time a causal relationship between NF-kB2 mutations and lymphomagenesis. Currently we are investigating the downstream target genes and signaling pathways that mediate the oncogenic activity of NF-kB2 mutation and signaling in the pathogenesis of human lymphomas in cell and animal models.