Dr.Hu-Dan Liu:  My laboratory has been interested in cellular signaling implicated in tumorigenesis with a long term goal to determine novel therapeutic targets for cancer treatment. Specifically we are studying the dual roles of NOTCH signaling pathway in tumor development, using combined approaches of molecular biology, cellular biology and animal modeling. NOTCH is primarily oncogenic whereas tumor suppressive in some circumstances. Using acute T-cell lymphoblastic leukemia (T-ALL) as a model system, in which NOTCH1 has a definitive function as a major oncogenic driver, we tempt to understand the mechanism how NOTCH transcriptionally activates downstream target genes that mediates leukemogenesis as well as how aberrant NOTCH1 signaling is sustained in leukemia. Meanwhile, we are also keen on the tumor suppressive role of NOTCH1 in acute myeloid leukemia (AML) and try to determine the interplays of NOTCH with other oncogenic pathways in AML. With these efforts to decipher the functional modes of NOTCH in distinct hematological malignancies, we hope to identify more effective and specific therapeutic targets that will lead to drug development to benefit leukemia patients.


Dr.Guo-Liang Qing:  We are proposing the following three avenues of investigation: (1) how deregulated metabolism impacts tumor initiation, maintenance and aggressive progression; (2) how metabolism regulates cancer cell stem cells and drug resistance; and (3) high throughput drug screening against key metabolic enzymes and examination whether inhibition of this programming event confers therapeutic advantages. Using human tumor cell lines, animal tumor models and primary human tumor samples as model systems, our laboratory aims to address these questions by combining genetic, biochemical, metabolic and genomic approaches. 


Dr.Hao-Jian ZhangThe research in our laboratory is focused on the exploration of the mechanism of cancer immunology, mechanisms of cancer stem cell self-renewal and differentiation, the mechanistic study of blood diseases, and the establishment of mouse models for cancer and blood diseases based on genome-editing technology (CRISPR).


Dr. Qiang Chen: DNA damage repair; Epigenetic modification and cancer.        



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