Dr. Li is Professor at University of Massachusetts Medical School, Division of Hematology and Oncology. His research career in studying BCR-ABL-induced leukemia began in 1996 at Harvard Medical School where he established a retroviral transduction/transplantation mouse model for human chromic myeloid leukemia (CML). He also developed a B-ALL mouse model and began to identify and functionally test critical target genes that regulate survival and self-renewal of LSCs by comparing gene expression profiles between LSCs and normal HSCs. He discovered that Src family kinases are only required for BCR-ABL-induced B-ALL but not CML (Hu et al. Nature Genetics 36(5):453-461, 2004). This work has a huge impact on understanding how BCR-ABL signals, and indicates that BCR-ABL utilizes distinct signaling pathways to induce myeloid and lymphoid leukemias. Dr. Li identified the first lipid metabolic gene the arachidonate 5-lipoxygenase gene (Alox5) and showed that 5-lipoxygenase is essential for LSC survival and CML development. Importantly, this research also showed that 5lipoxygenase is not required for survival regulation of normal HSCs. This finding provides the first evidence showing that it is possible and feasible to identify and target key genes specific for LSCs.
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