My laboratory studies the biology of glioblastoma multiforme (GBM), the most aggressive subtype of brain tumors. Cardinal features of GBM tumor cells include their stem cell-like behaviors and highly infiltrative/migratory nature, which are main reasons why GBM is such a fetal disease. Given the importance of “stemness” and cell infiltration/migration in gliomagenesis, we study two key molecular pathways that control the above biological processes both in normal stem cells and cancer cells; 1) roles of Polycomb-mediated epigenetic gene silencing in the tumor initiation, maintenance, and invasion, 2) roles of c-Met (receptor tyrosine kinase) signal transduction pathways in stemness and migration of these tumor cells. By employing various aspects of stem cell biology into neuro oncology, we hope to better understand the underlying molecular mechanisms of GBM and provide potential therapeutic options.
Lee et al., Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines (2006). Cancer Cell 9, 391-403.
Lee et al., Epigenetic-mediated dysfunction of the bone morphogenetic protein pathway inhibits differentiation of glioblastomas-initiating cells (2008). Cancer Cell 13, 69-80.
Son M., Woolard K., Lee J.*, and Fine, H.A.*, SSEA-1 is an enrichment marker for tumor-initiating cells in human glioblastoma (2009). Cell Stem Cell 4, 440-452.
(* corresponding authors)
