|開催日時：||2019年4月8日 16：00 ～ 17:30|
|所属：||Salk Institute for Biological Studies, Research Associate|
|演題：||Exploring phenotypic mosaicism in a mouse model of glioma to understand intratumoral heterogeneity and cellular states in GBM.|
We employ a mouse model of glioma that recapitulates the pathophysiology and gene expression signatures of human GBM. While initiated with identical oncogenic drivers, this mouse model unexpectedly displays heterogeneous phenotypes between animals. Our data using time-series single-cell transcriptomics approach shows that transformed cells, even without acquiring additional genetic alterations, switch cellular states at the beginning of tumor formation and one population commit themselves to expand to establish gliomas that are mainly comprised of one cell type. We further observe the strong association of microenvironmental cues with glioma cell populations and their roles in the state transitioning of glioma cells. Through the characterization of mechanisms that drive phenotypic mosaicism, we hope to uncover general principles that govern tumor progression and heterogeneity, and then ultimately provide novel therapeutic strategies to cure GBM.
|世話人：||〇井上 純一郎 （分子発癌分野）
山梨 裕司 （腫瘍抑制分野）