Stanford University School of Medicine
Palo Alto, United States
Claudia K. Petritsch is an Associate Professor in Research at Stanford University School of Medicine, and a biochemist and and stem cell biologist by trainings. Her experience with successfully leveraging access to primary brain tissue has led to functional characteriztion of the heterogeneity of adult brain (tumor) cells (Persson et al, Cancer Cell, 2010) and paved the way for strategies to combat intra-tumoral heterogeneity. Her team was the first to show that oligodendrocyte progenitor cells use an evolutionary conserved mechanism of asymmetric cell division (Sugiarto et al, Cancer Cell, 2011), thereby identifying mechanisms for self-renewal, differentiation, and neoplastic transformation in the largest progenitor population in the human brain. Her findings that asymmetrically dividing cancer stem cells require Polo-like kinase 1 (PLK1) activity revealed a novel therapeutic vulnerability in pediatric brain cancer and identified novel synergies between inhibition of two pathways providing the rationale for combining Plk1 and MAPK pathway inhibitors to treat brain cancer. Her team recently generated several syngeneic orthotopic mouse models for a very challenging brain tumor type (BRAF V600E mutated glioma), and plans using these preclinical models to conduct experimental therapeutics (Huillard et al., 2014 PNAS; Lerner et al., 2015; Grossauer et al., 2016 Oncotarget). She directs a team of scientists that develops 3D patient-derived brain tumor models with the long-standing goal to model each pediatric brain cancer entity and distribute cancer cell lines to facilitate research. As a director of the Stanford Pediatrics Cancer Model Development Center she coordinate the development of next-generataion pediatric brain cancer models. Ongoing reserch activities are i. investigating the effects of molecular targeted therapies on the tumor/immune microenvironment crosstalk, and ii. the regulation of cell fate in the brain, and the ii. role for stem cells and oligodendrocyte progenitor cells in brain tumors, including immunesuppression (Daynac et al., 2018 Nature Comm).