Martine Roussel is a molecular oncologist recognized for landmark studies on the etiology of cancer and for translational development of strategies for the treatment of pediatric medulloblastoma. She identified several of the earliest recognized retroviral oncogenes, and elucidated their physiologic functions in signal transduction, regulation of gene expression, cell cycle dynamics, and organismal development. Together with her long-standing collaborator Charles Sherr, she identified the FMS oncogene as the receptor for colony-stimulating factor-1, discovered the D-type cyclins, cyclin-dependent kinase-4, two of the INK4 family of CDK4 inhibitors, and the ARF tumor suppressor. Her work revealed the essential involvement of CDK inhibitors in governing neuronal cell cycle exit, and as suppressors of pediatric brain tumor development. Roussel was born and educated in France and received her Master’s degree from Universite Paris VII and her Ph.D. (These d’Etat) from the Universite de Lille. She joined the National Cancer Institute, National Institutes of Health, as a Fogarty International postdoctoral fellow in 1980 and the faculty of St. Jude Children’s Research Hospital and the University of Tennessee in 1983, where she has remained until the present. She is a member of the American Academy of Arts & Sciences and the National Academy of Sciences.

Research Interests

Roussel's laboratory is currently interested in the development and treatment of pediatric medulloblastoma, the most common malignant brain tumor of childhood. Her previous work helped to identify the roles of specific polypeptide inhibitors of cyclin-dependent kinases in regulating neuronal development in the central nervous system and in suppressing cerebellar tumor development in response to oncogenic stress. She has developed pre-clinical mouse models of different molecular subgroups of medulloblastoma, initially demonstrating that the tumor suppressors Ink4c and p53 antagonize the pro-proliferative effects of
N-Myc in inhibiting tumor formation in response to sonic hedgehog signaling. Subsequent studies modeling a distinct and highly aggressive molecular subgroup of medulloblastoma revealed a role for c-Myc (but not N-Myc) activation in contributing to a currently incurable anaplastic disease. Molecular analysis of medulloblastomas revealed distinct requirements for the repressive
c-Myc co-factor Miz1 in defining subgroup identity and demonstrated roles for additional epigenetic regulators in driving Myc-driven disease. High throughput screening of a library of FDA-approved drugs identified several chemotherapeutic compounds that have been advanced into ongoing clinical trials for the treatment of c-Myc-driven medulloblastoma.

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Primary Section

Section 41: Medical Genetics, Hematology, and Oncology

Secondary Section

Section 24: Cellular and Molecular Neuroscience