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[Cancer Research 63, 5428-5437, September 1, 2003]
© 2003 American Association for Cancer Research

Regular Articles

A Molecular Fingerprint for Medulloblastoma1

Youngsoo Lee, Heather L. Miller, Patricia Jensen, Roberto Hernan, Michele Connelly, Cynthia Wetmore, Frederique Zindy, Martine F. Roussel, Tom Curran, Richard J. Gilbertson and Peter J. McKinnon2

Departments of Genetics and Tumor Cell Biology [Y. L., H. L. M., F. Z., M. R., P. J. M.] and Developmental Neurobiology [P. J., R. H., M. C., T. C., R. G.], Saint Jude Children’s Research Hospital, Memphis, Tennessee 38105, and Division of Pediatric Hematology/Oncology, Mayo Clinic, Rochester, Minnesota 55905 [C. W.]

Medulloblastoma is the most common malignant pediatric brain tumor. In mice, Ptc1 haploinsufficiency and disruption of DNA repair (DNA ligase IV inactivation) or cell cycle regulation (Kip1, Ink4d, or Ink4c inactivation), in conjunction with p53 dysfunction, predispose to medulloblastoma. To identify genes important for this tumor, we evaluated gene expression profiles in medulloblastomas from these mice. Unexpectedly, medulloblastoma expression profiles were very similar among tumors and also to those of developing cerebellum. However, 21 genes were specifically up-regulated in medulloblastoma, including sFrp1, Ptc2, and Math1, members of signaling pathways that regulate cerebellar development. Coordinated deregulation of these same genes also occurred in a large subset of human medulloblastomas. These data identify a group of genes that is central to medulloblastoma tumorigenesis.




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