期刊
CANCER CELL
卷 14, 期 2, 页码 123-134出版社
CELL PRESS
DOI: 10.1016/j.ccr.2008.07.005
关键词
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资金
- Dr. Mildred-Scheel-Stiftung for Knebsforschung and by the Max-Eder-Nachwuchsgruppenprogramm of the Deutsche Krebshilfe
- Charles King Trust/Medical Foundation
- American Brain Tumor Association
- NIH [NS047213, NS040828, NS033642, NS047527]
- NS047527)
- the James S. McDonnell Foundation
- he March of Dimes Foundation
- Pediatric Brain Tumor Foundation of the United States
Whether the brain tumor medulloblastoma originates from stem cells or restricted progenitor cells is unclear. To investigate this, we activated oncogenic Hedgehog (Hh) signaling in multipotent and lineage-restricted central nervous system (CNS) progenitors. We observed that normal unipotent cerebellar granule neuron precursors (CGNPs) derive from hGFAP(+) and Olig2(+) rhombic lip progenitors. Hh activation in a spectrum of early-and late-stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hh signaling promotes medulloblastoma from lineage-restricted granule cell progenitors.
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