Abstract：
:The Rb/E2F pathway is deregulated in most human brain tumors, and the finding that loss of E2F1 reduced pituitary tumorigenesis in Rb(+/-) mice suggests that loss of pRb induces brain tumors by activating E2F1. We therefore investigated the role of E2F1 in the development and maintenance of brain cancer using a transgenic mouse model engineered to express E2F1 specifically within glial cells (GFAP-tgE2F1). GFAP-tgE2F1 mice developed a highly penetrant phenotype characterized by neurologic defects, and examination of the brains revealed the presence of brain tumors in 20% of these animals. Importantly, the distribution of tumors according to mouse age suggests the existence of a bimodal pattern of tumor development, forcing a comparison with the human disease. Mice, at an early age, with deregulated E2F1 show the formation of embryonal brain tumors such as medulloblastoma, choroid plexus carcinoma, and primary neuroectodermal tumor. Conversely, at an older age, mice escaping embryonal tumor formation present with malignant gliomas, which are typically identified in the human adult population. Thus, this study offers the first evidence for a global role of E2F1 in the formation and maintenance of multilineage brain tumors, irrefutably establishing E2F1 as an oncogene in the brain.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Olson MV,Johnson DG,Jiang H,Xu J,Alonso MM,Aldape KD,Fuller GN,Bekele BN,Yung WK,Gomez-Manzano C,Fueyo Jdoi
10.1158/0008-5472.CAN-06-2973subject
Has Abstractpub_date
2007-05-01 00:00:00pages
4005-9issue
9eissn
0008-5472issn
1538-7445pii
67/9/4005journal_volume
67pub_type
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