rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
7
|
pubmed:dateCreated |
2003-4-2
|
pubmed:abstractText |
Oligodendrogliomas of all grades overexpress epidermal growth factor receptor (EGFR), whereas deletion of ink4a/arf is found only in high-grade tumors. We used the S100 beta promoter to generate transgenic mice expressing v-erbB, a transforming allele of EGFR. These mice developed low-grade oligodendroglioma. Transgenic animals heterozygous for ink4a/arf or p53 developed high-grade tumors. Comparative genomic hybridization revealed loss of distal mouse chromosome 4, a region orthologous with human chromosome 1p, which is commonly lost in oligodendroglioma. Our results demonstrate that overexpression of EGFR, an epigenetic observation of uncertain significance in human oligodendroglioma, can initiate oligodendroglioma in the mouse. Furthermore, p53 pathway mutations can mediate the transition from low to high grade. These models hold promise for studying tumor lineage, identifying contributing genetic alterations and evaluating preclinical therapies in this important neoplasm.
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0008-5472
|
pubmed:author |
pubmed-author:AldapeKenK,
pubmed-author:BurnsMichael JMJ,
pubmed-author:DePinhoRonR,
pubmed-author:HackettChristopherC,
pubmed-author:HillJohn RJR,
pubmed-author:IsraelMark AMA,
pubmed-author:KuriyamaHirokoH,
pubmed-author:KuriyamaNagatoN,
pubmed-author:MilshteynNadezhdaN,
pubmed-author:RobertsTimT,
pubmed-author:WeissWilliam AWA,
pubmed-author:WendlandMichael FMF
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
63
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1589-95
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:12670909-Animals,
pubmed-meshheading:12670909-Brain Neoplasms,
pubmed-meshheading:12670909-Chromosome Aberrations,
pubmed-meshheading:12670909-Chromosomes, Mammalian,
pubmed-meshheading:12670909-Cyclin-Dependent Kinase Inhibitor p16,
pubmed-meshheading:12670909-Disease Models, Animal,
pubmed-meshheading:12670909-Genes, erbB-1,
pubmed-meshheading:12670909-Genes, p53,
pubmed-meshheading:12670909-Humans,
pubmed-meshheading:12670909-Mice,
pubmed-meshheading:12670909-Mice, Inbred C57BL,
pubmed-meshheading:12670909-Mice, Inbred DBA,
pubmed-meshheading:12670909-Mice, Transgenic,
pubmed-meshheading:12670909-Mutation,
pubmed-meshheading:12670909-Nerve Growth Factors,
pubmed-meshheading:12670909-Oligodendroglioma,
pubmed-meshheading:12670909-Oncogene Proteins v-erbB,
pubmed-meshheading:12670909-Promoter Regions, Genetic,
pubmed-meshheading:12670909-Receptor, Epidermal Growth Factor,
pubmed-meshheading:12670909-S100 Proteins,
pubmed-meshheading:12670909-Tumor Cells, Cultured
|
pubmed:year |
2003
|
pubmed:articleTitle |
Genetic determinants of malignancy in a mouse model for oligodendroglioma.
|
pubmed:affiliation |
Department of Neurology, University of California, San Francisco, California 94143-0663, USA. weiss@cglucsf.edu
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|