Frequent met oncogene amplification in a Brca1/Trp53 mouse model of mammary tumorigenesis

In a screen for gene copy number alterations in mouse mammary tumors initiated by loss of the Brca1 and Trp53 genes, we observed that the majority (11 of 15; 73%) had high-level amplification of wild-type Met, encoding a growth factor receptor implicated in tumor progression. Met amplification was l...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2006-04, Vol.66 (7), p.3452-3455
Main Authors: SMOLEN, Gromoslaw A, MUIR, Beth, GARBER, Judy E, BELL, Daphne W, SGROI, Dennis C, CHIN, Lynda, DENG, Chu-Xia, HABER, Daniel A, MOHAPATRA, Gayatry, BARMETTLER, Anne, KIM, Woo J, RIVERA, Miguel N, HASERLAT, Sara M, OKIMOTO, Ross A, KWAK, Eunice, DAHIYA, Sonika
Format: Article
Language:English
Subjects:
Animals
Antineoplastic agents
Biological and medical sciences
Cell Line, Tumor
Disease Models, Animal
Female
Gene Amplification
Gene Deletion
Genes, BRCA1
Mammary Neoplasms, Experimental - genetics
Medical sciences
Mice
Pharmacology. Drug treatments
Proto-Oncogene Proteins c-met - genetics
Tumor Suppressor Protein p53 - genetics
Tumors
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Summary:In a screen for gene copy number alterations in mouse mammary tumors initiated by loss of the Brca1 and Trp53 genes, we observed that the majority (11 of 15; 73%) had high-level amplification of wild-type Met, encoding a growth factor receptor implicated in tumor progression. Met amplification was localized to unstable double minute chromosomes and was uniquely found in mouse breast tumors driven by loss of Brca1 and Trp53. Whereas analogous MET amplification was not found in human breast cancers, the identification of a dominant somatic genetic lesion in the Brca1/Trp53 mouse model suggests that recurrent secondary hits may also exist in BRCA1-initiated human breast cancer.
ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.CAN-05-4181