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Vol. 12, Issue 6, 969-975, June 2002

METHODS
A Bioinformatics-Based Strategy Identifies c-Myc and Cdc25A as Candidates for the Apmt Mammary Tumor Latency Modifiers

Diana Cozma,1 Luanne Lukes,1 Jessica Rouse,1 Ting Hu Qiu,2 Edison T. Liu,2,3 and Kent W. Hunter1,4

1 Laboratory of Population Genetics, 2 Molecular Signaling and Oncogenesis Section, Medicine Branch, Center for Cancer Research, National Cancer Institute/National Institutes of Health, Bethesda, Maryland 20892, USA

The epistatically interacting modifier loci (Apmt1 and Apmt2) accelerate the polyoma Middle-T (PyVT)-induced mammary tumor. To identify potential candidate genes loci, a combined bioinformatics and genomics strategy was used. On the basis of the assumption that the loci were functioning in the same or intersecting pathways, a search of the literature databases was performed to identify molecular pathways containing genes from both candidate intervals. Among the genes identified by this method were the cell cycle-associated genes Cdc25A and c-Myc, both of which have been implicated in breast cancer. Genomic sequencing revealed noncoding polymorphism in both genes, in the promoter region of Cdc25A, and in the 3' UTR of c-Myc. Molecular and in vitro analysis showed that the polymorphisms were functionally significant. In vivo analysis was performed by generating compound PyVT/Myc double-transgenic animals to mimic the hypothetical model, and was found to recapitulate the age-of-onset phenotype. These data suggest that c-Myc and Cdc25A are Apmt1 and Apmt2, and suggest that, at least in certain instances, bioinformatics can be utilized to bypass congenic construction and subsequent mapping in conventional QTL studies.

3 Present address: National University of Singapore, Singapore 117604.

4 Corresponding author.

12:969-975 ©2002 by Cold Spring Harbor Laboratory Press  ISSN 1088-9051/02 $5.00
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