C-Myc and Cdc25A are candidates for the mammary tumor latency modifier genes Apmt1 and Apmt2
Kent Hunter
Laboratory of Population Genetics CCR/NCI/NIH
Bldg 41 Rm 702
41 Library Drive
Bethesda, MD 20892 USA
ABSTRACT
The epistatically interacting modifier loci (Apmt1 and Apmt2) accelerate the
polyoma Middle-T (PyMT) induced mammary tumor. Using a bioinformatics
strategy Cdc25A and c-Myc were identified as candidate genes. Molecular and
in vitro analysis revealed functional differences for both genes between the
mouse-inbred strains in question. Compound PyMT/Myc double transgenic
animals were generated to mimic the hypothetical model and were 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.