BALB/c mice are more susceptible than C57BL/6 mice to radiation-induced instability and it is hypothesized that this difference determines transformation frequency differences in the two mouse strains. Analysis of F1 progeny suggests that the difference in susceptibility for induction of mammary cancer is a heritable trait and Preliminary Data suggests a similar pattern for inheritance of susceptibility to the induction of cytogenetic instability. Experiments are proposed which will: 1) use F1 and F2 progeny of BALB/c and C57BL/6 mice to determine the pattern of inheritance for susceptibility to genetic instability and radiation transformation; 2) use these recombinant inbred strains to examine co-segregation of the loci controlling the phenotypic traits; and 3) map the loci that determine the susceptibility differences. It is hoped that mapping of these loci will ultimately lead to cloning of the involved genes. Identification of such genes should help identify pathways mechanistically involved in the induction of instability and transformation and may be useful in identifying sub-populations of people who are at increased risk for radiation-induced cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
7R01CA043322-16
Application #
6435531
Study Section
Radiation Study Section (RAD)
Project Start
1986-01-01
Project End
2002-11-30
Budget Start
2001-03-01
Budget End
2002-11-30
Support Year
16
Fiscal Year
2000
Total Cost
$143,550
Indirect Cost
Name
Colorado State University-Fort Collins
Department
Public Health & Prev Medicine
Type
Schools of Veterinary Medicine
DUNS #
112617480
City
Fort Collins
State
CO
Country
United States
Zip Code
80523
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Bailey, Susan M; Brenneman, Mark A; Goodwin, Edwin H (2004) Frequent recombination in telomeric DNA may extend the proliferative life of telomerase-negative cells. Nucleic Acids Res 32:3743-51
Bailey, Susan M; Cornforth, Michael N; Ullrich, Robert L et al. (2004) Dysfunctional mammalian telomeres join with DNA double-strand breaks. DNA Repair (Amst) 3:349-57

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