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[Cancer Research 63, 2361-2363, May 15, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Adenoma Multiplicity in Irradiated ApcMin Mice Is Modified by Chromosome 16 Segments from BALB/c1

Natalie L. Degg, Michael M. Weil, Alan Edwards, Jackie Haines, Margaret Coster, John Moody, Michele Ellender, Roger Cox and Andrew Silver2

Radiation Effects Department, National Radiological Protection Board, Chilton, Didcot, Oxon, OX11 0RQ, United Kingdom [N. L. D., A. E., J. H., M. C., J. M., M. E., R. C., A. S.]; Department of Pathology and Microbiology, School of Medical Sciences, University Of Bristol, University Walk, Bristol BS8 1TD, United Kingdom [N. L. D.]; and Department of Experimental Radiation Oncology, M. D. Anderson Cancer Center, Houston, Texas 77030 [M. M. W.]

Ionizing radiation (IR) is a well-characterized carcinogen in humans and mice. The BALB/c mouse strain is unusually sensitive to IR-induced tissue damage and cancer development in a range of organs, suggestive of a partial defect in DNA damage response. This has been confirmed by finding BALB/c-specific functional polymorphism in Prkdc, a gene on mouse chromosome 16 that encodes the catalytic subunit of DNA-dependent protein kinase. PrkdcBALB has been associated with increased susceptibility to IR-induced mammary and lymphatic neoplasia. Here, we provide evidence that chromosome 16 segments from BALB/c interact with ApcMin (multiple intestinal neoplasia) and specifically enhance IR-induced adenoma development in the upper part of the small intestine.




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S. Pazzaglia, M. Mancuso, M. Tanori, M. J. Atkinson, P. Merola, S. Rebessi, V. Di Majo, V. Covelli, H. Hahn, and A. Saran
Modulation of Patched-Associated Susceptibility to Radiation Induced Tumorigenesis by Genetic Background
Cancer Res., June 1, 2004; 64(11): 3798 - 3806.
[Abstract] [Full Text] [PDF]


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Copyright © 2003 by the American Association for Cancer Research.