Adenoma multiplicity in irradiated ApcMin mice is modified by chromosome 16 segments from BALB/c

Natalie L. Degg, Michael M. Weil, Alan Edwards, Jacqueline Haines, Margaret Coster, John Moody, Michele Ellender, Roger Cox, Andrew Silver*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2361-2363
Number of pages3
JournalCancer Research
Volume63
Issue number10
Publication statusPublished - 15 May 2003

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