Xrcc2 modulates spontaneous and radiation-induced tumorigenesis in Apc min/+ mice

Jackie W. Haines, Margaret R. Coster, Julie Adam, Michael Cheeseman, Elizabeth A. Ainsbury, John Thacker, Simon D. Bouffler

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


XRCC2 has an important role in repair of DNA damage by homologous recombination. Adult Apcmin/+ (min, multiple intestinal neoplasia) mice, wild-type or heterozygous for Xrcc2 deficiency, were sham-irradiated or 2-Gy X-irradiated. Spontaneous mammary and intestinal tumor incidences are lower in Apcmin/+ Xrcc2+/- mice than in Apcmin/+ Xrcc2+/+ mice (mammary tumors: 14% and 38%, respectively, χ2 P = 0.03; intestinal adenomas in mice reaching full life span: 108.6 and 130.1, respectively, t-test P = 0.005). Following irradiation, the increase in mammary tumors was greatest in female mice heterozygous for Xrcc2 (7.25 ± 0.50-fold in Apcmin/+ Xrcc2+/- mice compared with 2.57 ± 0.35-fold in Apcmin/+ Xrcc2+/+ mice; t-test P < 0.001). The increase in intestinal tumor multiplicity following irradiation was significantly greater in Apcmin/+ Xrcc2+/- mice (Apcmin/+ Xrcc2+/-, 4.14 ± 0.05-fold, versus Apcmin/+ Xrcc2+/+, 3.30 ± 0.05-fold; t-test P < 0.001). Loss of heterozygosity of all chromosome 18 markers was greater in intestinal tumors from Apcmin/+ Xrcc2 +/- mice than in tumors from Apcmin/+ Xrcc2+/+ mice. These findings indicate that Xrcc2 haploinsufficiency reduces spontaneous tumor incidence on an Apcmin/+ background but increases the tumorigenic response to radiation.

Original languageEnglish
Pages (from-to)1227-1233
Number of pages7
JournalMolecular Cancer Research
Issue number9
Publication statusPublished - Sep 2010


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