| First Author | Haines JW | Year | 2010 |
| Journal | Mol Cancer Res | Volume | 8 |
| Issue | 9 | Pages | 1227-33 |
| PubMed ID | 20671066 | Mgi Jnum | J:205233 |
| Mgi Id | MGI:5544396 | Doi | 10.1158/1541-7786.MCR-10-0089 |
| Citation | Haines JW, et al. (2010) Xrcc2 modulates spontaneous and radiation-induced tumorigenesis in Apcmin/+ mice. Mol Cancer Res 8(9):1227-33 |
| abstractText | XRCC2 has an important role in repair of DNA damage by homologous recombination. Adult Apc(min/+) (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 Apc(min/+) Xrcc2(+/-) mice than in Apc(min/+) Xrcc2(+/+) mice (mammary tumors: 14% and 38%, respectively, chi(2) 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 Apc(min/+) Xrcc2(+/-) mice compared with 2.57 +/- 0.35-fold in Apc(min/+) Xrcc2(+/+) mice; t-test P < 0.001). The increase in intestinal tumor multiplicity following irradiation was significantly greater in Apc(min/+) Xrcc2(+/-) mice (Apc(min/+) Xrcc2(+/-), 4.14 +/- 0.05-fold, versus Apc(min/+) 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 Apc(min/+) Xrcc2(+/-) mice than in tumors from Apc(min/+) Xrcc2(+/+) mice. These findings indicate that Xrcc2 haploinsufficiency reduces spontaneous tumor incidence on an Apc(min/+) background but increases the tumorigenic response to radiation. |
