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- Title
Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma.
- Authors
Mao, J-H; Wu, D; Kim, I-J; Kang, H C; Wei, G; Climent, J; Kumar, A; Pelorosso, F G; DelRosario, R; Huang, E J; Balmain, A
- Abstract
A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53+/− and p53−/− mice showed frequent loss of heterozygosity (LOH) on chromosome 6. Fine mapping of these LOH regions revealed three non-overlapping regions, one of which was refined to a 0.2 Mb interval that contained only the gene encoding homeobox-interacting protein kinase 2 (Hipk2). More than 30% of radiation-induced tumors from both p53+/− and p53−/− mice showed heterozygous loss of one Hipk2 allele. Mice carrying a single inactive allele of Hipk2 in the germline were susceptible to induction of tumors by γ-radiation, but most tumors retained and expressed the wild-type allele, suggesting that Hipk2 is a haploinsufficient tumor suppressor gene for mouse lymphoma development. Heterozygous loss of both Hipk2 and p53 confers strong sensitization to radiation-induced lymphoma. We conclude that Hipk2 is a haploinsufficient lymphoma suppressor gene.
- Subjects
RADIATION carcinogenesis; THYMUS tumors; P53 antioncogene; PROTEIN kinases; LABORATORY mice; T-cell lymphoma; LOSS of heterozygosity; GERM cells
- Publication
Oncogene, 2012, Vol 31, Issue 9, p1176
- ISSN
0950-9232
- Publication type
Article
- DOI
10.1038/onc.2011.306