@article {185,
	title = {Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma.},
	journal = {Oncogene},
	volume = {31},
	year = {2012},
	month = {2012 Mar 1},
	pages = {1176-80},
	abstract = {<p>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.</p>},
	keywords = {Animals, Carrier Proteins, Cell Transformation, Neoplastic, Chromosomes, Mammalian, Gamma Rays, Gene Expression Regulation, Neoplastic, Loss of Heterozygosity, Lymphoma, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasms, Radiation-Induced, Protein Binding, Protein-Serine-Threonine Kinases, Thymus Neoplasms, Tumor Suppressor Protein p53},
	issn = {1476-5594},
	doi = {10.1038/onc.2011.306},
	author = {Jiang-Hua Mao and Wu, D and Kim, I-J and Kang, H C and Wei, G and Climent, J and Kumar, A and Pelorosso, F G and DelRosario, R and Huang, E J and Balmain, A}
}
