Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma
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 inte...
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| Vydané v: | Oncogene Ročník 31; číslo 9; s. 1176 - 1180 |
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| Hlavní autori: | , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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01.03.2012
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| 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. |
|---|---|
| AbstractList | 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. Oncogene (2012) 31, 1176-1180; doi:10.1038/onc.2011.306; published online 25 July 2011 Keywords: Hipk2; p53; radiation; tumorigenesis 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 gamma -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. 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. 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.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. 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. A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53 þ / 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 0.2Mb interval that contained only the gene encoding homeobox-interacting protein kinase 2 (Hipk2). More than 30% of radiation-induced tumors from both p53 þ / 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 c-radiation, but most tumors retained and expressed the wild-type allele, suggesting that Hipk2 is a haploin-sufficient 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 haploin-sufficient lymphoma suppressor gene. 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. |
| Audience | Academic |
| Author | Kim, I-J Kang, H C Huang, E J DelRosario, R Balmain, A Kumar, A Mao, J-H Pelorosso, F G Wu, D Wei, G Climent, J |
| Author_xml | – sequence: 1 givenname: J-H surname: Mao fullname: Mao, J-H organization: Life Sciences Division, Lawrence Berkeley National Laboratory – sequence: 2 givenname: D surname: Wu fullname: Wu, D organization: Helen Diller Family Comprehensive Cancer Center – sequence: 3 givenname: I-J surname: Kim fullname: Kim, I-J organization: Helen Diller Family Comprehensive Cancer Center – sequence: 4 givenname: H C surname: Kang fullname: Kang, H C organization: Helen Diller Family Comprehensive Cancer Center – sequence: 5 givenname: G surname: Wei fullname: Wei, G organization: Department of Pathology, University of California and Pathology Service 113B, Veterans Affairs Medical Center, Department of Anatomy, Shandong University School of Medicine – sequence: 6 givenname: J surname: Climent fullname: Climent, J organization: Helen Diller Family Comprehensive Cancer Center – sequence: 7 givenname: A surname: Kumar fullname: Kumar, A organization: Helen Diller Family Comprehensive Cancer Center – sequence: 8 givenname: F G surname: Pelorosso fullname: Pelorosso, F G organization: Helen Diller Family Comprehensive Cancer Center – sequence: 9 givenname: R surname: DelRosario fullname: DelRosario, R organization: Helen Diller Family Comprehensive Cancer Center – sequence: 10 givenname: E J surname: Huang fullname: Huang, E J organization: Department of Pathology, University of California and Pathology Service 113B, Veterans Affairs Medical Center – sequence: 11 givenname: A surname: Balmain fullname: Balmain, A email: abalmain@cc.ucsf.edu organization: Helen Diller Family Comprehensive Cancer Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21785465$$D View this record in MEDLINE/PubMed https://www.osti.gov/servlets/purl/1624017$$D View this record in Osti.gov |
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| Keywords | radiation tumorigenesis p53 |
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| Snippet | A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from
p53
+/− and
p53
−/− mice showed frequent loss of... A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53+/- and p53-/- mice showed frequent loss of heterozygosity... A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53 +/- and p53-/- mice showed frequent loss of... A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53 þ / and p53/ mice showed frequent loss of heterozygosity... A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53+/− and p53−/− mice showed frequent loss of heterozygosity... |
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| SubjectTerms | Animals Apoptosis BASIC BIOLOGICAL SCIENCES Biochemistry & Molecular Biology Carrier Proteins - genetics Carrier Proteins - metabolism Cell Biology Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - radiation effects chromosome 6 Chromosomes, Mammalian gamma Radiation Gamma rays Gamma Rays - adverse effects Gene Expression Regulation, Neoplastic Gene mapping Genetic aspects Genetics & Heredity Health aspects HIPK2 protein Human Genetics Internal Medicine Loss of Heterozygosity Lymphoma Lymphoma - genetics Lymphoma - metabolism Lymphomas Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Knockout Neoplasms, Radiation-Induced - genetics Neoplasms, Radiation-Induced - metabolism Oncology Original original-article p53 protein Peptide mapping Physiological aspects Protein Binding Protein kinase Protein kinases Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Risk factors Thymus Thymus Neoplasms - genetics Thymus Neoplasms - metabolism Tumor proteins Tumor suppressor genes Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Tumors |
| Title | Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma |
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