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KMID : 1098420060140020096
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Korean Journal of Medicinal Crop Science
2006 Volume.14 No. 2 p.96 ~ p.100
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Candidate Tumor-Suppressor Gene Regions Responsible for Radiation Lymphomagenesis in F1 Mice with Different p53 Status
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Hong Doo-Pyo
Choi Dong-Kug
Choi Wahn-Soo
Cho Bong-Gum
Park Tae-Kyu
Lim Byong-Ou
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Abstract
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Regions of allelic loss on chromosomes in many tumors of human and some experimental animals are generally considered to harbor tumor-suppressor genes involved in tumorigenesis. Allelotype analyses have greatly improved our under-standing of the molecular mechanism of radiation lymphomagenesis. Previously, we and others found frequent loss of heterozygosity (LOH) on chromosomes 4, 11, 12, 16 and 19 in radiation-induced lymphomas from several F_1, hybrid mice. To examine possible contributions of individual tumor-suppressor genes to tumorigenesis in p53 heterozygous deficiency, we investigated the genome-wide distribution and status of LOH in radiation-induced lymphomas from F_1 mice with different p53 status. In this study, we found frequent LOH (more than 20%) on chromosomes 4 and 12 and on chromosomes 11, 12, 16 and 19 in radiation-induced lymphomas from (STS/A{times}MSM/Ms)F_1 mice and (STS/A{times}MSM/Ms)F_1-p53^{KO/+} mice, respectively. Low incidences of LOH (10-20%) were also observed on chromosomes 11 in mice with wild-type p53, and chromosomes 1, 2, 9, 17 and X in p53 heterozygous-deficient mice. The frequency of LOH on chromosomes 9 and 11 increased in the (STS/A{times}MSM/Ms)F_1-p53^{KO/+} mice. Preferential losses of the STS-derived allele on chromosome 9 and wild-type p53 allele on chromosome 11 were also found in the p53 heterozygous-deficient mice. Thus, the putative tumor-suppressor gene regions responsible for lymphomagenesis might considerably differ due to the p53 status.
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KEYWORD
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p53, chromosome, lymphomaganesis, tumorigenesis, heterozygosity
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