Korean Journal of Medicinal Crop Science (한국약용작물학회지)

The Korean Society of Medicinal Crop Science (한국약용작물학회)
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Candidate Tumor-Suppressor Gene Regions Responsible for Radiation Lymphomagenesis in F1 Mice with Different p53 Status

  • Hong, Doo-Pyo (College of Biomedical & Health Science, Department of Life Science, Konkuk university) ;
  • Choi, Dong-Kug (College of Biomedical & Health Science, Department of Life Science, Konkuk university) ;
  • Choi, Wahn-Soo (Department of Immunology, College of Medicine and Institute of Biomedical Science and Technology, Konkuk University) ;
  • Cho, Bong-Gum (College of Biomedical & Health Science, Department of Life Science, Konkuk university) ;
  • Park, Tae-Kyu (College of Biomedical & Health Science, Department of Life Science, Konkuk university) ;
  • Lim, Beong-Ou (College of Biomedical & Health Science, Department of Life Science, Konkuk university)
  • Published : 2006.04.01
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Abstract

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.

Keywords

References

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