Matsumoto Y, Kosugi S, Shinbo T, Chou D, Ohashi M, Wakabayashi Y, Sakai K, Okumoto M, Mori N, Aizawa S, Niwa O, Kominami R
Department of Biochemistry, Niigata University School of Medicine, Asahimachi, Japan.
Oncogene. 1998 May 28;16(21):2747-54. doi: 10.1038/sj.onc.1201810.
A total of 429 gamma-ray-induced thymic lymphomas were obtained from F1 and backcross mice between BALB/c and MSM strains, about a half of which carried a p53-deficient allele. A genome-wide allelic loss analysis has revealed two loci exhibiting frequent allelic losses but no allelic preference, one is localized within a 2.9 cM region between D12Mit53 and D12Mit279 loci on chromosome 12, and the other is near the D16Mit122/D16Mit162 loci on chromosome 16. The frequency of allelic loss in the D12Mit279 region is 62% and does not differ in tumors between the presence and absence of the p53-deficient allele. In contrast, the loss frequency of D16Mit122 is raised by the existence of p53-deficient allele: 62% for p63(-/+) and 13% for p53(+/+), suggesting co-operative function of the two losses. The D12Mit279 and D16Mit122 regions probably harbor different types of tumor suppressor gene that play key roles in lymphoma development.
从BALB/c和MSM品系之间的F1代和回交小鼠中总共获得了429例γ射线诱导的胸腺淋巴瘤，其中约一半携带p53缺陷等位基因。全基因组等位基因缺失分析显示有两个位点频繁出现等位基因缺失，但无等位基因偏好，一个位于12号染色体上D12Mit53和D12Mit279位点之间2.9 cM的区域内，另一个位于16号染色体上D16Mit122/D16Mit162位点附近。D12Mit279区域的等位基因缺失频率为62%，在有和没有p53缺陷等位基因的肿瘤之间没有差异。相比之下，D16Mit122的缺失频率因p53缺陷等位基因的存在而升高：p63(-/+)为62%，p53(+/+)为13%，表明这两种缺失具有协同作用。D12Mit279和D16Mit122区域可能含有不同类型的肿瘤抑制基因，它们在淋巴瘤发展中起关键作用。
