Comparison of Properties of Spontaneous and Radiation-Induced Mouse Thymic Lymphomas: Role of Trp53 and Radiation
Comparison of Properties of Spontaneous and Radiation-Induced Mouse Thymic Lymphomas: Role of Trp53 and Radiation
复制标题
DOI：
10.1667/rr3303
复制
发表时间：
2005-02
期刊：
影响因子：
--
通讯作者：
T. Kubota;Yoshihiro Yoshikai;Y. Tamura;Y. Mishima;Y. Aoyagi;O. Niwa;R. Kominami
中科院分区：
文献类型：
--
作者：
T. Kubota;Yoshihiro Yoshikai;Y. Tamura;Y. Mishima;Y. Aoyagi;O. Niwa;R. Kominami
摘要久保田，T.，Yoshikai，Y.，Tamura，Y.，三岛，Y.，Aoyagi，Y.，丹羽岛和Kominami，R.自发性和辐射诱导小鼠胸腺淋巴瘤的性质比较：Trp 53和辐射的作用。Radiat. Res. 163，159-164（2005）。小鼠胸腺淋巴瘤容易由辐射诱导，并且当小鼠Trp 53功能无效时，也会在没有辐射的情况下出现。在本研究中，将Trp 53 −/−小鼠中的自发性胸腺淋巴瘤与辐照Trp 53 +/−小鼠中出现的淋巴瘤进行了比较，揭示了自发性淋巴瘤的三个特征。(1)Mp53 D2是一种影响Trp 53 +/−小鼠放射性胸腺淋巴瘤潜伏期的Trp 53修饰剂，对自发性淋巴瘤的发生没有影响。(2)（3）11号染色体上编码正常淋巴细胞发育和分化所需转录因子的Ikaros基因的等位基因丢失频率存在显著差异;在Trp 53 −/−小鼠的淋巴瘤中为2%，在Trp 53 +/−小鼠的放射性淋巴瘤中为78%，提示Trp 53的缺失可能降低淋巴瘤发生对Ikaros缺失的需要。此外，19号染色体上的等位基因缺失分析定位了一个可能含有未知肿瘤抑制基因的区域。这些结果表明淋巴瘤发生的复杂步骤受Trp 53的存在或不存在的影响。
Abstract Kubota, T., Yoshikai, Y., Tamura, Y., Mishima, Y., Aoyagi, Y., Niwa, O. and Kominami, R. Comparison of Properties of Spontaneous and Radiation-Induced Mouse Thymic Lymphomas: Role of Trp53 and Radiation. Radiat. Res. 163, 159–164 (2005). Mouse thymic lymphomas are readily induced by radiation and also arise without irradiation when the mice are null in Trp53 functions. In the present study, spontaneous thymic lymphomas in Trp53−/− mice were compared to those arising in irradiated Trp53+/− mice, revealing three features characteristic of the spontaneous lymphomas. (1) Mp53D2, a Trp53 modifier that affects the latent period of radiogenic thymic lymphomas in Trp53+/− mice, had no effect on the development of spontaneous lymphomas. (2) A sex difference in the latency was found. (3) A marked difference was noted in the frequency of allelic loss at the Ikaros gene on chromosome 11, encoding a transcription factor required for normal lymphocyte development and differentiation; 2% in the lymphomas of Trp53−/− mice and 78% in the radiogenic lymphomas of Trp53+/− mice, suggesting that loss of Trp53 may reduce the requirement for the loss of Ikaros for lymphomagenesis. Furthermore, allelic loss analysis on chromosome 19 localized a region that may harbor an unknown tumor suppressor gene. These results suggest intricate steps of lymphomagenesis influenced by the presence or absence of Trp53.