Abstract

We used 183 F1 CBA×C57Bl hybrid mice to study the delayed effects of low-power long-term γ-irradiation at a dose of 12.6 Gy (10 mGy/min) 8 and 10 months after the treatment. Eight months after the treatment we found the increased expression of the transcription factor NFκB and its target genes iNOS and G-SCF in the bone marrow (BM). Ten months after the treatment malignant lymphomas were revealed in 14 of 94 mice in the liver, abdominal cavity, and subcutaneously. In the BM of these mice, the transcription of the PTEN, NFκB, and iNOS genes was inhibited and the contents of long non-coding RNAs (lncRNAs) lnc p21, NEAT1, and microRNA miR-125b were decreased. The expression of the NFκB(p65) gene and miR-125b was inhibited in the BM of irradiated mice without tumors ten months after the treatment. These data show the deregulation of the P53 system supporting the genome stability in the BM of irradiated mice. These indices will be studied as potential markers of risk of development of irradiation-induced tumors.

中文翻译：

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辐射小鼠肿瘤发生过程中涉及造血调节的基因活性变化。

摘要

我们使用183只F1 CBA×C57B1杂种小鼠在治疗后8和10个月研究了以12.6 Gy（10 mGy / min）的剂量进行的低功率长期γ辐射的延迟效应。治疗八个月后，我们发现转录因子NFκB及其靶基因iNOS和G - SCF在骨髓（BM）中表达增加。治疗后十个月，在肝，腹腔和皮下的94只小鼠中有14只发现了恶性淋巴瘤。在这些小鼠中的BM，所述的转录PTEN，NF κ乙，和iNOS的基因受到抑制和长的非编码RNA（lncRNAs）LNC P21，利落，和微小RNA的miR-125b的含量减少。的表达NF κ B（p65）表达基因和miR-125b的照射小鼠的BM被抑制而不肿瘤治疗后十个月。这些数据表明，P53系统的失控支持了辐射小鼠的BM中的基因组稳定性。这些指标将作为潜在的标志物进行研究，这些标志物可能是辐射诱发的肿瘤发展的风险。