Rb and p53 gene deletions in lung adenocarcinomas from irradiated and control mice.
Rb and p53 gene deletions in lung adenocarcinomas from irradiated and control mice.
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受辐射小鼠和对照小鼠的肺腺癌中 Rb 和 p53 基因缺失。
作者：
Y. Zhang;G. Woloschak
本研究对25年前用福尔马林处理并包埋在石蜡中的小鼠肺腺癌组织进行了研究，以研究B6 CF 1雄性小鼠中Rb和p53的大基因缺失。在本研究的Rb部分中，随机选择了总共80个来自辐照小鼠的肺组织样本和40个来自未辐照对照组的肺组织样本，并进行了检查。结果显示，在低剂量和低剂量率下，每周60次γ射线照射组小鼠肺腺癌Rb基因缺失率高于每周24次γ射线照射组（P < 0.05）;但是，在此情况下，百分比没有显著差异（P > 0.05）与自发性肺腺癌或暴露于相同总剂量单剂量γ射线照射的小鼠肺腺癌相比。Rb片段3（71%）和5（67%）是编码Rb蛋白与腺病毒E1 A和SV 40 T抗原的口袋结合区的基因部分，是最常见的缺失片段。p53基因缺失的分析进行了正常肺和肺腺癌，最初发现携带Rb缺失。选择外显子1、4、5、6和9进行分析。31例正常肺和肺腺癌中有30例（97%）存在p53缺失。外显子4（83%）和5（90%）是最常见的测试外显子中删除。每周一次暴露于中子60次的小鼠的p53完全缺失百分比（5/8; 63%）高于每周一次暴露于伽马射线60次的小鼠（2/8; 25%）。我们的结论是，p53基因缺失可能是一个主要的突变事件在照射B6 CI，小鼠肺腺癌的肿瘤发生。
This study was conducted on mouse lung adenocarcinoma tissues that were treated with formalin and embedded in paraffin 25 years ago to investigate the large gene deletions of Rb and p53 in B6CF1 male mice. A total of 80 lung tissue samples from irradiated mice and 40 lung samples from nonirradiated controls were selected randomly and examined in the Rb portion of this study. The results showed a significantly (P < 0.05) higher percentage of Rb deletions in lung adenocarcinomas from mice exposed to 60 once-weekly gamma-ray doses than those from mice receiving 24 once-weekly gamma-ray doses at low doses and low dose rates; however, the percentage was not significantly different (P > 0.05) from that for spontaneous lung adenocarcinomas or lung adenocarcinomas from mice exposed to single-dose gamma irradiation at a similar total dose. Rb fragments 3 (71%) and 5 (67%), the parts of the gene that encoded the pocket binding region of Rb protein to adenovirus E1A and SV40 T-antigen, were the most frequently deleted fragments. Analysis of p53 gene deletion was carried out on normal lungs and lung adenocarcinomas that were initially found to bear Rb deletions. Exons 1, 4, 5, 6 and 9 were chosen to be analyzed. The data showed that 30 (97%) of 31 normal lungs and lung adenocarcinomas had p53 deletions. Exons 4 (83%) and 5 (90%) were the most frequently deleted among tested exons. Mice exposed to neutrons 60 times on a once-weekly schedule had a higher percentage of complete p53 deletions (5/8; 63%) than those exposed to gamma rays 60 times on a once-weekly schedule (2/8; 25%). We conclude that p53 deletions may be one of the major mutational events in the tumorigenesis of lung adenocarcinomas in the irradiated B6CI, mice.
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