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背景与目的 Rb作为重要的抑癌基因,调控细胞周期的进程。各种原因导致的Rb功能异常均可导致细胞的持续过度增殖从而导致肿瘤的发生。Rb蛋白表达缺失或减弱及过度磷酸化是Rb功能异常的重要机制。具有突变的表皮生长因子受体(epidermal growth factor receptor,EGFR)基因是肺腺癌重要的驱动基因,在肺癌的发生发展中起着重要的作用。本研究目的在于探讨Rb在EGFR突变的肺腺癌中的存在状态。方法取23例具有EGFR突变的肺腺癌标本,用免疫组化的方法分析Rb、p Rb-780、p Rb-795表达状态及临床特征。结果在23例EGFR突变的肺腺癌患者中Rb蛋白表达缺失/减弱频率为69.6%,p Rb-780、p Rb-795过表达的频率分别为73.9%、69.6%。23例患者均存在Rb表达缺失/减弱或Rb过度磷酸化。进一步分析发现,p Rb-780过表达在晚期患者中发生更多(P=0.022);p Rb-795过表达在晚期患者中发生更多,但无统计学差异(P=0.074)。结论在EGFR突变的肺腺癌患者中,频繁发生Rb的表达缺失/减弱或过度磷酸化,Rb功能异常是EGFR突变肺腺癌患者重要的发病机制。
Background and objective Rb as an important tumor suppressor gene regulates the progression of the cell cycle. Various causes of Rb dysfunction can lead to sustained over-proliferation of cells leading to the occurrence of tumors. The loss or decrease of Rb protein expression and hyperphosphorylation are important mechanisms of Rb dysfunction. The mutant epidermal growth factor receptor (EGFR) gene is an important driving gene of lung adenocarcinoma and plays an important role in the development of lung cancer. The purpose of this study was to investigate the presence of Rb in lung adenocarcinomas with EGFR mutations. Methods Twenty-three lung adenocarcinoma specimens with EGFR mutations were obtained and the expression and clinical features of Rb, p Rb-780 and p Rb-795 were analyzed by immunohistochemistry. Results The frequency of expression / deletion of Rb protein was 69.6% in 23 cases of EGFR mutant lung adenocarcinoma, and 73.9% and 69.6% respectively of pRb-780 and pRb-795 overexpression. All 23 patients had Rb expression loss / attenuation or Rb hyperphosphorylation. Further analysis showed that pRb-780 overexpression occurred more frequently in patients with advanced disease (P = 0.022); pRb-795 overexpression occurred more frequently in patients with advanced disease, but without statistical difference (P = 0.074). Conclusions In patients with EGFR mutant lung adenocarcinoma, the expression of Rb is frequently absent / weakened or hyperphosphorylated, and the abnormal function of Rb is an important pathogenesis of EGFR mutant lung adenocarcinoma.