背景:流行病学研究表明肺癌与结核病之间存在因果关系,尤其患有结核病的患者往往更容易患上肺腺癌,但其中的作用机制尚不清楚。前期研究发现,肺结核患者中EGFR突变和FHIT甲基化水平较高,本研究旨在查明肺腺癌和结核病患者中EGFR突变和F...背景:流行病学研究表明肺癌与结核病之间存在因果关系,尤其患有结核病的患者往往更容易患上肺腺癌,但其中的作用机制尚不清楚。前期研究发现,肺结核患者中EGFR突变和FHIT甲基化水平较高,本研究旨在查明肺腺癌和结核病患者中EGFR突变和FHIT甲基化的遗传相关性。方法:在肺腺癌和肺结核患者中,分析了表皮生长因子受体(EGFR)突变及FHIT基因的甲基化状态,并检查了结核病状态与遗传/表观遗传变异之间的关系。结果:结核患病状态与EGFR突变频率有很强的相关性,而结核患病状态与FHIT甲基化之间的关系较弱。EGFR突变与FHIT甲基化之间呈反相关关系。结论:结核病可能在增加FHIT甲基化率的同时会阻碍EGFR突变,导致患结核病后发展肺腺癌的患者对EGFR抑制剂治疗疗效不佳。Background: Epidemiological studies have shown a causal relationship between lung cancer and tuberculosis, especially in patients with tuberculosis, who are more likely to develop lung adenocar-cinoma, but the mechanism of action is not clear. Previous studies have found that EGFR mutation and FHIT methylation levels are higher in pulmonary tuberculosis patients, and this study aims to identify the genetic association of EGFR mutation and FHIT methylation in lung adenocarcinoma and tuberculosis patients. Methods: In patients with lung adenocarcinoma and tuberculosis, epidermal growth factor receptor (EGFR) mutations and methylation status of FHIT gene were analyzed, and the relationship between tuberculosis status and genetic/epigenetic variants was examined. Results: There was a strong correlation between tuberculosis prevalence and EGFR mutation frequency, while the relationship between tuberculosis prevalence and FHIT methylation was weak. There was an inverse correlation between EGFR mutations and FHIT methylation. Conclusion: Tuberculosis may hinder EGFR mutations while increasing the methylation rate of FHIT, resulting in poor response to EGFR inh展开更多
文摘背景:流行病学研究表明肺癌与结核病之间存在因果关系,尤其患有结核病的患者往往更容易患上肺腺癌,但其中的作用机制尚不清楚。前期研究发现,肺结核患者中EGFR突变和FHIT甲基化水平较高,本研究旨在查明肺腺癌和结核病患者中EGFR突变和FHIT甲基化的遗传相关性。方法:在肺腺癌和肺结核患者中,分析了表皮生长因子受体(EGFR)突变及FHIT基因的甲基化状态,并检查了结核病状态与遗传/表观遗传变异之间的关系。结果:结核患病状态与EGFR突变频率有很强的相关性,而结核患病状态与FHIT甲基化之间的关系较弱。EGFR突变与FHIT甲基化之间呈反相关关系。结论:结核病可能在增加FHIT甲基化率的同时会阻碍EGFR突变,导致患结核病后发展肺腺癌的患者对EGFR抑制剂治疗疗效不佳。Background: Epidemiological studies have shown a causal relationship between lung cancer and tuberculosis, especially in patients with tuberculosis, who are more likely to develop lung adenocar-cinoma, but the mechanism of action is not clear. Previous studies have found that EGFR mutation and FHIT methylation levels are higher in pulmonary tuberculosis patients, and this study aims to identify the genetic association of EGFR mutation and FHIT methylation in lung adenocarcinoma and tuberculosis patients. Methods: In patients with lung adenocarcinoma and tuberculosis, epidermal growth factor receptor (EGFR) mutations and methylation status of FHIT gene were analyzed, and the relationship between tuberculosis status and genetic/epigenetic variants was examined. Results: There was a strong correlation between tuberculosis prevalence and EGFR mutation frequency, while the relationship between tuberculosis prevalence and FHIT methylation was weak. There was an inverse correlation between EGFR mutations and FHIT methylation. Conclusion: Tuberculosis may hinder EGFR mutations while increasing the methylation rate of FHIT, resulting in poor response to EGFR inh
