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针对表皮生长因子受体(epidermal growth factor receptor,EGFR)的靶向治疗已成为继手术、放疗和化疗后治疗非小细胞肺癌(non-small-cell lung cancer,NSCLC)的又一重要手段,但EGFR特异性抑制剂gefitinib对NSCLC的有效率远低于EGFR在NSCLC中的表达率。NSCLC EGFR酪氨酸激酶结构域突变的发现揭示了肺癌对gefitinib敏感的分子机制,并为预测gefitinib疗效提供了极佳的预测指标。这种突变主要发生在EGFR基因的19和21外显子,尽管突变种类较多,19外显子上的突变主要为缺失突变,21外显子上的突变均为错义突变,且集中在EGFR酪氨酸激酶的关键部位。这种突变主要见于东亚人种、不吸烟的肺腺癌患者。
Targeted treatment of epidermal growth factor receptor (EGFR) has become another important tool in the treatment of non-small-cell lung cancer (NSCLC) following surgery, radiotherapy and chemotherapy The efficiency of EGFR-specific inhibitor gefitinib in NSCLC is much lower than that of EGFR in NSCLC. The discovery of EGFR tyrosine kinase domain mutations in NSCLC revealed the molecular mechanism of lung cancer sensitivity to gefitinib and provided an excellent predictor of the efficacy of gefitinib. This mutation occurs mainly in exons 19 and 21 of the EGFR gene, although the mutations are numerous and the mutations in exon 19 are mainly deletion mutations. The mutations in exon 21 are missense mutations and are concentrated in The key site of EGFR tyrosine kinase. This mutation is mainly seen in East Asian ethnic, non-smoking lung adenocarcinoma patients.