| 张睿琳,王孟超,王超然,等.非小细胞肺癌表皮生长因子受体酪氨酸激酶抑制剂获得性耐药机制及临床研究进展[J].肿瘤学杂志,2026,32(10):846-852. |
| 非小细胞肺癌表皮生长因子受体酪氨酸激酶抑制剂获得性耐药机制及临床研究进展 |
| Acquired Resistance Mechanisms to EGFR-TKIs in Non-Small Cell Lung Cancer and Advances in Clinical Research |
| 投稿时间：2026-06-27 |
| DOI：10.11735/j.issn.1671-170X.2026.10.B005 |
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| 中文关键词: 癌，非小细胞肺 表皮生长因子受体 酪氨酸激酶抑制剂 获得性耐药 靶向治疗 |
| 英文关键词:carcinoma, non-small cell lung epidermal growth factor receptor tyrosine kinase inhibitor acquired resistance targeted therapy |
| 基金项目:天津市南开区中医药传承创新发展示范试点项目（20240204020） |
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| 中文摘要: |
| 摘 要：非小细胞肺癌是肺癌中最常见的病理类型，表皮生长因子受体（epidermal growth factor receptor，EGFR）突变是其重要驱动事件之一。表皮生长因子受体酪氨酸激酶抑制剂（epidermal growth factor receptor-tyrosine kinase inhibitor，EGFR-TKI）的应用显著改善了EGFR突变型晚期非小细胞肺癌患者的生存获益，但多数患者在持续治疗后仍不可避免地出现获得性耐药，限制了靶向治疗的长期疗效。EGFR-TKI获得性耐药机制具有显著异质性，主要涉及EGFR二次突变、旁路信号激活、融合基因获得、下游信号通路异常，以及表型或组织学转化等。同时，仍存在现有检测条件下无法明确具体的耐药机制的情况。全文围绕EGFR-TKI获得性耐药的主要分子机制及相应临床研究进展进行综述，旨在为未来开展机制指导下的前瞻性联合治疗研究提供参考，进一步推动EGFR突变耐药后治疗由经验性序贯走向精准分层处置。 |
| 英文摘要: |
| Abstract： Non-small cell lung cancer(NSCLC) is the most common histological subtype of lung cancer， and epidermal growth factor receptor (EGFR) mutations represent an important oncogenic driver. The use of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) has significantly improved survival outcomes in patients with advanced EGFR-mutant NSCLC； however， most patients inevitably develop acquired resistance during continued treatment， limiting the long-term efficacy of targeted therapy. The mechanisms of acquired resistance to EGFR-TKIs are highly heterogeneous and mainly include secondary EGFR mutations， activation of bypass signaling pathways， acquisition of gene fusions， abnormalities in downstream signaling pathways， and phenotypic or histological transformation. Meanwhile， certain resistance mechanisms remain elusive under current detection conditions. This review summarizes the major molecular mechanisms underlying acquired resistance to EGFR-TKIs and the corresponding clinical research advances， aiming to provide a reference for future mechanism-guided prospective combination therapy studies and to further promote the transition of post-resistance treatment for EGFR-mutant cancers from empirical sequential strategies to precision-based stratification. |
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