Royal Marsden Hospital NHS Foundation Trust, London, and Surrey, UK.
Lung Cancer. 2013 Apr;80(1):1-4. doi: 10.1016/j.lungcan.2012.12.019. Epub 2013 Jan 10.
Several different acquired resistance mechanisms of EGFR mutant lung adenocarcinoma to EGFR-tyrosine kinase inhibitor (TKI) therapy have been described, most recently transformation to small cell lung carcinoma (SCLC). We describe the case of a 46-year-old female with relapsed EGFR exon 19 deletion lung adenocarcinoma treated with erlotinib, and on resistance, cisplatin-pemetrexed. Liver rebiopsy identified an afatinib-resistant combined SCLC and non-small cell carcinoma with neuroendocrine morphology, retaining the EGFR exon 19 deletion. This case highlights acquired EGFR-TKI resistance through transformation to the high-grade neuroendocrine carcinoma spectrum and that that such transformation may not be evident at time of progression on TKI therapy.
已经描述了几种不同的表皮生长因子受体（EGFR）突变型肺腺癌对 EGFR-酪氨酸激酶抑制剂（TKI）治疗的获得性耐药机制，最近的一种是转化为小细胞肺癌（SCLC）。我们描述了一例 46 岁女性复发性 EGFR 外显子 19 缺失肺腺癌患者，接受厄洛替尼治疗，耐药后接受顺铂-培美曲塞治疗。肝再活检发现一种阿法替尼耐药的 SCLC 和非小细胞癌，具有神经内分泌形态，保留 EGFR 外显子 19 缺失。本病例强调了通过向高级别神经内分泌癌谱转化获得 EGFR-TKI 耐药，并且这种转化在 TKI 治疗进展时可能不明显。
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