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表皮生长因子受体突变型肺腺癌中鳞状细胞癌“转化”和 EGFR 外显子 20 S768I 突变的同步发生是一种新的耐药机制。

Synchronous occurrence of squamous-cell carcinoma "transformation" and EGFR exon 20 S768I mutation as a novel mechanism of resistance in EGFR-mutated lung adenocarcinoma.

机构信息

Medical Oncology Unit, Azienda USL, Hospital "Ramazzini", Carpi, Italy.

Section of Pathologic Anatomy, Modena University Hospital, Modena, Italy.

出版信息

Lung Cancer. 2017 Jan;103:24-26. doi: 10.1016/j.lungcan.2016.11.012. Epub 2016 Nov 17.

DOI:10.1016/j.lungcan.2016.11.012
PMID:28024692
Abstract

The occurrence of secondary EGFR mutation T790M in exon 20 and histologic "transformation" are common mechanisms underlying resistance to EGFR first- or second-generation tyrosine kinase inhibitors (TKI). We describe here on a hitherto unreported mechanism of EGFR TKI resistance synchronously combining squamous-cell carcinoma change and occurrence of the EGFR exon 20 S768I secondary mutation in a 43 year-old woman with stage IV adenocarcinoma harbouring EGFR exon 21 L858R mutation. After 8 months of response to gefitinib, the patient experienced EGFR TKI resistance and died of leptomeningeal neoplastic dissemination.

摘要

继发 EGFR 突变 T790M 发生于 20 号外显子及组织学“转化”是 EGFR 第一代或第二代酪氨酸激酶抑制剂(TKI)耐药的常见机制。我们在此描述了一种此前尚未报道的机制,即同步合并鳞状细胞癌改变及 EGFR 外显子 20 继发性 S768I 突变的 EGFR TKI 耐药,发生于一位 43 岁女性,其患有 EGFR 外显子 21 L858R 突变的 IV 期腺癌。在吉非替尼治疗 8 个月后,患者出现 EGFR TKI 耐药并死于脑膜肿瘤扩散。

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