Transformation to small-cell carcinoma as an acquired resistance mechanism to AZD9291: A case report

被引：51

作者：

Li, Lin ^{[1
]}

Wang, Hui ^{[1
]}

Li, Chao ^{[1
]}

Wang, Zheng ^{[2
]}

Zhang, Ping ^{[1
]}

Yan, Xu ^{[1
]}

机构：

[1] Natl Ctr Gerontol, Beijing Hosp, Dept Oncol, Beijing, Peoples R China

[2] Natl Ctr Gerontol, Beijing Hosp, Dept Pathol, Beijing, Peoples R China

来源：

ONCOTARGET | 2017年 / 8卷 / 11期

关键词：

NSCLC; EGFR-TKI; AZD9291; acquired resistance; transformation; LUNG-CANCER; EGFR-INHIBITOR; ADENOCARCINOMA; PATIENT; LEVEL;

D O I：

10.18632/oncotarget.14506

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

AZD9291, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), benefits patients with T790M mutant non-small-cell lung cancer who fail treatment with first-generation EGFR TKIs. Acquisition of resistance to AZD9291 occurs inevitable and mechanisms need to be explored. We reported an advanced lung adenocarcinoma female with EGFR exon19 deletion treated on AZD9291 after failure of erlotinib and chemotherapy. Disease progressed again after 6 months' treatment of AZD9291 with hepatic metastasis. Re-biopsy of the hepatic lesion showed histopathology transformation to small cell lung cancer, which harbored EGFR exon19 deletion. Therefore, small cell carcinoma transformation is one of potential resistance mechanisms to AZD9291 and regimen for small cell carcinoma may be one of the treatment options.

引用

页码：18609 / 18614

页数：6

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