Transformation to small-cell carcinoma as an acquired resistance mechanism to AZD9291: A case report
Metrics: PDF 1814 views | HTML 1255 views | ?
Lin Li1, Hui Wang1, Chao Li1, Zheng Wang2, Ping Zhang1 and Xu Yan1
1 Department of Oncology, Beijing Hospital, National Center of Gerontology, Beijing, China
2 Department of Pathology, Beijing Hospital, National Center of Gerontology, Beijing, China
Lin Li, email:
Keywords: NSCLC; EGFR-TKI; AZD9291; acquired resistance; transformation
Received: October 11, 2016 Accepted: December 27, 2016 Published: January 04, 2017
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.