Small-Cell Lung Cancer Transformation In A Pulmonary Adenocarcinoma Patient As An Acquired Resistance Mechanism To Icotinib: A Case Report And Review

Icotinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), benefits patients with exon 19 deletion advanced non-small-cell lung cancer who have failed treatment with platinum-based chemotherapy. Acquisition of resistance to icotinib occurs inevitably and mechanisms need to be explored. We reported an advanced lung adenocarcinoma female with EGFR exon 19 deletion treated with icotinib after failure of gemcitabine plus cisplatin. Disease progressed again after 10 months' treatment of icotinib. Then the second bronchoscopy was performed and a histological examination confirmed histopathology transformation to small cell lung cancer, which harbored EGFR exon 19 deletion. Therefore, small cell carcinoma transformation is one of potential resistance mechanisms to icotinib and regimen for small cell carcinoma may be one of the treatment options. However, disease progressed after four cycles of etoposide plus carboplatin (EC) chemotherapy and adenocarcinoma emerged again. Amplification refractory mutation system (ARMS) analyses still revealed EGFR exon 19 deletions in third bronchoscopy biopsy. So the patient continued icotinib combined with EC chemotherapy and achieved good response. It is important for SCLC transformation patients to take the repeat biopsy after TKI resistance; Furthermore, patients with SCLC transformation may still benefit from classic anti-SCLC therapies and effective comprehensive treatment for the combined NSCLC component.