Gefitinib
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Acquired drug resistance: case report A 68-year-old man acquired resistance during treatment with gefitinib for lung adenocarcinoma. The man was diagnosed with metastatic lung adenocarcinoma (stage IV) in October 2015. Subsequently, EGFR exon 19 deletion was detected by next-generation sequencing (NGS). Therefore, he started receiving gefitinib 250mg daily [route not stated]. A partial response was eventually obtained, that lasted 11 months. In September 2016, a disease progression was observed in the form of an enlargement of the lung neoplasm and increased pleural effusion. Adenocarcinoma was eventually identified in the pleural effusion. NGS of cell blocks showed known EGFR exon 19 deletion and MET amplification. Therefore, a combination therapy comprising gefitinib [dosage not stated] and crizotinib was initiated. A partial response was eventually observed. After a progression-free survival of 9 months, a disease progression was noted in June 2017. The plasma circulating tumour DNA genomic analysis by NGS showed the known EGFR exon 19 deletion along with a BRAF N581S missense mutation. Development of BRAF N581S mutation indicated acquired resistance to gefitinib. In June 2017, crizotinib was stopped, and off-label therapy with oral dabrafenib 150mg twice a day and oral trametinib 2mg once a day were added to the man’s ongoing gefitinib. A subsequent partial response was observed. In March 2018, gefitinib was also stopped, and dabrafenib and trametinib were continued. The response was maintained for 33 months. Liu Y, et al. Acquired BRAF N581S mutation mediated resistance to gefitinib and responded to dabrafenib plus trametinib. Lung Cancer 146: 355-357, Aug 2020. Available 803505192 from: URL: http://doi.org/10.1016/j.lungcan.2020.06.004
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Reactions 3 Oct 2020 No. 1824
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