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Successful Treatment with Gefitinib in Advanced Non–Small Cell Lung Cancer after Acquired Resistance to Osimertinib Nuria Chic, MD Journal of Thoracic Oncology Volume 12, Issue 6, Pages e78-e80 (June 2017) DOI: /j.jtho Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions
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Figure 1 Clinical course of the patient and subsequent biopsies. (A) Thoracic assessment by computed tomography and molecular characterization at diagnosis (p.E746_S752delinsV) showing response to the second-generation EGFR tyrosine kinase inhibitor afatinib. (B) Response to the third-generation tyrosine kinase inhibitor osimertinib after acquisition of a p.T790M mutation (DelE19 positive/T790M positive). (C) Outstanding response to the first-generation EGFR tyrosine kinase inhibitor after onset of osimertinib resistance with EGFR p.C797S mutation (DelE19 positive/T790M negative/C797S positive). Journal of Thoracic Oncology , e78-e80DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions
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Figure 2 (A) Chest radiograph showing right pleural effusion. (B) Sanger sequencing chromatogram confirming a 2389T>A transversion resulting in a p.C797S amino acid substitution in DNA obtained from pleural effusion cytologic examination. The arrow indicates the base change. (C) Allelic discrimination plot of the peptide nucleic acid (PNA) probe–based real-time polymerase chain reaction performed on blood and showing negativity for p.T790M (left panel) and positivity for the p.C797S (right panel). Del, deletion; Neg, negative; WT, wild type; MUT, mutation. Journal of Thoracic Oncology , e78-e80DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions
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