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Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification  Justin.

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Presentation on theme: "Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification  Justin."— Presentation transcript:

1 Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification  Justin F. Gainor, MD, Matthew J. Niederst, PhD, Jochen K. Lennerz, MD, PhD, Ibiayi Dagogo-Jack, MD, Sara Stevens, NP, Alice T. Shaw, MD, PhD, Lecia V. Sequist, MD, MPH, Jeffrey A. Engelman, MD, PhD  Journal of Thoracic Oncology  Volume 11, Issue 7, Pages e83-e85 (July 2016) DOI: /j.jtho Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions

2 Figure 1 Axial and coronal computed tomography images of a patient with advanced non–small cell lung cancer harboring a concurrent epidermal growth factor receptor gene (EGFR) L858R mutation and MET proto-oncogene, receptor tyrosine kinase gene (MET) amplification, depicting (A) baseline disease assessment with prominent pleural thickening and nodularity (blue arrows), (B) interval progression of disease after 4 weeks of single-agent erlotinib, and (C) dramatic interval improvement in pleural thickening and intralobular septal thickening after 4 weeks of combination erlotinib and crizotinib. Journal of Thoracic Oncology  , e83-e85DOI: ( /j.jtho ) Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions

3 Figure 2 Molecular genetic workup. (A) Single-nucleotide extension Sanger sequencing as an orthogonal method to confirm the epidermal growth factor receptor gene (EGFR) thymine > guanine (T > G) transversion. (B) Pile-up view of the EGFR mutation by NGS-sequencing. (C) Fluorescent hybridization for the anaplastic lymphoma receptor tyrosine kinase gene (ALK) shows no rearrangement. (D) Copy number assessment by next-generation sequencing shows amplification of the MET proto-oncogene, receptor tyrosine kinase gene (MET) on chromosome 7 (inset). (E) Fluorescent hybridization for MET and corresponding centromeric enumeration probe for chromosome 7 (CEP7). The MET probe signals are clustered and too numerous to count, which is diagnostic of MET gene amplification. WT, wild type; SMO, smoothened, frizzled class receptor; BRAF, B-Raf proto-oncogene, serine/threonine kinase. Journal of Thoracic Oncology  , e83-e85DOI: ( /j.jtho ) Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions


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