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Coexistence of Tyrosine Kinase Inhibitor-Sensitizing and Resistant EGFR Mutations in an Untreated Lung Adenocarcinoma Patient and Response to Erlotinib Gagan Mathur, MD, Deqin Ma, MD, PhD Journal of Thoracic Oncology Volume 9, Issue 7, Pages e55-e57 (July 2014) DOI: /JTO Copyright © 2014 International Association for the Study of Lung Cancer Terms and Conditions
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FIGURE 1 Identification of EGFR exon 19 compound mutation by massively parallel sequencing. Genomic DNA was extracted from formalin-fixed, paraffin-embedded tissue. EGFR mutation analysis was performed using the Ion AmpliSeq Cancer Hotspot Panel v2 (Life Technologies, Carlsbad, CA) at our molecular pathology laboratory. The hollow arrow indicates point mutation and the solid arrow indicates the region of the15 base-pair deletion. Journal of Thoracic Oncology 2014 9, e55-e57DOI: ( /JTO ) Copyright © 2014 International Association for the Study of Lung Cancer Terms and Conditions
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FIGURE 2 Identification of EGFR exon 19 compound mutation by Sanger sequencing. Exons18-21 of the EGFR gene was polymerase chain reaction amplified and Sanger sequencing was performed. The hollow arrow indicates the c.2240T>C point mutation and the solid arrow marks the beginning of the15 base-pair deletion (c.2246_2260de15). Journal of Thoracic Oncology 2014 9, e55-e57DOI: ( /JTO ) Copyright © 2014 International Association for the Study of Lung Cancer Terms and Conditions
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FIGURE 3 Computed Tomography images of the initial presentation (A) and 2 months post-Erlotinib treatment (B) of the lung nodule. Journal of Thoracic Oncology 2014 9, e55-e57DOI: ( /JTO ) Copyright © 2014 International Association for the Study of Lung Cancer Terms and Conditions
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