PMC4977654_01
a Diagnostic imaging from September 2013, 2 cm left lower lobe lesion, multilevel mediastinal involvement, and numerous hypermetabolic skeletal lesions. b May 2014 PET-CT demonstrating new hypermetabolic lesion at T12. c January 2015 attempted CT guided biopsy of T12 lesion. d August 2015 PET-CT demonstrating response to third generation TKI following identification of EGFR resistance mutation
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Fig1
Chest X-ray and positron emission tomography-computed tomography (PET-CT) were notable for a 2.0 cm dominant left lower lung lobe lesion with multilevel mediastinal disease and widespread involvement of the axial skeleton (Fig. 1a).  T12 (Fig. 1b). The option of re-biopsy was discussed, specifically to identify emergence of acquired resistance mechanisms for consideration of alternative therapies, but the patient declined and opted to continue with erlotinib therapy. T12, she agreed to a core needle biopsy of the skeletal lesion (Fig. 1c). The sample was submitted for massively parallel sequencing, but was insufficient for comprehensive genomic evaluation. She showed good symptomatic and radiographic response (Figs. 1d, 3).
Urine ctDNA test results confirming presence of EGFR L858R activating mutation and emergence of EGFR T790M resistance mutation
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Fig2
The analysis was also positive for EGFR T790M (217 copies per 100,000 GEq) (Fig. 2).
Timeline of therapy, diagnostic evaluation, and patient status
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Fig3
She showed good symptomatic and radiographic response (Figs. 1d, 3).