1. Receptor Tyrosine Kinase Fusions and BRAF Kinase Fusions are Rare but Actionable Resistance Mechanisms to EGFR Tyrosine Kinase Inhibitors 
Alexa B. Schrock, PhD, Viola W. Zhu, MD, PhD, Wen-Son Hsieh, MD, PhD, Russell Madison, BS, Benjamin Creelan, MD, Jeffrey Silberberg, MD, Dan Costin, MD, Anjali Bharne, MD, Ioana Bonta, MD, Thangavijayan Bosemani, MD, Petros Nikolinakos, MD, Jeffrey S. Ross, MD, Vincent A. Miller, MD, Siraj M. Ali, MD, PhD, Samuel J. Klempner, MD, Sai-Hong Ignatius Ou, MD, PhD 
Journal of Thoracic Oncology 
Volume 13, Issue 9, Pages (September 2018)
DOI: /j.jtho
Copyright © 2018 International Association for the Study of Lung Cancer Terms and Conditions

2. Figure 1 Flow diagram of the patients analyzed.
RTK, receptor tyrosine kinase; TKI, tyrosine kinase inhibitor; MET, mesenchymal epithelial transition factor receptor gene.
Journal of Thoracic Oncology  , DOI: ( /j.jtho )
Copyright © 2018 International Association for the Study of Lung Cancer Terms and Conditions

3. Figure 2
Treatment timeline for 31 NSCLC patients with EGFR mutations + BRAF or RTK fusions. Includes available records of EGFR targeted therapy and other therapy received during the relevant interval between EGFR molecular testing. Tick marks indicate 2 months. Grey boxes indicate unknown or approximate duration of treatment. Negative ALK FISH test results are noted when appropriate. Green arrow: known time of CGP. Red arrow: known time of local molecular testing. Orange circle: approximate time of local molecular testing. Pink arrows: radiation therapy.
*CGP was performed retrospectively on an initial biopsy at the time of progression on EGFR targeted therapy.
#CGP of ctDNA at this time would not have detected the BRAF fusion that was later detected in a tissue sample, so this is not considered a case with a paired pre-treatment sample.
C, carboplatin; p, pemetrexed; b, bevacizumab; cis, cisplatin; n, navelbine; ab, cetuximab; d, docetaxel; A, alectinib; a, afatinib; e, erlotinib; z, crizotinib; osi, osimertinib; bri, brigatinib; cabo, cabozantinib; t, clinical trial of EGFR unspecified inhibitor; N, nivolumab; r, rocelitinib; WT, wild-type; ALK, ALK receptor tyrosine kinase; FISH, fluorescent in situ hybridization; CGP, comprehensive genome profiling; RTK, receptor tyrosine kinase.
Journal of Thoracic Oncology  , DOI: ( /j.jtho )
Copyright © 2018 International Association for the Study of Lung Cancer Terms and Conditions

4. Figure 3
Schematic of the genomic rearrangements of all the RTK- and BRAF- fusions. Included exons are numbered and the involved kinase is colored purple (ALK), orange (FGFR3), pink (RET), teal (BRAF), green (NTRK1), or blue (EGFR). Exons encoding a portion of the kinase domain are colored in red. *Breakpoint within the indicated exon. RTK, receptor tyrosine kinase; ALK, ALK receptor tyrosine kinase; RET, ret proto-oncogene; NTRK1, neurotrophic receptor tyrosine kinase 1.
Journal of Thoracic Oncology  , DOI: ( /j.jtho )
Copyright © 2018 International Association for the Study of Lung Cancer Terms and Conditions

5. Figure 4
Treatment evolution and genomic profiling in a patient with EGFR+ NSCLC with an acquired PLEKHA7-ALK fusion. (A) Schema of the PLEKHA7-ALK fusion protein. (B) Radiographic response to osimertinib + alectinib. Pre- (left) and 16 weeks post- (right) initiation of combination treatment with osimertinib + alectinib. ALK, ALK receptor tyrosine kinase; WW, tryptophan tryptophan; TKI, tyrosine kinase inhibitor.
Journal of Thoracic Oncology  , DOI: ( /j.jtho )
Copyright © 2018 International Association for the Study of Lung Cancer Terms and Conditions