PATIENT Name MRN DOB Gender ORDER INFORMATION Order ID Provider Practice Indication C34.90, Malignant neoplasm of unsp part of unsp bronchus or Report Date lung, Stage IIIA TEST SPECIMEN Specimen ID Specimen core biopsy, LLL lung Collected Source mass Specimen Received Facility

DETECTED VARIANTS Therapies Priority Additional Variants of Associated Precision Precision Potential Potential Unknown Variant Exon VAF With Tumor Medicine Medicine Off-Label Hereditary Therapeutic Type Trials Trials Therapies Variants Significance EML4e6-ALKe20 Fusion - - ◊ ◊ ◊ TP53 c.604C>G (R202G) 6 0.12 ◊ ◊ STK11 c.242delA (K81RfsX15) 1 0.13 ◊ VAF = Variant Allele Frequency

THERAPEUTIC BENEFIT SUMMARY Therapies Associated with Non-Small Cell Lung Cancer Variant Detected: EML4e6-ALKe20 Fusion Therapies Level of Evidence Evidence Sources alectinib Consensus EMA-alectinib, ESMO-Metastatic Non-Small- Cell Lung Cancer, FDA-alectinib, NCCN-Non- Small Cell Lung Cancer brigatinib Consensus FDA-brigatinib, NCCN-Non-Small Cell Lung Cancer ceritinib Consensus EMA-ceritinib, ESMO-Metastatic Non-Small- Cell Lung Cancer, FDA-ceritinib, NCCN-Non- Small Cell Lung Cancer crizotinib Consensus EMA-crizotinib, ESMO-Metastatic Non- Sample ReportSmall-Cell Lung Cancer, FDA-crizotinib, NCCN-Non-Small Cell Lung Cancer crizotinib + radiation therapy Consensus ESMO-Metastatic Non-Small-Cell Lung Cancer crizotinib + surgical intervention Consensus ESMO-Metastatic Non-Small-Cell Lung Cancer EGFR tyrosine kinase inhibitor Not Recommended NCCN-Non-Small Cell Lung Cancer Not For Clinical Use

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 1 of 7 Roswell Park Cancer Institute Priority Precision Medicine Trials in Non-Small Cell Lung Cancer Variant Detected: EML4e6-ALKe20 Fusion Trial Name Phase NCT ID Location* Crizotinib in Treating Patients With Stage IB-IIIA Non-small Cell Lung 3 NCT02201992 1-24 miles Cancer That Has Been Removed by Surgery and ALK Fusion Mutations Buffalo, NY (An ALCHEMIST Treatment Trial) Ceritinib and Combination Chemotherapy in Treating Patients With 1 NCT02227940 1-24 miles Advanced Solid Tumors or Locally Advanced or Metastatic Pancreatic Buffalo, NY Cancer Disclaimer: Clinical Trial information is current as of 09/25/2017. For the most up to date information regarding a particular trial, search www.clinicaltrials.gov by NCT ID. *Location range provides an approximate distance from the physician billing zip code to the nearest location of a trial. Visit www.clinicaltrials.gov for specific trial location information.

Additional Precision Medicine Trials in Non-Small Cell Lung Cancer Variant Detected: EML4e6-ALKe20 Fusion Trial Name Phase NCT ID Location* A Study Of Lorlatinib Versus Crizotinib In First Line Treatment Of Patients 3 NCT03052608 Over 200 miles With ALK-Positive NSCLC Columbus, OH Erlotinib Hydrochloride or Crizotinib and Chemoradiation Therapy in 2 NCT01822496 50-100 miles Treating Patients With Stage III Non-small Cell Lung Cancer Rochester, NY A Study Of PF-06463922 An ALK/ROS1 Inhibitor In Patients With 2 NCT01970865 Over 200 miles Advanced Non Small Cell Lung Cancer With Specific Molecular Detroit, MI Alterations S1300: Pemetrexed Disodium With or Without Crizotinib in Treating 2 NCT02134912 Over 200 miles Patients With Stage IV Non-Small Cell Lung Cancer That Has Progressed Omaha, NE After Crizotinib A Phase II Study to Evaluate the Efficacy and Safety of Oral Ceritinib in 2 NCT02336451 Over 200 miles Patients With ALK-positive NSCLC Metastatic to the Brain and/or to Columbus, OH Leptomeninges Ceritinib in Combination With Stereotactic Ablative Radiation Metastatic 2 NCT02513667 Over 200 miles Lung Adenocarcinoma Dallas, TX Basket Study of Entrectinib (RXDX-101) for the Treatment of Patients 2 NCT02568267 100-200 miles With Solid Tumors Harboring NTRK 1/2/3 (Trk A/B/C), ROS1, or ALK Cleveland, OH Gene Rearrangements (Fusions) Study to Evaluate Safety, Efficacy, Pharmacokinetics And 2 NCT02584634 Over 200 miles Pharmacodynamics Of Avelumab In Combination With Either Crizotinib Boston, MA Or PF-06463922 In Patients With NSCLC. (Javelin Lung 101) TAPUR: Testing the Use of Food and Drug Administration (FDA) 2 NCT02693535 Over 200 miles Approved Drugs That Target a Specific Abnormality in a Tumor Gene in Ann Arbor, MI People With AdvancedSample Stage Cancer Report A Study of Lorlatinib in Advanced ALK and ROS1 Rearranged Lung Cancer 2 NCT02927340 Over 200 miles With CNS Metastasis in the Absence of Measurable Extracranial Lesions Boston, MA Targeted Therapy in Treating Patients With Incurable Non-Small Cell 2 NCT02949843 Over 200 miles Lung Cancer With Genetic Mutations Winston-Salem, NC Evaluating Crizotinib in the Neoadjuvant Setting in Patients With Non- 2 NCT03088930 Over 200 miles small Cell Lung Cancer Aurora, CO Phase 1/2 Study of X-396, an Oral ALK Inhibitor, in Patients With ALK- 1/ 2 NCT01625234 Over 200 miles positive Non-Small CellNot Lung Cancer For Clinical UseMorgantown, WV

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| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 2 of 7 Additional Precision Medicine Trials in Non-Small Cell Lung Cancer Variant Detected: EML4e6-ALKe20 Fusion Trial Name Phase NCT ID Location* Phase I/II Trial of Alectinib and Bevacizumab in Patients With Advanced, 1/ 2 NCT02521051 Over 200 miles Anaplastic Lymphoma Kinase (ALK)-Positive, Non-Small Cell Lung Cancer Boston, MA A Study of ALK Inhibitor, Ensartinib, and Anti-PD-L1, Durvalumab, in 1/ 2 NCT02898116 Over 200 miles Subjects With ALK-rearranged Non-small Cell Lung Cancer New York, NY A Study of TPX-0005 in Patients With Advanced Solid Tumors Harboring 1/ 2 NCT03093116 Over 200 miles ALK, ROS1, or NTRK1-3 Rearrangements New York, NY A Phase IB/II Study of Alectinib Combined With Cobimetinib in Advanced 1/ 2 NCT03202940 Over 200 miles ALK-Rearranged (ALK+) NSCLC Boston, MA A Study Of Oral PF-02341066, A C-Met/Hepatocyte Growth Factor 1 NCT00585195 100-200 miles Tyrosine Kinase Inhibitor, In Patients With Advanced Cancer Pittsburgh, PA Study of Oral RXDX-101 in Adult Patients With Locally Advanced or 1 NCT02097810 Over 200 miles Metastatic Cancer Targeting NTRK1, NTRK2, NTRK3, ROS1, or ALK New York, NY Molecular Alterations. A Phase I, Multi-center, Open Label, Drug-drug Interaction Study to 1 NCT02422589 Over 200 miles Assess the Effect of Ceritinib on the Pharmacokinetics of Warfarin and Detroit, MI Midazolam in Patients With ALK-positive Advanced Tumors Crizotinib Plus Pembrolizumab In Alk-Positive Advanced Non Small Cell 1 NCT02511184 100-200 miles Lung Cancer Patients Cleveland, OH Preoperative Ceritinib (LDK378) in Glioblastoma Multiforme and CNS Early Phase 1 NCT02605746 Over 200 miles Metastasis Phoenix, AZ Variant Detected: TP53 c.604C>G (R202G) VAF: 0.12 Exon: 6 Protein Prediction: Deleterious/Benign Trial Name Phase NCT ID Location* OLAParib COmbinations 2 NCT02576444 Over 200 miles New Haven, CT Pazopanib in Molecularly Selected Patients With Advanced NSCLC 1 NCT02193152 Over 200 miles Saint Louis, MO Nintedanib in Molecularly Selected Patients With Advanced Non-Small 1 NCT02299141 Over 200 miles Cell Lung Cancer Saint Louis, MO Disclaimer: Clinical Trial information is current as of 09/25/2017. For the most up to date information regarding a particular trial, search www.clinicaltrials.gov by NCT ID. *Location range provides an approximate distance from the physician billing zip code to the nearest location of a trial. Visit www.clinicaltrials.gov for specific trial location information.

Potential Off-Label Therapies SampleNo therapeutic variant associations wereReport identified for other tumor types.

POTENTIAL HEREDITARY VARIANTS FOR FOLLOW UP No potential hereditary variants were identified. Not For Clinical Use

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 3 of 7 VARIANTS OF UNKNOWN THERAPEUTIC SIGNIFICANCE Mutations Variant Exon VAF Gene Type Protein Domain/Prediction STK11 c.242delA (K81RfsX15) 1 0.13 Tumor Suppressor Gene Deleterious TP53 c.604C>G (R202G) 6 0.12 Tumor Suppressor Gene Deleterious/Benign

THERAPY DETAILS ALECTINIB Indications and Use ALECENSA is indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive, metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial. Mechanism of Action Alectinib is a tyrosine kinase inhibitor that targets ALK and RET. In nonclinical studies, alectinib inhibited ALK phosphorylation and ALK-mediated activation of the downstream signaling proteins STAT3 and AKT, and decreased tumor cell viability in multiple cell lines harboring ALK fusions, amplifications, or activating mutations. The major active metabolite of alectinib, M4, showed similar in vitro potency and activity. Alectinib and M4 demonstrated in vitro and in vivo activity against multiple mutant forms of the ALK enzyme, including some mutations identified in NSCLC tumors in patients who have progressed on crizotinib. BRIGATINIB Indications and Use ALUNBRIG is indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial. Mechanism of Action Brigatinib is a tyrosine kinase inhibitor with in vitro activity at clinically achievable concentrations against multiple kinases including ALK, ROS1, insulin-like growth factor-1 receptor (IGF-1R), and FLT-3 as well as EGFR deletion and point mutations. Brigatinib inhibited autophosphorylation of ALK and ALK-mediated phosphorylation of the downstream signaling proteins STAT3, AKT, ERK1/2, and S6 in in vitro and in vivo assays. CERITINIB Indications and Use ZYKADIA is indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. An improvement in survival or disease-related symptoms has not been established. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. Mechanism of Action Ceritinib is a kinase inhibitor. Targets of ceritinib inhibition identified in either biochemical or cellular assays at clinically relevant concentrations include ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1. Among these, ceritinib is most active against ALK. CRIZOTINIB Indications and Use XALKORI is indicated for the treatment of patients with metastatic non-small cell lung cancer (NSCLC) whose tumors are anaplastic lymphoma kinase (ALK)-positive as detected by an FDA-approved test. Mechanism of Action Crizotinib is an inhibitor of receptor tyrosine kinases including ALK, Hepatocyte Growth Factor Receptor (HGFR, c-Met), ROS1 (c-ros), and Recepteur d'Origine Nantais (RON). Translocations can affect the ALK gene resulting in the expression of oncogenic fusion proteins. The formation of ALK fusion proteins results in activation and dysregulation of the gene's expression and signaling which can contribute to increased cell proliferation and survival in tumors expressing these proteins. Disclaimer: Therapy Details information provided in this report represents abstracted partial drug label content, where available, for drugs that are approved by the FDA for human use in either the tumor type tested orSample other tumor types. It is not intended to replace full drug label contentReport and does not address potential contraindications, precautions, warnings, or adverse reactions. For complete drug label information, refer to www.FDA.gov.

SURGICAL PATHOLOGY REVIEW SUMMARY Submitted Pathology Reviewed Pathologic Lung / Malignant Epithelial / Adenocarcinoma Report Diagnosis Sample Procurement Date Tissue Metastatic Tumor Nuclei 70% Tumor Reviewed Pathologic NotHematopoietic /For Lymph node NOS Clinical Use Tissue Site Continued on next page

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 4 of 7 SURGICAL PATHOLOGY REVIEW SUMMARY Summary of Received Samples for Testing Received Sample Label Type Quantity Unit Purpose FFPE Block 1.0 Block Testing

Sample Report

Not For Clinical Use

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 5 of 7 ABOUT OMNISEQ COMPREHENSIVE SM OmniSeq Comprehensive SM is a next generation sequencing assay that uses multiplexed PCR-based DNA-seq and RNA-seq technologies to detect somatic variants in tumors (mutations, copy number variants and fusions) for 144 genes (118 oncogenes and 26 tumor suppressor genes) to guide cancer therapeutic management. The DNA-seq component detects mutations (single nucleotide variants, insertions and deletions) and copy number variants in both oncogenes and tumor suppressor genes, while the RNA-seq component performs fusion analysis in oncogenes. DNA-seq mutational analysis detects gain-of-function mutations in oncogenes using a hotspot coverage strategy while copy number analysis detects high level amplification. DNA-seq mutational analysis also detects loss-of-function mutations in tumor suppressor genes using a complete coding sequence coverage strategy, while copy number analysis detects homozygous deletions. The RNA-seq component is focused on fusion analysis. OmniSeq Comprehensive SM Genes and Next Generation Sequencing Technologies DNA-Seq RNA-Seq Mutations (SNVs, insertions and deletions) Copy Number Variants Fusions Coding Hotspot Sequence Loss Gain Gene ABL1 GNA11 MYD88 APC APC ACVRL1 IL6 ABL1 AKT1 GNAQ NFE2L2 ATM ATM AKT1 KIT AKT3 ALK GNAS NPM1 BAP1 BAP1 APEX1 KRAS ALK AR HNF1A NRAS BRCA1 BRCA1 AR MCL1 AXL ARAF HRAS PAX5 BRCA2 BRCA2 ATP11B MDM2 BRAF BRAF IDH1 PDGFRA CDH1 CDH1 BCL2L1 MDM4 EGFR BTK IDH2 PIK3CA CDKN2A CDKN2A BCL9 MET ERBB2 CBL IFITM1 PPP2R1A FBXW7 FBXW7 BIRC2 MYC ERG CDK4 IFITM3 PTPN11 GATA3 GATA3 BIRC3 MYCL ETV1 CHEK2 JAK1 RAC1 MSH2 MSH2 CCND1 MYCN ETV4 CSF1R JAK2 RAF1 NF1 NF1 CCNE1 MYO18A ETV5 CTNNB1 JAK3 RET NF2 NF2 CD274 NKX2-1 FGFR1 DDR2 KDR RHEB NOTCH1 NOTCH1 CD44 NKX2-8 FGFR2 DNMT3A KIT RHOA PIK3R1 PIK3R1 CDK4 PDCD1LG2 FGFR3 EGFR KNSTRN SF3B1 PTCH1 PTCH1 CDK6 PDGFRA MET ERBB2 KRAS SMO PTEN PTEN CSNK2A1 PIK3CA NTRK1 ERBB3 MAGOH SPOP RB1 RB1 DCUN1D1 PNP NTRK2 ERBB4 MAP2K1 SRC SMAD4 SMAD4 EGFR PPARG NTRK3 ESR1 MAP2K2 STAT3 SMARCB1 SMARCB1 ERBB2 RPS6KB1 PDGFRA EZH2 MAPK1 U2AF1 STK11 STK11 FGFR1 SOX2 PPARG FGFR1 MAX XPO1 TET2 TET2 FGFR2 TERT RAF1 FGFR2 MED12 TP53 TP53 FGFR3 TIAF1 RET FGFR3Sample MET TSC1 Report TSC1 FGFR4 ZNF217 ROS1 FLT3 MLH1 TSC2 TSC2 FLT3 FOXL2 MPL VHL VHL GAS6 GATA2 MTOR WT1 WT1 IGF1R

OmniSeq Comprehensive SM reports mutations at the protein level based on the Life Technology Oncomine TM Assay Knowledgebase. Standard Human Genome Variation Society (HGVS) nomenclature (http://www.hgvs.org/varnomen) is used in reporting coding DNA and predicted protein changes. OmniSeq Comprehensive SM reports detected variants with therapeutic associations for the tumor type tested and for other tumor types as described by the OmniSeq Knowledgebase SM, which contains international and US practice guidelines from sources such as NCCN and EMSO, approved FDA and EMA drug label content, and genomic content from multiple sources such as COSMIC, 1000 GenomesNot Project, dbSNP, SIFT,For PolyPhen, and ClinVar.Clinical This information is proprietarily curated Use by OmniSeq for final clinical and genomic content. While OmniSeq reviews this information to help ensure accuracy, decisions about patient Continued on next page

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 6 of 7 ABOUT OMNISEQ COMPREHENSIVE SM care and treatment must be based on the independent medical judgment of the treating physician, taking into consideration all applicable information concerning the patient's condition, such as patient and family history, physical examinations, information from other diagnostic tests, and patient preferences, in accordance with the standard of care in a given community. There is no guarantee that detection of any variant by this test will result in therapeutic efficacy or lack of efficacy. The absence of detected variants by this test does not confer a lack of therapeutic efficacy for any drug or therapy known to target genes in this test. It is possible that therapeutic implications associated with variants detected by this test are not suitable for a specific patient. OmniSeq Comprehensive SM reports detected variants as having unknown therapeutic significance when they do not have a match to the OmniSeq Knowledgebase SM, are non-synonymous, and are not reported in the 1,000 Genomes database at a prevalence of 1% or greater. In addition, variants detected in tumor suppressor genes must be deleterious in at least one protein modeling database (SIFT or PolyPhen) to be reportable as having unknown therapeutic significance. OmniSeq Comprehensive SM reports wild type for some genes and tumor types where appropriate, such as EGFR for NSCLC, KIT/PDGFRA for GIST, and NRAS/KRAS for colorectal cancer. When wild type analysis does not meet criteria for 95% confidence in the wild type call for a specific variant position, the results are reported as indeterminate for wild type for that specific sample. OmniSeq Comprehensive SM testing includes mutational analysis of 15 genes (APC, BRCA1, BRCA2, MLH1, MSH2, NF2, PTEN, RB1, RET, STK11, TP53, TSC1, TSC2, VHL, and WT1) designated by the American College of Medical Genetics and Genomics (ACMG) as harboring potential germline mutations that may result in incidental findings related to hereditary susceptibility to disease. While OmniSeq Comprehensive SM does not sequence matching non-tumor tissue from tested patients, it is possible that germline mutations can be identified from tumor-only sequencing results without direct analysis of germline DNA. OmniSeq Comprehensive SM reports detected mutations in ACMG genes as potentially hereditary when they are identified as pathogenic or likely pathogenic in ClinVar (http://www.ncbi.nlm.nih.gov/clinvar) at the nucleotide level. If clinically applicable, these results should be further investigated by additional germline testing at the discretion of the ordering or treating physician. For single nucleotide variants, OmniSeq Comprehensive SM has an assay sensitivity and PPV of 97.0% and 97.9%, respectively, for formalin fixed paraffin embedded specimens. For insertions and deletions, OmniSeq Comprehensive SM has an assay sensitivity and positive predictive value (PPV) of 82.0% and 96.7%, respectively. OmniSeq Comprehensive SM detects single nucleotide variants, insertions and deletions with 95% sensitivity at a minimum VAF of 14.6% and an analytical sensitivity of 79.8% at a VAF of 5%. OmniSeq Comprehensive SM can reliably detect single nucleotide variants, insertions and deletions in samples with 20% or greater neoplastic nuclei. For copy number variants, OmniSeq Comprehensive SM has an assay sensitivity and PPV of 93% and 90%, respectively. OmniSeq Comprehensive SM can reliably detect copy number variants in samples with 50% or greater neoplastic nuclei. For gene fusions, OCP has an assay sensitivity and PPV of 100% and 100%, respectively, for the known fusions in this assay. Knowledge of known fusion partners is required for detection by OmniSeq Comprehensive SM. Percent neoplastic nuclei has minimal to no influence on the detection of gene fusions in OmniSeq Comprehensive SM due to the RNA-based method of detection. This test was developed and its performance characteristics determined by OmniSeq. The U.S. Food and Drug Administration (FDA) has not approved or cleared this test; however, FDA approval or clearance is currently not required for clinical use of this test. The results are not intended to be used as the sole means for clinical diagnosis or patient management decisions. This test should not be regarded as investigational or for research use. OmniSeq Inc. is authorized under the Clinical Laboratory Improvement Amendments and by the New York State Clinical Laboratory Evaluation Program to perform high-complexity testing. Sample Report

Not For Clinical Use

| Report electronically signed by Antonios Papanicolau, MD | CLIA ID: 33D2098748 | OmniSeq Inc., 700 Ellicott Street, Buffalo NY 14203 | 1 (800) 781-1259 Page 7 of 7