Sample Report. Result: POSITIVE Mutations Detected: NRAS-G13V, TP53-R282W, TP53-G245D, TP53-R175H, BRAF-V600M, MSI-High

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1 Sample Report PATIENT INFORMATION Name: DOB: Age: Sex: Address: Doe, John 09/04/ Male South Plainfield, NJ, SAMPLE INFORMATION Date Collected: Date Received: Date of Report: lab ID: Testing Method: 09/20/ /21/ /12/2018 REFERING PHYSICIAN Name: Institution: Address: COPY TO (if different from ordering) Name: Address: Contact: NGS on blood Contact: Tumor Profile for Doe, John ICD-10: C18.9: Malignant neoplasm of colon, unspecified Result: POSITIVE Mutations Detected: NRAS-G13V, TP53-R282W, TP53-G245D, TP53-R175H, BRAF-V600M, MSI-High Pembrolizumab, Nivolumab Panitumumab, Cetuximab LiquidGx Report for Doe, John Microsatellite Instability-MSI-High NRAS-G13V Dabrafenib BRAF-V600M Vemurafenib + Cobimetinib BRAF-V600M Dabrafenib + Trametinib BRAF-V600M Dabrafenib, Vemurafenib BRAF-V600M BRAF-V600M 5 TP53-R175H 1 NRAS-G13V 4 TP53-R282W 1 Laboratory Director: James Dermody, PhD CLIS ID: CLIA ID: 31D Rev1 Page 1 of 17

2 KEY FINDINGS 1. Potential Clinical Benefit in Cancer with Pembrolizumab, Nivolumab due to Microsatellite Instability MSI-High. 2. Potential Clinical Benefit in Melanoma with Dabrafenib due to BRAF V600M. 3. Potential Clinical Benefit in Melanoma with Vemurafenib + Cobimetinib due to BRAF V600M. 4. Potential Clinical Benefit in Melanoma with Dabrafenib + Trametinib due to BRAF V600M. 5. Potential Clinical Benefit in Non-Small Cell Lung Cancer with Dabrafenib, Vemurafenib due to BRAF V600M. 6. Potential Drug Resistance in Colorectal Cancer with Panitumumab, Cetuximab due to NRAS G13V. * The Key Findings section is an overview of potential therapeutic benefit or lack thereof. Please refer to the information below for details. Medically Actionable Alterations THERAPIES WITH POTENTIAL CLINICAL BENEFIT - SAME TUMOR TYPE Gene Alteration Detected Therapies Tumor Type Reference Microsat ellite Instability MSI-High Pembrolizumab, Nivolumab Cancer FDA THERAPIES WITH POTENTIAL CLINICAL BENEFIT - DIFFERENT TUMOR TYPE Gene Alteration Detected Therapies Tumor Type Reference BRAF V600M Dabrafenib Melanoma Hauschild A, et al BRAF V600M Vemurafenib + Cobimetinib Melanoma Larkin J, et al BRAF V600M Dabrafenib + Trametinib Melanoma BRAF V600M Dabrafenib, Vemurafenib Non-Small Cell Lung Cancer Johnson DB, et al Gautschi O, et al. 2015, Hyman DM, et al THERAPIES WITH POTENTIAL DRUG RESISTANCE - SAME TUMOR TYPE Gene Alteration Detected Therapies Tumor Type Reference NRAS G13V Panitumumab, Cetuximab Colorectal Cancer FDA Page 2 of 17

3 CLINICAL TRIALS TO CONSIDER 1. BRAF-V600M Associated Clinical Trials Therapies NCT ID Title Phase Locations# Vemurafenib Vemurafenib Panitumumab Vitamin C Panitumumab, Trametinib NCT NCT NCT NCT NCT A Phase IV, PostMarketing, Open-Label, Extension (Rollover) Study of Vemurafenib in Patients With BRAF V600 Mutation-Positive Malignancies Previously Enrolled in an Antecedent Vemurafenib Protocol NCI-COG Pediatric MATCH (Molecular Analysis for Therapy Choice)- Phase 2 Subprotocol of Vemurafenib in Patients With Tumors Harboring Braf V600 Mutations A Randomized Phase II Study of Hepatic Arterial Infusion With Intravenous Irinotecan, 5FU and Leucovorin With or Without Panitumumab, in Patients With Wild Type RAS Who Have Resected Hepatic Metastases From Colorectal Cancer A Phase II Study of High Dose Vitamin C Intravenous Infusion in Patients With Resectable or Metastatic Solid Tumor Malignancies A Phase II Enrichment Study of Panitumumab as a Single Agent or in Combination With Trametinib in Cetuximab-Refractory Stage IV Colorectal Cancer Patients Pennsylvania, New York New Jersey, Delaware New Jersey, New York 2 New York 2 Texas 2. TP53-R175H Associated Clinical Trials Therapies NCT ID Title Phase Locations# AZD1775, Olaparib NCT A Phase II Study of the PARP Inhibitor Olaparib (AZD2281) Alone and in Combination With AZD1775, AZD5363, or AZD6738 in Advanced Solid Tumors 2 Connecticut, Massachusetts Page 3 of 17

4 3. NRAS-G13V Associated Clinical Trials Therapies NCT ID Title Phase Locations# Panitumumab Panitumumab, Trametinib Binimetinib Navitoclax, Trametinib NCT NCT NCT NCT A Randomized Phase II Study of Hepatic Arterial Infusion With Intravenous Irinotecan, 5FU and Leucovorin With or Without Panitumumab, in Patients With Wild Type RAS Who Have Resected Hepatic Metastases From Colorectal Cancer A Phase II Enrichment Study of Panitumumab as a Single Agent or in Combination With Trametinib in Cetuximab-Refractory Stage IV Colorectal Cancer Patients Molecular Analysis for Therapy Choice (MATCH) An Open Label, Two-Part, Phase Ib/II Study to Investigate the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of the MEK Inhibitor Trametinib and the BCL2-Family Inhibitor Navitoclax (ABT-263) in Combination in Subjects With KRAS or NRAS Mutation-Positive Advanced Solid Tumors 2 New Jersey, New York 2 Texas 2 New Jersey, Delaware 1,2 Massachusetts 4. TP53-R282W Associated Clinical Trials Therapies NCT ID Title Phase Locations# AZD1775, Olaparib NCT A Phase II Study of the PARP Inhibitor Olaparib (AZD2281) Alone and in Combination With AZD1775, AZD5363, or AZD6738 in Advanced Solid Tumors 2 Connecticut, Massachusetts # The locations closest to the patient s address based on zip code are shown (for US locations, otherwise show all locations). Note: Select clinical trials are shown. For a full list of clinical trials, please search the ClinicalTrials.gov website. Page 4 of 17

5 ALTERATION DETAILS WITH THERAPEUTIC IMPLICATIONS BY TUMOR TYPE BRAF Gene: BRAF Nucleotide: c.1798g>a Pathways: RAS/RAF/MEK/ERK signaling pathway Alteration Detected: V600M Response to Dabrafenib: Response to Vemurafenib + Cobimetinib: Response to Dabrafenib + Trametinib: Response to Dabrafenib,Vemurafenib: Variation Type: Missense Potential Clinical Benefit in Melanoma Potential Clinical Benefit in Melanoma Potential Clinical Benefit in Melanoma Potential Clinical Benefit in Non-Small Cell Lung Cancer TP53 Gene: TP53 Nucleotide: c.524g>a Pathways: p53 signaling pathway Alteration Detected: R175H Variation Type: Missense Response Unknown NRAS Gene: NRAS Nucleotide: c.38g>t Pathways: RAS/RAF/MEK/ERK signaling pathway Alteration Detected: G13V Variation Type: Missense Response to Panitumumab, Cetuximab: Potential Drug Resistance in Colorectal Cancer TP53 Gene: TP53 Nucleotide: c.844c>t Pathways: p53 signaling pathway Alteration Detected: R282W Variation Type: Missense Response Unknown TP53 Gene: TP53 Nucleotide: c.734g>a Pathways: p53 signaling pathway Alteration Detected: G245D Variation Type: Missense Response Unknown Page 5 of 17

6 MEDICALLY ACTIONABLE MUTATIONS INFORMATION Gene Position Alteration Detected Nucleotide Read Depth Allele Freq RG AD NRAS chr1: G13V c.38g>t TP53 chr17: R282W c.844c>t TP53 chr17: G245D c.734g>a TP53 chr17: R175H c.524g>a BRAF chr7: V600M c.1798g>a MSI Result:MSI-High Microsatellite instability (MSI) is determined by detecting the length of mononucleotide repeats at five genomic sites (BAT-25, BAT-26, NR-21, NR-24, and NR-27) indicating a defect in DNA repair. Anti-PD-1 therapy has been FDA approved for patients classified as MSI-High. A positive call at 3 sites is required for a patient to be classified as MSI-High. Repeat Site BAT-25 BAT-26 NR-21 NR-24 NR-27 Result Positive Negative Positive Positive Negative Page 6 of 17

7 LIST OF ALL ALTERATIONS AND RESULTS Gene Alteration Coverage Alteration Type Result D594G SNV Negative(-) BRAF D594V SNV Negative(-) L597R SNV Negative(-) L597Q SNV Negative(-) L597S SNV Negative(-) L597V SNV Negative(-) V600D SNV Negative(-) V600E SNV Negative(-) V600G SNV Negative(-) V600K SNV Negative(-) V600M SNV Positive(+) V600R SNV Negative(-) K601E SNV Negative(-) G719A SNV Negative(-) EGFR G719C SNV Negative(-) G719S SNV Negative(-) K745_A750del Indel Negative(-) E746_A750del Indel Negative(-) E746_A750delELREA Indel Negative(-) E746_S752delinsA Indel Negative(-) L747_S752del Indel Negative(-) L747_P753delinsS Indel Negative(-) A763_Y764insFQEA Indel Negative(-) D770_N771insSVD Indel Negative(-) T790M SNV Negative(-) C797S SNV Negative(-) L858R SNV Negative(-) L861Q SNV Negative(-) L861R SNV Negative(-) Exon19_del Indel Negative(-) Exon19_ins Indel Negative(-) Exon20_ins Indel Negative(-) / CNV Negative(-) Page 7 of 17

8 G776L SNV Negative(-) ERBB2 A775_G776insYVMA Indel Negative(-) G776_777insVC Indel Negative(-) / CNV Negative(-) G12A SNV Negative(-) KRAS G12C SNV Negative(-) G12D SNV Negative(-) G12R SNV Negative(-) G12S SNV Negative(-) G12V SNV Negative(-) G13A SNV Negative(-) G13C SNV Negative(-) G13D SNV Negative(-) G13R SNV Negative(-) G13S SNV Negative(-) G13V SNV Negative(-) Q61H SNV Negative(-) Q61K SNV Negative(-) Q61L SNV Negative(-) Q61P SNV Negative(-) Q61R SNV Negative(-) K117N SNV Negative(-) A146P SNV Negative(-) A146T SNV Negative(-) A146V SNV Negative(-) AKT1 E17K SNV Negative(-) T1151_L1152insT Indel Negative(-) ALK F1174L SNV Negative(-) L1196M SNV Negative(-) G1202R SNV Negative(-) S1206Y SNV Negative(-) G1269A SNV Negative(-) EML4-ALK Fusion Negative(-) KIF5B-ALK Fusion Negative(-) TFG-ALK Fusion Negative(-) STRN-ALK Fusion Negative(-) Page 8 of 17

9 MET PIK3CA RET ROS1 Exon14_skipping Negative(-) / CNV Negative(-) E542K SNV Negative(-) E545K SNV Negative(-) E545G SNV Negative(-) H1047R SNV Negative(-) CCDC6-RET Fusion Negative(-) NCOA4-RET Fusion Negative(-) KIF5B-RET Fusion Negative(-) M918T SNV Negative(-) C634R SNV Negative(-) C634Y SNV Negative(-) C634W SNV Negative(-) LRIG3-ROS1 Fusion Negative(-) TPM3-ROS1 Fusion Negative(-) EZR-ROS1 Fusion Negative(-) SDC4-ROS1 Fusion Negative(-) GOPC-ROS1 Fusion Negative(-) SLC34A2-ROS1 Fusion Negative(-) CD74-ROS1 Fusion Negative(-) Page 9 of 17

10 G12C SNV Negative(-) NRAS G12S SNV Negative(-) G12A SNV Negative(-) G12D SNV Negative(-) G12V SNV Negative(-) G12R SNV Negative(-) G13R SNV Negative(-) G13C SNV Negative(-) G13A SNV Negative(-) G13D SNV Negative(-) G13V SNV Positive(+) Q61K SNV Negative(-) Q61R SNV Negative(-) Q61L SNV Negative(-) Q61H SNV Negative(-) Q61E SNV Negative(-) Q61P SNV Negative(-) W557R SNV Negative(-) KIT V559A SNV Negative(-) V559D SNV Negative(-) L576P SNV Negative(-) K642E SNV Negative(-) W557-L576 Indel Negative(-) I111S SNV Negative(-) MAP2K1 C121S SNV Negative(-) P124S SNV Negative(-) P124L SNV Negative(-) PDGFRA D842V SNV Negative(-) G12R SNV Negative(-) HRAS G12V SNV Negative(-) G13C SNV Negative(-) G13R SNV Negative(-) Q61R SNV Negative(-) Page 10 of 17

11 TP53 PTEN R175H SNV Positive(+) G245S SNV Negative(-) R248Q SNV Negative(-) R248W SNV Negative(-) R249S SNV Negative(-) R273H SNV Negative(-) R273C SNV Negative(-) R282W SNV Positive(+) R130G SNV Negative(-) R130* SNV Negative(-) R130Q SNV Negative(-) R159S SNV Negative(-) R233* SNV Negative(-) P248fs Indel Negative(-) K267fs Indel Negative(-) T319fs Indel Negative(-) N323fs Indel Negative(-) Page 11 of 17

12 ABOUT GENES TP53 TP53 (Tumor protein p53) is a gene that codes for a tumor suppressor protein. The protein regulates expression of genes involved in cell cycle arrest, apoptosis, senescence, DNA repair, and changes in metabolism. In cancer, TP53 s normal roles are not fulfilled, leading to cell survival, DNA damage, and cell proliferation. TP53 is the most frequently mutated gene in cancer; it is mutated in about one third of all cancers. TP53 is most frequently mutated in ovarian, colon, and esophageal cancers, although it is significantly mutated in many other cancer types. Mutation location in gene and/or protein R282W: Exon 8 G245D:. R175H:. Mutation prevalence TP53 mutation frequency in Cancer: 32.26%(26419/81895) TP53 mutation frequency in Lung Cancer: 38.46%(2489/6472) TP53 mutation frequency in Colorectal Cancer: 45.03%(5561/12350) TP53 mutation frequency in Liver Cancer: 35.89%(1101/3068) TP53 mutation frequency in Ovarian Cancer: 49.77%(1851/3719) TP53 mutation frequency in Breast Cancer: 24.99%(2753/11017) TP53-R282W mutation frequency from all TP53 mutations in Cancer: 2.62%(691/26419) TP53-G245D mutation frequency from all TP53 mutations in Cancer: 0.71%(187/26419) TP53-R175H mutation frequency from all TP53 mutations in Cancer: 6.03%(1594/26419) Effect of mutation TP53-R282W is a Gain-of-Function mutation. Unlike other inactivating mutations, this TP53 mutation is associated with earlier onset of familial cancers and poorer outcome of cancer patients, suggesting a more prominent GOF effect of this specific mutant (Zhang et al., 2016). TP53-R175H is an inactivating mutation. TP53 is a tumor suppressor that encodes the p53 protein; alterations in TP53 may result in a loss of p53 function, yet an increase in the expression and stability of the mutant p53 protein in the nucleus, sometimes leading to oncogenic effects, including genomic instability and excessive cell proliferation (Levine, 1997, Wang et al., 2005, Koga et al., 2001, Kato et al., 2003, Houben et al., 2011, Olivier et al., 2009). NRAS RAS proteins are small GTPases which cycle between inactive guanosine diphosphate (GDP)-bound and active guanosine triphosphate (GTP)-bound forms. RAS proteins are central mediators downstream of growth factor receptor signaling and therefore are critical for cell proliferation, survival, and differentiation. RAS can activate several downstream effectors, including the PI3K-AKT-mTOR pathway, which is involved in cell survival, and the RAS-RAF-MEK-ERK pathway, which is involved in cell proliferation.ras has been implicated in the pathogenesis of several cancers. Activating mutations within the RAS gene result in constitutive activation of the RAS GTPase, even in the absence of growth factor signaling. The result is a sustained proliferation signal within the cell.specific RAS genes are recurrently mutated in different malignancies. NRAS mutations are particularly common in melanoma, hepatocellular carcinoma, myeloid leukemias, and thyroid carcinoma. Mutation location in gene and/or protein G13V: Codon 13 Mutation prevalence NRAS mutation frequency in Colorectal Cancer: 4.42%(312/7065) NRAS mutation frequency in Melanoma: 18.52%(1604/8662) NRAS mutation frequency in Non-Small Cell Lung Cancer: 0.76%(80/10494) NRAS mutation frequency in Thyroid Cancer: 7.15%(475/6642) Page 12 of 17

13 NRAS-G13V mutation frequency from all NRAS mutations in Colorectal Cancer: 0.64%(2/312) NRAS-G13V mutation frequency from all NRAS mutations in Melanoma: 1.06%(17/1604) Effect of mutation BRAF BRAF (B-Raf proto-oncogene, serine/threonine kinase) is a gene that encodes the serine/threonine-protein kinase B-raf. Mutant BRAF has been implicated in the pathogenesis of several cancers, including melanoma, non-small cell lung cancer, colorectal cancer, papillary thyroid cancer, and ovarian cancer. BRAF is involved in many cellular processes, including cell proliferation, differentiation, and transcriptional regulation. Mutation location in gene and/or protein V600M: Kinase domain (exon 15) Mutation prevalence BRAF mutation frequency in Colorectal Cancer: 12.63%(9280/73480) BRAF mutation frequency in Gastrointestinal Stromal Tumor: 3.45%(33/957) BRAF mutation frequency in Glioma: 8.47%(268/3164) BRAF mutation frequency in Histiocytosis: 51.3%(237/462) BRAF mutation frequency in Melanoma: 45.33%(8447/18636) BRAF mutation frequency in Non-Small Cell Lung Cancer: 2.43%(312/12840) BRAF mutation frequency in Ovarian Cancer: 7.66%(270/3524) BRAF mutation frequency in Thyroid Cancer: 41.79%(19375/46360) BRAF-V600M mutation frequency from all BRAF mutations in Melanoma: 0.11%(9/8447) Effect of mutation CANCER DRUG INFORMATION ZELBORAF (Vemurafenib) ERBITUX (Cetuximab) TAFINLAR (Dabrafenib) MEKINIST (Trametinib) COTELLIC (Cobimetinib) VECTIBIX (Panitumumab) Page 13 of 17

14 Table 1: LiquidGx Panel Genes LiquidGx is an amplicon-based cancer test panel designed to provide sensitive and accurate genomic analysis on genes frequently mutated in cancers, EGFR, ERBB2, KRAS, BRAF, MET, ALK, ROS1, RET, PIK3CA, AKT1, NRAS, HRAS, KIT, MAP2K1, PDGFRA, TP53, and PTEN. Using Next Generation Sequencing (NGS) based technology, this test detects point mutations and small insertions/deletions for EGFR, ERBB2, KRAS, BRAF, ALK, PIK3CA, AKT1, NRAS, HRAS, KIT, MAP2K1, PDGFRA, TP53, and PTEN. It detects copy number variation for EGFR, ERBB2, and MET. Additionally, it detects fusions for ALK, ROS1, and RET and Exon14 skipping for MET. Finally, the test detects if microsatellite instability (MSI) is present by detecting repeat length at BAT-25, BAT-26, NR-21, NR-24, and NR-27. Page 14 of 17

15 HGNC gene name RefSeq Accession Detectable Exons BRAF NM_ E15 EGFR NM_ E18, E19, E20, E21 KRAS NM_ E2, E3, E4 ERBB2 NM_ E3, E12, E16, E20, E23, E29 ALK NM_ E22, E23, E25 PIK3CA NM_ E10, E21 AKT1 NM_ E4 MET NM_ E2, E3, E17, E18, E19 RET NM_ E11, E16 NRAS NM_ E2, E3 KIT NM_ E11, E13 PDGFRA NM_ E18 HRAS NM_ E2, E3 TP53 NM_ E5, E7, E8 PTEN NM_ E5, E7, E8 MAP2K1 NM_ E3 HGNC gene name RefSeq Accession Detectable fusion partner genes ROS1 NM_ CD74, SLC34A2, GOPC, EZR, SDC4, TPM3, LRIG3 ALK NM_ KIF5B, TFG, EML4, STRN RET NM_ CCDC6, NCOA4, KIF5B HGNC gene name RefSeq Accession Detectable fusion partner genes MET NM_ E14 skipping Repeat name BAT-25 BAT-26 NR-21 NR-24 NR-27 hg19 Genomic coordinates chr4:55,598, chr2:47,641, chr14:23,652, chr2:95,849, chr11:102,193, Page 15 of 17

16 References: NCCN Biomarkers Compendium at: U.S. Food and Drug Administration, Table of Pharmacogenomic Biomarkers in Drug Labeling. Available online at: My Cancer Genome at: Knowledge Base of Precision Oncology at: Catalogue Of Somatic Mutations In Cancer (COSMIC) at: cancer.sanger.ac.uk Zhang Y, et al. Gain of function of mutant p53: R282W on the peak? Oncogenesis Feb 15;5:e196. (PMID: ) Levine AJ, et al. p53, the cellular gatekeeper for growth and division. Cell Feb 7;88(3): (PMID: ) Wang YC, et al. Wild-type p53 overexpression and its correlation with MDM2 and p14arf alterations: an alternative pathway to non-small-cell lung cancer. J Clin Oncol Jan 1;23(1): (PMID: ) Koga T, et al. Heterogeneous distribution of P53 immunoreactivity in human lung adenocarcinoma correlates with MDM2 protein expression, rather than with P53 gene mutation. Int J Cancer Jul 20;95(4): (PMID: ) Kato S, et al. Understanding the function-structure and function-mutation relationships of p53 tumor suppressor protein by high-resolution missense mutation analysis. Proc Natl Acad Sci U S A Jul 8;100(14): (PMID: ) Houben R, et al. High-level expression of wild-type p53 in melanoma cells is frequently associated with inactivity in p53 reporter gene assays. PLoS One. 2011;6(7):e (PMID: ) Olivier M, et al. Recent advances in p53 research: an interdisciplinary perspective. Cancer Gene Ther Jan;16(1):1-12. (PMID: ) Hauschild A, et al. Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre, open-label, phase 3 randomised controlled trial. Lancet Jul 28;380(9839): (PMID: ) Larkin J, et al. Combined vemurafenib and cobimetinib in BRAF-mutated melanoma. N Engl J Med Nov 13;371(20): (PMID: ) Johnson DB, et al. Combined BRAF (Dabrafenib) and MEK inhibition (Trametinib) in patients with BRAFV600-mutant melanoma experiencing progression with single-agent BRAF inhibitor. J Clin Oncol Nov 20;32(33): (PMID: ) Gautschi O, et al. Targeted Therapy for Patients with BRAF-Mutant Lung Cancer: Results from the European EURAF Cohort. J Thorac Oncol Oct;10(10): (PMID: ) Hyman DM, et al. Vemurafenib in Multiple Nonmelanoma Cancers with BRAF V600 Mutations. N Engl J Med Aug 20;373(8): (PMID: ) Page 16 of 17

17 Test Methodology and Limitations for LiquidGx : Target regions of interest were sequenced using tagging of individual molecules followed by amplicon library generation and massive parallel sequencing (Illumina platform). The detected mutations are annotated based on hg19 reference genome assembly. The LiquidGx test was developed by Admera Health, including determination and validation of performance characteristics. The limit of detection is between 0.05% and 0.1%, dependent on initial cfdna concentration. This test has not been approved by the U.S. Food and Drug Administration (FDA) and is for research purposes only. The Admera Health clinical laboratory is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), accredited by the College of American Pathologists, and is qualified to perform high complexity clinical laboratory testing. Disclaimer of Liability: The information contained in this report is provided as a service and does not constitute medical advice. At the time of report generation this information is believed to be current and is based upon published research; however, research data evolves and amendments to the prescribing information of the drugs listed will change over time. While this report is believed to be accurate and complete as of the date issued, THE DATA IS PROVIDED "AS IS", WITHOUT WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING WITHOUT LIMITATION, THE IMPLIED WARRANTIES OF MERCHANTABILITY AND FITNESS FOR A PARTICULAR PURPOSE. As medical advice must be tailored to the specific circumstances of each case, the treating health care professional has ultimate responsibility for all treatment decisions made with regard to a patient including any made on the basis of a patient's genotype. I certify that these lab results are accurate. Signatures: James J. Dermody, Ph.D. Laboratory Director Admera Health LLC Testing and interpretation performed by: Admera Health LLC, 126 Corporate Blvd, South Plainfield, NJ Tel.# James Dermody Ph.D. Laboratory Director LiquidGx is a trademark of. Page 17 of 17