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DAMODARAN, BERGER, AND ROYCHOWDHURY IMPACT OF CANCER GENOMIC TESTING IN THE CLINIC Although the availability of cancer genomic testing in the clinic has led to opportunities in oncology such as drug target discovery, it has also led to challenges including how to develop targeted therapies for small populations of patients with rare mutations. For example, in contrast to the frequency of ERBB2 amplifıcation in breast cancer and BRAF mutations in melanoma (20% and 45%, respectively), the majority of actionable genomic alterations revealed by clinical tumor sequencing typically occur at frequencies of 2% to 5%. This has raised several challenges for delivering treatment to patients and developing novel therapies in clinical trials. For example, cancer genomic sequencing enabled discovery of novel activating somatic point mutations the ERBB2 gene in patients with breast cancer who were negative for ERBB2 gene (HER2) amplifıcation, but these mutations are only found in 1% to 2% of patients with breast cancer. 36 In vitro studies demonstrated that these activating mutations conferred resistance to reversible inhibitor lapatinib but were sensitive to neratinib, an irreversible ERBB2 inhibitor. 36 This has led to a phase II study of neratinib for patients with metastatic ERBB2-mutant breast cancer. 2 Although this strategy appears rational for a disease- and mutation-specifıc trial, moving forward for other uncommon genomic alterations within a single tumor type, typical large randomized phase III trials will not be pragmatic for each disease and each mutation subset. Meanwhile predictive biomarker selection has led to exceptional tumor responses to matching therapies, and phase II trials may provide convincing evidence of clinical activity and benefıt. 37-39 The low prevalence of actionable oncogenic mutations has led to the evolution of “basket trials.” Unlike a conventional tumor histology–based clinical trial, patient selection is based on a specifıc genomic alteration and not on tumor type. 40 This is different from BATTLE or I-SPY trials in which adaptive design is utilized to enrich patients into specifıc molecular cohorts based on initial effıcacy results, while restricted to a single tumor type. Presently, basket trial approaches will unlikely lead to regulatory drug approval in a specifıc tumor type, but they help assess whether all or selected cancer types with specifıc genomic alterations (e.g., FGFR, BRAF) would indeed respond to a matching targeted therapy, and they help consider other endpoints, such as magnitude of response, duration of responses, and the study of novel predictive biomarkers for sensitivity and resistance. 41 Finally, basket trials enable enrollment of multiple tumor types and facilitate patient accrual for both rare cancers and genomic alterations. In addition to prospective trials, cancer genomic testing may help us understand clinical responses retrospectively based on patients who have exceptional responses to therapy. Iyer et al observed a complete, durable response of more than 2 years in a single patient with metastatic bladder cancer with everolimus treatment on a clinical trial that did not meet its primary endpoint. They performed whole-genome sequencing of the tumor, which revealed a mutation in TSC1, a gene involved in the mTOR pathway. They subsequently demonstrated a basis for clinical response to everolimus, an mTOR inhibitor. 34 Similarly, whole-exome sequencing on a patient with metastatic anaplastic thyroid cancer, who had an exceptional response to everolimus, identifıed a mutation in TSC2, a negative regulator of the mTOR pathway. 42 These individual patients highlight an application of genomic sequencing to understand how we can learn from exceptional responders to guide further development of targeted therapies. The National Cancer Institute and academic cancer centers are actively seeking to apply this approach in ongoing clinical trials across the country to guide drug development based on novel predictive biomarkers. Finally, as we learn to identify the correct genomic alteration that can predict response to a therapy, we must also prospectively consider how cancers become resistant to therapy. Although targeted therapies may lead to remarkable initial responses for patients with selected biomarkers, metastatic cancers inevitably acquire resistance. NGS has been utilized to characterize mechanisms of secondary resistance to identify potential combinatorial therapies that can prevent or delay emergence of resistance. Wagle et al performed NGS in a patient with metastatic melanoma who developed resistance to vemurafenib after showing initial response. They identifıed an acquired mutation in MEK1, conferring resistance to RAF or MEK inhibition. 43 Tumor sequencing has also helped identify resistance mechanisms in long-established therapies, such as estrogen blockade in breast cancer, where ligandbinding domain mutations in ESR1 (the estrogen receptor) mediate acquired resistance to antihormonal therapy. 44,45 Similarly, whole-exome sequencing has been utilized to study acquired resistance to the recently approved BTK inhibitor ibrutinib in relapsed chronic lymphocytic leukemia and has identifıed a mutation in BTK that limits drug binding. 46 CONCLUSION Although the application of clinical tumor sequencing has enabled identifıcation of actionable genomic alterations that could provide molecular eligibility to matching targeted therapies, clinical application and interpretation does have some challenges. Intratumor heterogeneity, discerning drivers from passenger mutations, lack of sustained response, and acquired resistance to targeted therapies are some of the issues that limit the potential of genomics-driven targeted therapies. Further, responses to targeting tend to vary across tumors and within a tumor depending on the treatment context. Biopsies at multiple time points, rational combination therapies, and basket trial designs can help address some of these issues. As oncology is migrating to a more molecularly matched therapy paradigm, a strong collaboration between basic scientists, molecular pathologists, bioinformaticians, and oncologists is paramount in an effort to identify novel cancer therapies that lead to improvement in patient survival. e180 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
OPPORTUNITIES AND CHALLENGES FOR CLINICAL TUMOR SEQUENCING ACKNOWLEDGMENT Thanks to Cassie Hershberger for administrative support. Thanks to ASCO for organizing this education session. Disclosures of Potential Conflicts of Interest Relationships are considered self-held and compensated unless otherwise noted. Relationships marked “L” indicate leadership positions. Relationships marked “I” are those held by an immediate family member; those marked “B” are held by the author and an immediate family member. Institutional relationships are marked “Inst.” Relationships marked “U” are uncompensated. Employment: None. Leadership Position: None. Stock or Other Ownership Interests: Sameek Roychowdhury, Johnson and Johnson (I). Honoraria: None. Consulting or Advisory Role: Michael F. Berger, Cancer Genetics, Inc. Speakers’ Bureau: None. Research Funding: Sameek Roychowdhury, Ariad Pharmaceuticals, Novartis. Patents, Royalties, or Other Intellectual Property: None. Expert Testimony: None. Travel, Accommodations, Expenses: None. Other Relationships: None. References 1. Weiss GJ, Liang WS, Izatt T, et al. Paired tumor and normal whole genome sequencing of metastatic olfactory neuroblastoma. PLoS One. 2012;7:e37029. 2. NCT01670877. Neratinib in Metastatic HER2 Non-amplifıed But HER2 Mutant Breast Cancer. https://clinicaltrials.gov/ct2/show/NCT01670877. Accessed February 8, 2015. 3. Welch JS, Westervelt P, Ding L, et al. Use of whole-genome sequencing to diagnose a cryptic fusion oncogene. JAMA. 2011;305:1577-1584. 4. Roychowdhury S, Iyer MK, Robinson DR, et al. Personalized oncology through integrative high-throughput sequencing: a pilot study. Sci Transl Med. 2011;3:111ra121. 5. Link DC, Schuettpelz LG, Shen D, et al. Identifıcation of a novel TP53 cancer susceptibility mutation through whole-genome sequencing of a patient with therapy-related AML. JAMA. 2011;305:1568-1576. 6. Jones SJ, Laskin J, Li YY, et al. Evolution of an adenocarcinoma in response to selection by targeted kinase inhibitors. Genome Biol. 2010;11: R82. 7. Frampton GM, Fichtenholtz A, Otto GA, et al. Development and validation of a clinical cancer genomic profıling test based on massively parallel DNA sequencing. Nat Biotechnol. 2013;31:1023-1031. 8. Xuan J, Yu Y, Qing T, et al. Next-generation sequencing in the clinic: promises and challenges. Cancer Lett. 2013;340:284-295. 9. Van Allen EM, Wagle N, Stojanov P, et al. Whole-exome sequencing and clinical interpretation of formalin-fıxed, paraffın-embedded tumor samples to guide precision cancer medicine. Nat Med. 2014;20:682-688. 10. Shyr D, Liu Q. Next generation sequencing in cancer research and clinical application. Biol Proced Online. 2013;15:4. 11. Gerlinger M, Rowan AJ, Horswell S, et al. Intratumor heterogeneity and branched evolution revealed by multiregion sequencing. N Engl J Med. 2012;366:883-892. 12. Everett JN, Gustafson SL, Raymond VM. Traditional roles in a nontraditional setting: genetic counseling in precision oncology. J Genet Couns. 2014;23:655-660. 13. Cottrell CE, Al-Kateb H, Bredemeyer AJ, et al. Validation of a nextgeneration sequencing assay for clinical molecular oncology. J Mol Diagn. 2014;16:89-105. 14. Pritchard CC, Salipante SJ, Koehler K, et al. Validation and implementation of targeted capture and sequencing for the detection of actionable mutation, copy number variation, and gene rearrangement in clinical cancer specimens. J Mol Diagn. 2014;16:56-67. 15. Wagle N, Berger MF, Davis MJ, et al. High-throughput detection of actionable genomic alterations in clinical tumor samples by targeted, massively parallel sequencing. Cancer Discov. 2012;2:82-93. 16. Won HH, Scott SN, Brannon AR, et al. Detecting somatic genetic alterations in tumor specimens by exon capture and massively parallel sequencing. J Vis Exp. 2013;e50710. 17. Lipson D, Capelletti M, Yelensky R, et al. Identifıcation of new ALK and RET gene fusions from colorectal and lung cancer biopsies. Nat Med. 2012;18:382-384. 18. Takeuchi K, Soda M, Togashi Y, et al. RET. ROS1 and ALK fusions in lung cancer. Nat Med. 2012;18:378-381. 19. Roberts KG, Li Y, Payne-Turner D, et al. Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia. N Engl J Med. 2014;371: 1005-1015. 20. Zheng Z, Liebers M, Zhelyazkova B, et al. Anchored multiplex PCR for targeted next-generation sequencing. Nat Med. 2014;20:1479-1484. 21. Qadir MA, Zhan SH, Kwok B, et al. ChildSeq-RNA: a next-generation sequencing-based diagnostic assay to identify known fusion transcripts in childhood sarcomas. J Mol Diagn. 2014;16:361-370. 22. Iyer MK, Niknafs YS, Malik R, et al. The landscape of long noncoding RNAs in the human transcriptome. Nat Genet. Epub 2015 Jan 19. 23. Quinodoz S, Guttman M. Long noncoding RNAs: An emerging link between gene regulation and nuclear organization. Trends Cell Biol. 2014;24:651-663. 24. Garzon R, Marcucci G, Croce CM. Targeting microRNAs in cancer: rationale, strategies and challenges. Nat Rev Drug Discov. 2010;9:775-789. 25. Rosenfeld N, Aharonov R, Meiri E, et al. MicroRNAs accurately identify cancer tissue origin. Nat Biotechnol. 2008;26:462-469. 26. Pentheroudakis G, Pavlidis N, Fountzilas G, et al. Novel microRNAbased assay demonstrates 92% agreement with diagnosis based on clinicopathologic and management data in a cohort of patients with carcinoma of unknown primary. Mol Cancer. 2013;12:57. 27. Sozzi G, Boeri M, Rossi M, et al. Clinical utility of a plasma-based miRNA signature classifıer within computed tomography lung cancer screening: a correlative MILD trial study. J Clin Oncol. 2014;32:768-773. 28. Van Allen EM, Wagle N, Levy MA. Clinical analysis and interpretation of cancer genome data. J Clin Oncol. 2013;31:1825-1833. 29. Tran B, Brown AM, Bedard PL, et al. Feasibility of real time next generation sequencing of cancer genes linked to drug response: results from a clinical trial. Int J Cancer. 2013;132:1547-1555. 30. Levy MA, Lovly CM, Pao W. Translating genomic information into clinical medicine: lung cancer as a paradigm. Genome Res. 2012;22:2101-2108. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e181
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2015 ASCO Annual Meeting Disclosure
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2015 Educational Book Expert Panel
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James Marshall, PhD Roswell Park Ca
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2015 Annual Meeting Supporters* MIS
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David Yurman Corporate Allies Conqu
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CD19 CAR THERAPY FOR ALL FIGURE 1.
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LILENBAUM, LEIGHL, AND NEUBAUER Exp
Page 608 and 609:
LILENBAUM, LEIGHL, AND NEUBAUER tha
Page 610 and 611:
LILENBAUM, LEIGHL, AND NEUBAUER Ref
Page 612 and 613:
BERNARDO H.L. GOULART The Value of
Page 614 and 615:
BERNARDO H.L. GOULART TABLE 1. Expe
Page 616 and 617:
BERNARDO H.L. GOULART every 6 month
Page 618 and 619:
BERNARDO H.L. GOULART lung-cancer/l
Page 620 and 621:
LUNG CANCER Updates in the Multimod
Page 622 and 623:
WOODARD AND JABLONS section, becaus
Page 624 and 625:
WOODARD AND JABLONS mediastinum is
Page 626 and 627:
WOODARD AND JABLONS FIGURE 1. Molec
Page 628 and 629:
NASSER HANNA Current Standards and
Page 630 and 631:
NASSER HANNA At the 2014 ASCO Annua
Page 632 and 633:
NASSER HANNA culty of this task. Va
Page 634 and 635:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 636 and 637:
NOWAKOWSKI AND CZUCZMAN sociated wi
Page 638 and 639:
NOWAKOWSKI AND CZUCZMAN trial is in
Page 640 and 641:
NOWAKOWSKI AND CZUCZMAN TABLE 2. DH
Page 642 and 643:
NOWAKOWSKI AND CZUCZMAN 15. Aragon-
Page 644 and 645:
DAVID W. SCOTT Cell-of-Origin in Di
Page 646 and 647:
DAVID W. SCOTT FIGURE 1. The Origin
Page 648 and 649:
DAVID W. SCOTT FIGURE 2. Immunohist
Page 650 and 651:
DAVID W. SCOTT FIGURE 3. The Lymph2
Page 652 and 653:
DAVID W. SCOTT 10. Shaffer AL 3rd,
Page 654 and 655:
CHEAH, OKI, AND FANALE Novel Treatm
Page 656 and 657:
CHEAH, OKI, AND FANALE an ongoing G
Page 658 and 659:
CHEAH, OKI, AND FANALE a similar me
Page 660 and 661:
CHEAH, OKI, AND FANALE TABLE 3. Sel
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CHEAH, OKI, AND FANALE eral T cell
Page 664 and 665:
CHEAH, OKI, AND FANALE 77. Cairns R
Page 666 and 667:
STEPHEN ANSELL associated with pati
Page 668 and 669:
STEPHEN ANSELL Disclosures of Poten
Page 670 and 671:
MATEOS AND SAN MIGUEL Smoldering Mu
Page 672 and 673:
MATEOS AND SAN MIGUEL years. This f
Page 674 and 675:
MATEOS AND SAN MIGUEL previously me
Page 676 and 677:
MATEOS AND SAN MIGUEL TABLE 2. Risk
Page 678 and 679:
MATEOS AND SAN MIGUEL 30. Rajkumar
Page 680 and 681:
BHUTANI, LANDGREN, AND USMANI of th
Page 682 and 683:
BHUTANI, LANDGREN, AND USMANI bette
Page 684 and 685:
BHUTANI, LANDGREN, AND USMANI fıne
Page 686 and 687:
BHUTANI, LANDGREN, AND USMANI FIGUR
Page 688 and 689:
BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
Page 692 and 693:
MOREAU AND TOUZEAU other effıcacy
Page 694 and 695:
MOREAU AND TOUZEAU was able to indu
Page 696 and 697:
MOREAU AND TOUZEAU Group consensus
Page 698 and 699:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 700 and 701:
MANAGEMENT OF CLL Up-Front Manageme
Page 702 and 703:
MANAGEMENT OF CLL than 17p-/TP53mut
Page 704 and 705:
MANAGEMENT OF CLL could be associat
Page 706 and 707:
MANAGEMENT OF CLL tion by nonmalign
Page 708 and 709:
MANAGEMENT OF CLL fludarabine and c
Page 710 and 711:
MANAGEMENT OF CLL lymphocytic leuke
Page 712 and 713:
PROGNOSTIC FACTORS AND ADJUVANT RAD
Page 714 and 715:
Page 716 and 717:
Page 718 and 719:
MERKEL CELL CARCINOMA Merkel Cell C
Page 720 and 721:
MERKEL CELL CARCINOMA tions in PIK3
Page 722 and 723:
MERKEL CELL CARCINOMA treating MCC
Page 724 and 725:
MERKEL CELL CARCINOMA 32. Leonard J
Page 726 and 727:
MELANOMA/SKIN CANCERS Locoregional
Page 728 and 729:
PERFUSION AND INFUSION IN THE ERA O
Page 730 and 731:
Page 732 and 733:
Page 734 and 735:
NEOADJUVANT THERAPY OF MELANOMA Neo
Page 736 and 737:
NEOADJUVANT THERAPY OF MELANOMA TAB
Page 738 and 739:
NEOADJUVANT THERAPY OF MELANOMA ity
Page 740 and 741:
NEOADJUVANT THERAPY OF MELANOMA 4.
Page 742 and 743:
MELANOMA/SKIN CANCERS Targeted Mole
Page 744 and 745:
SULLIVAN ET AL FIGURE 1. Relevant S
Page 746 and 747:
SULLIVAN ET AL Resistance to BRAF i
Page 748 and 749:
SULLIVAN ET AL TABLE 1. Clinical Tr
Page 750 and 751:
SULLIVAN ET AL 17. Halait H, Demart
Page 752 and 753:
SULLIVAN ET AL NRAS-mutant melanoma
Page 754 and 755:
KLEPIN, RODIN, AND HURRIA Treating
Page 756 and 757:
KLEPIN, RODIN, AND HURRIA plication
Page 758 and 759:
KLEPIN, RODIN, AND HURRIA plan was
Page 760 and 761:
KLEPIN, RODIN, AND HURRIA patient-s
Page 762 and 763:
KLEPIN, RODIN, AND HURRIA 62. Blanc
Page 764 and 765:
PERIPHERAL NEUROTOXICITY IN CANCER
Page 766 and 767:
Page 768 and 769:
Page 770 and 771:
Page 772 and 773:
PARTRIDGE, JACOBSEN, AND ANDERSEN C
Page 774 and 775:
PARTRIDGE, JACOBSEN, AND ANDERSEN c
Page 776 and 777:
PARTRIDGE, JACOBSEN, AND ANDERSEN w
Page 778 and 779:
PARTRIDGE, JACOBSEN, AND ANDERSEN v
Page 780 and 781:
LESLIE R. SCHOVER Sexual Healing in
Page 782 and 783:
LESLIE R. SCHOVER tinuous ADT in pr
Page 784 and 785:
LESLIE R. SCHOVER 12. Potosky AL, H
Page 786 and 787:
CATHERINE H. VAN POZNAK TABLE 1. Wo
Page 788 and 789:
CATHERINE H. VAN POZNAK (tamoxifen,
Page 790 and 791:
CATHERINE H. VAN POZNAK TABLE 3. FD
Page 792 and 793:
CATHERINE H. VAN POZNAK premenopaus
Page 794 and 795:
SHARI GOLDFARB KEY POINTS Brea
Page 796 and 797:
SHARI GOLDFARB and friction with va
Page 798 and 799:
SHARI GOLDFARB importance both duri
Page 800 and 801:
PATIENT AND SURVIVOR CARE Moving Su
Page 802 and 803:
MAYER ET AL TABLE 1. Quality Metric
Page 804 and 805:
MAYER ET AL to enhance the quality
Page 806 and 807:
MAYER ET AL FIGURE 2. (A) Infertili
Page 808 and 809:
MAYER ET AL efıcial suggests that
Page 810 and 811:
PATIENT AND SURVIVOR CARE The Chall
Page 812 and 813:
BRUERA AND PAICE Choice of Opioid a
Page 814 and 815:
BRUERA AND PAICE toxicity and proce
Page 816 and 817:
BRUERA AND PAICE effective. Basic s
Page 818 and 819:
PEDIATRIC ONCOLOGY Real-Time Molecu
Page 820 and 821:
CARROLL, RAETZ, AND MEYER KEY POINT
Page 822 and 823:
CARROLL, RAETZ, AND MEYER most are
Page 824 and 825:
CARROLL, RAETZ, AND MEYER markers a
Page 826 and 827:
PEDIATRIC ONCOLOGY Translating Surv
Page 828 and 829:
REDUCING THE BURDEN OF LATE EFFECTS
Page 830 and 831:
Page 832 and 833:
Page 834 and 835:
Page 836 and 837:
PROFESSIONAL DEVELOPMENT The Challe
Page 838 and 839:
ADVANCES IN WEBSITE INFORMATION RES
Page 840 and 841:
Page 842 and 843:
Page 844 and 845:
Page 846 and 847:
COMMUNICATION AND TECHNOLOGY: IT’
Page 848 and 849:
Page 850 and 851:
Page 852 and 853:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 854 and 855:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 856 and 857:
PROFESSIONAL DEVELOPMENT Trends, An
Page 858 and 859:
CLINICAL ONCOLOGY PRACTICE 2015 FIG
Page 860 and 861:
CLINICAL ONCOLOGY PRACTICE 2015 (6.
Page 862 and 863:
CLINICAL ONCOLOGY PRACTICE 2015 Pro
Page 864 and 865:
ADJUVANT/NEOADJUVANT MEDICAL THERAP
Page 866 and 867:
Page 868 and 869:
Page 870 and 871:
INDICATIONS FOR ADJUVANT RADIATION
Page 872 and 873:
Page 874 and 875:
Page 876 and 877:
Page 878 and 879:
SARCOMA Latest Advances in Systemic
Page 880 and 881:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 882 and 883:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 884 and 885:
RETHINKING TREATMENT FOR CHONDROSAR
Page 886 and 887:
Page 888 and 889:
Page 890 and 891:
Page 892 and 893:
BONE SARCOMAS IN ADULTS local disea
Page 894 and 895:
BONE SARCOMAS IN ADULTS structure a
Page 896 and 897:
SARCOMA Well-Differentiated and Ded
Page 898 and 899:
ABBAS MANJI ET AL ticular region. 7
Page 900 and 901:
ABBAS MANJI ET AL MYXOID (ROUND CEL
Page 902 and 903:
ABBAS MANJI ET AL versus doxorubici
Page 904 and 905:
SHLUSH AND HERSHKOVITZ Clonal Evolu
Page 906 and 907:
SHLUSH AND HERSHKOVITZ FIGURE 1. Ti
Page 908 and 909:
TUMOR BIOLOGY New Strategies to Und
Page 910 and 911:
KNAPP, DHAWAN, AND OSTRANDER in dog
Page 912 and 913:
KNAPP, DHAWAN, AND OSTRANDER TABLE
Page 914 and 915:
KNAPP, DHAWAN, AND OSTRANDER 14. Fe
Page 916 and 917:
SOURBIER, SRINIVASAN, AND LINEHAN M
Page 918 and 919:
SOURBIER, SRINIVASAN, AND LINEHAN F
Page 920 and 921:
SOURBIER, SRINIVASAN, AND LINEHAN T
Page 922:
Author Index Abbas Manji, Gulam ...
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