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MICHAEL W. DEININGER 30. Hughes T, Saglio G, Branford S, et al. Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. J Clin Oncol. 2009;27:4204-4210. 31. Apperley JF. Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol. 2007;8:1018-1029. 32. O’Hare T, Eide CA, Deininger MW. Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia. Blood. 2007;110:2242-2249. 33. O’Hare T, Zabriskie MS, Eiring AM, et al. Pushing the limits of targeted therapy in chronic myeloid leukaemia. Nat Rev Cancer. 2012;12:513- 526. 34. Donato NJ, Wu JY, Stapley J, et al. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood. 2003;101:690-698. 35. Warsch W, Kollmann K, Eckelhart E, et al. High STAT5 levels mediate imatinib resistance and indicate disease progression in chronic myeloid leukemia. Blood. 2011;117:3409-3420. 36. Burchert A, Wang Y, Cai D, et al. Compensatory PI3-kinase/Akt/mTor activation regulates imatinib resistance development. Leukemia. 2005; 19:1774-1782. 37. Aceves-Luquero CI, Agarwal A, Callejas-Valera JL, et al. ERK2, but not ERK1, mediates acquired and “de novo” resistance to imatinib mesylate: implication for CML therapy. PLoS One. 2009;4:e6124. 38. Gioia R, Leroy C, Drullion C, et al. Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells. Blood. 2011;118:2211-2221. 39. Wang Y, Cai D, Brendel C, et al. Adaptive secretion of granulocytemacrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL progenitors via JAK-2/STAT-5 pathway activation. Blood. 2007;109:2147-2155. 40. Weisberg E, Wright RD, McMillin DW, et al. 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RISK STRATIFICATION IN PATIENTS WITH MPN From Philadelphia-Negative to JAK2-Positive: Effect of Genetic Discovery on Risk Stratification and Management Naveen Pemmaraju, MD, and Alison R. Moliterno, MD OVERVIEW The 2005 discovery of the JAK2 mutation redefined the diagnosis and natural history of myeloproliferative neoplasms (MPNs). Most importantly, this improvement in the pathobiologic conceptualization has focused our evolution of this field from being defined as what it is not (e.g., Philadelphia [Ph]-negative) to what it is (e.g., JAK2-positive, CALR-positive) in the majority of MPN cases. In the ensuing 10 years, the field has experienced a paradigm shift in terms of understanding of the biologic basis of the development of MPNs, an explosion of knowledge of the genetics of MPNs, and has translated disease knowledge into effective targeted therapies. With greater uniformity and agreement on the diagnosis and differences among the individual MPNs, augmented by improved cytogenetic and molecular classification, attention has turned now to addressing the need for uniformity in risk stratification of patients in the clinic for both disease complications and disease transformation. This article will highlight the developments in the field with regard to risk stratification and prognostication in MPNs with focus on the clinical aspects of the patient who presents with either essential thrombocytosis (ET), polycythemia vera (PV), or myelofibrosis (MF). Myeloproliferative neoplasms represent a family of clonal hematopoietic stem cell disorders that exhibit a wide variety of clinical, biologic, and phenotypic heterogeneity. MPNs serve as the model of acquired somatic genetic lesions as the causal basis of cancer (so-called drivers), from the fırst genetic lesion ascribed to cancer, the Philadelphia (Ph) chromosome in chronic myelogenous leukemia (CML), to the more recent discoveries of lesions in JAK2, MPL, and CALR in what were previously called Ph-chromosome–negative MPN. MPNs cause a substantial amount of morbidity and mortality during a patient’s lifetime, including increased cardiovascular, thrombotic, and hemorrhagic events, and increased lifetime risk for transformation to acute myeloid leukemia (AML), bone marrow failure, or MF. In the 10 years since the JAK2V617F discovery, the MPN fıeld has experienced a profound increase in both clinical and basic research with regard to further understanding of the pathobiologic basis for the disease, especially illustrated by the more recent discoveries of diagnostic and prognostic signifıcance of JAK2, MPL, CALR, ASXL1, and other molecular markers. Importantly, genetic discovery in CML and MPN have been translated to effective, targeted therapy, capable of altering the natural history of the MPN. 1-6 This review will focus on the most recent advances in risk stratifıcation of the patient with MPN, and how risk stratifıcation can be translated to disease- and patient-specifıc therapy. ACQUIRED SOMATIC MUTATION IN THE MPN: IDENTIFICATION OF CAUSAL LESIONS Chronic myeloproliferative disorders (MPDs) were recognized as clinical entities in the 19th century, but the 20th century brought precise clinical classifıcation and their genetic basis into being. The 21st century has, and continues to, unravel their causal genetic basis. The primary nature of bone marrow’s overproduction was compared with that of leukemia, and both CML and PV were considered as neoplasms of the hematopoietic tissue. William Dameshek theorized that these entities might be driven by a shared stimulus intrinsic to the marrow itself, and coined the term MPDs. 7 The identifıcation of the Ph chromosome as specifıc to CML and not to the rest of the MPD class was not only an advance in disease classifıcation within MPNs, but, ultimately, confırmed the causal association of an acquired genetic lesion in the generation of human cancer. 8 Given the similarities of Ph-chromosome–negative MPN to Ph-positive–MPN (stem cell basis, overproduction of mature myeloid elements, tendency to evolve to MF or acute leukemia), lesions in tyrosine kinase pathways critical to erythropoietin, thrombopoietin, and granulocyte-colony stimulating factor signal transduction were investigated. Advances in DNA sequencing technology led several investigators to resequence the JAK2 gene in patients with PV because of its specifıc activity in primary PV cells, its identity as a ty- From the Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD; the Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Alison R. Moliterno, MD, Department of Medicine, The Johns Hopkins Hospital, 720 Rutland Ave., Ross Research Building Room 1025, Baltimore, MD 21205; email: amoliter@jhmi.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK 139
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Controversies in Neoadjuvant Therap
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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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EGIDIO DEL FABBRO tion of precachex
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GYNECOLOGIC CANCER Cervical Cancer
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CHEMOTHERAPY FOR PATIENTS WITH BMOC
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CANCER CARE QUALITY: CURRENT STATE
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Page 592 and 593: GERBER, PAIK, AND DOWLATI squamous
Page 594 and 595: GERBER, PAIK, AND DOWLATI FIGURE 2.
Page 596 and 597: GERBER, PAIK, AND DOWLATI TABLE 1.
Page 598 and 599: GERBER, PAIK, AND DOWLATI gression
Page 600 and 601:
GERBER, PAIK, AND DOWLATI Disclosur
Page 602 and 603:
GERBER, PAIK, AND DOWLATI enzyme in
Page 604 and 605:
GERBER, PAIK, AND DOWLATI receptor
Page 606 and 607:
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
Page 662 and 663:
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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