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MICHAEL W. DEININGER broad range effıcacy of ponatinib must be balanced against its substantial cardiovascular toxicity, which is enhanced by preexisting risk factors such as diabetes, hypercholesterolemia, and hypertension. 54 Failure of ponatinib indicates a patient is a candidate for non-TKI therapies, including omacetaxine, a clinical trial, or HSCT. 44 This is particularly true for patients with compound mutations that include T315I as one component and may confer resistance to all currently approved TKIs. 28 Dense qPCR monitoring is critical for patients in whom second-generation TKIs failed, and those in whom multiple TKIs have failed. When to proceed to HSCT in a patient with CP-CML is a diffıcult clinical decision that must take into account the transplant risk as well as the risk of progression to AP/BC-CML. It is good clinical practice to refer any transplant-eligible patient with progression on fırstline therapy to a transplant center for an initial evaluation and preliminary clarifıcation of donor options. Progression to Accelerated-Phase/Blastic-Phase Chronic Myeloid Leukemia Patients who progress to AP/BP-CML are treated with the appropriate TKI, taking into account prior TKI exposure history and BCR-ABL1 mutation status. Given the limited therapeutic options, more TKI toxicity is acceptable. Decisions whether or not to combine TKI salvage with chemotherapy must be individualized based on performance status and the availability of allogeneic stem cell transplant as a potentially curative salvage strategy. 19 Given the absence of controlled studies in this fortunately rare patient population, the value of adding chemotherapy is not completely clear, particularly in patients with myeloid transformation. All eligible patients should be offered an allogeneic stem cell transplant, and avoiding unnecessary toxicity in potential transplant patients is an important consideration. ALLOGENEIC STEM CELL TRANSPLANTATION Allogeneic HSCT was the fırst treatment modality that restored Ph-negative hematopoiesis and induced durable responses. 55 Before the introduction of imatinib, allografting was recommended to all eligible patients and even today it is still regarded as the only therapy with curative potential. Only one study prospectively compared allotransplant versus drug therapy. Newly diagnosed patients with CML-CP were biologically randomly assigned to a matched sibling transplant versus IFN-based drug therapy, the best nontransplant treatment available when the trial was initiated. 56 Patients managed with drug therapy had superior survival, with the biggest difference observed in low-risk patients. After approximately 8 years, the survival curves crossed, suggesting that transplant would be superior in the long-term if IFN was the alternative. However, given the effıcacy of TKIs in the fırst-line setting, and that early transplant-related mortality is clearly higher than the risk of early disease progression, allotransplant is no longer justifıable in newly diagnosed patients with CML-CP, except in unusual circumstances. 57 Risk scores for allografting in CML were developed by the European Group for Blood and Marrow Transplantation (EBMT) in the pre-imatinib era and identifıed disease duration of longer than 12 months, more advanced disease, higher age, unrelated donor type, and the combination of a male recipient with a female donor as adverse prognostic factors. 58 Disease phase had the greatest effect on outcome. Although somewhat historic, the EBMT score is still useful for prognostication. There is consensus that allotransplant should be offered to all patients with progression to AP/BP. A more individualized approach is required for patients in whom dasatinib or nilotinib have failed in chronic phase, given that ponatinib is effective, albeit at the cost of cardiovascular toxicity. 54 Fortunately, there is no evidence that imatinib or other TKIs before allografting negatively affect the outcome. On the contrary, for unknown reasons, imatinib before allotransplant seems to reduce the risk of chronic graft-versus-host disease and possibly relapse risk. 59-61 Results from the German CML study group reassert the importance of transplanting patients while they are still in chronic phase: 3-year OS was 91% for patients transplanted in CP after imatinib failed versus 59% for patients transplanted in AP/BP. 62 There is an emerging consensus that bone marrow is preferred over peripheral blood stem cells in patients with CML-CP, in whom graft-versus-host disease is a greater concern than disease control. 63 This assessment is different for patients with transformation to AP/BP, even if they have achieved a second chronic phase. High relapse–risk patients should receive a TKI post-transplant; BCR-ABL1 mutation analysis at the time of resistance will help match the optimal TKI to individual patients. Given the high median age at the time of diagnosis, many patients will be eligible only for reduced intensity conditioning regimens. An in-depth discussion of the various conditioning regimens, selection of bone marrow versus peripheral blood stem cells, and post-transplant immunosuppression is presented elsewhere. PERSPECTIVE Despite the unparalleled success of TKI in CML, progression during fırst-line TKI therapy, and transformation to accelerated- or blastic-phase continue to carry a poor prognosis. Although BCR-ABL1 mutations are a well-established mechanism of TKI resistance, many cases of clinical resistance remained mechanistically unexplained and are thought to be a result of activation of alternative signaling pathways. In these patients, salvage therapies are currently nonspecifıc. The hope is that diverse upstream pathways may activate a limited set of downstream effector molecules, thus providing an opportunity for rationally targeted therapies that are applicable to a wider population of patients. Early identifıcation of patients with TKI failure or at risk of transformation is critical, so that therapy can be adjusted in a timely fashion to maximize the chances of successful salvage therapy. Despite the introduction of new TKIs such as ponatinib, the prediction is that allogeneic stem cell transplant will retain its position as the salvage therapy of choice for patients who progress to AP/BC-CML. e386 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
RECOGNIZING AND MANAGING HIGH-RISK CML 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: None. Honoraria: Michael W. Deininger, ARIAD, BMS, Incyte, Novartis, Pfizer. Consulting or Advisory Role: Michael W. Deininger, ARIAD, BMS, Incyte, Novartis, Pfizer. Speakers’ Bureau: None. Research Funding: Michael W. Deininger, BMS (Inst), Celgene (Inst), Incyte (Inst), Novartis (Inst). Patents, Royalties, or Other Intellectual Property: None. Expert Testimony: Michael W. Deininger, BMS. Travel, Accommodations, Expenses: Michael W. Deininger, ARIAD, BMS, Novartis, Pfizer. Other Relationships: None. References 1. Tanaka K, Takechi M, Hong J, et al. 9;22 translocation and bcr rearrangements in chronic myelocytic leukemia patients among atomic bomb survivors. J Radiat Res. 1989;30:352-358. 2. Schmidt M, Rinke J, Schäfer V, et al. Molecular-defıned clonal evolution in patients with chronic myeloid leukemia independent of the BCR- ABL status. Leukemia. 2014;28:2292-2299. 3. Deininger MW, Goldman JM, Melo JV. The molecular biology of chronic myeloid leukemia. Blood. 2000;96:3343-3356. 4. Kantarjian HM, Deisseroth A, Kurzrock R, et al. Chronic myelogenous leukemia: a concise update. Blood. 1993;82:691-703. 5. Talpaz M, Silver RT, Druker BJ, et al. Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. Blood. 2002;99: 1928-1937. 6. Baccarani M, Deininger MW, Rosti G, et al. European LeukemiaNet recommendations for the management of chronic myeloid leukemia: 2013. Blood. 2013;122:872-884. 7. Sokal JE, Cox EB, Baccarani M, et al. Prognostic discrimination in “good-risk” chronic granulocytic leukemia. Blood. 1984;63:789-799. 8. Hasford J, Pfırrmann M, Hehlmann R, et al. A new prognostic score for survival of patients with chronic myeloid leukemia treated with interferon alfa. Writing Committee for the Collaborative CML Prognostic Factors Project Group. J Natl Cancer Inst. 1998;90:850-858. 9. Hasford J, Baccarani M, Hoffmann V, et al. Predicting complete cytogenetic response and subsequent progression-free survival in 2060 patients with CML on imatinib treatment: the EUTOS score. Blood. 2011; 118:686-692. 10. Jabbour E, Cortes J, Nazha A, et al. EUTOS score is not predictive for survival and outcome in patients with early chronic phase chronic myeloid leukemia treated with tyrosine kinase inhibitors: a single institution experience. Blood. 2012;119:4524-4526. 11. McWeeney SK, Pemberton LC, Loriaux MM, et al. A gene expression signature of CD34 cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib. Blood. 2010;115:315-325. 12. Yong AS, Szydlo RM, Goldman JM, et al. Molecular profıling of CD34 cells identifıes low expression of CD7, along with high expression of proteinase 3 or elastase, as predictors of longer survival in patients with CML. Blood. 2006;107:205-212. 13. Radich JP, Dai H, Mao M, et al. Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad SciUSA.2006;103:2794-2799. 14. Fabarius A, Leitner A, Hochhaus A, et al. Impact of additional cytogenetic aberrations at diagnosis on prognosis of CML: long-term observation of 1151 patients from the randomized CML Study IV. Blood. 2011; 118:6760-6768. 15. Eiring AM, Deininger MW. Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia. Genome Biol. 2014; 15:461. 16. Perrotti D, Cesi V, Trotta R, et al. BCR-ABL suppresses C/EBPalpha expression through inhibitory action of hnRNP E2. Nat Genet. 2002;30: 48-58. 17. Eiring AM, Harb JG, Neviani P, et al. miR-328 functions as an RNA decoy to modulate hnRNP E2 regulation of mRNA translation in leukemic blasts. Cell. 2010;140:652-665. 18. Cortes J, Kim DW, Raffoux E, et al. Effıcacy and safety of dasatinib in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blast phase. Leukemia. 2008;22:2176-2183. 19. Hehlmann R. How I treat CML blast crisis. Blood. 2012;120:737-747. 20. La Rosée P, Deininger MW. Resistance to imatinib: mutations and beyond. Semin Hematol. 2010;47:335-343. 21. Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI- 571 cancer therapy caused by BCR-ABL gene mutation or amplifıcation. Science. 2001;293:876-880. 22. Schindler T, Bornmann W, Pellicena P, et al. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science. 2000;289:1938- 1942. 23. Deininger M, Buchdunger E, Druker BJ. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood. 2005;105: 2640-2653. 24. Tokarski JS, Newitt JA, Chang CY, et al. The Structure of dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Cancer Res. 2006;66:5790-5797. 25. Bradeen HA, Eide CA, O’Hare T, et al. Comparison of imatinib mesylate, dasatinib (BMS-354825), and nilotinib (AMN107) in an N-ethyl- N-nitrosourea (ENU)-based mutagenesis screen: high effıcacy of drug combinations. Blood. 2006;108:2332-2338. 26. Azam M, Latek RR, Daley GQ. Mechanisms of autoinhibition and STI- 571/imatinib resistance revealed by mutagenesis of BCR-ABL. Cell. 2003;112:831-843. 27. von Bubnoff N, Veach DR, van der Kuip H, et al. A cell-based screen for resistance of Bcr-Abl-positive leukemia identifıes the mutation pattern for PD166326, an alternative Abl kinase inhibitor. Blood. 2005;105: 1652-1659. 28. Zabriskie MS, Eide CA, Tantravahi SK, et al. BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia. Cancer Cell. 2014;26:428-442. 29. Müller MC, Cortes JE, Kim DW, et al. Dasatinib treatment of chronicphase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations. Blood. 2009;114:4944-4953. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e387
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American Society of Clinical Oncolo
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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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INDUSTRY AND ONCOLOGY KEY POINTS F
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INDUSTRY AND ONCOLOGY 42. World Hea
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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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