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BONE SARCOMAS IN ADULTS structure and calcifıcation in the soft tissue, so combining the CT images from the PET-CT with the MRI gives the best overall assessment. Until recently, new agents with clear activity in the treatment of metastatic osteosarcoma have not been identifıed in the past 2 decades. Anecdotal evidence for the effıcacy of gemcitabine with or without docetaxel was not confırmed in a clinical trial. 25 Recently, however, Grignani et al 26 reported a study from the Italian Sarcoma Group using the combination of sorafenib and everolimus. 26 The median progression-free survival (PFS) was 5 months, with a 6-month PFS rate of 45% despite an objective response rate of only 10%. It has long been known that primary osteosarcoma may not shrink when it responds. The use of PFS as an endpoint in this study is novel and important, and it throws into question some of the negative clinical trials of the past. 25 EWING SARCOMA It is even harder to fınd studies on Ewing sarcoma in adults than it is to fınd studies on osteosarcoma. Our initial data on the treatment of Ewing sarcoma in adults is, unfortunately, published only in abstract form, 27 and the logistics of transition from paper to electronic medical records and fılm to digital images makes a new review of the data cumbersome at best. The major lessons from our initial patients treated with VAdriaC (vincristine, doxorubicin, and cyclophosphamide) or CyVADIC (cyclophosphamide, vincristine, doxorubicin, and dacarbazine) were that any residual viable tumor in excess of scattered cells carried a high risk of recurrence and that, the more doxorubicin given, the better the patients faired. Therefore, it has become our practice to add additional postoperative chemotherapy with an alternative regimen to any patient who has less than 99% tumor necrosis. The role of ifosfamide, questioned in the treatment of osteosarcoma, is well established in the treatment of Ewing sarcoma in pediatrics. 2,3 Because ifosfamide is one of the most active agents in the treatment of adult sarcomas, we have considerable experience in its use. The standard soft tissue sarcoma chemotherapy regimen is doxorubicin and ifosfamide, which we have studied extensively. 28 Ifosfamide is superior to cyclophosphamide in the treatment of sarcomas, 29 so we saw no reason to alternate cyclophosphamide with ifosfamide and have thus adopted VAI as our primary treatment regimen for Ewing sarcoma by simply adding vincristine to our standard soft tissue sarcoma regimen. We give 2 mg of vincristine on day 1, 75 to 90 mg/m 2 of doxorubicin as a 72-hour infusion, and 2.5 g/m 2 of ifosfamide over 3 hours daily for four doses. We reviewed the data on a series of 24 patients with primary Ewing sarcoma of bone treated with VAI. The median age was 23 (range, 17 to 54); 17% of patients were younger than 20, and 17% of patients were older than 30. The 5-year CDFS was 70%, and all relapses but one occurred within 1 year of treatment. The primary sites of relapse were local recurrence in bone and adjacent soft tissue, with only a single case of pulmonary metastasis as the fırst site. Two patients experienced relapse during induction therapy. No patient who experienced relapse survived. Twenty of the 24 patients underwent surgery after induction chemotherapy. Eleven patients (55%) who had more than 95% tumor necrosis in the resected specimen had an 80% 5-year CDFS compared with a 44% 5-year CDFS for the nine patients (45%) who had less than 95% tumor necrosis. All patients with more than scattered residual tumor cells after induction therapy underwent variable consolidation chemotherapy, including high-dose ifosfamide, ifosfamide/etoposide (IE), and irinotecan/temozolomide with or without vincristine. Although this is a small series, the results compare favorably with the commonly used regimen of alternating VAdriaC and IE used in the pediatric literature, for which event-free survival for patients older than age 18 was 44% 2 and was 47% in the study of compressed-interval dosing. 3 MRI is the best modality to defıne an anatomic abnormality within bone or bone marrow. A screening MRI of the spine and pelvis can detect subtle metastatic sites missed by other imaging modalities, even PET-CT, or blind bone marrow biopsies. PET-CT is the best imaging modality to assess response to therapy, but it is not as critical as in osteosarcoma, because Ewing sarcoma tends to shrink or disappear as it responds. New approaches to the therapy of Ewing sarcoma with insulin-like growth factor 1 receptor (IGF-1R) blockade with 30 or without 31 mammalian target of rapamycin inhibitors hold some promise, but thus far have been effective in only a minority of patients. Unfortunately, the IGF-1R target has relatively little interest to most pharmaceutical companies, and further studies to select the subset of patients who might benefıt most have been stymied by the lack of drug supply and pharmaceutical support. Other new approaches, interesting from a theoretical point of view, have yet to undergo formal study. CONCLUSION Treatment of primary bone tumors in adults presents challenges and opportunities. The fırst challenge is fınding effective therapy for chondrosarcomas. These tumors are like the gastrointestinal stromal tumors of the 1990s. We have no medical treatment. There are some interesting targets. How do we turn it around? For giant cell tumor of bone, we have a wonderful new agent, but is it curative? How long does therapy need to continue? How can we take advantage of the great activity of denosumab to design better treatments for the future? In treating osteosarcoma and Ewing sarcoma in adults, we do not do as well as our pediatric colleagues, perhaps because younger patients can tolerate more intensive chemotherapy and perhaps because of the differing mix of variant histologies. The VAI regimen for Ewing sarcoma seems promising, but formal studies and larger numbers will be required. The tragedy of near certain death with relapse in Ewing sarcoma needs to be addressed with better strategies, perhaps aimed at directly inhibiting the effects of its causative translocation. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e659
BENJAMIN ET AL 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: Robert S. Benjamin, Express Scripts (I), Gilead Sciences (I), Johnson and Johnson (I), Merck Serono (I), Pfizer (I). Honoraria: None. Consulting or Advisory Role: Shreyaskumar Patel, Novartis, Johnson & Johnson/Janssen Research & Development, CytRx Corp., EMD Serono, Daiichi Sankyo. Speakers’ Bureau: None. Research Funding: Shreyaskumar Patel, Johnson & Johnson/Janssen R&D, Morphotek, Eisai, PharmaMar. Patents, Royalties, or Other Intellectual Property: None. Expert Testimony: None. Travel, Accommodations, Expenses: Robert S. Benjamin, PharmaMar. Other Relationships: None. References 1. Longhi A, Errani C, Gonzales-Arabio D, et al. Osteosarcoma in patients older than 65 years. J Clin Oncol. 2008;26:5368-5373. 2. Grier HE, Krailo MD, Tarbell NJ, et al. Addition of ifosfamide and etoposide to standard chemotherapy for Ewing’s sarcoma and primitive neuroectodermal tumor of bone. N Engl J Med. 2003;348:694-701. 3. Womer RB, West DC, Krailo MD, et al. Randomized controlled trial of interval-compressed chemotherapy for the treatment of localized Ewing sarcoma: a report from the Children’s Oncology Group. J Clin Oncol. 2012;30: 4148-4154. 4. Bovée J, Hogendoorn PCW, Wunder JS, et al. Cartilage tumours and bone development: molecular pathology and possible therapeutic targets. Nat Rev Cancer. 2010;10:481-488. 5. Tiet TD, Hopyan S, Nadesan P, et al. Constitutive hedgehog signaling in chondrosarcoma up-regulates tumor cell proliferation. Am J Path. 2006; 168:321-330. 6. Italiano A, Le Cesne A, Bellera C, et al. GDC-0449 in patients with advanced chondrosarcomas: a French Sarcoma Group/US and French National Cancer Institute single-arm phase II collaborative study. Ann Oncol. 2013;24:2922-2926. 7. Amary MF, Bacsi K, Maggiani F, et al. IDH1 and IDH2 mutations are frequent events in central chondrosarcoma and central and periosteal chondromas but not in other mesenchymal tumours. J Pathol. 2011;224:334-343. 8. Johnson S, Têtu B, Ayala AG, et al. Chondrosarcoma with additional mesenchymal component (dedifferentiated chondrosarcoma). I. A clinicopathologic study of 26 cases. Cancer. 1986;58:278-286. 9. Benjamin RS, Chu P, Patel SR, et al. Dedifferentiated chondrosarcoma: a treatable disease. Proc Amer Assoc Cancer Res. 1995;36:243a. 10. Italiano A, Mir O, Cioffı A, et al. Advanced chondrosarcomas: role of chemotherapy and survival. Ann Oncol. 2013;24:2916-2922. 11. Dahlin DC. Caldwell Lecture. Giant cell tumor of bone: highlights of 407 cases. AJR Am J Roentgenol. 1985;144:955-960. 12. Eckardt JJ, Grogan TJ. Giant cell tumor of bone. Clin Orthop. 1986;204:45-58. 13. Wallace S, Granmayeh M, deSantos LA, et al. Arterial occlusion of pelvic bone tumors. Cancer. 1979;43:322-328. 14. Lin PP, Guzel VB, Moura MF, et al. Long-term follow-up of giant cell tumor of the sacrum treated with selective arterial embolization. Cancer. 2002;95: 1317-1325. 15. Benjamin RS, Patel SR, Gutterman JU, et al. Interferon alfa-2b as antiangiogenesis therapy of giant cell tumors of bone: implications for the study of newer angiogenesis-inhibitors. Proc Am Soc Clin Oncol. 1999;18:548a. 16. Kaban LB, Troulis MJ, Ebb D, et al. Antiangiogenic therapy with interferon alpha for giant cell lesions of the jaws. J Oral Maxillofac Surg. 2002;60:1103-1111. 17. Thomas DM. RANKL, denosumab, and giant cell tumor of bone. Curr Opin Oncol. 2012;24:397-403. 18. Thomas D, Henshaw R, Skubitz K, et al. Denosumab in patients with giant-cell tumour of bone: an open-label, phase 2 study. Lancet Oncol. 2010;11:275-280. 19. Chawla S, Henshaw R, Seeger L, et al. Safety and effıcacy of denosumab for adults and skeletally mature adolescents with giant cell tumour of bone: interim analysis of an open-label, parallel-group, phase 2 study. Lancet Oncol. 2013;14:901-908. 20. Raymond AK, Chawla SP, Carrasco CH, et al. Osteosarcoma chemotherapy effect: a prognostic factor. Semin Diagn Pathol. 1987;4:212-236. 21. Benjamin RS, Patel SR. Pediatric and adult osteosarcoma: comparison and contrasts in presentation and therapy. Cancer Treat Res. 2009;152:355-363. 22. Marina N, Smeland S, Bielack SS, et al. MAPIE vs MAP as postoperative chemotherapy in patients with a poor response to preoperative chemotherapy for newly-diagnosed osteosarcoma: results from EURAMOS-1. Presented at: CTOS; October 2014; Berlin, Germany. Paper 032. 23. Rosen G, Caparros B, Huvos AG, et al. Preoperative chemotherapy for osteogenic sarcoma: selection of postoperative adjuvant chemotherapy based on the response of the primary tumor to preoperative chemotherapy. Cancer. 1982;49:1221-1230. 24. Bacci G, Picci P, Ferrari S, et al. Primary chemotherapy and delayed surgery for nonmetastatic osteosarcoma of the extremities: results in 164 patients preoperatively treated with high doses of methotrexate followed by cisplatin and doxorubicin. Cancer. 1993;72:3227-3238. 25. Fox E, Patel S, Wathen JK, et al. Phase II study of sequential gemcitabine followed by docetaxel for recurrent Ewing sarcoma, osteosarcoma, or unresectable or locally recurrent chondrosarcoma: results of Sarcoma Alliance for Research through Collaboration Study 003. Oncologist. 2012;17:321. 26. Grignani G, Palmerini E, Ferraresi V, et al. Sorafenib and everolimus combination in unresectable high-grade osteosarcoma progressing after standard treatment: a non-randomized phase II clinical trial from the Italian Sarcoma Group. Lancet Oncol. 2015;16:98-107. 27. PapadopoulosNEJ,BenjaminRS,PlagerC,etal.SkeletalEwingsarcoma(ES)in adults: an over 40 years’ experience. Proc Am Assoc Cancer Res. 1989;30:288a. 28. Patel SR, Vadhan-Raj S, Burgess MA, et al. Results of two consecutive trials of dose-intensive chemotherapy with doxorubicin and ifosfamide in patients with sarcomas. Am J Clin Oncol. 1998;21:317-321. 29. Bramwell VH, Mouridsen HT, Santoro A, et al. Cyclophosphamide versus ifosfamide: fınal report of a randomized phase II trial in adult soft tissue sarcomas. Eur J Cancer Clin Oncol. 1987;23:311-321. 30. Naing A, LoRusso P, Fu S, et al. Insulin growth factor-receptor (IGF-1R) antibody cixutumumab combined with the mTOR inhibitor temsirolimus in patients with refractory Ewing sarcoma family tumors. Clin Cancer Res. 2012;18: 2625-2631. 31. Pappo AS, Patel SR, Crowley J, et al. R1507, a monoclonal antibody to the insulin-like growth factor 1 receptor, in patients with recurrent or refractory Ewing sarcoma family of tumors: results of a phase II Sarcoma Alliance for Research through Collaboration study. J Clin Oncol. 2011;29:4541-4547. e660 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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American Society of Clinical Oncolo
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Controversies in Neoadjuvant Therap
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Clinical Trials of Precision Medici
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Managing Ovarian Cancer in the Olde
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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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INVITED ARTICLES This year’s invi
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ENG ET AL colorectal cancer. Indeed
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WILLIAM M. SIKOV gational treatment
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MICHAEL W. DEININGER broad range ef
Page 550 and 551:
MICHAEL W. DEININGER 30. Hughes T,
Page 552 and 553:
PEMMARAJU AND MOLITERNO TABLE 1. Ac
Page 554 and 555:
PEMMARAJU AND MOLITERNO drome (BCS)
Page 556 and 557:
PEMMARAJU AND MOLITERNO 13. Xing S,
Page 558 and 559:
THERAPIES AND INDICATIONS FOR PH-NE
Page 560 and 561:
Page 562 and 563:
Page 564 and 565:
Page 566 and 567:
LEUKEMIA, MYELODYSPLASIA, AND TRANS
Page 568 and 569:
RECENT UPDATES IN MDS AND MDS/MPNS
Page 570 and 571:
Page 572 and 573:
Page 574 and 575:
Page 576 and 577:
Page 578 and 579:
Page 580 and 581:
Page 582 and 583:
LUNG CANCER Beyond Second-Line Trea
Page 584 and 585:
BEYOND SECOND-LINE TREATMENT FOR LU
Page 586 and 587:
BEYOND SECOND-LINE TREATMENT FOR LU
Page 588 and 589:
LUNG CANCER New Therapies for Histo
Page 590 and 591:
GERBER, PAIK, AND DOWLATI a tumor t
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: ADVANCES IN WEBSITE INFORMATION RES
Page 846 and 847: COMMUNICATION AND TECHNOLOGY: IT’
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 870 and 871: INDICATIONS FOR ADJUVANT RADIATION
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 892 and 893: BONE SARCOMAS IN ADULTS local disea
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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