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ISAACSSON VELHO, CASTRO JR, AND CHUNG Table 1. Active Clinical Trials Evaluating PI3K/AKT/mTOR Targeted Agents in Patients with Locally Advanced, Recurrent, and/or Metastatic HNSCC* Targeted Agent Additional Targeted Agent Additional Therapy Inclusion Criteria Phase Clinical Trial Identifier PI3K Inhibitor PX-866 - Docetaxel Recurrent or metastatic HNSCC/NSCLC I/II NCT01204099 PX-866 Cetuximab - Recurrent or metastatic HNSCC/CRC I/II NCT01252628 BYL-719 - - Recurrent or metastatic HNSCC II NCT02145312 BYL-719 Cetuximab - Recurrent or metastatic HNSCC I/II NCT01602315 BYL-719 Paclitaxel Recurrent or metastatic HNSCC/BRC I NCT02051751 Buparlisib - - Recurrent or metastatic HNSCC II NCT01527877 Buparlisib Cetuximab - Recurrent or metastatic HNSCC I/II NCT01816984 Buparlisib - Paclitaxel Recurrent or metastatic HNSCC II NCT01852292 Buparlisib - IMRT, cisplatin Locally advanced HNSCC Ib NCT02113878 PI3K/mTOR Inhibitor NVP-BEZ235 - - Recurrent or metastatic solid tumors I NCT01343498 NVP-BEZ235 NVP-BKM120 Paclitaxel Recurrent or metastatic solid tumors I NCT01285466 NVP-BEZ235 MEK-162 - Recurrent or metastatic solid tumors I NCT01337765 NVP-BEZ235 Everolimus - Recurrent or metastatic solid tumors I/II NCT01508104 mTOR Inhibitor Everolimus - - Recurrent or metastatic HNSCC II NCT01111058 Everolimus - - Recurrent or metastatic HNSCC II NCT01051791 Everolimus Cetuximab Carboplatin Recurrent or metastatic HNSCC I/II NCT01283334 Everolimus Erlotinib - Recurrent or metastatic HNSCC II NCT00942734 Everolimus Vatalinib - Recurrent or metastatic solid tumors I NCT00655655 Everolimus - IMRT, cisplatin Locally advanced HNSCC I NCT00858663 Everolimus - Docetaxel, cisplatin Locally advanced HNSCC I NCT00935961 Everolimus - Carboplatin, paclitaxel Locally advanced HNSCC I/II NCT01333085 Everolimus Cetuximab Cisplatin, paclitaxel Locally advanced HNSCC II NCT01133678 Temsirolimus - - Recurrent or metastatic HNSCC II NCT01172769 Temsirolimus - Carboplatin, paclitaxel Recurrent or metastatic HNSCC I/II NCT01016769 Temsirolimus Cetuximab - Recurrent or metastatic HNSCC II NCT01256385 Temsirolimus Cetuximab Cisplatin Recurrent or metastatic HNSCC I/II NCT01015664 Temsirolimus Erlotinib - Recurrent or metastatic HNSCC II NCT01009203 Sirolimus - - Recurrent or metastatic HNSCC I/II NCT01195922 Sirolimus - Grapefruit juice Recurrent or metastatic solid tumors I NCT00375245 Ridaforolimus Cetuximab - Recurrent or metastatic HNSCC/NSCLC/CRC I NCT01212627 Metformin - Paclitaxel Recurrent or metastatic HNSCC II NCT01333852 Abbreviations: HNSCC, head and neck squamous cell carcinoma; IMRT, intensity modulated radiation therapy; NSCLC, non-small cell lung cancer; CRC, colorectal cancer; BRC, breast cancer. *All trial data are available at www.clinicaltrials.gov. toxicity. Because of the ease of tumor DNA testing for PIK3CA mutations, many have proposed that the PIK3CA mutations are an integral biomarker for screening patient populations with PI3K pathway activation for future clinical trials. 37 Some studies suggest that patients with HPV-positive HNSCC would be more sensitive because of frequent PIK3CA mutations and enrich the trial. 17 However, in a recent study of cetuximab with or without PX-866, tumor HPV status was assessed by p16 immunohistochemistry. 25 Twenty-six patients (57%) of 46 with available tissue were HPV positive and 20 patients (43%) were HPV negative. There was no association between the tumor HPV status and response. PIK3CA mutations were detected in 17% of patients, but no response was seen in these eight patients with the PIK3CA mutation-harboring tumors. In addition, the PI3K pathway activation through compensatory receptor tyrosine kinase activation, such as MET and HER3, has been proposed as one of the resistance mechanisms of EGFR inhibitors in preclinical studies, suggesting PI3K/mTOR inhibitors may be developed in patients who are EGFR inhibitor–resistant in addition to patients with the PIK3CA mutations. 38,39 In a recent preclinical study, the combined activity of cetuximab and mTOR inhibitors in patients with HNSCC was evaluated. Cetuximab-sensitive 126 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
TARGETING THE PI3K PATHWAY IN HNSCC HNSCC cells were transduced to express PIK3CA and RAS oncogenes, and tumor xenografts were treated with control, cetuximab, or rapamycin. The in vivo study showed that patients with HNSCC tumor xenografts expressing mutant PI3K and Ras proteins relapsed a few weeks after the initial response to cetuximab treatments. However, the addition of rapamycin dramatically increased antitumor activity in these cetuximab-resistant tumors, supporting the rationale to evaluate a combination of cetuximab/mTOR inhibitors for treatment of patients with HNSCC. 39 However, a vast majority of the model systems use the H1047R PI3KCA mutation that does not reflect the most commonly seen mutations. 5 For example, there are differences in the PIK3CA mutation hotspots between patients with HPV-positive and HPV-negative HNSCC. Greater than 90% of HPV-positive patients with HNSCC have mutations in the helical domain (i.e., E542K or E545K), whereas patients with HPV-negative HNSCC have mutations throughout the entire gene, although the hotspot mutations in the helical and kinase domains (i.e., H1047R) are relatively more frequent. 14 The site of the mutations and resulting amino acid substitutions might produce functionally different mutant proteins and further differ depending on the genetic background of patients with HPV-positive and HPVnegative HNSCC. These phenotypical differences may result in varied responses to the PI3K targeted agents and substantially affect the development of predictive biomarkers. This concern is validated in the PX-866 trial in which the PIK3CA mutations were not associated with response to cetuximab or cetuximab and PX-866 combination. 25 In addition, patients with HNSCC have PTEN loss and other functional gain or loss of genes/proteins within the pathway that may affect the pathway in the absence of the PIK3CA mutations. 14 The functional signifıcance of these features must be adequately characterized before applying them to clinical trials. CONCLUSION Advancements in genomic and proteomic technology are providing a glimpse of the complexity of cancer biology and generating rich hypotheses for potential therapeutic targets. In addition, respective companion diagnostic biomarkers are being developed for clinical application. Currently, a large body of preclinical data indicate the PI3K pathway is important and a promising therapeutic target in patients with HNSCC. However, they have not always translated to clinically meaningful effıcacy in clinical studies. Additional studies to determine an appropriate method of patient selection with the activation of PI3K pathway and to develop targeted agents with favorable toxicity profıles are required. Existing data on PIK3CA mutations as a predictive biomarker to PI3K/mTOR inhibitor response or the EGFR inhibitor resistance are not yet fully developed. Potential differences in the gene/protein function based on the location and amino acid changes resulting from the PIK3CA mutations in appropriate genetic context of other coexisting pathologic signaling network, must be delineated further before proceeding with a broader clinical application. 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: None. Consulting or Advisory Role: Christine H. Chung, Novartis. Gilberto Castro, Teva, Boehringer Ingelheim, Eurofarma, Pfizer, Bayer. Speakers’ Bureau: Gilberto Castro, Speakers’ Bureau (Lilly, AstraZeneca, Bayer, Novartis, Roche, Eurofarma, Merck Serono). Research Funding: Christine H. Chung, Boehringer Ingelheim, Immunogen. Patents, Royalties, or Other Intellectual Property: None. Expert Testimony: None. Travel, Accommodations, Expenses: Christine H. Chung, Merck. Gilberto Castro, Merck Sharp & Dohme, Lilly, Novartis, Pfizer, Roche, AstraZeneca, Boehringer Ingelheim, Eurofarma, Bayer. Other Relationships: None. References 1. Maier H, Dietz A, Gewelke U, et al. Tobacco and alcohol and the risk of head and neck cancer. Clin Investig. 1992;70:320-327. 2. D’Souza G, Kreimer AR, Viscidi R, et al. Case-control study of human papillomavirus and oropharyngeal cancer. N Engl J Med. 2007;356: 1944-1956. 3. Ang KK, Harris J, Wheeler R, et al. Human papillomavirus and survival of patients with oropharyngeal cancer. N Engl J Med. 2010;363:24-35. 4. Gillison ML, D’Souza G, Westra W, et al. Distinct risk factor profıles for human papillomavirus type 16-positive and human papillomavirus type 16-negative head and neck cancers. J Natl Cancer Inst. 2008;100:407- 420. 5. Cancer Genome Atlas Network. Comprehensive genomic characterization of head and neck squamous cell carcinomas. Nature. 2015;517:576- 582. 6. Thorpe LM, Yuzugullu H, Zhao JJ. PI3K in cancer: divergent roles of isoforms, modes of activation and therapeutic targeting. Nat Rev Cancer. 2015;15:7-24. 7. Lee JY, Engelman JA, Cantley LC. Biochemistry. PI3K charges ahead. Science. 2007;317:206-207. 8. Clarke PA, Workman P. Phosphatidylinositide-3-kinase inhibitors: addressing questions of isoform selectivity and pharmacodynamic/predictive biomarkers in early clinical trials. J Clin Oncol. 2012;30:331-333. 9. Hardt M, Chantaravisoot N, Tamanoi F. Activating mutations of TOR (target of rapamycin). Genes Cells. 2011;16:141-151. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK 127
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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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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Updates in the Multimodality Manage
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PEDIATRIC ONCOLOGY Real-Time Molecu
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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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WONG, CAPASSO, AND ECKHARDT 3 3 sc
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STEPHEN T. SONIS portantly, patient
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STEPHEN T. SONIS Defıning the clin
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HUSSAIN AND DIPAOLA TABLE 1. U.S. F
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EDWARD S. KIM TABLE 1. Selected Umb
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EDWARD S. KIM platform that plans t
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INVITED ARTICLES HEAD AND NECK CANC
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GROSS AND COHEN treatments are poor
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GILBERT ET AL tional scholars, lead
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ENG ET AL colorectal cancer. Indeed
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WILLIAM M. SIKOV gational treatment
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BREAST CANCER Individualizing the A
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CANCER PREVENTION, GENETICS, AND EP
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DECISION MAKING IN THE CONTEXT OF B
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REFORMING THE BUY-AND-BILL CHEMOTHE
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CARE DELIVERY AND PRACTICE MANAGEME
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INTEGRATING ICD-10 IN YOUR PRACTICE
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ZARDAVAS AND PICCART-GEBHART TABLE
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MICHAEL A. POSTOW Managing Immune C
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AHN ET AL Pancreatic cancer has bee
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EGIDIO DEL FABBRO tion of precachex
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LEUKEMIA, MYELODYSPLASIA, AND TRANS
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MICHAEL W. DEININGER TABLE 1. Defin
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GERBER, PAIK, AND DOWLATI a tumor t
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GERBER, PAIK, AND DOWLATI squamous
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GERBER, PAIK, AND DOWLATI gression
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BERNARDO H.L. GOULART The Value of
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LUNG CANCER Updates in the Multimod
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WOODARD AND JABLONS section, becaus
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WOODARD AND JABLONS mediastinum is
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NASSER HANNA Current Standards and
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NASSER HANNA culty of this task. Va
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LYMPHOMA AND PLASMA CELL DISORDERS
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NOWAKOWSKI AND CZUCZMAN sociated wi
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NOWAKOWSKI AND CZUCZMAN TABLE 2. DH
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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
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CHEAH, OKI, AND FANALE an ongoing G
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CHEAH, OKI, AND FANALE a similar me
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CHEAH, OKI, AND FANALE TABLE 3. Sel
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CHEAH, OKI, AND FANALE eral T cell
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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
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MATEOS AND SAN MIGUEL Smoldering Mu
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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
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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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