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RIMAWI, DE ANGELIS, AND SCHIFF phase III ALTTO trial (BIG 2-06; NCCTG [Alliance] N063D) comparing one year of anti-HER2 therapy with lapatinib alone (L), trastuzumab alone (T), their sequence (T3L), or their combination (TL) in the adjuvant treatment of HER2-positive early breast cancer (EBC). J Clin Oncol. 2014;32:18s (suppl; abstr LBA4). 49. Rimawi MF, Mayer IA, Forero A, et al. Multicenter phase II study of neoadjuvant lapatinib and trastuzumab with hormonal therapy and without chemotherapy in patients with human epidermal growth factor receptor 2-overexpressing breast cancer: TBCRC 006. J Clin Oncol. 2013;31:1726-1731. 50. Krop IE, Kim SB, González-Martín A, et al. Trastuzumab emtansine versus treatment of physician’s choice for pretreated HER2-positive advanced breast cancer (TH3RESA): a randomised, open-label, phase 3 trial. Lancet Oncol. 2014;15:689-699. 51. Verma S, Miles D, Gianni L, et al. Trastuzumab emtansine for HER2- positive advanced breast cancer. N Engl J Med. 2012;367:1783-1791. 52. Berns K, Horlings HM, Hennessy BT, et al. A functional genetic approach identifıes the PI3K pathway as a major determinant of trastuzumab resistance in breast cancer. Cancer Cell. 2007;12:395-402. 53. Miller TW, Rexer BN, Garrett JT, et al. Mutations in the phosphatidylinositol 3-kinase pathway: Role in tumor progression and therapeutic implications in breast cancer. Breast Cancer Res. 2011;13:224. 54. Brady SW, Zhang J, Seok D, et al. Enhanced PI3K p110 signaling confers acquired lapatinib resistance that can be effectively reversed by a p110-selective PI3K inhibitor. Mol Cancer Ther. 2014;13:60-70. 55. Xia W, Husain I, Liu L, et al. Lapatinib antitumor activity is not dependent upon phosphatase and tensin homologue deleted on chromosome 10 in ErbB2-overexpressing breast cancers. Cancer Res. 2007;67:1170- 1175. 56. Loibl S, von Minckwitz G, Schneeweiss A, et al. PIK3CA mutations are associated with lower rates of pathologic complete response to antihuman epidermal growth factor receptor 2 (HER2) therapy in primary HER2-overexpressing breast cancer. J Clin Oncol. 2014:32:3212-3220. 57. Majewski IJ, Nuciforo P, Mittempergher L, et al. PIK3CA mutations are associated with decreased benefıt to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer. J Clin Oncol. Epub 2015 Jan 5. 58. Contreras A, Herrera S, Wang T, et al. PIK3CA mutations and/or low PTEN predict resistance to combined anti-HER2 therapy with lapatinib and trastuzumab and without chemotherapy in TBCRC006, a neoadjuvant trial of HER2-positive breast cancer patients. Cancer Research. 2013;73:24s (suppl; abstr PD1-2). 59. Perez EA, Dueck AC, McCullough AE, et al. Impact of PTEN protein expression on benefıt from adjuvant trastuzumab in early-stage human epidermal growth factor receptor 2-positive breast cancer in the North Central Cancer Treatment Group N9831 trial. J Clin Oncol. 2013;31:2115-2122. 60. Schiff R, Massarweh SA, Shou J, et al. Cross-talk between estrogen receptor and growth factor pathways as a molecular target for overcoming endocrine resistance. Clin Cancer Res. 2004;10:331S-336S. 61. Wang YC, Morrison G, Gillihan R, et al. Different mechanisms for resistance to trastuzumab versus lapatinib in HER2-positive breast cancers-role of estrogen receptor and HER2 reactivation. Breast Cancer Res. 2011;13:R121. 62. Dave B, Migliaccio I, Gutierrez MC, et al. Loss of phosphatase and tensin homolog or phosphoinositol-3 kinase activation and response to trastuzumab or lapatinib in human epidermal growth factor receptor 2-overexpressing locally advanced breast cancers. J Clin Oncol. 2011;29:166-173. 63. Bhargava R, Dabbs DJ, Beriwal S, et al. Semiquantitative hormone receptor level influences response to trastuzumab-containing neoadjuvant chemotherapy in HER2-positive breast cancer. Mod Pathol. 2011; 24:367-374. 64. Finn RS, Press MF, Dering J, et al. Estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2 (HER2), and epidermal growth factor receptor expression and benefıt from lapatinib in a randomized trial of paclitaxel with lapatinib or placebo as fırst-line treatment in HER2-negative or unknown metastatic breast cancer. J Clin Oncol. 2009;27:3908-3915. 65. Vaz-Luis I, Winer EP, Lin NU. Human epidermal growth factor receptor-2-positive breast cancer: does estrogen receptor status defıne two distinct subtypes? Ann Oncol. 2013;24:283-291. 66. Rimawi MF, Niravath PA, Wang T, et al. TBCRC023: a randomized multicenter phase II neoadjuvant trial of lapatinib, trastuzumab, with or without endocrine therapy for 12 weeks vs. 24 weeks in patients with HER2 overexpressing breast cancer. Paper presented at: San Antonio Breast Cancer Symposium; December 2014; San Antonio, TX. 67. Untch M, Loibl S, Bischoff J, et al. Lapatinib versus trastuzumab in combination with neoadjuvant anthracycline-taxane-based chemotherapy (GeparQuinto, GBG 44): a randomised phase 3 trial. Lancet Oncol. 2012; 13:135-144. e164 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
THE BATTLE AGAINST TKI RESISTANCE IN LUNG CANCER Combating Acquired Resistance to Tyrosine Kinase Inhibitors in Lung Cancer Christine M. Lovly, MD, PhD OVERVIEW The prospective identification and therapeutic targeting of oncogenic tyrosine kinases with tyrosine kinase inhibitors (TKIs) has revolutionized the treatment for patients with non–small cell lung cancer (NSCLC). TKI therapy frequently induces dramatic clinical responses in molecularly defined cohorts of patients with lung cancer, paving the way for the implementation of precision medicine. Unfortunately, acquired resistance, defined as tumor progression after initial response, seems to be an inevitable consequence of this treatment approach. This brief review will provide an overview of the complex and heterogeneous problem of acquired resistance to TKI therapy in NSCLC, with a focus on EGFR-mutant and ALK-rearranged NSCLC. In vitro models of TKI resistance and analysis of tumor biopsy samples at the time of disease progression have generated breakthroughs in our understanding of the spectrum of mechanisms by which a tumor can thwart TKI therapy and have provided an important rationale for the development of novel approaches to delay or overcome resistance. Numerous ongoing clinical trials implement strategies, including novel, more potent TKIs and rational combinations of targeted therapies, some of which have already proven effective in surmounting therapeutic resistance. Therapeutic targeting of oncogenes has emerged as a preeminent treatment paradigm for patients with non– small cell lung cancer (NSCLC). Beginning in 2004 with the initial identifıcation of epidermal growth factor receptor (EGFR) mutations in a subset of lung adenocarcinomas, 1-3 molecular profıling of lung cancer, particularly lung adenocarcinoma, has evolved into a complex spectrum of clinically relevant and therapeutically actionable genomic alterations. These alterations occur at varying frequencies and, at present, have varying levels of clinical evidence to support the use of targeted inhibitors in each setting. To date, the most welldescribed molecular cohorts of NSCLC are those defıned by the presence of EGFR mutations and ALK rearrangements. Treatment for patients with EGFR-mutant and ALKrearranged NSCLC with specifıc tyrosine kinase inhibitors (TKIs) that target the EGFR and ALK tyrosine kinases, respectively, has led to remarkable clinical responses, including often-dramatic tumor shrinkage and increased progressionfree survival (PFS) compared with standard cytotoxic chemotherapy. 4-10 Unfortunately, despite the exciting results, virtually every patient who receives TKI therapy and has an antitumor response will eventually experience disease progression. This tumor relapse while the patient is still receiving drug therapy is called acquired resistance and typically occurs within 1 to 2 years after the initiation of the TKI. 4-8,11,12 The development of drug resistance remains a major limitation to the successful treatment for patients with advanced NSCLC. Therefore, numerous preclinical and clinical studies have been directed at identifying and understanding on a mechanistic level the tumor-specifıc factors that lead to acquired resistance in NSCLC. Given the complexity of the topic, we will specifıcally focus in this review on EGFRmutant and ALK-rearranged NSCLC as paradigms for the use of targeted therapies and the battle to overcome acquired TKI resistance in this disease. EGFR-MUTANT NSCLC EGFR is the gene that encodes for the EGFR tyrosine kinase. EGFR propagates growth and survival signals through several downstream pathways within the cell, including the RAS-RAF- MEK-ERK (mitogen-activated protein [MAP] kinase) and the phosphoinositide 3-kinase (PI3K)–AKT–mammalian target of rapamycin (mTOR) pathways. In NSCLC, EGFR mutations are typically detected in exons 18 to 21, which encode part of the EGFR tyrosine kinase domain. Approximately 90% of these mutations are small in-frame deletions in exon 19 or point mutations in exon 21 (L858R). 13 These mutations activate EGFR kinase activity and are typically detected in lung adenocarcinomas with a frequency of approximately 10% of patients with NSCLC in the United States and of approximately 35% in Asia. 1-3 EGFR mutations confer sensitivity to and are strong predictors of effıcacy for the EGFR TKIs. Several classes of EGFR From the Division of Hematology-Oncology, Vanderbilt University School of Medicine, Nashville, TN. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Christine M. Lovly, MD, PhD, Division of Hematology-Oncology, Vanderbilt University School of Medicine, 2220 Pierce Ave. South, 777 Preston Research Building, Nashville, TN 37232; email: christine.lovly@vanderbilt.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e165
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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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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
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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
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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
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BHUTANI, LANDGREN, AND USMANI fıne
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BHUTANI, LANDGREN, AND USMANI FIGUR
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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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