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HEAD AND NECK CANCER PI3-Kinase: Genomics to Clinical Practice CHAIR Christine H. Chung, MD The Johns Hopkins Medical Institutions Baltimore, MD SPEAKERS Matthew G. Fury, MD Memorial Sloan Kettering Cancer Center New York, NY J. Silvio Gutkind, PhD National Institute of Dental and Craniofacial Research at the National Institutes of Health Bethesda, MD
TARGETING THE PI3K PATHWAY IN HNSCC Targeting the PI3K Pathway in Head and Neck Squamous Cell Carcinoma Pedro Henrique Isaacsson Velho, MD, Gilberto Castro Jr, MD, PhD, and Christine H. Chung, MD OVERVIEW Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous disease arising from the mucosal epithelia in the head and neck region. The most common risk factors are tobacco use, alcohol consumption, and HPV infection, particularly in the oropharynx. The HPV-positive HNSCC is biologically and clinically distinct from the HPV-negative HNSCC; however, deregulations within the phosphatidylinositol 3-kinase (PI3K) pathway are frequent in both HPV-positive and HPV-negative HNSCC as it is the most frequently altered oncogenic pathway with a gain-of-function in HNSCC. This article reviews the basic biology and clinical data from the trials involving anticancer agents targeting the PI3K pathway in HNSCC. It also discusses the difficulties of translating the preclinical data to tangible clinical efficacy of these agents in patients with HNSCC even when there is significant preclinical data suggesting the PI3K pathway is a promising therapeutic target in HNSCC. We conclude that additional studies to determine appropriate patient selection for the activation of PI3K pathway and to develop targeted agents either as a monotherapy or combination therapy with favorable toxicity profiles are required before a broader clinical application. Head and neck squamous cell carcinoma is a heterogeneous disease originating from the mucosal epithelia in the head and neck region, most commonly the oral cavity, oropharynx, hypopharynx, and larynx. The risk factors are tobacco use, alcohol consumption, and HPV infection, particularly in the oropharynx. 1,2 The HPV-positive HNSCC is now established as a separate entity with distinct clinical characteristics, including younger age of onset, better performance status, less smoking history, and its association with high-risk sexual behaviors compared to the HPV-negative HNSCC. 3,4 In addition, the HPV-positive HNSCC has a distinct molecular profıle compared to the HPV-negative HNSCC, including lack of TP53 and CDKN2A mutations; however, mutations or copy number variations of genes within the PI3K pathway are frequent in both HPV-positive and HPV-negative HNSCC as it is the most frequently altered oncogenic pathway with a gain-of-function in HNSCC. 5 This article reviews the basic biology and clinical data from trials involving the PI3K pathway inhibitors in patients with HNSCC. BASIC BIOLOGY OF THE PI3K PATHWAY P13Ks are divided into three classes: class I, II, and III. The differences in these classes are comprehensively reviewed by Thorpe et al. 6 Class I is further divided into subclass IA and IB in mammals. Class IA PI3Ks are heterodimeric kinases consisting of a p110 catalytic subunit (p110-alpha, p110-beta, and p110-delta encoded by PIK3CA, PIK3CB, and PIK3CD, respectively) and a p85 regulatory subunit (p85-alpha and its splice variants, p55-alpha and p50-alpha, encoded by PIK3R1; p85-beta encoded by PIK3R2; and p55-gamma encoded by PIK3R3). These three p110 catalytic subunit isoforms can form a heterodimer with any of the fıve p85 regulatory subunits. Class IB PI3Ks are heterodimeric kinases consisting of a p110-gamma catalytic subunit encoded by PIK3CG and a p101 or p87 regulatory subunit encoded by PIK3R5 and PIK3R6, respectively. Unlike class I PI3Ks, class II PI3Ks are monomeric lipid kinases without a regulatory subunit. There are three class II isoforms, including PI3K- C2-alpha, PIK3-C2-beta, and PIK3-C2-gamma encoded by PIK3C2A, PIK3C2B, and PIK3C2G, respectively. VPS34 is the sole Class III PI3K encoded by PIK3C3 and forms a heterodimer with VPS15 encoded by PIK3R4. Activation of the PI3K signaling pathway is highly regulated. PI3K activation is initiated by activated receptor tyrosine kinases such as ErbB family receptors, fıbroblast growth factor receptors, insulin-like growth factor 1 receptor and others, as well as G protein-coupled receptors. 6,7 On activation, class I PI3Ks translocate to the plasma membrane where inhibition by the p85 regulatory subunit is relieved, and the p110 catalytic subunit catalyzes the phosphorylation From the Department of Clinical Oncology, Instituto do Câncer do Estado de São Paulo, Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil; Department of Oncology and Department of Head and Neck Surgery-Otolaryngology, The Johns Hopkins Medical Institutions, Baltimore, MD. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Christine H. Chung, MD, Department of Oncology and Department of Head and Neck Surgery-Otolaryngology, Johns Hopkins University School of Medicine, Sidney Kimmel Comprehensive Cancer Center, 1550 Orleans St. CRB-2 Room 546, Baltimore, MD 21287-0014; email: cchung11@jhmi.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK 123
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2015 Educational Book Expert Panel
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James Marshall, PhD Roswell Park Ca
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CD19 CAR THERAPY FOR ALL 5. Zhou G,
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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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SULLIVAN ET AL 17. Halait H, Demart
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SULLIVAN ET AL NRAS-mutant melanoma
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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
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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
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MAYER ET AL to enhance the quality
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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
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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
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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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