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GASTROINTESTINAL (NONCOLORECTAL) CANCER Hepatocellular Carcinoma Tumor Board: Making Sense of the Technologies CHAIR Ghassan K. Abou-Alfa, MD Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College New York, NY SPEAKERS Riccardo Lencioni, MD, PhD Pisa University Hospital and School of Medicine Pisa, Italy John Renz, MD, PhD The University of Chicago Chicago, IL Jorge Marrero, MD The University of Texas Southwestern Medical Center Dallas, TX
HCC TUMOR BOARD: MAKING SENSE OF THE TECHNOLOGIES Hepatocellular Carcinoma Tumor Board: Making Sense of the Technologies Ghassan K. Abou-Alfa, MD, Jorge Marrero, MD, John Renz, MD, PhD, and Riccardo Lencioni, MD, PhD OVERVIEW Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death, with a rising global incidence. The vast majority of HCC cases occur in the setting of liver cirrhosis, mainly due to chronic hepatitis C (HCV) or hepatitis B (HBV) viral infections, alcohol consumption, and nonalcoholic fatty liver disease. The new approval of curative therapy with two NS5A inhibitors, ledipasvir and sofosbuvir, for the treatment of HCV will no doubt affect HCC incidence and outcome. No studies have evaluated the use of the new antivirals in patients with HCC. Staging and scoring remain an integral part of the management of patients with advanced HCC. Curative therapies for the treatment of HCC are evolving. Improvements in surgical techniques and risk stratification for orthotopic liver transplantation (OLT) have expanded access and improved the outlook for patients suffering from HCC. Interventional locoregional treatments continue to play a key role in the management of HCC. Transarterial chemoembolization is considered the standard of care for patients with noninvasive multinodular tumors at the intermediate stage. Bland embolization appears to have similar virtues in some studies. Y90 radioembolization represents a promising treatment option for patients unfit or refractory to transarterial chemoembolization. The advent of sorafenib as a standard of care with an improvement in survival sadly remain the only major breakthrough in the treatment of advanced HCC, with mounting negative data from multiple clinical trials. Advances in immunotherapy and customized therapy may hopefully help reverse this tide. Hepatocellular carcinoma is a leading cause of cancerrelated death, with a rising global incidence. 1 The vast majority of HCC cases occur in the setting of liver cirrhosis, usually because of chronic HCV or HBV, alcohol consumption, nonalcoholic fatty liver disease, among others. Because the majority of patients with HCC have cirrhosis, it is important to understand it and its complications, while we focus on the recent advancements in prevention of cirrhosis-causing etiologies, specifıcally HCV. This manuscript also addresses the recent developments in the curative and palliative whole treatment armamentarium for HCC from surgery and transplant through local therapies, up to systemic treatment including targeted and immunotherapies. CIRRHOSIS AND LIVER DYSFUNCTION Cirrhosis is the outcome of a relentless inflammatory event that ultimately leads to hepatic fıbrosis in response to a chronic liver disease (e.g., HCV), to the point where most of the liver parenchyma is replaced by scar. This starts a steady hepatic decompensation phenomenon, along with a risk of developing HCC. Hepatic decompensation includes the development of jaundice, ascites, variceal hemorrhage, hepatic encephalopathy, hepatopulmonary syndrome, or portopulmonary hypertension. Cirrhosis can be compensated or decompensated, with a 2-year survival of 90% compared with 54%, respectively. 2 HCC is the other important complication of cirrhosis and occurs at an annual incidence rate of 2% to 3%. 3 The presence of cirrhosis and its complications will affect the prognosis and management of patients with HCC. Multidisciplinary management including hepatology is critical in the care for patients with advanced HCC. The Child-Turcotte classifıcation system was developed in 1964 to risk-stratify patients undergoing shunt surgery for portal decompression at the University of Michigan. In 1972, Pugh modifıed the Child-Turcotte system, and it became known as the Child-Turcotte-Pugh score, also known for short as the Child-Pugh score. The Child-Pugh score is composed of levels of albumin, prothrombin time, and total bilirubin and also with the presence or absence of clinical hepatic encephalopathy and ascites. Based on these variables, points are assigned and patients are classifıed as A, B, or C. Although empirically derived, the Child-Pugh has been shown to accurately predict outcomes in patients with cirrhosis and portal hypertension, and it continues to be used today. Because it is simple and does not require complicated calculation, this tool is widely used by clinicians to assess the risk of mortality in patients with cirrhosis. Another important system to as- From the Memorial Sloan Kettering Cancer Center, New York, NY; Weill Cornell Medical College, New York, NY; The University of Texas Southwestern, Dallas, TX; The University of Chicago, Chicago, IL; and Pisa University Hospital and School of Medicine, Pisa, Italy. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Ghassan K. Abou-Alfa, MD, Memorial Sloan Kettering Cancer Center, 300 East 66th St., New York, NY: 10065; email: abou-alg@mskcc.org. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e213
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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Controversies in Neoadjuvant Therap
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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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GYNECOLOGIC CANCER Cervical Cancer
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GYNECOLOGIC CANCER Managing Ovarian
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GYNECOLOGIC CANCER Treatment of the
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CANCER CARE QUALITY: CURRENT STATE
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TREATMENT OF PHILADELPHIA CHROMOSOM
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CD19 CAR THERAPY FOR ALL FIGURE 1.
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CD19 CAR THERAPY FOR ALL 5. Zhou G,
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LYMPHOMA AND PLASMA CELL DISORDERS
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NOWAKOWSKI AND CZUCZMAN sociated wi
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MANAGEMENT OF CLL Up-Front Manageme
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MANAGEMENT OF CLL than 17p-/TP53mut
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MANAGEMENT OF CLL could be associat
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MERKEL CELL CARCINOMA Merkel Cell C
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PERFUSION AND INFUSION IN THE ERA O
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SULLIVAN ET AL FIGURE 1. Relevant S
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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
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KLEPIN, RODIN, AND HURRIA plication
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KLEPIN, RODIN, AND HURRIA plan was
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KLEPIN, RODIN, AND HURRIA patient-s
Page 762 and 763:
KLEPIN, RODIN, AND HURRIA 62. Blanc
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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
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PARTRIDGE, JACOBSEN, AND ANDERSEN w
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PARTRIDGE, JACOBSEN, AND ANDERSEN v
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LESLIE R. SCHOVER Sexual Healing in
Page 782 and 783:
LESLIE R. SCHOVER tinuous ADT in pr
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LESLIE R. SCHOVER 12. Potosky AL, H
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CATHERINE H. VAN POZNAK TABLE 1. Wo
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CATHERINE H. VAN POZNAK (tamoxifen,
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CATHERINE H. VAN POZNAK TABLE 3. FD
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CATHERINE H. VAN POZNAK premenopaus
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SHARI GOLDFARB KEY POINTS Brea
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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
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MAYER ET AL efıcial suggests that
Page 810 and 811:
PATIENT AND SURVIVOR CARE The Chall
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BRUERA AND PAICE Choice of Opioid a
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BRUERA AND PAICE toxicity and proce
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BRUERA AND PAICE effective. Basic s
Page 818 and 819:
PEDIATRIC ONCOLOGY Real-Time Molecu
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CARROLL, RAETZ, AND MEYER KEY POINT
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CARROLL, RAETZ, AND MEYER most are
Page 824 and 825:
CARROLL, RAETZ, AND MEYER markers a
Page 826 and 827:
PEDIATRIC ONCOLOGY Translating Surv
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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.
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CLINICAL ONCOLOGY PRACTICE 2015 Pro
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ADJUVANT/NEOADJUVANT MEDICAL THERAP
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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
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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
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BONE SARCOMAS IN ADULTS structure a
Page 896 and 897:
SARCOMA Well-Differentiated and Ded
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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
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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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