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GASTROINTESTINAL (COLORECTAL) CANCER Sequence, Duration, and Cost of Treating Metastatic Unresectable Colorectal Cancer CHAIR John Marshall, MD Lombardi Comprehensive Cancer Center, Georgetown University Washington, DC SPEAKERS Marwan Fakih, MD City of Hope Comprehensive Cancer Center Duarte, CA Cornelis J.A. Punt, MD, PhD University of Amsterdam Amsterdam, Netherlands
BIOLOGIC THERAPIES IN COLORECTAL CANCER Biologic Therapies in Colorectal Cancer: Indications and Contraindications Marwan Fakih, MD OVERVIEW The role of antiangiogenic and anti-epidermal growth factor receptor (EGFR) agents has been investigated extensively in colorectal cancer in the palliative, adjuvant, and neoadjuvant settings. Although the role of biologic agents has become well-defined in the first, second, and subsequent lines of treatment of metastatic colorectal cancer (mCRC), considerable debate continues around the optimal sequencing and around optimal patient selection. The benefits from integrating bevacizumab or cetuximab in the adjuvant setting have been investigated in several randomized phase III clinical trials in stage II/III disease, all with disappointing results. Neoadjuvant approaches incorporating biologic therapy in patients with liver metastatic disease have led to mixed results. Although the current evidence does suggest increased down-staging and increased resectability with the addition of cetuximab in patients with initially unresectable or borderline resectable liver metastases, a positive effect of anti-EGFR therapy on the overall survival (OS) in this setting is not conclusive. Patients with resectable liver metastases derive no benefit and may experience potential harm from the addition of cetuximab to neoadjuvant chemotherapy. Similarly, there is neither rationale nor adequate data to support the addition of bevacizumab to neoadjuvant chemotherapy in patients with resectable liver metastases. In this review, we examine the role of antiangiogenesis and anti-EGFR therapies across the spectrum of adjuvant, neoadjuvant, and metastatic disease. Signifıcant progress has been made in the last decade in the management of mCRC, with median OS of patients with mCRC now at or exceeding 30 months. 1,2 The improvements in outcome are at least partially credited to the integration of biologic therapies, whether antiangiogenic or anti-EGFR, in the mainstream treatment of metastatic disease. Although signifıcant progress has been made with the addition of these classes in advanced noncurable disease, their role has been disappointing in the adjuvant setting and continues to evolve in the neoadjuvant setting. In this review, we will summarize the current clinical data for biologic and targeted agents in adjuvant CRC, neoadjuvant, and nonresectable mCRC. BIOLOGIC THERAPY IN THE ADJUVANT TREATMENT OF COLORECTAL CANCER Bevacizumab in Stage II and III Colon Cancer Several randomized phase III clinical trials have evaluated bevacizumab in combination with systemic chemotherapy in the adjuvant treatment of colorectal cancer. The NSABP C-08 clinical trial randomized 2,710 patients with stage II or III colon cancer to receive 6 months (12 cycles) of modifıed FOLFOX6 regimen with or without 1 year of bevacizumab. 3,4 No signifıcant effect on disease-free survival (DFS) or OS was noted in the study population or within the stage II or stage III subgroups. Interestingly, the effect of bevacizumab on DFS was different before and after the 15-month time point from study treatment. The hazard ratio (HR) for recurrence within 15 months from start of study treatment was 0.61 (95% CI, 0.48 to 0.78) in favor of bevacizumab. In contrast, a trend toward increased recurrence rate was noted after 15 months on the bevacizumab arm. A post hoc analysis of the NSABP-CO8 population by mismatch repair status suggested a benefıt from bevacizumab in the mismatch defıcient cohort (HR 0.52; 95% CI, 0.29 to 0.94). 5 The AVANT phase III clinical trial randomized patients with stage II or III colon cancer to receive 6 months of oxaliplatin plus a fluoropyrimidine with or without bevacizumab. 6 Patients were randomly assigned in a 1:1:1 ratio to three arms of treatment: FOLFOX4, FOLFOX4 plus 1 year of bevacizumab, XELOX plus 1 year of bevacizumab. No benefıts in DFS were noted with the addition of bevacizumab to chemotherapy. The HR for DFS for bevacizumab/FOLFOX4 and bevacizumab/XELOX compared with FOLFOX4 were 1.17 (95% CI, 0.98 to 1.39) and 1.07 (95% CI, 0.9 to 1.28), respectively. Similar to the NSABP-C08 study, bevacizumab was associated with an improved DFS in the initial period of follow-up. In the fırst year of the study, the HR for DFS was 0.63 and 0.61 on the bevacizumab/FOLFOX4 and bevacizumab/XELOX arms in comparison with FOLFOX4. This initial improvement in DFS From the City of Hope Comprehensive Cancer Center, Duarte, CA. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Marwan Fakih, MD, City of Hope Comprehensive Cancer Center, Building 51, Room 127, 1500 E. Duarte Rd., Duarte, CA 91010; email: mfakih@coh.org. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e197
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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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GILBERT ET AL tional scholars, lead
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INVITED ARTICLES GASTROINTESTINAL C
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ENG ET AL colorectal cancer. Indeed
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INVITED ARTICLES BREAST CANCER I Wi
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WILLIAM M. SIKOV gational treatment
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BREAST CANCER Individualizing the A
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CAN DIET AND LIFESTYLE PREVENT BREA
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MAWRIN, CHUNG, AND PREUSSER Biology
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THE SPECTRUM OF NEUROENDOCRINE TUMO
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CHALLENGING THE TREATMENT PARADIGM
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STAGE I TESTICULAR GERM CELL CANCER
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STAGE I TESTICULAR GERM CELL CANCER
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GERM CELL TUMORS: LOOKING TO THE FU
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SALVAGE CHEMOTHERAPY Salvage Therap
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SALVAGE CHEMOTHERAPY References 1.
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EARLY CHEMOTHERAPY IN MEN WITH META
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RADIUM 223 AND METASTATIC CASTRATIO
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RADIUM 223 AND METASTATIC CASTRATIO
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IMMUNOTHERAPY FOR PROSTATE TUMORS I
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EVOLVING IMMUNOTHERAPY STRATEGIES I
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NOVEL IMMUNOTHERAPY AGENTS IN METAS
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PROMISING STRATEGIES IN BLADDER CAN
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GYNECOLOGIC CANCER Cervical Cancer
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MACKAY, WENZEL, AND MILESHKIN ing s
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MACKAY, WENZEL, AND MILESHKIN 59. F
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GYNECOLOGIC CANCER Managing Ovarian
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DUSKA, TEW, AND MOORE KEY POINTS A
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DUSKA, TEW, AND MOORE FIGURE 2. Sur
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DUSKA, TEW, AND MOORE FIGURE 4. Ger
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DUSKA, TEW, AND MOORE 10. Griffıth
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GYNECOLOGIC CANCER Treatment of the
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CHEMOTHERAPY FOR PATIENTS WITH BMOC
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PROGRESS IN HEAD AND NECK SQUAMOUS
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HEAD AND NECK CANCER PI3-Kinase: Ge
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ISAACSSON VELHO, CASTRO JR, AND CHU
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SHARON H. GIORDANO Comparative Effe
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HEALTH SERVICES RESEARCH AND QUALIT
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INDUSTRY AND ONCOLOGY KEY POINTS F
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INDUSTRY AND ONCOLOGY has been “l
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INDUSTRY AND ONCOLOGY by (covered)
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INDUSTRY AND ONCOLOGY 42. World Hea
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CANCER CARE QUALITY: CURRENT STATE
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MANAGING OLDER PATIENTS WITH ALL Th
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MANAGING OLDER PATIENTS WITH ALL TA
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MANAGING OLDER PATIENTS WITH ALL FI
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MANAGING OLDER PATIENTS WITH ALL FI
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MANAGING OLDER PATIENTS WITH ALL ra
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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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NEW TARGETED THERAPIES FOR iNHL New
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NEW TARGETED THERAPIES FOR iNHL TAB
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NEW TARGETED THERAPIES FOR iNHL a P
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HEMATOPOIETIC CELL TRANSPLANTATION
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LEUKEMIA, MYELODYSPLASIA, AND TRANS
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MICHAEL W. DEININGER TABLE 1. Defin
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MICHAEL W. DEININGER the ATP-bindin
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MICHAEL W. DEININGER broad range ef
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MICHAEL W. DEININGER 30. Hughes T,
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PEMMARAJU AND MOLITERNO TABLE 1. Ac
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PEMMARAJU AND MOLITERNO drome (BCS)
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PEMMARAJU AND MOLITERNO 13. Xing S,
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THERAPIES AND INDICATIONS FOR PH-NE
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LEUKEMIA, MYELODYSPLASIA, AND TRANS
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RECENT UPDATES IN MDS AND MDS/MPNS
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LUNG CANCER Beyond Second-Line Trea
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BEYOND SECOND-LINE TREATMENT FOR LU
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BEYOND SECOND-LINE TREATMENT FOR LU
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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 TABLE 1.
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GERBER, PAIK, AND DOWLATI gression
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GERBER, PAIK, AND DOWLATI Disclosur
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GERBER, PAIK, AND DOWLATI enzyme in
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GERBER, PAIK, AND DOWLATI receptor
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LILENBAUM, LEIGHL, AND NEUBAUER Exp
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LILENBAUM, LEIGHL, AND NEUBAUER Ref
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BERNARDO H.L. GOULART The Value of
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BERNARDO H.L. GOULART every 6 month
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BERNARDO H.L. GOULART lung-cancer/l
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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 FIGURE 1. Molec
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NASSER HANNA Current Standards and
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NASSER HANNA At the 2014 ASCO Annua
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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 trial is in
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NOWAKOWSKI AND CZUCZMAN 15. Aragon-
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DAVID W. SCOTT Cell-of-Origin in Di
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DAVID W. SCOTT FIGURE 1. The Origin
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DAVID W. SCOTT FIGURE 2. Immunohist
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DAVID W. SCOTT FIGURE 3. The Lymph2
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DAVID W. SCOTT 10. Shaffer AL 3rd,
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CHEAH, OKI, AND FANALE Novel Treatm
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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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STEPHEN ANSELL associated with pati
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STEPHEN ANSELL Disclosures of Poten
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MATEOS AND SAN MIGUEL Smoldering Mu
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MATEOS AND SAN MIGUEL previously me
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MATEOS AND SAN MIGUEL TABLE 2. Risk
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MATEOS AND SAN MIGUEL 30. Rajkumar
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BHUTANI, LANDGREN, AND USMANI of th
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MOREAU AND TOUZEAU Multiple Myeloma
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LYMPHOMA AND PLASMA CELL DISORDERS
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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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MANAGEMENT OF CLL tion by nonmalign
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MANAGEMENT OF CLL fludarabine and c
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MANAGEMENT OF CLL lymphocytic leuke
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PROGNOSTIC FACTORS AND ADJUVANT RAD
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MERKEL CELL CARCINOMA Merkel Cell C
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MERKEL CELL CARCINOMA tions in PIK3
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MERKEL CELL CARCINOMA treating MCC
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MERKEL CELL CARCINOMA 32. Leonard J
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MELANOMA/SKIN CANCERS Locoregional
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PERFUSION AND INFUSION IN THE ERA O
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NEOADJUVANT THERAPY OF MELANOMA Neo
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NEOADJUVANT THERAPY OF MELANOMA TAB
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NEOADJUVANT THERAPY OF MELANOMA ity
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NEOADJUVANT THERAPY OF MELANOMA 4.
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MELANOMA/SKIN CANCERS Targeted Mole
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SULLIVAN ET AL FIGURE 1. Relevant S
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SULLIVAN ET AL Resistance to BRAF i
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SULLIVAN ET AL TABLE 1. Clinical Tr
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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
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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
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
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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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