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CENTRAL NERVOUS SYSTEM TUMORS Brain Metastases: From Clinical Trials to Clinical Practice CHAIR Manmeet S. Ahluwalia, MD Cleveland Clinic Cleveland, OH SPEAKERS Frank Winkler, MD University of Heidelberg Heidelberg, Germany Minesh P. Mehta, MD University of Maryland School of Medicine Baltimore, MD
APPROACHES IN BRAIN METASTASES Targeted and Immunotherapeutic Approaches in Brain Metastases Manmeet S. Ahluwalia, MD, and Frank Winkler, MD OVERVIEW Brain metastases are a common and devastating complication of cancer. The approach to the management of brain metastases is often multidisciplinary and includes surgery, whole-brain radiation therapy (WBRT), stereotactic radiosurgery (SRS), and systemic therapeutic agents. Until recently, systemic therapy has had a limited role in the management of brain metastases because of a lack of activity, challenges of blood-brain barrier penetration, the heterogeneous patient population, and a heavily pretreated patient population. Advances in the understanding of the biology of brain metastases and molecularly defined disease subsets have facilitated an emerging role of novel therapeutic agents, including targeted therapies and immunotherapy, in the management of brain metastases. Brain metastases are serious complications of systemic cancer that occur in 10% to 30% of adults with cancer. 1 The most common malignancies that metastasize to the brain are lung, breast, and melanoma. 2-5 Eighty percent of patients present with brain metastases within the cerebral hemispheres; 15% are within the cerebellar hemispheres and 5% are within the brainstem. 6 Key determinants in the management of brain metastases include the tumor histology, number, size, and site of lesions; the status of extracranial metastases; and the performance status of the patient. One of the challenges in the development of effective therapies for brain metastases is the presence of the blood-brain barrier, a highly selective permeability barrier made of capillary endothelial cells connected by tight junctions and astrocyte foot processes that limit entry of systemic therapies into the brain. 7,8 In addition, active transport mechanisms of drug efflux and high plasma protein binding of agents further lower the volume of distribution of agents in the brain parenchyma. 8 An additional challenge is that patients who develop brain metastases often are heavily pretreated with tumors that are more likely to be resistant to therapy at diagnosis of the brain metastases. The role of systemic therapy (chemotherapy, targeted agents, or immunotherapy) in brain metastases is not well defıned, because there is no level-1 evidence favoring the use of systemic therapy compared with local approaches. However, in recent years, the development of novel cytotoxic agents and targeted therapies with better blood-brain barrier penetration have increased the interest in use of systemic therapies in brain metastases. TARGETING BRAIN HOST CELLS Another potential mechanism of resistance in metastatic tumor cells in the brain is their interaction with brain resident cells. The brain metastatic process depends on the perpetuation of a perivascular niche, at least during the early steps, 9 and this niche has been associated with promotion and/or maintenance of a stem-like and resistant cellular phenotype, per se, in brain tumors. The components of the blood-brain barrier (endothelial cells, pericytes, astrocytic foot processes, and/or the vascular basement membrane) 10 are likely candidates to provide this supportive niche for cancer cells. Conversely, the high ineffıciency of the brain metastatic process (with 95% to 99% of brain-arrested cancer cells failing to successfully grow to a macrometastasis 9 ) raises the question of whether some of these components are more foe than friend for extravasating cancer cells in the brain. A recent report suggested that the astrocyte-produced plasminogen activator forces brain metastatic cancer cells into apoptosis and that cancer cells need to inhibit this process to survive this brain protective mechanism. 11 In contrast, astrocytes might protect brain metastatic cancer cells from the adverse effects of chemotherapy by buffering intracellular calcium increases via gap junction coupling and other mechanisms. 12 Thus, the role of many brain resident cells appears to be complex, and further research is required to understand the potential to target them for brain metastasis prevention or treatment. The brain endothelial cell (the main cell type reacting to angiogenic growth factors produced by tumor cells) appears to be among the most promising cellular target that is emerging, as detailed in this review. From the Burkhardt Brain Tumor Neuro-Oncology Center, Neurological Institute, Cleveland Clinic, Cleveland, OH; Neurology Clinic, University of Heidelberg and German Cancer Research Center, Heidelberg, Germany. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Manmeet S. Ahluwalia, MD, Burkhardt Brain Tumor and Neuro-Oncology Center, Neurological Institute, Cleveland Clinic, 9500 Euclid Ave., S70, Cleveland, OH 44195; email: ahluwam@ccf.org. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK 67
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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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AHN ET AL Making Sense of Current a
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AHN ET AL Pancreatic cancer has bee
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AHN ET AL Disclosures of Potential
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EGIDIO DEL FABBRO tion of precachex
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EGIDIO DEL FABBRO FIGURE 3. Mechani
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EGIDIO DEL FABBRO II RCT of ghrelin
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SALVAGE CHEMOTHERAPY Salvage Therap
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NOVEL IMMUNOTHERAPY AGENTS IN METAS
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GYNECOLOGIC CANCER Cervical Cancer
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GYNECOLOGIC CANCER Managing Ovarian
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DUSKA, TEW, AND MOORE KEY POINTS A
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GYNECOLOGIC CANCER Treatment of the
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CHEMOTHERAPY FOR PATIENTS WITH BMOC
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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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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 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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HEMATOPOIETIC CELL TRANSPLANTATION
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MICHAEL W. DEININGER TABLE 1. Defin
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PEMMARAJU AND MOLITERNO drome (BCS)
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THERAPIES AND INDICATIONS FOR PH-NE
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GERBER, PAIK, AND DOWLATI a tumor t
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GERBER, PAIK, AND DOWLATI gression
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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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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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DAVID W. SCOTT Cell-of-Origin in Di
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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 TABLE 3. Sel
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CHEAH, OKI, AND FANALE 77. Cairns R
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STEPHEN ANSELL Disclosures of Poten
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MATEOS AND SAN MIGUEL Smoldering Mu
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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 lymphocytic leuke
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MERKEL CELL CARCINOMA Merkel Cell C
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MERKEL CELL CARCINOMA 32. Leonard J
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PERFUSION AND INFUSION IN THE ERA O
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NEOADJUVANT THERAPY OF MELANOMA Neo
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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 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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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
Page 816 and 817:
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
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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’
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Page 850 and 851:
Page 852 and 853:
PATIENT-REPORTED OUTCOMES IN ONCOLO
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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
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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
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
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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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