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GYNECOLOGIC CANCER Treatment of the BRCA Mutation Carrier: Screening, Surveillance, and Management CHAIR Elise C. Kohn, MD National Cancer Institute at the National Institutes of Health Bethesda, MD SPEAKERS Judy Ellen Garber, MD, MPH Dana-Farber Cancer Institute Boston, MA Stanley B. Kaye, MD, FRCP, FRSE The Royal Marsden NHS Foundation Trust London, United Kingdom
TAN AND KAYE Chemotherapy for Patients with BRCA1 and BRCA2–Mutated Ovarian Cancer: Same or Different? David S.P. Tan, PhD, MBBS, BSc, MRCP, and Stanley B. Kaye, MD, FRCP, FRSE OVERVIEW Retrospective studies have shown an improved prognosis, higher response rates to platinum-containing regimens, and longer treatment-free intervals between relapses in patients with BRCA 1 and BRCA 2 (BRCA1/2)–mutated ovarian cancer (BMOC) compared with patients who are not carriers of this mutation. These features of BMOC are attributed to homologous-recombination repair (HR) deficiency in the absence of BRCA1/2 function, which results in an impaired ability of tumor cells to repair platinum-induced double-strand breaks (DSBs), thereby conferring increased chemosensitivity and increased sensitivity to poly(ADP-ribose) polymerase (PARP) enzyme inhibition and other DNA-damaging chemotherapeutic agents such as pegylated liposomal doxorubicin (PLD). Therefore, the chemotherapeutic approach for patients with BMOC should focus on treatment with platinum-based chemotherapy at first-line and recurrent-disease settings and measures to increase the platinum-free interval following early platinum-resistant relapse (i.e., progression-free survival of less than 6 months from last platinum-based chemotherapy) by using nonplatinum cytotoxic agents, with the aim of reintroducing platinum again at a later date. The role of first-line intraperitoneal platinum-based therapy in the specific context of BMOC also merits further analysis. Other than platinum, alternative DNA-damaging agents (including PLD and trabectedin) also may have a therapeutic role in patients with recurrent BMOC. The recent approval of olaparib for clinical use in Europe and the United States will also affect chemotherapeutic strategies for these patients. Further work to clarify the precise relationship between BRCA1/2 mutation genotype and clinical phenotype is crucial to delineating the optimal therapeutic choices in the future for patients with BMOC. The BRCA1/2 tumor suppressor genes are critical for the maintenance of cellular genomic stability through the error-free repair of DNA double-strand breaks (DSBs) via the high-fıdelity homologous-recombination repair (HR) pathway. 1,2 Loss of BRCA1/2 function may occur because of somatic mutations or epigenetic silencing, which results in a dependency on alternative error-prone (low-fıdelity) DNA repair pathways and potential genomic instability. 2 The absence of BRCA1/2 function is associated with a cumulative lifetime risk for developing epithelial ovarian cancer (EOC) of 40% to 50% in patients who are BRCA1-mutation carriers and 20% to 25% in patients who are BRCA2-mutationcarriers. 3 Germ-linemutationsinBRCA1/2have been observed in 14% of patients with nonmucinous EOC, including 17% of patients with high-grade serous histology, with 44% of thesepatientshavingnoreportedfamilyhistoryofbreastorovarian cancer,whereassomaticmutationsinBRCA1/2havebeenfoundin 6% of patients with high-grade serous EOCs. 4,5 PLATINUM SENSITIVITY AND IMPROVED SURVIVAL ARE HALLMARKS OF BRCA-NESS IN EOC Improved prognosis in terms of progression-free survival (PFS) and overall survival (OS), with higher partial response (PR) and complete response (CR) rates to platinumcontaining regimens and longer treatment-free intervals, has been observed in retrospective studies of patients who are BRCA1/2-mutant carriers with ovarian cancer compared with patients who are non-BMOC. 5-10 This “BRCAness” phenotype, with superior outcomes following platinumbased therapy in patients with BMOC, has been attributed to HR defıciency in the absence of BRCA1/2 function. This results in an impaired ability of BRCA-defıcient tumor cells to repair platinum-induced DSBs, which confers increased sensitivity to chemotherapy. 8,9,11 Similarly, inhibition of poly(ADP-ribose) polymerase (PARP) enzymes (which repair single-stranded DNA breaks mainly through the baseexcision repair pathway) in HR-defıcient cells by PARP inhibitors (PARPi) results in DSBs that are subjected to lowfıdelity repair by nonhomologous end joining. 2,12 The absence of high-fıdelity DNA-repair mechanisms following PARPi treatment in HR-defıcient cells leads to synthetic lethality through an accumulation of DNA damage that results in mitotic catastrophe and cell death. 13 PARP inhibitors are active agents in patients with BMOC, but they also may be effective in a subset of sporadic ovarian cancers. 14 Mutations From the National University Cancer Institute, Singapore; National University Hospital, Singapore; The Royal Marsden Hospital NHS Foundation Trust, London, United Kingdom. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Stanley B. Kaye, MD, FRCP, FRSE, The Royal Marsden NHS Foundation Trust, London, United Kingdom; email: stan.kaye@rmh.nhs.uk. © 2015 by American Society of Clinical Oncology. 114 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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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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WONG, CAPASSO, AND ECKHARDT terize
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ABOU-ALFA ET AL HCC (Anti-Programme
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AHN ET AL Pancreatic cancer has bee
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EGIDIO DEL FABBRO tion of precachex
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EGIDIO DEL FABBRO FIGURE 3. Mechani
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GERM CELL TUMORS: LOOKING TO THE FU
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SALVAGE CHEMOTHERAPY Salvage Therap
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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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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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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 squamous
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GERBER, PAIK, AND DOWLATI gression
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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 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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MOREAU AND TOUZEAU Multiple Myeloma
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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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PROGNOSTIC FACTORS AND ADJUVANT RAD
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MERKEL CELL CARCINOMA Merkel Cell C
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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 ity
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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 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
Page 760 and 761:
KLEPIN, RODIN, AND HURRIA patient-s
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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
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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