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LESLIE R. SCHOVER 12. Potosky AL, Haque R, Cassidy-Bushrow AE, et al. Effectiveness of primary androgen-deprivation therapy for clinically localized prostate cancer. J Clin Oncol. 2014;32:1324-1330. 13. Elliott S, Latini DM, Walker LM, et al. Androgen deprivation therapy for prostate cancer: recommendations to improve patient and partner quality of life. J Sex Med. 2010;7:2996-3010. 14. Denham JW, Wilcox C, Joseph D, et al. Quality of life in men with locally advanced prostate cancer treated with leuprorelin and radiotherapy with or without zoledronic acid (TROG 03.04 RADAR): secondary endpoints from a randomised phase 3 factorial trial. Lancet Oncol. 2012;13: 1260-1270. 15. Son CH, Chennupati SK, Kunnavakkam R, et al. The impact of hormonal therapy on sexual quality of life in men receiving intensity modulated radiation therapy for prostate cancer. Pract Radiat Oncol. Epub 2014 Dec 6. 16. Benedict C, Traeger L, Dahn JR, et al. Sexual bother in men with advanced prostate cancer undergoing androgen deprivation therapy. J Sex Med. 2014;11:2571-2580. 17. Schover LR, Fouladi RT, Warneke CL, et al. Defıning sexual outcomes after treatment for localized prostate carcinoma. Cancer. 2002;95:1773- 1785. 18. Sevilla C, Maliski SL, Kwan L, et al. Long-term quality of life in disadvantaged men with prostate cancer on androgen-deprivation therapy. Prostate Cancer Prostatic Dis. 2012;15:237-243. 19. Mazzola CR, Deveci S, Heck M, et al. Androgen deprivation therapy before radical prostatectomy is associated with poorer postoperative erectile function outcomes. BJU Int. 2012;110:112-116. 20. Harden J, Sanda MG, Wei JT, et al. Survivorship after prostate cancer treatment: spouses’ quality of life at 36 months. Oncol Nurs Forum. 2013;40:567-573. 21. Klotz L, Nabid A, Higano C, et al. Effect of dutasteride in men receiving intermittent androgen ablation therapy: the AVIAS trial. Can Urol Assoc J. 2014;8:E789-E794. 22. Traish AM, Mulgaonkar A, Giordano N. The dark side of 5-reductase inhibitors’ therapy: sexual dysfunction, high Gleason grade prostate cancer and depression. Korean J Urol. 2014;55:367-379. 23. Klotz L. Intermittent versus continuous androgen deprivation therapy in advanced prostate cancer. Curr Urol Rep. 2013;14:159-167. 24. Langenhuijsen JF, Badhauser D, Schaaf B, et al. Continuous vs. intermittent androgen deprivation therapy for metastatic prostate cancer. Urol Oncol. 2013;31:549-556. 25. Wibowo E, Wassersug RJ. The effect of estrogen on the sexual interest of castrated males: implications to prostate cancer patients on androgendeprivation therapy. Crit Rev Oncol Hematol. 2013;87:224-238. 26. Ng E, Woo HH, Turner S, et al. The influence of testosterone suppression and recovery on sexual function in men with prostate cancer: observations from a prospective study in men undergoing intermittent androgen suppression. J Urol. 2012;187:2162-2166. 27. Carani C, Bancroft J, Granata A, et al. Testosterone and erectile function, nocturnal penile tumescence and rigidity, and erectile response to visual erotic stimuli in hypogonadal and eugonadal men. Psychoneuroendocrinology. 1992;17:647-654. 28. Schover LR, Canada AL, Yuan Y, et al. A randomized trial of Internetbased versus traditional sexual counseling for couples after localized prostate cancer treatment. Cancer. 2012; 118:500-509. 29. Basal S, Wambi C, Acikel C, et al. Optimal strategy for penile rehabilitation after robot-assisted radical prostatectomy based on preoperative erectile function. BJU Int. 2013;111:658-665. 30. Tal R, Valenzuela R, Aviv N, et al. Persistent erectile dysfunction following radical prostatectomy: the association between nerve-sparing status and the prevalence and chronology of venous leak. J Sex Med. 2009;6: 2813-2819. 31. Dowsett GW, Lyons A, Duncan D, et al. Flexibility in men’s sexual practices in response to iatrogenic erectile dysfunction after prostate cancer treatment. Sex Med. 2014;2:115-120. 32. Frey AU, Sønksen J, Fode M. Neglected side effects after radical prostatectomy: a systematic review. J Sex Med. 2014;11:374-385. 33. Mehta A, Deveci S, Mulhall JP. Effıcacy of a penile variable tension loop for improving climacturia after radical prostatectomy. BJU Int. 2013; 111:500-504. 34. Carmack Taylor CL, Demoor C, Smith MA, et al. Active for life after cancer: a randomized trial examining a lifestyle physical activity program for prostate cancer patients. Psychooncology. 2006;15:847-862. 35. Jones LW, Hornsby WE, Freedland SJ, et al. Effects of nonlinear aerobic training on erectile dysfunction and cardiovascular function following radical prostatectomy for clinically localized prostate cancer. Eur Urol. 2014;65:852-855. 36. Cormie P, Newton RU, Taaffe DR, et al. Exercise maintains sexual activity in men undergoing androgen suppression for prostate cancer: a randomized controlled trial. Prostate Cancer Prostatic Dis. 2013;16:170- 175. e566 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
BONE HEALTH AND ENDOCRINE THERAPY IN BREAST OR PROSTATE CANCER Bone Health in Adults Treated with Endocrine Therapy for Early Breast or Prostate Cancer Catherine H. Van Poznak, MD OVERVIEW Bone is a hormonally responsive organ. Sex hormones and calcium regulating hormones, including parathyroid hormone, 1–25 dihydroxy vitamin D, and calcitonin, have effects on bone resorption and bone deposition. These hormones affect both bone quality and bone quantity. The sex hormone estrogen inhibits bone resorption, and estrogen therapy has been developed to prevent and treat osteoporosis. Androgens are an important source of estrogen through the action of the enzyme aromatase and may themselves stimulate bone formation. Hence, the sex steroids play a role in bone metabolism. Breast cancer and prostate cancer are frequently hormonally responsive and may be treated with antiestrogens or antiandrogens respectfully. In addition, chemotherapy and supportive medications may alter the patient’s endocrine system. In general, the suppression of sex hormones has a predictable affect on bone health, as seen by loss of bone mineral density and increased risk of fragility fractures. The bone toxicity of cancer-directed endocrine therapy can be mitigated through screening, counseling on optimization of calcium and vitamin D intake, exercise, and other lifestyle/behavioral actions, as well as the use of medications when the fracture risk is high. Maintaining bone health in patients who are treated with endocrine therapy for breast and prostate cancer is the focus of this review. In the United States, approximately one in eight women will be affected by breast cancer and one in seven men will be affected by prostate cancer. Screening techniques and excellent therapies exist for both of these cancers. Although there remains room for improvement, the cure and survival rates for both of these cancers are high. It is estimated that there are more than 2.8 million breast cancer survivors and more than 2.7 million prostate cancer survivors alive today in the United States. 1,2 Breast cancer and prostate cancer are frequently hormonally responsive and may be treated with antiestrogens or antiandrogens. In general, the suppression of sex hormones during cancer therapy has a predictable affect on bone health, as seen by loss of bone mineral density and increased risk of fragility fractures. Hence, in terms of survivorship of these patients, long-term bone health issues, including osteoporosis, are a public health concern. When treating breast and prostate cancer in the adjuvant setting, the goals of care are curative. For metastatic breast or prostate cancer, the goals of care are palliative. Metastatic breast and prostate cancers typically affect life expectancy and often cause bone metastases. Although the following discussion of bone health includes much that is applicable to both adjuvant and metastatic care, the focus is on the nonmetastatic setting. OSTEOPENIA AND OSTEOPOROSIS IN THE OLDER ADULT POPULATION In the United States, approximately 10 million people have osteoporosis and an additional 43 million have low bone density. 3,4 Low bone mass correlates with an increased risk for fracture, and fractures are associated with substantial morbidity and mortality. Approximately one in two women and one in fıve men in the United States will experience an osteoporotic fracture. 3 A particularly disconcerting fact is that a hip fracture is associated with 8% to 36% excess mortality within 1 year. In addition, 20% of patients with a fracture of the hip require long-term nursing home care, and 60% will not regain their prefracture level of independence. 3 In addition to the pain and suffering associated with fractures, they are also is a substantial burden to health care expenditure. A standard technique for measuring bone mineral density (BMD) is dual energy X-ray absorptiometry (DXA). The World Health Organization 5 has defıned conditions of low bone mass using BMD as outlined in Table 1. The T score represents the standard deviation from an ideal bone mass. The BMD measurement provides the diagnostic criteria of osteoporosis as well as a threshold for pharmaceutical intervention. 4 Although the T score provides the operational definition of osteoporosis, the underlying health concern is the risk for fracture, not simply having a low DXA T score. There From the Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan, Ann Arbor, MI 5848. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Catherine Van Poznak, MD, Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan, 1500 E Medical Center Dr., Ann Arbor, MI 48109; email: cvanpoz@med.umich.edu. © 2015 by American Society of Clinical Oncology. asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e567
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Controversies in Neoadjuvant Therap
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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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LYMPHOMA AND PLASMA CELL DISORDERS
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DAVID W. SCOTT Cell-of-Origin in Di
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DAVID W. SCOTT FIGURE 1. The Origin
Page 648 and 649:
DAVID W. SCOTT FIGURE 2. Immunohist
Page 650 and 651:
DAVID W. SCOTT FIGURE 3. The Lymph2
Page 652 and 653:
DAVID W. SCOTT 10. Shaffer AL 3rd,
Page 654 and 655:
CHEAH, OKI, AND FANALE Novel Treatm
Page 656 and 657:
CHEAH, OKI, AND FANALE an ongoing G
Page 658 and 659:
CHEAH, OKI, AND FANALE a similar me
Page 660 and 661:
CHEAH, OKI, AND FANALE TABLE 3. Sel
Page 662 and 663:
CHEAH, OKI, AND FANALE eral T cell
Page 664 and 665:
CHEAH, OKI, AND FANALE 77. Cairns R
Page 666 and 667:
STEPHEN ANSELL associated with pati
Page 668 and 669:
STEPHEN ANSELL Disclosures of Poten
Page 670 and 671:
MATEOS AND SAN MIGUEL Smoldering Mu
Page 672 and 673:
MATEOS AND SAN MIGUEL years. This f
Page 674 and 675:
MATEOS AND SAN MIGUEL previously me
Page 676 and 677:
MATEOS AND SAN MIGUEL TABLE 2. Risk
Page 678 and 679:
MATEOS AND SAN MIGUEL 30. Rajkumar
Page 680 and 681:
BHUTANI, LANDGREN, AND USMANI of th
Page 682 and 683:
BHUTANI, LANDGREN, AND USMANI bette
Page 684 and 685:
BHUTANI, LANDGREN, AND USMANI fıne
Page 686 and 687:
BHUTANI, LANDGREN, AND USMANI FIGUR
Page 688 and 689:
BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
Page 692 and 693:
MOREAU AND TOUZEAU other effıcacy
Page 694 and 695:
MOREAU AND TOUZEAU was able to indu
Page 696 and 697:
MOREAU AND TOUZEAU Group consensus
Page 698 and 699:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 700 and 701:
MANAGEMENT OF CLL Up-Front Manageme
Page 702 and 703:
MANAGEMENT OF CLL than 17p-/TP53mut
Page 704 and 705:
MANAGEMENT OF CLL could be associat
Page 706 and 707:
MANAGEMENT OF CLL tion by nonmalign
Page 708 and 709:
MANAGEMENT OF CLL fludarabine and c
Page 710 and 711:
MANAGEMENT OF CLL lymphocytic leuke
Page 712 and 713:
PROGNOSTIC FACTORS AND ADJUVANT RAD
Page 714 and 715:
Page 716 and 717:
Page 718 and 719:
MERKEL CELL CARCINOMA Merkel Cell C
Page 720 and 721:
MERKEL CELL CARCINOMA tions in PIK3
Page 722 and 723:
MERKEL CELL CARCINOMA treating MCC
Page 724 and 725:
MERKEL CELL CARCINOMA 32. Leonard J
Page 726 and 727:
MELANOMA/SKIN CANCERS Locoregional
Page 728 and 729:
PERFUSION AND INFUSION IN THE ERA O
Page 730 and 731:
Page 732 and 733:
Page 734 and 735: NEOADJUVANT THERAPY OF MELANOMA Neo
Page 736 and 737: NEOADJUVANT THERAPY OF MELANOMA TAB
Page 738 and 739: NEOADJUVANT THERAPY OF MELANOMA ity
Page 740 and 741: NEOADJUVANT THERAPY OF MELANOMA 4.
Page 742 and 743: MELANOMA/SKIN CANCERS Targeted Mole
Page 744 and 745: SULLIVAN ET AL FIGURE 1. Relevant S
Page 746 and 747: SULLIVAN ET AL Resistance to BRAF i
Page 748 and 749: SULLIVAN ET AL TABLE 1. Clinical Tr
Page 750 and 751: SULLIVAN ET AL 17. Halait H, Demart
Page 752 and 753: SULLIVAN ET AL NRAS-mutant melanoma
Page 754 and 755: 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 772 and 773: PARTRIDGE, JACOBSEN, AND ANDERSEN C
Page 774 and 775: 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 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
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 834 and 835:
REDUCING THE BURDEN OF LATE EFFECTS
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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