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GASTROINTESTINAL (NONCOLORECTAL) CANCER The Many Faces of Neuroendocrine Cancers CHAIR Emily Bergsland, MD UCSF Helen Diller Family Comprehensive Cancer Center San Francisco, CA SPEAKERS David S. Klimstra, MD Memorial Sloan Kettering Cancer Center New York, NY Rogerio Lilenbaum, MD Yale Cancer Center New Haven, CT Himisha Beltran, MD Weill Cornell Medical College New York, NY
KLIMSTRA ET AL The Spectrum of Neuroendocrine Tumors: Histologic Classification, Unique Features and Areas of Overlap David S. Klimstra, MD, Himisha Beltran, MD, Rogerio Lilenbaum, MD, and Emily Bergsland, MD OVERVIEW Neuroendocrine neoplasms are diverse in terms of sites of origin, functional status, and degrees of aggressiveness. This review will introduce some of the common features of neuroendocrine neoplasms and will explore the differences in pathology, classification, biology, and clinical management between tumors of different anatomic sites, specifically, the lung, pancreas, and prostate. Despite sharing neuroendocrine differentiation and histologic evidence of the neuroendocrine phenotype in most organs, well-differentiated neuroendocrine tumors (WD-NETs) and poorly differentiated neuroendocrine carcinomas (PD-NECs) are two very different families of neoplasms. WD-NETs (grade 1 and 2) are relatively indolent (with a natural history that can evolve over many years or decades), closely resemble non-neoplastic neuroendocrine cells, and demonstrate production of neurosecretory proteins, such as chromogranin A. They arise in the lungs and throughout the gastrointestinal tract and pancreas, but WD-NETs of the prostate gland are uncommon. Surgical resection is the mainstay of therapy, but treatment of unresectable disease depends on the site of origin. In contrast, PD-NECs (grade 3, small cell or large cell) of all sites often demonstrate alterations in P53 and Rb, exhibit an aggressive clinical course, and are treated with platinum-based chemotherapy. Only WD-NETs arise in patients with inherited neuroendocrine neoplasia syndromes (e.g., multiple endocrine neoplasia type 1), and some common genetic alterations are site-specific (e.g., TMPRSS2-ERG gene rearrangement in PD-NECs arising in the prostate gland). Advances in our understanding of the molecular basis of NETs should lead to new diagnostic and therapeutic strategies and is an area of active investigation. Neuroendocrine neoplasms are a diverse group of neoplasms. Although these share certain pathologic features regardless of where they arise, they have largely been studied and classifıed in an organ-specifıc manner (which has led to a variety of different terminological variations) and their grading and staging remain site specifıc. Nonetheless, conceptual commonalities cross organ boundaries. This review will introduce some of the common features of neuroendocrine neoplasms and will also explore the differences in pathology, classifıcation, biology, and clinical management between tumors of different anatomic sites, specifıcally the lungs, pancreas, and prostate. PATHOLOGIC CONCEPTS IN NEUROENDOCRINE TUMORS The concept of neuroendocrine differentiation in tumors can be defıned as the secretion into the bloodstream of bioactive substances, usually peptide hormones or bioamines, by the neoplastic cells. The histologic similarity of the cells composing many neuroendocrine neoplasms and non-neoplastic neuroendocrine cells suggests that the tumors may arise from these mature counterparts. Although this concept is likely overly simplistic even in the case of WD-NETs, which bear the closest resemblance to their normal cell counterparts. Pathologically, neuroendocrine differentiation has come to be defıned as architectural and cytological patterns reminiscent of non-neoplastic neuroendocrine cells (such as a nesting or trabecular growth pattern and coarsely stippled nuclear chromatin) and the production of characteristic neurosecretory proteins that can be detected by immunohistochemistry. These include most importantly chromogranin A and synaptophysin, although some authorities accept the expression of CD56 (neural cell adhesion molecule or even neuron specifıc enolase (NSE) as adequate evidence of neuroendocrine differentiation. 1-3 However, NSE has been widely questioned as a neuroendocrine marker, based on the lack of specifıcity. Thus, in practice, WD-NETs are usually readily recognizable as having neuroendocrine differentiation based on their routine histologic features, and proof can be obtained with universally available immunohistochemical stains. The historic terms for WD-NETs was a carcinoid tumor or, in the pancreas, an islet cell tumor, although recent practice in the gastroenteropancreatic system has been to replace these terms with NET to avoid the connotation that a carcinoid tumor is a benign neoplasm. 1-3 From the Memorial Sloan Kettering Cancer Center, New York, NY; Weill Cornell Medical College, New York, NY; Yale Cancer Center, New Haven, CT; UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA. Disclosures of potential conflicts of interest are found at the end of this article. Corresponding author: Emily Bergsland, MD, UCSF Helen Diller Family Comprehensive Cancer Center, 1600 Divisadero St., Room A727, San Francisco, CA 94143; email: emily.bergsland@ucsf.edu. © 2015 by American Society of Clinical Oncology. 92 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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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
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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
Page 786 and 787:
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
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
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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
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
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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.
Page 862 and 863:
CLINICAL ONCOLOGY PRACTICE 2015 Pro
Page 864 and 865:
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
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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