Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive(1653 views) Dynkevich Y, Rother KI, Whitford I, Qureshi S, Galiveeti S, Szulc AL, Danoff A, Breen TL, Kaviani N, Shanik MH, LeRoith D, Vigneri R, Koch CA, Roth J
Queens Long Island Medical Group, North Shore-Long Island Jewish (NS-LIJ) Health System, Hicksville, NY 11801, United States
National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, United States
Laboratory of Diabetes and Diabetes-Related Research, Feinstein Institute for Medical Research, NS-LIJ Health System, Manhasset, NY 11030, United States
Albert Einstein College of Medicine, Yeshiva University, Bronx, NY 10461, United States
Division of Endocrinology, Diabetes, and Metabolism, New York University, School of Medicine, New York 10016, NY, United States
Veterans Administration New York Harbor Healthcare System, New York 10010, NY, United States
Hofstra NS-LIJ School of Medicine, NS-LIJ Health System, Manhasset, NY 11549, United States
Endocrinology and Metabolism, Geisinger Health System, State College, Pennsylvania 16801, United States
Endocrine Associates of Long Island, Smithtown, NY 11787, United States
Stony Brook University Hospital, Stony Brook, NY 11794, United States
Diabetes and Metabolism Clinical Research Center of Excellence, Clinical Research Institute at Rambam, Haifa 31096, Israel
Endocrine Unit, Department of Clinical and Molecular Biomedicine, University of Catania, Garibaldi-Nesima Hospital, Catania, Italy
Istituto di Biostrutture e Bioimmagini-Consilgio Nazionale delle Richerche Catania Section, Catania 95131, Italy
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Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive
Tumors of mesenchymal and epithelial origin produce IGF-2, which activates pathways in the tumors. In a minority of patients, the tumors (hepatomas, fibromas, and fibrosarcomas are the most common among many) release into the circulation enough IGF-2-related peptides to mimic the fasting hypoglycemia characteristic of patients with insulin-producing islet-cell tumors. Rarely, markedly elevated IGF-2 levels produce somatic changes suggestive of acromegaly. Typically, the elevated IGF-2 levels are associated with suppressed plasma levels of insulin, IGF-1, and GH. Complicating the pathophysiology are the IGF binding proteins (IGFBPs) that can bind IGF-2 and IGF-1, modifying hormone metabolism and action. IGFBP concentrations are often altered in the presence of these tumors. At the cellular level, the 3 hormone-related ligands, IGF-2, IGF-1, and insulin, all bind to 4 (or more) types of IGF-1 receptor (IGF-1R) and insulin receptor (IR). Each receptor has its own characteristic affinity for each ligand, a tyrosine kinase, and overlapping profiles of action in the target cells. The IGF-2R, in addition to binding mannose-6-phosphate-containing proteins, provides an IGF-2 degradation pathway. Recent evidence suggests IGF-2R involvement also in signal transduction. Surgery, the treatment of choice, can produce a cure. For patients not cured by surgery, multiple therapies exist, for the tumor and for hypoglycemia. Potential future therapeutic approaches are sketched. From 1910 to 1930, hypoglycemia, insulin, insulinomas, and non-islet-cell tumors were recognized. The latter third of the century witnessed the emergence of the immunoassay for insulin; the IGFs, their binding proteins, and assays to measure them; and receptors for the insulin-related peptides as well as the intracellular pathways beyond the receptor. In closing, we replace non-islet-cell tumor hypoglycemia, an outdated and misleading label, with IGF-2-oma, self-explanatory and consistent with names of other hormone-secreting tumors.
Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive
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Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive
Petraglia F, Singh AA, Carafa V, Nebbioso A, Conte M, Scisciola L, Valente S, Baldi A, Mandoli A, Petrizzi VB, Ingenito C, De Falco S, Cicatiello V, Apicella I, Janssen-megens EM, Kim B, Yi G, Logie C, Heath S, Ruvo M, Wierenga ATJ, Flicek P, Yaspo ML, Della Valle V, Bernard O, Tomassi S, Novellino E, Feoli A, Sbardella G, Gut I, Vellenga E, Stunnenberg HG, Mai A, Martens JHA, Altucci L * Combined HAT/EZH2 modulation leads to cancer-selective cell death(284 views) Oncotarget (ISSN: 1949-2553electronic, 1949-2553linking), 2018 May 22; 9(39): 25630-25646. Impact Factor:5.008 ViewExport to BibTeXExport to EndNote