REFERENCES
- Fraser WD. Hyperparathyroidism. Lancet 2009;374:145–158.
- Adami S, Marcocci C, Gatti D. Epidemiology of primary hyperparathyroidism in Europe. J Bone Miner. 2002;17(Suppl 2):18–23.
- Silverberg SJ, Bilezikian JP. Evaluation and management of primary hyperparathyroidism. J Clin Endocrinol Metab. 1996;81:2036–2040.
- Irvin GL, Carneiro D. Management changes in primary hyperparathyroidism. JAMA 2000;284:934–936.
- Clark OH.Surgical treatment of primary hyperparathyroidism. Adv Endocrinol Metab. 1995;6:1–9.
- Kimberley FC, Screaton GR. Following a TRAIL: update on a ligand and its five receptors. Cell Res. 2004;14:359–372.
- Tecchio C, Huber V, Scapini P, et al. IFNalpha-stimulated neutrophils and monocytes release a soluble form of TNF-related apoptosis-inducing ligand (TRAIL/Apo-2 ligand) displaying apoptotic activity on leukemic cells. Blood 2004;103:3837–3844.
- Corazza N, Kassahn D, Jakob S, et al. TRAIL-induced apoptosis: between tumor therapy and immunopathology. Ann N Y Acad Sci. 2009;1171:50–58.
- Stuckey DW, Shah K. TRAIL on trial: preclinical advances in cancer therapy. Trends Mol Med. 2013;19:685–694.
- Mori K, Emoto M, Inaba M. Multifunctional role of TRAIL in atherosclerosis and cardiovascular disease. In: Advances in the Diagnosis of Coronary Atherosclerosis, Kiraç SF, ed. Rijeka, Croatia: In Tech; 2011:19–32.
- Mori K, Ikari Y, Jono S, et al. Association of serum TRAIL level with coronary artery disease. Thromb Res. 2010;125:322–325.
- Michowitz Y, Goldstein E, Roth A, et al. The involvement of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in atherosclerosis. J Am Coll Cardiol. 2005;45:1018–1024.
- Guicciardi ME, Gores GJ. Life and death by death receptors. FASEB J. 2009;23:1625–1637.
- Son JK, Varadarajan S, Bratton SB. TRAIL-activated stress kinases suppress apoptosis through transcriptional upregulation of MCL-1. Cell Death Differ. 2010;17:1288–1301.
- Schneider P, Thome M, Burns K, et al. TRAIL receptors 1 (DR4) and 2 (DR5) signal FADD-dependent apoptosis and activate NF-kappaB. Immunity 1997;7:831–836.
- Peter ME, Krammer PH. The CD95(APO-1/Fas) DISC and beyond. Cell Death Differ. 2003;10:26–35.
- Nagata S.Apoptosis by death factor. Cell 1997;88:355–365.
- Krammer PH.CD95′s deadly mission in the immune system. Nature 2000;407:789–795.
- Peter ME, Barnhart BC, Algeciras-Schimnich A. The cytokine handbook: CD95L/FasL and its receptor CD95 (APO-1/Fas). Cytokine Handbook 2003;2:885–911.
- Árvai K, Nagy K, Barti-Juhász H et al. Molecular profiling of parathyroid hyperplasia, adenoma and carcinoma. Pathol Oncol Res. 2012;18(3):607–614.
- Szende B, Árvai K, Peták I, et al. Changes in gene expression in the course of proliferative processes in the parathyroid gland. Magy Onkol. 2006;50(2):137–140.
- Wang W, Johansson H, Kvasnicka T, et al. Detection of apoptotic cells and expression of Ki-67 antigen, bcl-2, p53 oncoproteins in human parathyroid adenoma. Acta Pathol Microbiol Scand. 1996;104:789–796.
- Thomopoulou GE, Tseleni-Balafouta S, Lazaris AC, et al. Immunohistochemical detection of cell cycle regulators, Fhit protein and apoptotic cells in parathyroid lesions. Eur J Endocrinol. 2003;148(1):81–87.
- Szende B, Farid P, Vegso G, et al. Apoptosis and P53, Bcl-2 and Bax gene expression in parathyroid glands of patients with hyperparathyroidism. Pathol Oncol Res. 2004;10(2):98–103.
- Kvasnicka T, Wang W, Johansson H, et al. Apoptosis and growth factors in parathyroid adenomas. Horm Metab Res. 1997;29(11):544–548.
- Hadar T, Shvero J, Yaniv E, et al. Expression of p53, Ki-67 and Bcl-2 in parathyroid adenoma and residual normal tissue. Pathol Oncol Res. 2005;11(1):45–49.
- Martinou JC, Youle RJ. Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics. Dev Cell 2011;21:92–101.
- Vargas MP, Vargas HI, Kleiner DE, Merino MJ. The role of prognostic markers (MiB-1, RB, and bcl-2) in the diagnosis of parathyroid tumors. Mod Pathol. 1997;10(1):12–17.