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Review Article

Apoptosis in Primary Hyperparathyroidism

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Pages 328-332 | Received 05 Feb 2017, Accepted 02 Mar 2017, Published online: 31 Mar 2017

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.
  • DeLellis RA, Lloyd RV, Heitz PU. Pathology and genetics of the tumours of endocrine organs. In: WHO Classification of Tumours. DeLellis RA, Lloyd RV, Heitz PU, Eng C, eds. Lyon, France: IARC Press; 2006:124–127.
  • Kim HK, Oh YL, Kim SH. Parafibromin immunohistochemical staining to differentiate parathyroid carcinoma from parathyroid adenoma. Head Neck 2012;34(2):201–206.
  • Tan MH, Morrison C, Wang P, et al. Loss of parafibromin immunoreactivity is a distinguishing feature of parathyroid carcinoma. Clin Cancer Res. 2004;10:6629–6637.
  • Juhlin CC, Haglund F, Obara T, et al. Absence of nucleolar parafibromin immunoreactivity in subsets of parathyroid malignant tumours. Virchows Arch. 2011;459:47–53.
  • Juhlin CC, Nilson IL, Johansson K, et al. Parafibromin and APC as screening markers for malignant potential in atypical parathyroid adenomas. Endocr Pathol. 2010;21:166–177.
  • Wang O, Wang CY, Shi J, et al. Expression of Ki-67, galectin-3, fragile histidine triad, and parafibromin in malignant and benign parathyroid tumors. Chin Med J (Engl). 2012;125(16):2895–2901.
  • Cetani F, Ambrogini E, Viacava P, et al. Should parafibromin staining replace HRPT2 gene analysis as an additional tool for histologic diagnosis of parathyroid carcinoma? Eur J Endocrinol. 2007;156:547–554.
  • Shattuck TM, Välimäki S, Obara T, et al. Somatic and germ-line mutations of the HRPT2 gene in sporadic parathyroid carcinoma. N Engl J Med. 2003;349:1722–1729.
  • Howell VM, Haven CJ, Kahnoski K, et al. HRPT2 mutations are associated with malignancy in sporadic parathyroid tumours. J Med Genet. 2003;40:657–663.
  • Gill AJ, Clarkson A, Gimm O, et al. Loss of nuclear expression of parafibromin distinguishes parathyroid carcinomas and hyperparathyroidism–jaw tumour (HPT-JT) syndrome-related adenomas from sporadic parathyroid adenomas and hyperplasias. Am J Surg Pathol. 2006;30:1140–1149.
  • Alò PL, Visca P, Mazzaferro S, et al. Immunohistochemical study of fatty acid synthase, Ki67, proliferating cell nuclear antigen, and p53 expression in hyperplastic parathyroids. Ann Diagn Pathol. 1999;3(5):287–293.
  • Stojadinovic A, Hoos A, Nissan A, et al. Parathyroid neoplasms: clinical, histopathological, and tissue microarraybased molecular analysis. Hum Pathol. 2003;34:54–64.
  • Lloyd RV, Carney JA, Ferreiro JA, et al. Immunohistochemical analysis of the cell cycle-associated antigens Ki-67 and retinoblastoma protein in parathyroid carcinomas and adenomas. Endocr Pathol. 1995;6:279–287.
  • 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.
  • Kebebew E, Arici C, Duh QY, et al. Localization and reoperation results for persistent and recurrent parathyroid carcinoma. Arch Surg. 2001;136:878–885.
  • Fuchs Y, Steller H. Programmed cell death in animal development and disease. Cell. 2011;147(4):742–758.
  • Kerr JF, Wyllie AH, Currie AR. Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer. 1972;26:239–257.
  • Muzio M, Stockwell BR, Stennicke HR, et al. An induced proximity model for caspase-8 activation. J Biol Chem. 1998;273(5):2926–2930.
  • Boatright KM, Salvesen GS. Mechanisms of caspase activation. Curr Opin Cell Biol. 2003;15(6):725–731.
  • Chang DW, Ditsworth D, Liu H, et al. Oligomerization is a general mechanism for the activation of apoptosis initiator and inflammatory procaspases. J Biol Chem. 2003;278(19):16466–16469.
  • Riedl SJ, Shi Y. Molecular mechanisms of caspase regulation during apoptosis. Nat Rev Mol Cell Biol. 2004;5(11):897–907.
  • Taylor RC, Cullen SP, Martin SJ. Apoptosis: controlled demolition at the cellular level. Nat Rev Mol Cell Biol. 2008;9(3):231–241.
  • 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.
  • 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 Pathologica Microbiologica Scandinavica. 1996;104:789–796.
  • Kvasnicka T, Wang W, Johansson H, et al. Apoptosis and growth factors in parathyroid adenomas. Horm Metab Res. 1997;29(11):544–548.
  • 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.
  • 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.
  • Segiet OA, Deska M, Mielańczyk Ł, et al. Expression of TRAIL and fas in primary hyperparathyroidism. J Invest Surg. doi:10.1080/08941939.2016.1236159
  • 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, Arvai 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.
  • 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: InTech; 2011:19–32.
  • Mori K, Ikari Y, Jono S, et al. ssociation 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.
  • Ritter CS, Haughey BH, Miller B, et al. Differential gene expression by oxyphil and chief cells of human parathyroid glands. J Clin Endocrinol Metab. 2012;97(8):E1499–E1505.
  • 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, et al. The role of prognostic markers (MiB-1, RB, and bcl-2) in the diagnosis of parathyroid tumors. Mod Pathol. 1997;10(1):12–17.
  • 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.
  • Ricci F, Mingazzini PL, Sebastiani V, et al. P53 as a marker of differentiation between hyperplastic and adenomatous parathyroids. J Endocrinol Invest. 1998;21(3):136–141.
  • Naccarato AG, Marcocci C, Miccoli P, et al. Bcl-2, p53 and MIB-1 expression in normal and neoplastic parathyroid tissues. J Endocrinol Invest. 1998;21(3):136–141.
  • Kaczmarek E, Lacka K, Majewski P, et al. Selected markers of proliferation and apoptosis in the parathyroid lesions: a spatial visualization and quantification. J Mol Histol. 2008;39(5):509–517.
  • Dijkers PF, Medema RH, Lammers JW. Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1. Curr Biol. 2000;10(19):1201–1204.
  • Muller PA, Vousden KH. p53 mutations in cancer. Nat Cell Biol. 2013;15:2–8.
  • Rivlin N, Brosh R, Oren M, et al. Mutations in the p53 tumor suppressor gene: important milestones at the various steps of tumorigenesis. Genes Cancer. 2011;2:466–474.
  • Bosari S, Viale G. The clinical significance of p53 aberrations in human tumours. Virchows Arch. 1995;427:229–241.
  • Kayath MJ, Martin LC, Vieira JG, et al. A comparative study of p53 immunoexpression in parathyroid hyperplasias secondary to uremia, primary hyperplasias, adenomas and carcinomas. Eur J Endocrinol. 1998;139(1):78–83.
  • Kishikawa S, Shan L, Ogihara K, et al. Overexpression and genetic abnormality of p53 in parathyroid adenomas. Pathol Int. 1999;49(10):853–857.
  • Gülkesen KH, Kiliçarslan B, Altunbaş HA, et al. EGFR and p53 expression and proliferative activity in parathyroid adenomas; an immunohistochemical study. APMIS. 2001;109(12):870–874.
  • Cryns VL, Rubio MP, Thor AD, et al. p53 abnormalities in human parathyroid carcinoma. J Clin Endocrinol Metab. 1994;78(6):1320–1324.
  • Alò PL, Visca P, Mazzaferro S, et al. Immunohistochemical study of fatty acid synthase, Ki67, proliferating cell nuclear antigen, and p53 expression in hyperplastic parathyroids. Ann Diagn Pathol. 1999;3(5):287–293.
  • Hakim JP, Levine MA. Absence of p53 point mutations in parathyroid adenoma and carcinoma. J Clin Endocrinol Metab. 1994;78(1):103–106.

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