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65 - The parathyroid glands

from Part 3.4 - Molecular pathology: endocrine cancers

Published online by Cambridge University Press:  05 February 2015

By
Edward M. Brown  and
Andrew Arnold
Edited by
Edward P. Gelmann ,
Charles L. Sawyers  and
Frank J. Rauscher, III
Edward M. Brown
Affiliation:
Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA
Andrew Arnold
Affiliation:
Center for Molecular Medicine and Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT, USA
Edward P. Gelmann
Affiliation:
Columbia University, New York
Charles L. Sawyers
Affiliation:
Memorial Sloan-Kettering Cancer Center, New York
Frank J. Rauscher, III
Affiliation:
The Wistar Institute Cancer Centre, Philadelphia
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Summary

Introduction

In this chapter we will examine the molecular genetic basis of parathyroid gland tumorigenesis across a spectrum of heritable and sporadic disorders (Table 65.1). Two genetic predispositions to parathyroid (and other) tumors, multiple endocrine neoplasia types 1 and 2, are addressed in a separate chapter. We begin with a brief review of parathyroid gland physiology, because a major effect of parathyroid neoplasia involves its disruption, and because of its relevance to modern molecular-targeted therapeutics.

Role of the parathyroid glands in maintaining mineral ion homeostasis

The parathyroid glands, usually four in number, are located near the posterior surface of the thyroid gland and play a central role in maintaining homeostasis of mineral ions – especially extra-cellular calcium (Ca2+o), through the regulated release of parathyroid hormone (PTH; 3). This is achieved through the parathyroids’ ability to carefully orchestrate movements of Ca2+ into or out of the body via the intestines and kidneys, respectively. In addition, the skeleton provides a nearly inexhaustible supply of calcium that can be accessed by PTH action (3,4). A central element in this homeostatic system is the capacity of the parathyroid glands to sense minute (i.e. 1–2%) changes in Ca2+o via the Ca2+o-sensing receptor, a G-protein coupled, cell-surface receptor whose principal physiological ligand is Ca2+o (4). A drop in Ca2+o evokes a brisk increase in PTH secretion, and parathyroid glands have the capacity to increase their mass 10–100-fold or more in response to chronic hypocalcemia, so-called secondary hyperparathyroidism (SHPT). Parathyroid glands that have undergone secondary parathyroid hyperplasia, however, only regress in size and cell number very slowly, owing, at least in part, to the limited capacity of even normal parathyroid cells to undergo apoptosis (5).

Type
Chapter
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Molecular Oncology
Causes of Cancer and Targets for Treatment
 , pp. 712 - 719
Publisher: Cambridge University Press
Print publication year: 2013

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References

Nesbit, MA, Hannan, FM, Howles, SA, et al. Mutations affecting G-protein submit α11 in hypercalcemia and hypocalcemia. New England Journal of Medicine 2013:368:2476–86.CrossRefGoogle Scholar
Nesbit, MA, Hannan, FM, Howles, SA, et al. Mutations in APZS1 cause familial hypocalciuric hypercalcemia type 3. Nature Genetics 2013:45:93–7.CrossRefGoogle ScholarPubMed
Bringhurst, FR, Demay, MB, Kronenberg, HM. Hormones and disorders of mineral metabolism. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, editors, Williams Textbook of Endocrinology, ninth edn. Philadelphia, PA: W.B. Saunders; 1998:1155–209.Google Scholar
Brown, EM.Clinical lessons from the calcium-sensing receptor. Nature Clinical Practice in Endocrinology and Metabolism 2007;3:122–33.CrossRefGoogle ScholarPubMed
Lewin, E, Olgaard, K.Influence of parathyroid mass on the regulation of PTH secretion. Kidney International Supplement 2006:S16–21.CrossRefGoogle ScholarPubMed
Dusso, A, Cozzolino, M, Lu, Y, Sato, T, Slatopolsky, E.1,25-Dihydroxyvitamin D downregulation of TGFalpha/EGFR expression and growth signaling: a mechanism for the antiproliferative actions of the sterol in parathyroid hyperplasia of renal failure. Journal of Steroid Biochemistry and Molecular Biology 2004;89–90:507–11.CrossRefGoogle ScholarPubMed
Silver, J, Sela, SB, Naveh-Many, T.Regulation of parathyroid cell proliferation. Current Opinion in Nephrology and Hypertension 1997;6:321–6.CrossRefGoogle ScholarPubMed
Arcidiacono, MV, Sato, T, Alvarez-Hernandez, D, et al. EGFR activation increases parathyroid hyperplasia and calcitriol resistance in kidney disease. Journal of the American Society of Nephrology 2008;19:310–20.CrossRefGoogle ScholarPubMed
Dusso, AS, Pavlopoulos, T, Naumovich, L, et al. p21(WAF1) and transforming growth factor-alpha mediate dietary phosphate regulation of parathyroid cell growth. Kidney International 2001;59:855–65.CrossRefGoogle ScholarPubMed
Gogusev, J, Duchambon, P, Stoermann-Chopard, C, et al. De novo expression of transforming growth factor-alpha in parathyroid gland tissue of patients with primary or secondary uraemic hyperparathyroidism. Nephrology Dialysis Transplantation 1996;11:2155–62.CrossRefGoogle ScholarPubMed
Cozzolino, M, Lu, Y, Finch, J, Slatopolsky, E, Dusso, AS.p21WAF1 and TGF-alpha mediate parathyroid growth arrest by vitamin D and high calcium. Kidney International 2001;60:2109–17.CrossRefGoogle ScholarPubMed
Cozzolino, M, Lu, Y, Sato, T, et al. A critical role for enhanced TGF-alpha and EGFR expression in the initiation of parathyroid hyperplasia in experimental kidney disease. American Journal of Physiology, Renal Physiology 2005;289:F1096–102.CrossRefGoogle ScholarPubMed
Lin, SY, Makino, K, Xia, W, et al. Nuclear localization of EGF receptor and its potential new role as a transcription factor. Nature Cell Biology 2001;3:802–8.CrossRefGoogle ScholarPubMed
Ritter, CS, Martin, DR, Lu, Y, Slatopolsky, E, Brown, AJ.Reversal of secondary hyperparathyroidism by phosphate restriction restores parathyroid calcium-sensing receptor expression and function. Journal of Bone and Mineral Research 2002;17:2206–13.CrossRefGoogle ScholarPubMed
Mallya, SM, Gallagher, JJ, Wild, YK, et al. Abnormal parathyroid cell proliferation precedes biochemical abnormalities in a mouse model of primary hyperparathyroidism. Molecular Endocrinology 2005;19:2603–9.CrossRefGoogle Scholar
Gogusev, J, Duchambon, P, Hory, B, et al. Depressed expression of calcium receptor in parathyroid gland tissue of patients with hyperparathyroidism. Kidney International 1997;51:328–36.CrossRefGoogle ScholarPubMed
Kifor, O, Moore, FD, Jr., Wang, P, et al. Reduced immunostaining for the extracellular Ca2+-sensing receptor in primary and uremic secondary hyperparathyroidism [see comments]. Journal of Clinical Endocrinology and Metabolism 1996;81:1598–606.Google Scholar
Fukuda, N, Tanaka, H, Tominaga, Y, et al. Decreased 1,25-dihydroxyvitamin D3 receptor density is associated with a more severe form of parathyroid hyperplasia in chronic uremic patients. Journal of Clinical Investigation 1993;92:1436–43.CrossRefGoogle ScholarPubMed
Tokumoto, M, Tsuruya, K, Fukuda, K, et al. Reduced p21, p27 and vitamin D receptor in the nodular hyperplasia in patients with advanced secondary hyperparathyroidism. Kidney International 2002;62:1196–207.CrossRefGoogle ScholarPubMed
Hosokawa, Y, Pollak, MR, Brown, EM, Arnold, A.Mutational analysis of the extracellular Ca(2+)-sensing receptor gene in human parathyroid tumors. Journal of Clinical Endocrinology and Metabolism 1995;80:3107–10.Google ScholarPubMed
Brown, SB, Brierley, TT, Palanisamy, N, et al. Vitamin D receptor as a candidate tumor-suppressor gene in severe hyperparathyroidism of uremia. Journal of Clinical Endocrinology and Metabolism 2000;85:868–72.Google ScholarPubMed
Tominaga, Y, Kohara, S, Namii, Y, et al. Clonal analysis of nodular parathyroid hyperplasia in renal hyperparathyroidism. World Journal of Surgery 1996;20:744–50; discussion 750–2.CrossRefGoogle ScholarPubMed
Arnold, A, Brown, MF, Urena, P, et al. Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia. Journal of Clinical Investigation 1995;95:2047–53.CrossRefGoogle ScholarPubMed
Nagy, A, Chudek, J, Kovacs, G.Accumulation of allelic changes at chromosomes 7p, 18q, and 2 in parathyroid lesions of uremic patients. Laboratory Investigation 2001;81:527–33.CrossRefGoogle ScholarPubMed
Harach, HR, Jasani, B.Parathyroid hyperplasia in tertiary hyper-parathyroidism: a pathological and immunohistochemical reappraisal. Histopathology 1992;21:513–19.CrossRefGoogle Scholar
Brown, EM, Wilson, RE, Eastman, RC, Pallotta, J, Marynick, SP.Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure. Journal of Clinical Endocrinology and Metabolism 1982;54:172–9.CrossRefGoogle ScholarPubMed
Brown, EM.Four parameter model of the sigmoidal relationship between parathyroid hormone release and extracellular calcium concentration in normal and abnormal parathyroid tissue. Journal of Clinical Endocrinology and Metabolism 1983;56:572–81.CrossRefGoogle ScholarPubMed
Imanishi, Y, Tahara, H, Palanisamy, N, et al. Clonal chromosomal defects in the molecular pathogenesis of refractory hyperparathyroidism of uremia. Journal of the American Society of Nephrology 2002;13:1490–8.CrossRefGoogle ScholarPubMed
Tahara, H, Imanishi, Y, Yamada, T, et al. Rare somatic inactivation of the multiple endocrine neoplasia type 1 gene in secondary hyperparathyroidism of uremia. Journal of Clinical Endocrinology and Metabolism 2000;85:4113–17.Google ScholarPubMed
Afonso, S, Santamaria, I, Guinsburg, ME, et al. Chromosomal aberrations, the consequence of refractory hyperparathyroidism: its relationship with biochemical parameters. Kidney International Supplement 2003:S32–3.CrossRefGoogle ScholarPubMed
Farnebo, F, Teh, BT, Dotzenrath, C, et al. Differential loss of heterozygosity in familial, sporadic, and uremic hyperparathyroidism. Human Genetics 1997;99:342–9.CrossRefGoogle ScholarPubMed
Koshiishi, N, Chong, JM, Fukasawa, T, et al. Microsatellite instability and loss of heterozygosity in primary and secondary proliferative lesions of the parathyroid gland. Laboratory Investigation 1999;79:1051–8.Google ScholarPubMed
Hendy, GN, D’Souza-Li, L, Yang, B, Canaff, L, Cole, DE.Mutations of the calcium-sensing receptor (CASR) in familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, and autosomal dominant hypocalcemia. Human Mutation 2000;16:281–96.3.0.CO;2-A>CrossRefGoogle ScholarPubMed
Hu, J, Spiegel, AM.Naturally occurring mutations in the extracellular Ca2+-sensing receptor: implications for its structure and function. Trends in Endocrinology and metabolism 2003;14:282–8.CrossRefGoogle ScholarPubMed
Pollak, MR, Brown, EM, Chou, YH, et al. Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. Cell 1993;75:1297–303.CrossRefGoogle ScholarPubMed
Ho, C, Conner, DA, Pollak, MR, et al. A mouse model of human familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism [see comments]. Nature Genetics 1995;11:389–94.CrossRefGoogle Scholar
Law, Jr WM, Heath, III H. Familial benign hypercalcemia (hypocalciuric hypercalcemia). Clinical and pathogenetic studies in 21 families. Annals of Internal Medicine 1985;105:511–19.CrossRefGoogle Scholar
Marx, SJ, Attie, MF, Levine, MA, et al. The hypocalciuric or benign variant of familial hypercalcemia: clinical and biochemical features in fifteen kindreds. Medicine (Baltimore) 1981;60:397–412.CrossRefGoogle ScholarPubMed
Hauache, OM.Extracellular calcium-sensing receptor: structural and functional features and association with diseases. Brazilian Journal of Medical and Biological Research 2001;34:577–84.CrossRefGoogle ScholarPubMed
Law, WM, Jr, Carney, JA, Heath, H. Parathyroid glands in familial benign hypercalcemia (familial hypocalciuric hypercalcemia). American Journal of Medicine 1984;76:1021–6.CrossRefGoogle Scholar
Thogeirsson, U, Costa, J, Marx, SJ.The parathyroid glands in familial hypocalciuric hypercalcemia. Human Pathology 1981;12:229–37.CrossRefGoogle Scholar
Lietman, SA, Tenenbaum-Rakover, Y, Jap, TS, et al. A novel loss-of-function mutation, Gln459Arg, of the calcium-sensing receptor gene associated with apparent autosomal recessive inheritance of familial hypocalciuric hypercalcemia. Journal of Clinical Endocrinology and Metabolism 2009;94:4372–9.CrossRefGoogle ScholarPubMed
Hannan, FM, Nesbit, MA, Christie, PT, et al. A homozygous inactivating calcium-sensing receptor mutation, Pro339Thr, is associated with isolated primary hyperparathyroidism: correlation between location of mutations and severity of hypercalcaemia. Clinical Endocrinology (Oxford) 2010;73:715–22.CrossRefGoogle ScholarPubMed
Ward, DT, Brown, EM, Harris, HW. Disulfide bonds in the extracellular calcium-polyvalent cation-sensing receptor correlate with dimer formation and its response to divalent cations in vitro. Journal of Biological Chemistry 1998;273:14476–83.CrossRefGoogle ScholarPubMed
Bai, M, Trivedi, S, Brown, EM.Dimerization of the extracellular calcium-sensing receptor (CaR) on the cell surface of CaR-transfected HEK293 cells. Journal of Biological Chemistry 1998;273:23605–10.CrossRefGoogle ScholarPubMed
Bai, M, Pearce, SH, Kifor, O, et al. In vivo and in vitro characterization of neonatal hyperparathyroidism resulting from a de novo, heterozygous mutation in the Ca2+-sensing receptor gene: normal maternal calcium homeostasis as a cause of secondary hyperpara-thyroidism in familial benign hypocalciuric hypercalcemia. Journal of Clinical Investigation 1997;99:88–96.CrossRefGoogle Scholar
Carling, T, Szabo, E, Bai, M, et al. Familial hypercalcemia and hypercalciuria caused by a novel mutation in the cytoplasmic tail of the calcium receptor [see comments]. Journal of Clinical Endocrinology and Metabolism 2000;85:2042–7.Google Scholar
Burski, K, Torjussen, B, Paulsen, AQ, Boman, H, Bollerslev, J.Parathyroid adenoma in a subject with familial hypocalciuric hypercalcemia: coincidence or causality? Journal of Clinical Endocrinology and Metabolism 2002;87:1015–16.CrossRefGoogle ScholarPubMed
Heath, DA.Familial hypocalciuric hypercalcemia. In: Bilezikian, JP, Marcus, R, Levine, MA, editors, The Parathyroids. New York, NY: Raven Press; 1994:699–710.Google Scholar
Marx, SJ, Fraser, D, Rapoport, A.Familial hypocalciuric hypercalcemia. Mild expression of the gene in heterozygotes and severe expression in homozygotes. American Journal of Medicine 1985;78:15–22.CrossRefGoogle ScholarPubMed
Spiegel, AM, Harrison, HE, Marx, SJ, Brown, EM, Aurbach, GD.Neonatal primary hyperparathyroidism with autosomal dominant inheritance. Journal of Pediatrics 1977;90:269–72.CrossRefGoogle ScholarPubMed
Cetani, F, Pinchera, A, Pardi, E, et al. No evidence for mutations in the calcium-sensing receptor gene in sporadic parathyroid adenomas. Journal of Bone and Mineral Research 1999;14:878–82.CrossRefGoogle ScholarPubMed
Arnold, A, Marx, SJ.Familial hyperparathyroidism including MEN, FHH, HPT-JT. In: Rosen, CJ, editor, Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, seventh edn. Washington, DC: American Society for Bone and Mineral Research; 2008:361–6.CrossRefGoogle Scholar
Rozenblatt-Rosen, O, Hughes, CM, Nannepaga, SJ, et al. The parafibromin tumor suppressor protein is part of a human Paf1 complex. Molecular and Cellular Biology 2005;25:612–20.CrossRefGoogle ScholarPubMed
Carpten, JD, Robbins, CM, Villablanca, A, et al. HRPT2, encoding parafibromin, is mutated in hyperparathyroidism-jaw tumor syndrome. Nature Genetics 2002;32:676–80.CrossRefGoogle ScholarPubMed
Simonds, WF, Robbins, CM, Agarwal, SK, et al. Familial isolated hyperparathyroidism is rarely caused by germline mutation in HRPT2, the gene for the hyperparathyroidism-jaw tumor syndrome. Journal of Clinical Endocrinology and Metabolism 2004;89:96–102.CrossRefGoogle ScholarPubMed
Warner, JV, Nyholt, DR, Busfield, F, et al. Familial isolated hyperparathyroidism is linked to a 1.7 Mb region on chromosome 2p13.3–14. Journal of Medical Genetics 2006;43:e12.CrossRefGoogle ScholarPubMed
Pellegata, NS, Quintanilla-Martinez, L, Siggelkow, H, et al. Germ-line mutations in p27Kip1 cause a multiple endocrine neoplasia syndrome in rats and humans. Proceedings of the National Academy of Sciences USA 2006;103:15 558–63.CrossRefGoogle Scholar
Agarwal, SK, Mateo, CM, Marx, SJ.Rare germline mutations in cyclin-dependent kinase inhibitor genes in multiple endocrine neoplasia type 1 and related states. Journal of Clinical Endocrinology and Metabolism 2009;94:1826–34.CrossRefGoogle ScholarPubMed
Bernards, R.CDK-independent activities of D type cyclins. Biochimica et Biophysica Acta 1999;1424:M17–22.Google ScholarPubMed
Lamb, J, Ramaswamy, S, Ford, HL, et al. A mechanism of cyclin D1 action encoded in the patterns of gene expression in human cancer. Cell 2003;114:323–34.CrossRefGoogle ScholarPubMed
Arnold, A, Papanikolaou, A.Cyclin D1 in breast cancer pathogenesis. Journal of Clinical Oncology 2005;23:4215–24.CrossRefGoogle ScholarPubMed
Imanishi, Y, Hosokawa, Y, Yoshimoto, K, et al. Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice. Journal of Clinical Investigation 2001;107:1093–102.CrossRefGoogle ScholarPubMed
Heppner, C, Kester, MB, Agarwal, SK, et al. Somatic mutation of the MEN1 gene in parathyroid tumours. Nature Genetics 1997;16:375–8.CrossRefGoogle ScholarPubMed
Farnebo, F, Teh, BT, Kytola, S, et al. Alterations of the MEN1 gene in sporadic parathyroid tumors. Journal of Clinical Endocrinology and Metabolism 1998;83:2627–30.Google ScholarPubMed
Carling, T, Correa, P, Hessman, O, et al. Parathyroid MEN1 gene mutations in relation to clinical characteristics of nonfamilial primary hyperpara-thyroidism. Journal of Clinical Endocrinology and Metabolism 1998;83:2960–3.Google Scholar
Yang, Y, Hua, X.In search of tumor suppressing functions of menin. Molecular and Cellular Endocrinology 2007;265–6:34–41.CrossRefGoogle Scholar
Yokoyama, A, Cleary, ML.Menin critically links MLL proteins with LEDGF on cancer-associated target genes. Cancer Cell 2008;14:36–46.CrossRefGoogle ScholarPubMed
Tahara, H, Smith, AP, Gaz, RD, Cryns, VL, Arnold, A.Genomic localization of novel candidate tumor suppressor gene loci in human parathyroid adenomas. Cancer Research 1996;56:599–605.Google ScholarPubMed
Palanisamy, N, Imanishi, Y, Rao, PH, et al. Novel chromosomal abnormalities identified by comparative genomic hybridization in parathyroid adenomas. Journal of Clinical Endocrinology and Metabolism 1998;83:1766–70.Google ScholarPubMed
Farnebo, F, Kytola, S, Teh, BT, et al. Alternative genetic pathways in parathyroid tumorigenesis. Journal of Clinical Endocrinology and Metabolism 1999;84:3775–80.Google ScholarPubMed
Agarwal, SK, Schrock, E, Kester, MB, et al. Comparative genomic hybridization analysis of human parathyroid tumors. Cancer Genetics and Cytogenetics 1998;106:30–6.CrossRefGoogle ScholarPubMed
Dwight, T, Nelson, AE, Theodosopoulos, G, et al. Independent genetic events associated with the development of multiple parathyroid tumors in patients with primary hyperparathyroidism. American Journal of Pathology 2002;161:1299–306.CrossRefGoogle ScholarPubMed
Costa-Guda, J, Marinoni, I, Molatore, S, Pellegata, NS, Arnold, A.Somatic mutation and germline sequence abnormalities in CDKN1B, encoding p27Kip1, in sporadic parathyroid adenomas. Journal of Clinical Endocrinology and Metabolism 2011;96:E701–6.CrossRefGoogle ScholarPubMed
Starker, LF, Fonseca, A, Akerström, G, et al. Evidence of a stabilizing mutation of β-catenin encoded by CTNNB1 exon 3 in a large series of sporadic parathyroid adenomas. Endocrine 2012;42:612–15.CrossRefGoogle Scholar
Cromer, MK, Starker, LF, Choi, M, et al. Identification of somatic mutations in parathyroid tumors using whole-exome sequencing. Journal of Clinical Endocrinology and Metabolism 2012;97:E1774–81.CrossRefGoogle ScholarPubMed
Newey, PJ, Nesbit, MA, Rimmer, AJ, et al. Whole-exome sequencing studies of nonhereditary (sporadic) parathyroid adenomas. Journal of Clinical Endocrinology and Metabolism 2012;97:E1995–2005.CrossRefGoogle ScholarPubMed
Shattuck, TM, Valimaki, S, Obara, T, et al. Somatic and germ-line mutations of the HRPT2 gene in sporadic parathyroid carcinoma. New England Journal of Medicine 2003;349:1722–9.CrossRefGoogle ScholarPubMed
Howell, VM, Haven, CJ, Kahnoski, K, et al. HRPT2 mutations are associated with malignancy in sporadic parathyroid tumours. Journal of Medical Genetics 2003;40:657–63.CrossRefGoogle ScholarPubMed
Cetani, F, Pardi, E, Borsari, S, et al. Genetic analyses of the HRPT2 gene in primary hyperparathyroidism: germline and somatic mutations in familial and sporadic parathyroid tumors. Journal of Clinical Endocrinology and Metabolism 2004;89:5583–91.CrossRefGoogle ScholarPubMed
El-Hajj Fuleihan, G, Arnold, A.Parathyroid carcinoma. In: Basow, DS, editor. UpToDate. Waltham, MA: UpToDate, Inc.;2013.Google Scholar
Krebs, LJ, Shattuck, TM, Arnold, A.HRPT2 mutational analysis of typical sporadic parathyroid adenomas. Journal of Clinical Endocrinology and Metabolism 2005;90:5015–17.CrossRefGoogle ScholarPubMed
Brown, EM.Clinical utility of calcimimetics targeting the extracellular calcium-sensing receptor (CaSR). Biochemical Pharmacology 2010;80:297–307.CrossRefGoogle Scholar

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  • The parathyroid glands
    • By Edward M. Brown, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA, Andrew Arnold, Center for Molecular Medicine and Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT, USA
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.066
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  • The parathyroid glands
    • By Edward M. Brown, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA, Andrew Arnold, Center for Molecular Medicine and Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT, USA
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.066
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  • The parathyroid glands
    • By Edward M. Brown, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA, Andrew Arnold, Center for Molecular Medicine and Department of Genetics and Developmental Biology, University of Connecticut School of Medicine, Farmington, CT, USA
  • Edited by Edward P. Gelmann, Columbia University, New York, Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, Frank J. Rauscher, III
  • Book: Molecular Oncology
  • Online publication: 05 February 2015
  • Chapter DOI: https://doi.org/10.1017/CBO9781139046947.066
Available formats
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