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1
European guidance for the molecular diagnosis of pseudohypoparathyroidism not caused by point genetic variants at GNAS: an EQA study.欧洲关于非由GNAS基因位点突变引起的假性甲状旁腺功能减退症分子诊断的指南:一项室间质量评价研究
Eur J Hum Genet. 2015 Apr;23(4):438-44. doi: 10.1038/ejhg.2014.127. Epub 2014 Jul 9.
2
Analysis of Multiple Families With Single Individuals Affected by Pseudohypoparathyroidism Type Ib (PHP1B) Reveals Only One Novel Maternally Inherited GNAS Deletion.对多个仅有一名个体受Ib型假性甲状旁腺功能减退症(PHP1B)影响的家族进行分析,仅发现一个新的母系遗传的GNAS缺失。
J Bone Miner Res. 2016 Apr;31(4):796-805. doi: 10.1002/jbmr.2731. Epub 2015 Nov 14.
3
Mosaicism for GNAS methylation defects associated with pseudohypoparathyroidism type 1B arose in early post-zygotic phases.GNAS 甲基化缺陷相关的假甲状旁腺功能减退症 1B 的镶嵌现象出现在合子后早期。
Clin Epigenetics. 2018 Feb 6;10:16. doi: 10.1186/s13148-018-0449-4. eCollection 2018.
4
Quantitative analysis of methylation defects and correlation with clinical characteristics in patients with pseudohypoparathyroidism type I and GNAS epigenetic alterations.假性甲状旁腺功能减退症 I 型和 GNAS 表观遗传学改变患者甲基化缺陷的定量分析及其与临床特征的相关性。
J Clin Endocrinol Metab. 2014 Mar;99(3):E508-17. doi: 10.1210/jc.2013-3086. Epub 2013 Jan 1.
5
Pseudohypoparathyroidism and GNAS epigenetic defects: clinical evaluation of albright hereditary osteodystrophy and molecular analysis in 40 patients.假性甲状旁腺功能减退症和 GNAS 表观遗传缺陷:阿利特遗传性骨营养不良的临床评估和 40 例患者的分子分析。
J Clin Endocrinol Metab. 2010 Feb;95(2):651-8. doi: 10.1210/jc.2009-0176. Epub 2010 Jan 8.
6
Genetic and epigenetic states of the GNAS complex in pseudohypoparathyroidism type Ib using methylation-specific multiplex ligation-dependent probe amplification assay.应用甲基化特异性多重连接依赖性探针扩增检测技术研究 Ib 型假性甲状旁腺功能减退症中 GNAS 复合物的遗传和表观遗传状态。
Eur J Endocrinol. 2013 Jan 17;168(2):169-75. doi: 10.1530/EJE-12-0548. Print 2013 Feb.
7
Genome-wide DNA methylation analysis of pseudohypoparathyroidism patients with GNAS imprinting defects.伴有GNAS印记缺陷的假性甲状旁腺功能减退症患者的全基因组DNA甲基化分析。
Clin Epigenetics. 2016 Jan 26;8:10. doi: 10.1186/s13148-016-0175-8. eCollection 2016.
8
Similar frequency of paternal uniparental disomy involving chromosome 20q (patUPD20q) in Japanese and Caucasian patients affected by sporadic pseudohypoparathyroidism type Ib (sporPHP1B).在散发型I b型假性甲状旁腺功能减退症(sporPHP1B)患者中,日本患者和高加索患者涉及20号染色体长臂的父源单亲二倍体(patUPD20q)频率相似。
Bone. 2015 Oct;79:15-20. doi: 10.1016/j.bone.2015.05.011. Epub 2015 May 19.
9
Clinical and genetic characterization of Portuguese patients with pseudohypoparathyroidism type Ib.葡萄牙假性甲状旁腺功能减退症 Ib 型患者的临床和遗传特征。
Endocrine. 2010 Jun;37(3):408-14. doi: 10.1007/s12020-010-9321-9. Epub 2010 Mar 30.
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Epigenetic defects of GNAS in patients with pseudohypoparathyroidism and mild features of Albright's hereditary osteodystrophy.假性甲状旁腺功能减退症患者GNAS的表观遗传缺陷及Albright遗传性骨营养不良的轻微特征
J Clin Endocrinol Metab. 2007 Jun;92(6):2370-3. doi: 10.1210/jc.2006-2287. Epub 2007 Apr 3.

引用本文的文献

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Heterodisomy in the locus is also a cause of pseudohypoparathyroidism type 1B (iPPSD3).该位点的异源二体也是1B型假性甲状旁腺功能减退症(iPPSD3)的一个病因。
Front Endocrinol (Lausanne). 2024 Dec 16;15:1505244. doi: 10.3389/fendo.2024.1505244. eCollection 2024.
2
, and Mutations and Methylation Changes Are Not a Common Cause of Isolated Early-Onset Severe Obesity Among Finnish Children.以及突变和甲基化变化并非芬兰儿童孤立性早发性严重肥胖的常见原因。
Front Pediatr. 2020 Apr 7;8:145. doi: 10.3389/fped.2020.00145. eCollection 2020.
3
Pseudohypoparathyroidism.假性甲状旁腺功能减退症。
Endocrinol Metab Clin North Am. 2018 Dec;47(4):865-888. doi: 10.1016/j.ecl.2018.07.011. Epub 2018 Oct 12.
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Genetic approaches to metabolic bone diseases.遗传方法治疗代谢性骨疾病。
Br J Clin Pharmacol. 2019 Jun;85(6):1147-1160. doi: 10.1111/bcp.13803. Epub 2018 Nov 28.
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Case report: An infantile lethal form of Albright hereditary osteodystrophy due to a mutation.病例报告:一例因基因突变导致的婴儿致死型奥尔布赖特遗传性骨营养不良。
Clin Case Rep. 2018 Aug 16;6(10):1933-1940. doi: 10.1002/ccr3.1739. eCollection 2018 Oct.
6
Diagnosis and management of pseudohypoparathyroidism and related disorders: first international Consensus Statement.假性甲状旁腺功能减退症及相关疾病的诊断与管理:第一份国际共识声明。
Nat Rev Endocrinol. 2018 Aug;14(8):476-500. doi: 10.1038/s41574-018-0042-0.
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Genetic and Epigenetic Defects at the GNAS Locus Lead to Distinct Patterns of Skeletal Growth but Similar Early-Onset Obesity.GNAS 基因座的遗传和表观遗传缺陷导致不同的骨骼生长模式,但具有相似的早发性肥胖。
J Bone Miner Res. 2018 Aug;33(8):1480-1488. doi: 10.1002/jbmr.3450. Epub 2018 Jun 7.
8
A novel deletion involving GNAS exon 1 causes PHP1A and further refines the region required for normal methylation at exon A/B.一个新的缺失涉及 GNAS 外显子 1,导致 PHP1A 并进一步精确定位 A/B 外显子正常甲基化所需的区域。
Bone. 2017 Oct;103:281-286. doi: 10.1016/j.bone.2017.07.013. Epub 2017 Jul 12.
9
An Update on Molecular Diagnostic Testing of Human Imprinting Disorders.人类印记障碍分子诊断检测的最新进展
J Pediatr Genet. 2017 Mar;6(1):3-17. doi: 10.1055/s-0036-1593840. Epub 2016 Nov 10.
10
Genome-wide DNA methylation analysis of pseudohypoparathyroidism patients with GNAS imprinting defects.伴有GNAS印记缺陷的假性甲状旁腺功能减退症患者的全基因组DNA甲基化分析。
Clin Epigenetics. 2016 Jan 26;8:10. doi: 10.1186/s13148-016-0175-8. eCollection 2016.

本文引用的文献

1
Autosomal dominant pseudohypoparathyroidism type Ib: a novel inherited deletion ablating STX16 causes loss of imprinting at the A/B DMR.常染色体显性假性甲状旁腺功能减退症 Ib 型:一种新型遗传性缺失导致 STX16 失活,从而导致 A/B DMR 印迹丢失。
J Clin Endocrinol Metab. 2014 Apr;99(4):E724-8. doi: 10.1210/jc.2013-3704. Epub 2014 Jan 17.
2
Selective methylation of CpGs at regulatory binding sites controls NNAT expression in Wilms tumors.CpG 位点的选择性甲基化在调节结合位点控制肾母细胞瘤中 NNAT 的表达。
PLoS One. 2013 Jun 25;8(6):e67605. doi: 10.1371/journal.pone.0067605. Print 2013.
3
Quantitative analysis of methylation status at 11p15 and 7q21 for the genetic diagnosis of Beckwith-Wiedemann syndrome and Silver-Russell syndrome.11p15 和 7q21 甲基化状态的定量分析用于 Beckwith-Wiedemann 综合征和 Silver-Russell 综合征的遗传学诊断。
J Hum Genet. 2013 Sep;58(9):604-10. doi: 10.1038/jhg.2013.67. Epub 2013 Jun 27.
4
Simultaneous hyper- and hypomethylation at imprinted loci in a subset of patients with GNAS epimutations underlies a complex and different mechanism of multilocus methylation defect in pseudohypoparathyroidism type 1b.在一部分伴 GNAS 外显子突变的假性甲状旁腺功能减退症 1b 患者中,印记基因座的同时高甲基化和低甲基化是多基因甲基化缺陷的一种复杂且不同的机制。
Hum Mutat. 2013 Aug;34(8):1172-80. doi: 10.1002/humu.22352. Epub 2013 May 28.
5
Genome-wide allelic methylation analysis reveals disease-specific susceptibility to multiple methylation defects in imprinting syndromes.全基因组等位基因甲基化分析揭示印记综合征中多种甲基化缺陷的疾病特异性易感性。
Hum Mutat. 2013 Apr;34(4):595-602. doi: 10.1002/humu.22276. Epub 2013 Feb 19.
6
IGF2/H19 hypomethylation is tissue, cell, and CpG site dependent and not correlated with body asymmetry in adolescents with Silver-Russell syndrome.IGF2/H19 低甲基化与组织、细胞和 CpG 位点相关,而与 Silver-Russell 综合征青少年的身体不对称无关。
Clin Epigenetics. 2012 Sep 18;4(1):15. doi: 10.1186/1868-7083-4-15.
7
Clinical utility gene card for: pseudohypoparathyroidism.假性甲状旁腺功能减退症的临床实用基因卡片
Eur J Hum Genet. 2013 Jun;21(6). doi: 10.1038/ejhg.2012.211. Epub 2012 Sep 12.
8
Detection of hypomethylation syndrome among patients with epigenetic alterations at the GNAS locus.检测 GNAS 基因座表观遗传学改变患者中的低甲基化综合征。
J Clin Endocrinol Metab. 2012 Jun;97(6):E1060-7. doi: 10.1210/jc.2012-1081. Epub 2012 Apr 4.
9
Prognostic value of three different methods of MGMT promoter methylation analysis in a prospective trial on newly diagnosed glioblastoma.在一项新诊断胶质母细胞瘤的前瞻性试验中,三种不同的 MGMT 启动子甲基化分析方法的预后价值。
PLoS One. 2012;7(3):e33449. doi: 10.1371/journal.pone.0033449. Epub 2012 Mar 13.
10
A new deletion ablating NESP55 causes loss of maternal imprint of A/B GNAS and autosomal dominant pseudohypoparathyroidism type Ib.一个新的缺失性 NESP55 导致 A/B GNAS 的母系印迹缺失和常染色体显性假性甲状旁腺功能减退症 Ib 型。
J Clin Endocrinol Metab. 2012 May;97(5):E863-7. doi: 10.1210/jc.2011-2804. Epub 2012 Feb 29.

欧洲关于非由GNAS基因位点突变引起的假性甲状旁腺功能减退症分子诊断的指南:一项室间质量评价研究

European guidance for the molecular diagnosis of pseudohypoparathyroidism not caused by point genetic variants at GNAS: an EQA study.

作者信息

Garin Intza, Mantovani Giovanna, Aguirre Urko, Barlier Anne, Brix Bettina, Elli Francesca M, Freson Kathleen, Grybek Virginie, Izzi Benedetta, Linglart Agnès, Perez de Nanclares Guiomar, Silve Caroline, Thiele Susanne, Werner Ralf

机构信息

Molecular (Epi)Genetics Laboratory, BioAraba National Health Institute, Hospital Universitario Araba-Txagorritxu, Vitoria-Gasteiz, Spain.

Endocrinology and Diabetology Unit, Department of Clinical Sciences and Community Health, University of Milan, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.

出版信息

Eur J Hum Genet. 2015 Apr;23(4):438-44. doi: 10.1038/ejhg.2014.127. Epub 2014 Jul 9.

DOI:10.1038/ejhg.2014.127
PMID:25005735
原文链接:
https://pmc.ncbi.nlm.nih.gov/articles/PMC4666570/
Abstract

Pseudohypoparathyroidism is a rare endocrine disorder that can be caused by genetic (mainly maternally inherited inactivating point mutations, although intragenic and gross deletions have rarely been reported) or epigenetic alterations at GNAS locus. Clinical and molecular characterization of this disease is not that easy because of phenotypic, biochemical and molecular overlapping features between both subtypes of the disease. The European Consortium for the study of PHP (EuroPHP) designed the present work with the intention of generating the standards of diagnostic clinical molecular (epi)genetic testing in PHP patients. With this aim, DNA samples of eight independent PHP patients carrying GNAS genetic and/or epigenetic defects (three patients with GNAS deletions, two with 20q uniparental disomy and three with a methylation defect of unknown origin) without GNAS point mutations were anonymized and sent to the five participant laboratories for their routine genetic analysis (methylation-specific (MS)-MLPA, pyrosequencing and EpiTYPER) and interpretations. All laboratories were able to detect methylation defects and, after the data analysis, the Consortium compared the results to define technical advantages and disadvantages of different techniques. To conclude, we propose as first-level investigation in PHP patients copy number and methylation analysis by MS-MLPA. Then, in patients with partial methylation defect, the result should be confirmed by single CpG bisulphite-based methods (ie pyrosequencing), whereas in case of a complete methylation defect without detectable deletion, microsatellites or SNP genotyping should be performed to exclude uniparental disomy 20.

摘要

假性甲状旁腺功能减退症是一种罕见的内分泌疾病,可由GNAS基因座的遗传(主要是母系遗传的失活点突变,尽管基因内和大片段缺失很少见报道)或表观遗传改变引起。由于该疾病两种亚型之间存在表型、生化和分子重叠特征,因此对这种疾病进行临床和分子特征分析并非易事。欧洲假性甲状旁腺功能减退症研究联盟(EuroPHP)开展了本研究,旨在制定假性甲状旁腺功能减退症患者诊断性临床分子(表观)遗传学检测的标准。为此,将8例携带GNAS基因和/或表观遗传缺陷(3例有GNAS缺失,2例有20号染色体单亲二倍体,3例有不明来源的甲基化缺陷)且无GNAS点突变的独立假性甲状旁腺功能减退症患者的DNA样本进行匿名处理,并送至5个参与实验室进行常规遗传分析(甲基化特异性(MS)-MLPA、焦磷酸测序和EpiTYPER)及解读。所有实验室均能检测到甲基化缺陷,数据分析后,联盟比较结果以确定不同技术的技术优缺点。总之,我们建议对假性甲状旁腺功能减退症患者进行一级检查时采用MS-MLPA进行拷贝数和甲基化分析。然后,对于部分甲基化缺陷的患者,结果应通过基于单CpG亚硫酸氢盐的方法(即焦磷酸测序)进行确认,而对于无可检测到的缺失的完全甲基化缺陷的情况,应进行微卫星或SNP基因分型以排除20号染色体单亲二倍体。