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Journal articles on the topic 'SDHE'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Lee, Hansong, Seongdo Jeong, Yeuni Yu, et al. "Risk of metastatic pheochromocytoma and paraganglioma in SDHx mutation carriers: a systematic review and updated meta-analysis." Journal of Medical Genetics 57, no. 4 (2019): 217–25. http://dx.doi.org/10.1136/jmedgenet-2019-106324.

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BackgroundPheochromocytoma and paraganglioma (PPGL) are tumours that arise from chromaffin cells. Some genetic mutations influence PPGL, among which, those in genes encoding subunits of succinate dehydrogenase (SDHA, SDHB, SDHC and SDHD) and assembly factor (SDHAF2) are the most relevant. However, the risk of metastasis posed by these mutations is not reported except for SDHB and SDHD mutations. This study aimed to update the metastatic risks, considering prevalence and incidence of each SDHx mutation, which were dealt formerly all together.MethodsWe searched EMBASE and MEDLINE and selected 27

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Maher, Megan J., Anuradha S. Herath, Saumya R. Udagedara, David A. Dougan, and Kaye N. Truscott. "Crystal structure of bacterial succinate:quinone oxidoreductase flavoprotein SdhA in complex with its assembly factor SdhE." Proceedings of the National Academy of Sciences 115, no. 12 (2018): 2982–87. http://dx.doi.org/10.1073/pnas.1800195115.

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Succinate:quinone oxidoreductase (SQR) functions in energy metabolism, coupling the tricarboxylic acid cycle and electron transport chain in bacteria and mitochondria. The biogenesis of flavinylated SdhA, the catalytic subunit of SQR, is assisted by a highly conserved assembly factor termed SdhE in bacteria via an unknown mechanism. By using X-ray crystallography, we have solved the structure of Escherichia coli SdhE in complex with SdhA to 2.15-Å resolution. Our structure shows that SdhE makes a direct interaction with the flavin adenine dinucleotide-linked residue His45 in SdhA and maintains

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3

Guzy, Robert D., Bhumika Sharma, Eric Bell, Navdeep S. Chandel, and Paul T. Schumacker. "Loss of the SdhB, but Not the SdhA, Subunit of Complex II Triggers Reactive Oxygen Species-Dependent Hypoxia-Inducible Factor Activation and Tumorigenesis." Molecular and Cellular Biology 28, no. 2 (2007): 718–31. http://dx.doi.org/10.1128/mcb.01338-07.

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ABSTRACT Mitochondrial complex II is a tumor suppressor comprised of four subunits (SdhA, SdhB, SdhC, and SdhD). Mutations in any of these should disrupt complex II enzymatic activity, yet defects in SdhA produce bioenergetic deficiency while defects in SdhB, SdhC, or SdhD induce tumor formation. The mechanisms underlying these differences are not known. We show that the inhibition of distal subunits of complex II, either pharmacologically or via RNA interference of SdhB, increases normoxic reactive oxygen species (ROS) production, increases hypoxia-inducible factor alpha (HIF-α) stabilization

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Moog, Sophie, Charlotte Lussey-Lepoutre, and Judith Favier. "Epigenetic and metabolic reprogramming of SDH-deficient paragangliomas." Endocrine-Related Cancer 27, no. 12 (2020): R451—R463. http://dx.doi.org/10.1530/erc-20-0346.

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Pheochromocytomas and paragangliomas (PPGL) are rare neuroendocrine tumors arising from the adrenal medulla or extra-adrenal paraganglia. Around 40% of all cases are caused by a germline mutation in a susceptibility gene, half of which being found in an SDHx gene (SDHA, SDHB, SDHC, SDHD or SDHAF2). They encode the four subunits and assembly factor of succinate dehydrogenase (SDH), a mitochondrial enzyme involved both in the tricarboxylic acid cycle and electron transport chain. SDHx mutations lead to the accumulation of succinate, which acts as an oncometabolite by inhibiting iron(II) and alph

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5

Timmers, Henri J. L. M., Anne-Paule Gimenez-Roqueplo, Massimo Mannelli, and Karel Pacak. "Clinical aspects of SDHx-related pheochromocytoma and paraganglioma." Endocrine-Related Cancer 16, no. 2 (2009): 391–400. http://dx.doi.org/10.1677/erc-08-0284.

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Paragangliomas (PGLs) derive from either sympathetic chromaffin tissue in adrenal and extra-adrenal abdominal or thoracic locations, or from parasympathetic tissue of the head and neck. Mutations of nuclear genes encoding subunits B, C, and D of the mitochondrial enzyme succinate dehydrogenase (SDHB 1p35-p36.1, SDHC 1q21, SDHD 11q23) give rise to hereditary PGL syndromes PGL4, PGL3, and PGL1 respectively. The susceptibility gene for PGL2 on 11q13.1 remains unidentified. Mitochondrial dysfunction due to SDHx mutations have been linked to tumorigenesis by upregulation of hypoxic and angiogenesis

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6

Kim, Se-Hyuk, Tae Hoon Roh, Hyunee Yim, et al. "GENE-05. THE LOSS OF SUCCINATE DEHYDROGENASE B EXPRESSION IS FREQUENTLY IDENTIFIED IN HEMANGIOBLASTOMA OF THE CENTRAL NERVOUS SYSTEM." Neuro-Oncology 21, Supplement_6 (2019): vi98. http://dx.doi.org/10.1093/neuonc/noz175.407.

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Abstract Succinate dehydrogenase (SDH) is a mitochondrial enzyme that plays an important role in both the Krebs cycle and the electron transport chain. SDH inactivation is associated with tumorigenesis in certain types of tumor. SDH consists of subunits A, B, C and D (SDHA, SDHB, SDHC, and SDHD, respectively). Immunohistochemistry for SDHB is a reliable method for detecting the inactivation of SDH by mutations in SDHA, SDHB, SDHC, SDHD and SDH complex assembly factor 2 (SDHAF2) genes with high sensitivity and specificity. SDHB immunohistochemistry has been used to examine the inactivation of S

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7

Ilanchezhian, Maran, Sarah N. Fuller, Margarita Raygada, et al. "Clinical characterization of patients with SDHC epimutation in gastrointestinal stromal tumors." Journal of Clinical Oncology 37, no. 15_suppl (2019): 11033. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.11033.

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11033 Background: Gastrointestinal Stromal Tumors are the most common malignancy in the GI tract. While the vast majority exhibit somatic mutations in KIT and PDGFRA, approximately 15% of GIST patients do not have this feature. This group of KIT and PDGFRA “wildtype” GISTs have in common a negative expression of SDHB when interrogated by immunohistochemistry. Succinate dehydrogenase (SDH) is a conserved enzyme that plays a critical role in cellular metabolism and energy production. A loss in SDH function is a mechanism observed in several types of cancers, and germline SDH mutations are consid

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Main, Ailsa Maria, Maria Rossing, Line Borgwardt, Birgitte Grønkær Toft, Åse Krogh Rasmussen, and Ulla Feldt-Rasmussen. "Genotype–phenotype associations in PPGLs in 59 patients with variants in SDHX genes." Endocrine Connections 9, no. 8 (2020): 793–803. http://dx.doi.org/10.1530/ec-20-0279.

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Phaeochromocytomas and paragangliomas (PPGLs) are tumours of the adrenal medulla and extra-adrenal sympathetic nervous system which often secrete catecholamines. Variants of the SDHX (SDHA, -AF2, -B, -C, -D) genes are a frequent cause of familial PPGLs. In this study from a single tertiary centre, we aimed to characterise the genotype–phenotype associations in patients diagnosed with germline variants in SDHX genes. We also assessed whether systematic screening of family members resulted in earlier detection of tumours. The study cohort comprised all individuals (n = 59) diagnosed with a rare

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9

Daniel, Eleni, Robert Jones, Matthew Bull, and John Newell-Price. "Rapid-sequence MRI for long-term surveillance for paraganglioma and phaeochromocytoma in patients with succinate dehydrogenase mutations." European Journal of Endocrinology 175, no. 6 (2016): 561–70. http://dx.doi.org/10.1530/eje-16-0595.

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Background Patients with SDHx mutations need long-term radiological surveillance for the development of paragangliomas and phaeochromocytomas, but no longitudinal data exist. The aim of the study was to assess the performance of rapid-sequence non-contrast magnetic resonance imaging (MRI) in the long-term monitoring of patients with SDHx mutations. Methods Retrospective study between 2005 and 2015 at a University Hospital and regional endocrine genetics referral centre. Clinical and imaging data of 47 patients with SDHx mutations (SDHB (36), SDHC (6) and SDHD (5)) who had surveillance for dete

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10

Amar, Laurence, Karel Pacak, Olivier Steichen, et al. "International consensus on initial screening and follow-up of asymptomatic SDHx mutation carriers." Nature Reviews Endocrinology 17, no. 7 (2021): 435–44. http://dx.doi.org/10.1038/s41574-021-00492-3.

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AbstractApproximately 20% of patients diagnosed with a phaeochromocytoma or paraganglioma carry a germline mutation in one of the succinate dehydrogenase (SDHx) genes (SDHA, SDHB, SDHC and SDHD), which encode the four subunits of the SDH enzyme. When a pathogenic SDHx mutation is identified in an affected patient, genetic counselling is proposed for first-degree relatives. Optimal initial evaluation and follow-up of people who are asymptomatic but might carry SDHx mutations have not yet been agreed. Thus, we established an international consensus algorithm of clinical, biochemical and imaging

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11

Snezhkina, Anastasiya V., Dmitry V. Kalinin, Vladislav S. Pavlov, et al. "Immunohistochemistry and Mutation Analysis of SDHx Genes in Carotid Paragangliomas." International Journal of Molecular Sciences 21, no. 18 (2020): 6950. http://dx.doi.org/10.3390/ijms21186950.

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Carotid paragangliomas (CPGLs) are rare neuroendocrine tumors often associated with mutations in SDHx genes. The immunohistochemistry of succinate dehydrogenase (SDH) subunits has been considered a useful instrument for the prediction of SDHx mutations in paragangliomas/pheochromocytomas. We compared the mutation status of SDHx genes with the immunohistochemical (IHC) staining of SDH subunits in CPGLs. To identify pathogenic/likely pathogenic variants in SDHx genes, exome sequencing data analysis among 42 CPGL patients was performed. IHC staining of SDH subunits was carried out for all CPGLs s

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12

Park, Sanghui, So Young Kang, Ghee Young Kwon, et al. "Clinicopathologic Characteristics and Mutational Status of Succinate Dehydrogenase Genes in Paraganglioma of the Urinary Bladder: A Multi-Institutional Korean Study." Archives of Pathology & Laboratory Medicine 141, no. 5 (2016): 671–77. http://dx.doi.org/10.5858/arpa.2016-0403-oa.

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Context.— Because of the limited number of available primary bladder paraganglioma (PBPG) cases, the rates of succinate dehydrogenase (SDH) mutations and the clinicopathologic characteristics of SDH-deficient tumors have not been fully studied. Objective.— To define the clinicopathologic and molecular characteristics of PBPGs. Design.— A total of 52 PBPGs were collected retrospectively. SDHA and SDHB immunohistochemical stains were performed. In cases of SDHB expression loss, mutation analyses of SDHB, SDHC, and SDHD were performed. Results.— The clinicopathologic features were analyzed for 52

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Vega, Byron, and Megan M. Dewdney. "Sensitivity of Alternaria alternata from Citrus to Boscalid and Polymorphism in Iron-Sulfur and in Anchored Membrane Subunits of Succinate Dehydrogenase." Plant Disease 99, no. 2 (2015): 231–39. http://dx.doi.org/10.1094/pdis-04-14-0374-re.

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Boscalid, a succinate dehydrogenase inhibitor (SDHI), was registered in 2011 to control Alternaria brown spot (ABS) of citrus, caused by Alternaria alternata. In this study, the effect of boscalid on mycelial growth, conidial germination, and resazurin reduction was established in a subset of 16 sensitive isolates using three different media. Conidial germination and mycelial growth inhibition were not suppressed even at higher concentrations of boscalid, although effective concentration to inhibit 50% growth (EC50) values were established with each method. Resazurin reduction produced the low

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Piccini, Valentina, Elena Rapizzi, Alessandra Bacca, et al. "Head and neck paragangliomas: genetic spectrum and clinical variability in 79 consecutive patients." Endocrine-Related Cancer 19, no. 2 (2012): 149–55. http://dx.doi.org/10.1530/erc-11-0369.

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Head and neck paragangliomas (HNPGLs) are neural crest-derived tumors. In comparison with paragangliomas located in the abdomen and the chest, which are generally catecholamine secreting (sPGLs) and sympathetic in origin, HNPGLs are, in fact, parasympathetic in origin and are generally nonsecreting. Overall, 79 consecutive patients with HNPGL were examined for mutations in SDHA, SDHB, SDHC, SDHD, SDHAF2, VHL, MAX, and TMEM127 genes by PCR/sequencing. According to a detailed family history (FH) and clinical, laboratory (including metanephrines), and instrumental examinations, patients were divi

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Bayley, Jean Pierre, Birke Bausch, Johannes Adriaan Rijken, et al. "Variant type is associated with disease characteristics in SDHB, SDHC and SDHD-linked phaeochromocytoma–paraganglioma." Journal of Medical Genetics 57, no. 2 (2019): 96–103. http://dx.doi.org/10.1136/jmedgenet-2019-106214.

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BackgroundPathogenic germline variants in subunits of succinate dehydrogenase (SDHB, SDHC and SDHD) are broadly associated with disease subtypes of phaeochromocytoma–paraganglioma (PPGL) syndrome. Our objective was to investigate the role of variant type (ie, missense vs truncating) in determining tumour phenotype.MethodsThree independent datasets comprising 950 PPGL and head and neck paraganglioma (HNPGL) patients were analysed for associations of variant type with tumour type and age-related tumour risk. All patients were carriers of pathogenic germline variants in the SDHB, SDHC or SDHD gen

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Bausch, Birke, Ulrich Wellner, Dirk Bausch, et al. "Long-term prognosis of patients with pediatric pheochromocytoma." Endocrine-Related Cancer 21, no. 1 (2013): 17–25. http://dx.doi.org/10.1530/erc-13-0415.

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A third of patients with paraganglial tumors, pheochromocytoma, and paraganglioma, carry germline mutations in one of the susceptibility genes, RET, VHL, NF1, SDHAF2, SDHA, SDHB, SDHC, SDHD, TMEM127, and MAX. Despite increasing importance, data for long-term prognosis are scarce in pediatric presentations. The European-American-Pheochromocytoma–Paraganglioma-Registry, with a total of 2001 patients with confirmed paraganglial tumors, was the platform for this study. Molecular genetic and phenotypic classification and assessment of gene-specific long-term outcome with second and/or malignant par

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Wu, Ben-Hong, Shao-Hua Li, Marta Nosarzewski, and Douglas D. Archbold. "Sorbitol Dehydrogenase Gene Expression and Enzyme Activity in Apple: Tissue Specificity during Bud Development and Response to Rootstock Vigor and Growth Manipulation." Journal of the American Society for Horticultural Science 135, no. 4 (2010): 379–87. http://dx.doi.org/10.21273/jashs.135.4.379.

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Sorbitol is the primary photosynthate and translocated carbohydrate in apple (Malus ×domestica), and most of it is converted to fructose by sorbitol dehydrogenase (SDH) in sink tissues. We studied the expression of nine SDH genes, SDH activity, and sorbitol content of apple 1) in buds and floral tissues from dormancy to bloom, 2) in leaves and shoot tips of trees on two rootstocks, the moderately vigorous ‘Malling Merton 111’ (MM.111) and the dwarfing ‘Malling 9’ (M.9), and 3) in shoot tips in response to application of prohexadione-Ca to suppress shoot growth and defoliation and girdling (D/G

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Yao, Shirley A., Elizabeth A. Wiley, Lisa R. Susswein, et al. "Germline pathogenic variants in patients with pheochromocytoma." Journal of Clinical Oncology 36, no. 6_suppl (2018): 668. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.668.

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668 Background: Approximately 25% of pheochromocytomas (PCC) have a hereditary basis, and germline variants in the SDHA, SDHB, SDHC, SDHD, SDHAF2, TMEM127, MAX, VHL, FH, RET, MEN1, and NF1 genes have been associated with a predisposition to PCC and paraganglioma (PGL). Multi-gene hereditary cancer panel testing for PCC has become increasingly more common than single-gene testing algorithms. Identification of a pathogenic or likely pathogenic variant (PV/LPV) in one of these genes has important implications for surveillance in patients and their family members. Here we describe the spectrum of

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Papathomas, Thomas G., Jose Gaal, Eleonora P. M. Corssmit, et al. "Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC–PGL syndromes: a clinicopathological and molecular analysis." European Journal of Endocrinology 170, no. 1 (2014): 1–12. http://dx.doi.org/10.1530/eje-13-0623.

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ObjectiveAlthough the succinate dehydrogenase (SDH)-related tumor spectrum has been recently expanded, there are only rare reports of non-pheochromocytoma/paraganglioma tumors in SDHx-mutated patients. Therefore, questions still remain unresolved concerning the aforementioned tumors with regard to their pathogenesis, clinicopathological phenotype, and even causal relatedness to SDHx mutations. Absence of SDHB expression in tumors derived from tissues susceptible to SDH deficiency is not fully elucidated.Design and methodsThree unrelated SDHD patients, two with pituitary adenoma (PA) and one wi

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Testa, Joseph R., David Malkin, and Joshua D. Schiffman. "Connecting Molecular Pathways to Hereditary Cancer Risk Syndromes." American Society of Clinical Oncology Educational Book, no. 33 (May 2013): 81–90. http://dx.doi.org/10.14694/edbook_am.2013.33.81.

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An understanding of the genetic causes and molecular pathways of hereditary cancer syndromes has historically informed our knowledge and treatment of all types of cancers. For this review, we focus on three rare syndromes and their associated genetic mutations including BAP1, TP53, and SDHx (SDHA, SDHB, SDHC, SDHD, SDHAF2). BAP1 encodes an enzyme that catalyzes the removal of ubiquitin from protein substrates, and germline mutations of BAP1 cause a novel cancer syndrome characterized by high incidence of benign atypical melanocytic tumors, uveal melanomas, cutaneous melanomas, malignant mesoth

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Boedeker, Carsten Christof, Hartmut P. H. Neumann, Wolfgang Maier, Birke Bausch, Jörg Schipper, and Gerd Jürgen Ridder. "Malignant Head and Neck Paragangliomas in SDHB Mutation Carriers." Otolaryngology–Head and Neck Surgery 137, no. 1 (2007): 126–29. http://dx.doi.org/10.1016/j.otohns.2007.01.015.

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OBJECTIVE: Three of four paraganglioma syndromes (PGLs) have been characterized on a molecular genetic basis. PGL 1 is associated with mutations of the succinate dehydrogenase subunit D ( SDHD) gene, PGL 3 is caused by SDHC gene mutations, and PGL 4 is caused by SDHB gene mutations. The objective of this study was to investigate whether PGLs are associated with malignant head and neck paragangliomas (HNPs). STUDY DESIGN AND SETTING: Through November 2005, we screened 195 HNP patients for mutations of the genes SDHB, SDHC, and SDHD. RESULTS: We detected 5 SDHC, 13 SDHB, and 45 SDHD gene mutatio

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Stanley, Kaitlin, Erika Friehling, Amy Davis, and Sarangarajan Ranganathan. "Succinate Dehydrogenase-Deficient Gastrointestinal Stromal Tumor With SDHC Germline Mutation and Bilateral Renal and Neck Cysts." Pediatric and Developmental Pathology 22, no. 3 (2018): 265–68. http://dx.doi.org/10.1177/1093526618805354.

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Gastrointestinal stromal tumors (GISTs) are rare in children. Succinate dehydrogenase (SDH)-deficient GISTs are wild type and lack KIT proto-oncogene receptor tyrosine kinase and platelet-derived growth factor receptor A ( KIT or PDGFRA) mutations. These tumors result from germline SDH mutations, somatic SDH mutations, or SDH epimutants. Germline mutations in SDH genes ( SDHA, SDHB, SDHC, or SDHD) suggest Carney–Stratakis syndrome, a paraganglioma syndrome with predisposition for GIST. Negative immunohistochemistry for SDHB indicates dysfunction of the mitochondrial complex regardless of the s

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Cass, Nathan D., Melissa A. Schopper, Jonathan A. Lubin, Lauren Fishbein, and Samuel P. Gubbels. "The Changing Paradigm of Head and Neck Paragangliomas: What Every Otolaryngologist Needs to Know." Annals of Otology, Rhinology & Laryngology 129, no. 11 (2020): 1135–43. http://dx.doi.org/10.1177/0003489420931540.

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Background: Recommendations regarding head and neck paragangliomas (HNPGL) have undergone a fundamental reorientation in the last decade as a result of increased understanding of the genetic and pathophysiologic basis of these disorders. Objective: We aim to provide an overview of HNPGL and recent discoveries regarding their molecular genetics, along with updated recommendations on workup, treatment, and surveillance, and their implications for otolaryngologists treating patients with these disorders. Results: SDHx susceptibility gene mutations, encoding subunits of the enzyme succinate dehydr

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Benn, Diana E., Ying Zhu, Katrina A. Andrews, et al. "Bayesian approach to determining penetrance of pathogenic SDH variants." Journal of Medical Genetics 55, no. 11 (2018): 729–34. http://dx.doi.org/10.1136/jmedgenet-2018-105427.

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BackgroundUntil recently, determining penetrance required large observational cohort studies. Data from the Exome Aggregate Consortium (ExAC) allows a Bayesian approach to calculate penetrance, in that population frequencies of pathogenic germline variants should be inversely proportional to their penetrance for disease. We tested this hypothesis using data from two cohorts for succinate dehydrogenase subunits A, B and C (SDHA–C) genetic variants associated with hereditary pheochromocytoma/paraganglioma (PC/PGL).MethodsTwo cohorts were 575 unrelated Australian subjects and 1240 unrelated UK su

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Kong, Grace, Tess Schenberg, Christopher J. Yates, et al. "The Role of 68Ga-DOTA-Octreotate PET/CT in Follow-Up of SDH-Associated Pheochromocytoma and Paraganglioma." Journal of Clinical Endocrinology & Metabolism 104, no. 11 (2019): 5091–99. http://dx.doi.org/10.1210/jc.2019-00018.

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Abstract Purpose Germline succinate dehydrogenase (SDHx) mutation carriers, especially SDHB, are at increased risk for malignancy and require life-long surveillance. Current guidelines recommend periodic whole-body MRI imaging. We assessed the incremental value of 68Ga-DOTA-octreotate (GaTate) positron emission tomography (PET)/CT compared with conventional imaging in such patients. Methods SDHx mutation carriers who had GaTate PET/CT were retrospectively reviewed. Detection of lesions were compared with MRI or CT on a per-patient and per-lesion basis. Proof of lesions were based on histopatho

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Andrews, Katrina A., David B. Ascher, Douglas Eduardo Valente Pires, et al. "Tumour risks and genotype–phenotype correlations associated with germline variants in succinate dehydrogenase subunit genes SDHB, SDHC and SDHD." Journal of Medical Genetics 55, no. 6 (2018): 384–94. http://dx.doi.org/10.1136/jmedgenet-2017-105127.

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BackgroundGermline pathogenic variants in SDHB/SDHC/SDHD are the most frequent causes of inherited phaeochromocytomas/paragangliomas. Insufficient information regarding penetrance and phenotypic variability hinders optimum management of mutation carriers. We estimate penetrance for symptomatic tumours and elucidate genotype–phenotype correlations in a large cohort of SDHB/SDHC/SDHD mutation carriers.MethodsA retrospective survey of 1832 individuals referred for genetic testing due to a personal or family history of phaeochromocytoma/paraganglioma. 876 patients (401 previously reported) had a g

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Bernardo-Castiñeira, Cristóbal, Nuria Valdés, Marta I. Sierra, et al. "SDHC Promoter Methylation, a Novel Pathogenic Mechanism in Parasympathetic Paragangliomas." Journal of Clinical Endocrinology & Metabolism 103, no. 1 (2017): 295–305. http://dx.doi.org/10.1210/jc.2017-01702.

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Abstract Context Germline mutations in the succinate dehydrogenase A, B, C, and D genes (collectively, SDHx) predispose to the development of paragangliomas (PGLs) arising at the parasympathetic or sympathetic neuroendocrine systems. SDHx mutations cause absence of tumoral immunostaining for SDHB. However, negative SDHB immunostaining has also been found in a subset of PGLs that lack SDHx mutations. Settings Here, we report the comprehensive molecular characterization of one such a tumor of parasympathetic origin compared with healthy paraganglia and other PGLs with or without SDHx mutations.

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Aldera, Alessandro Pietro, and Dhirendra Govender. "Gene of the month: SDH." Journal of Clinical Pathology 71, no. 2 (2017): 95–97. http://dx.doi.org/10.1136/jclinpath-2017-204677.

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Succinate dehydrogenase (SDH) is a heterotetrameric nuclear encoded mitochondrial protein complex which plays a role in the citric acid cycle and the electron transfer chain. Germline mutations in SDHA are associated with Leigh syndrome. Mutations in SDHB, SDHC and SDHD are found in an increasing number of neoplasms, most notably paragangliomas and wild-type gastrointestinal stromal tumours. SDH deficiency in these tumours has important prognostic implications, and also provides a novel target for molecular therapy. In this article, we outline the structure and function of SDH and provide a su

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Else, Tobias, Antonio Marcondes Lerario, Jessica Everett, et al. "Adrenocortical carcinoma and succinate dehydrogenase gene mutations: an observational case series." European Journal of Endocrinology 177, no. 5 (2017): 439–44. http://dx.doi.org/10.1530/eje-17-0358.

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Objective Germline loss-of-function mutations in succinate dehydrogenase (SDHx) genes results in rare tumor syndromes that include pheochromocytoma, paraganglioma, and others. Here we report a case series of patients with adrenocortical carcinoma (ACC) that harbor SDHx mutations. Patients and results We report four unrelated patients with ACC and SDHx mutations. All cases presented with Cushing syndrome and large adrenal masses that were confirmed to be ACC on pathology. All four ACC specimens were found to have truncating mutations in either SDHC or SDHA, while cases 1, 2 and 3 also had the m

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Montani, M., A. M. Schmitt, S. Schmid, et al. "No mutations but an increased frequency of SDHx polymorphisms in patients with sporadic and familial medullary thyroid carcinoma." Endocrine-Related Cancer 12, no. 4 (2005): 1011–16. http://dx.doi.org/10.1677/erc.1.00996.

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Germline mutations of the three succinate dehydrogenase subunits SDHB, SDHC and SDHD have recently been associated with familial pheochromocytoma and paraganglioma. Several reasons make these genes candidate tumor suppressor genes for medullary thyroid carcinoma (MTC): (1) SDHB lies on chromosome 1p, the region known to be deleted most frequently in MTC, (2) MTCs develop from neural crest-derived cells, as do pheochromocytomas and paragangliomas and (3) patients with germline mutations of the Ret-protooncogene develop MTCs as well as pheochromocytomas, indicating a relationship of these tumors

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Wagner, Andrew J., Stephen P. Remillard, Yixiang Zhang, and Jason L. Hornick. "Immunohistochemical identification of SDHA-mutant gastrointestinal stromal tumors (GISTs)." Journal of Clinical Oncology 30, no. 15_suppl (2012): 10029. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10029.

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10029 Background: GISTs are most commonly driven by activating mutations in KIT or PDGFRA. However, 15% of GISTs in adults and >90% in children lack such mutations. A subset of KIT/PDGFRA wild-type GISTs shows distinctive morphologic and clinical features and loss of expression of succinate dehydrogenase (SDH) B. Only a fraction of SDHB-deficient GISTs carry loss-of-function mutations in SDHB or SDHC. Due to the complexity of its locus and the presence of several pseudogenes, SDHA is rarely analyzed. Recently, mutations in SDHA were shown to lead to loss of expression of SDHA and SDHB in pa

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Gruber, Lucinda, and L. James Maher. "Predicted Succinated Dehydrogenase Subunit Variant Pathogenicity: Why Are SDHB Variants “Bad”?" Journal of the Endocrine Society 5, Supplement_1 (2021): A71—A72. http://dx.doi.org/10.1210/jendso/bvab048.144.

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Abstract Variants in the 4 genes encoding subunits A-D of succinate dehydrogenase (SDH) are associated with paraganglioma and pheochromocytoma. Intuitively, loss-of-function variants affecting any of the subunits should equally diminish SDH function leading to succinate accumulation and tumorigenesis after loss of heterozygosity. However, variants in SDHB are associated with a higher prevalence of metastatic disease and a more aggressive clinical course. Evaluation of the SDH protein structure shows the fraction of amino acids in contact with other subunits or essential prosthetic groups to be

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Choi, Hye-Ryeon, Ja-Seung Koo, Cho-Rok Lee, et al. "Efficacy of Immunohistochemistry for SDHB in the Screening of Hereditary Pheochromocytoma–Paraganglioma." Biology 10, no. 7 (2021): 677. http://dx.doi.org/10.3390/biology10070677.

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The most common genetic backgrounds of hereditary paraganglioma and pheochromocytoma (PPGL) are SDHx germline mutations. Given the fact that the immunohistochemistry (IHC) result for SDHB is always negative regardless of the type of SDHx mutation, we aimed to evaluate the efficacy of using SDHB IHC for screening SDHx mutations in PPGL cases. In total, 52 patients who underwent surgery for PPGL treatment between 2006 and 2020 and underwent genetic analysis at diagnosis were included. Tissue microarrays (TMAs) were constructed with PPGL tissues and IHC for SDHB was performed on TMA sections. All

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Zhou, Xiaoting, Yan Gao, Weiwei Wang, et al. "Architecture of the mycobacterial succinate dehydrogenase with a membrane-embedded Rieske FeS cluster." Proceedings of the National Academy of Sciences 118, no. 15 (2021): e2022308118. http://dx.doi.org/10.1073/pnas.2022308118.

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Complex II, also known as succinate dehydrogenase (SQR) or fumarate reductase (QFR), is an enzyme involved in both the Krebs cycle and oxidative phosphorylation. Mycobacterial Sdh1 has recently been identified as a new class of respiratory complex II (type F) but with an unknown electron transfer mechanism. Here, using cryoelectron microscopy, we have determined the structure of Mycobacterium smegmatis Sdh1 in the presence and absence of the substrate, ubiquinone-1, at 2.53-Å and 2.88-Å resolution, respectively. Sdh1 comprises three subunits, two that are water soluble, SdhA and SdhB, and one

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White, Gemma, Samantha Anandappa, Michael Masucci, et al. "Using Multimodal Functional Imaging in the Management of SDHx-Related Pheochromocytoma and Paraganglioma." Journal of the Endocrine Society 5, Supplement_1 (2021): A1034—A1035. http://dx.doi.org/10.1210/jendso/bvab048.2117.

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Abstract Background: Succinate Dehydrogenase (SDH) subunit pathogenic variants predispose to Pheochromocytoma and Paraganglioma (PPGL). Functional imaging harnesses the innate receptor expression and the aberrant cellular pathways in PPGLs to improve diagnostic accuracy & guide treatments, including nuclear medicine therapies. Currently commonly available functional imaging modalities include 18F-FDG PET, 123I-MIBG and 68Ga-DOTATATE. Aims: To analyze the use of 123I-MIBG, 18F-FDG PET and 68Ga-DOTATATE in patients harboring SDHB & SDHD pathogenic variants and determine the detection rat

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Clark, Graeme R., Marco Sciacovelli, Edoardo Gaude, et al. "Germline FH Mutations Presenting With Pheochromocytoma." Journal of Clinical Endocrinology & Metabolism 99, no. 10 (2014): E2046—E2050. http://dx.doi.org/10.1210/jc.2014-1659.

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Abstract Context: At least a third of the patients with pheochromocytoma (PCC) or paraganglioma (PGL) harbor an underlying germline mutation in a known PCC/PGL gene. Mutations in genes (SDHB, SDHD, SDHC, and SDHA) encoding a component of the tricarboxylic acid cycle, succinate dehydrogenase (SDH), are a major cause of inherited PCC and PGL. SDHB mutations are also, albeit less frequently, associated with inherited renal cell carcinoma. Inactivation of SDH and another tricarboxylic acid cycle component, fumarate hydratase (FH), have both been associated with abnormalities of cellular metabolism

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Korpershoek, Esther, Judith Favier, José Gaal, et al. "SDHA Immunohistochemistry Detects Germline SDHA Gene Mutations in Apparently Sporadic Paragangliomas and Pheochromocytomas." Journal of Clinical Endocrinology & Metabolism 96, no. 9 (2011): E1472—E1476. http://dx.doi.org/10.1210/jc.2011-1043.

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Abstract Context: Pheochromocytoma-paraganglioma syndrome is caused by mutations in SDHB, SDHC, and SDHD, encoding subunits of succinate dehydrogenase (SDH), and in SDHAF2, required for flavination of SDHA. A recent report described a patient with an abdominal paraganglioma, immunohistochemically negative for SDHA, and identified a causal germline mutation in SDHA. Objective: In this study, we evaluated the significance of SDHA immunohistochemistry in the identification of new patients with SDHA mutations. Setting: This study was performed in the Erasmus Medical Center in Rotterdam (The Nether

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Whitworth, James, Ruth T. Casey, Philip S. Smith, et al. "Familial wild-type gastrointestinal stromal tumour in association with germline truncating variants in both SDHA and PALB2." European Journal of Human Genetics 29, no. 7 (2021): 1139–45. http://dx.doi.org/10.1038/s41431-021-00862-5.

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AbstractGastrointestinal stromal tumour (GIST) is a mesenchymal neoplasm arising in the gastrointestinal tract. A rare subset of GISTs are classified as wild-type GIST (wtGIST) and these are frequently associated with germline variants that affect the function of cancer predisposition genes such as the succinate dehydrogenase subunit genes (SDHA, SDHB, SDHC, SDHD) or NF1. However, despite this high heritability, familial clustering of wtGIST is extremely rare. Here, we report a mother–son diad who developed wtGIST at age 66 and 34 years, respectively. Comprehensive genetic testing revealed ger

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Wang, Gang, and Priya Rao. "Succinate Dehydrogenase–Deficient Renal Cell Carcinoma: A Short Review." Archives of Pathology & Laboratory Medicine 142, no. 10 (2018): 1284–88. http://dx.doi.org/10.5858/arpa.2017-0199-rs.

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Succinate dehydrogenase (SDH) is a mitochondrial enzyme complex composed of 4 protein subunits (SDHA, SDHB, SDHC, and SDHD). Germ line mutations of the genes encoding these SDH subunits result in hereditary syndromes harboring pheochromocytomas/paragangliomas, gastrointestinal stromal tumors, renal cell carcinomas, and pituitary adenomas. SDH-deficient renal cell carcinomas are rare, with a mean age of 38 to 40 years. Histologically, these tumors show a characteristic appearance that includes a solid, nested, or tubular architecture with variable cysts. Cells are typically cuboidal, have indis

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Casey, Ruth, Aoife Garrahy, Antoinette Tuthill, et al. "Universal Genetic Screening Uncovers a Novel Presentation of an SDHAF2 Mutation." Journal of Clinical Endocrinology & Metabolism 99, no. 7 (2014): E1392—E1396. http://dx.doi.org/10.1210/jc.2013-4536.

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Context: Hereditary pheochromocytoma/paraganglioma (PC/PGL) accounts for up to 60% of previously considered sporadic tumors. Guidelines suggest that phenotype should guide genetic testing. Next-generation sequencing technology can simultaneously sequence 9 of the 18 known susceptibility genes in a timely, cost-efficient manner. Objective: Our aim was to confirm that universal screening is superior to targeted testing in patients with histologically confirmed PC and PGL. Methods: In two tertiary referral hospitals in Ireland, NGS was carried out on all histologically confirmed cases of PC/PGL d

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Nannini, Margherita, Milena Urbini, Valentina Indio, et al. "Identification of SDHA germline mutations in sporadic SDHA mutant gastrointestinal stromal tumors (GIST): The need of a genetic counselling." Journal of Clinical Oncology 38, no. 15_suppl (2020): 11537. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.11537.

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11537 Background: SDH- deficient GIST, as defined by the loss of expression of SDHB, account up to about 10% of all gastric GIST and generally affect younger population. Germline mutations in SDHB, SDHC, and SDHD occur in about 20–30% of SDH- deficient, that may be referred to a hereditary condition known as hereditary GIST-paraganglioma syndrome (Carney-Stratakis Syndrome), whereas germline SDHA mutations have been rarely described in apparently sporadic cases. Currently, even germline testing is recommended for SDH- deficient GIST, there are no clear guidelines for genetic counselling and fo

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De Sousa, Sunita M. C., Mark J. McCabe, Kathy Wu, et al. "Germline variants in familial pituitary tumour syndrome genes are common in young patients and families with additional endocrine tumours." European Journal of Endocrinology 176, no. 5 (2017): 635–44. http://dx.doi.org/10.1530/eje-16-0944.

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Objective Familial pituitary tumour syndromes (FPTS) account for 5% of pituitary adenomas. Multi-gene analysis via next-generation sequencing (NGS) may unveil greater prevalence and inform clinical care. We aimed to identify germline variants in selected patients with pituitary adenomas using a targeted NGS panel. Design We undertook a nationwide cross-sectional study of patients with pituitary adenomas with onset ≤40 years of age and/or other personal/family history of endocrine neoplasia. A custom NGS panel was performed on germline DNA to interrogate eight FPTS genes. Genome data were analy

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Abed, Firas M., Melissa A. Brown, Omar A. Al-Mahmood, and Michael J. Dark. "SDHB and SDHA Immunohistochemistry in Canine Pheochromocytomas." Animals 10, no. 9 (2020): 1683. http://dx.doi.org/10.3390/ani10091683.

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Pheochromocytomas (PCs) are tumors arising from the chromaffin cells of the adrenal glands and are the most common tumors of the adrenal medulla in animals. In people, these are highly correlated to inherited gene mutations in the succinate dehydrogenase (SDH) pathway; however, to date, little work has been done on the genetic basis of these tumors in animals. In humans, immunohistochemistry has proven valuable as a screening technique for SDH mutations. Human PCs that lack succinate dehydrogenase B (SDHB) immunoreactivity have a high rate of mutation in the SDH family of genes, while human PC

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Thompson, Michael JW, Venkat Parameswaran, and John R. Burgess. "Clinical utility of chromogranin A for the surveillance of succinate dehydrogenase B- and succinate dehydrogenase D-related paraganglioma." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 1 (2018): 163–69. http://dx.doi.org/10.1177/0004563218811865.

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Background Patients with mutations of succinate dehydrogenase B (SDHB) and succinate dehydrogenase D (SDHD) are at high risk of paraganglioma necessitating surveillance. Chromogranin A has been proposed as a biochemical marker of paraganglioma. We sought to determine the diagnostic utility of chromogranin A in a population-based SDHx sample. Methods Tasmania is an island state with one tertiary referral centre for endocrine neoplasia. We performed a cross-sectional analysis of all adult SDHB ( n = 52) and SDHD ( n = 10) patients undergoing paraganglioma surveillance between 2011 and 2017. Chro

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Pankratova, Iu V., E. G. Przhiyalkovskaya, E. A. Pigarova, and L. K. Dzeranova. "The enzyme succinate dehydrogenase (SDH) and its role in hereditary pituitary adenomas." Obesity and metabolism 10, no. 4 (2013): 10–15. http://dx.doi.org/10.14341/omet2013410-15.

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Despite active research involving familial pituitary adenomas and characterization of five hereditary syndromes, the genetic defects in more than 80 - 95% of patients remain not found. Besides, there is more than 25 cases of coexistence of pheochromocytomas and pituitary adenomas described in literature that up to date is not integrated in any syndrome; genetic defects of such coexistence also aren't defined. However it is supposed that in pituitary tumorigenesis, germline mutations of SDH can take part that is obviously important aspect of further investigation. Germline mutations of SDH were

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Malinoc, Angelica, Maren Sullivan, Thorsten Wiech, et al. "Biallelic inactivation of the SDHC gene in renal carcinoma associated with paraganglioma syndrome type 3." Endocrine-Related Cancer 19, no. 3 (2012): 283–90. http://dx.doi.org/10.1530/erc-11-0324.

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The etiology and pathogenesis of renal cell carcinoma (RCC) are only partially understood. Key findings in hereditary RCC, which may be site specific or a component of a syndrome, have contributed to our current understanding. Important heritable syndromes of RCC are those associated with pheochromocytoma, especially von Hippel–Lindau disease (VHL) associated with germline VHL mutations, and pheochromocytoma and paraganglioma syndrome (PGL) associated with mutations in one of the four genes (SDHA–D) encoding succinate dehydrogenase. A subset of individuals with SDHB and SDHD germline DNA mutat

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Bayley, Jean-Pierre, Marjan M. Weiss, Anneliese Grimbergen, et al. "Molecular characterization of novel germline deletions affecting SDHD and SDHC in pheochromocytoma and paraganglioma patients." Endocrine-Related Cancer 16, no. 3 (2009): 929–37. http://dx.doi.org/10.1677/erc-09-0084.

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A major cause of paraganglioma and pheochromocytoma is germline mutation of the tumor suppressor genes SDHB, SDHC, and SDHD, encoding subunits of succinate dehydrogenase (SDH). While many SDH missense/nonsense mutations have been identified, few large deletions have been described. We performed multiplex ligation-dependent probe amplification deletion analysis in 126 point mutation-negative patients, and here we describe four novel deletions of SDHD and SDHC. Long-range PCR was used for the fine mapping of deletions. One patient had a 10 kb AluSg–AluSx-mediated deletion including SDHD exons 1

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Benn, Diana E., Bruce G. Robinson, and Roderick J. Clifton-Bligh. "15 YEARS OF PARAGANGLIOMA: Clinical manifestations of paraganglioma syndromes types 1–5." Endocrine-Related Cancer 22, no. 4 (2015): T91—T103. http://dx.doi.org/10.1530/erc-15-0268.

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The paraganglioma (PGL) syndromes types 1–5 are autosomal dominant disorders characterized by familial predisposition to PGLs, phaeochromocytomas (PCs), renal cell cancers, gastrointestinal stromal tumours and, rarely, pituitary adenomas. Each syndrome is associated with mutation in a gene encoding a particular subunit (or assembly factor) of succinate dehydrogenase (SDHx). The clinical manifestations of these syndromes are protean: patients may present with features of catecholamine excess (including the classic triad of headache, sweating and palpitations), or with symptoms from local tumour

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Filonenko, Daria A., Andrey A. Meshcheryakov, Petr P. Arkhiri, Maxim P. Nikulin, and Evgeniia S. Kolobanova. "SDH-deficient gastrointestinal stromal tumors: paradoxical effect of imatinib." Journal of Modern Oncology 22, no. 2 (2020): 133–36. http://dx.doi.org/10.26442/18151434.2020.2.200053.

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Succinate dehydrogenase deficient gastrointestinal stromal tumors (dSDH GIST) is a unique group of GISTs with an energy metabolism defect as the key oncogenic mechanism without mutations in the proto-oncogene receptor tyrosine kinase (KIT) and platelet-derived growth factor receptor a (PDGFRA). SDH-deficiency is a result of mutations in SDHA, SDHB, SDHC, SDHD. There are three variants of dSDH GIST: sporadic dSDH GIST, Carney triad or Carney-Stratakis syndrome. dSDH GISTs are characterized by young age, female prevalence, gastric location, multiple tumors, lymph node metastases, indolent behavi

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Jafri, Mariam, and Eamonn R. Maher. "GENETICS IN ENDOCRINOLOGY: The genetics of phaeochromocytoma: using clinical features to guide genetic testing." European Journal of Endocrinology 166, no. 2 (2012): 151–58. http://dx.doi.org/10.1530/eje-11-0497.

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Phaeochromocytoma is a rare, usually benign, tumour predominantly managed by endocrinologists. Over the last decade, major advances have been made in understanding the molecular genetic basis of adrenal and extra-adrenal phaeochromocytoma (also referred to as adrenal phaeochromocytoma (aPCA) and extra-adrenal functional paraganglioma (eFPGL)). In contrast to the previously held belief that only 10% of cases had a genetic component, currently about one-third of all aPCA/eFPGL cases are thought to be attributable to germline mutations in at least nine genes (NF1, RET, SDHA, SDHB, SDHC, SDHD, TME

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