Tumor risks and genotypeâphenotypeâproteotype analysis in 358 patients with germline mutations in<i>SDHB</i>and<i>SDHD</i>

Christopher J. Ricketts(University of Birmingham), Julia Forman(University of Cambridge), Eleanor Rattenberry(Birmingham Women's Hospital), Nicola Bradshaw(Woolmanhill Hospital), Fiona Lalloo(National Health Service), Louise Izatt(Guy's Hospital), Trevor Cole(Birmingham Women's Hospital), Ruth Armstrong(Alder Hey Children's Hospital), V K Ajith Kumar(Great Ormond Street Hospital), Patrick J. Morrison(Belfast Health and Social Care Trust), A. Brew Atkinson(Royal Victoria Hospital), Fiona Douglas(Newcastle upon Tyne Hospitals NHS Foundation Trust), Steve Ball(Newcastle University), Jackie Cook(Sheffield Children's Hospital), Umasuthan Srirangalingam(St Bartholomew's Hospital), Pip Killick(University of Birmingham), Gail Kirby(University of Birmingham), Simon Aylwin(King's College Hospital), Emma R. Woodward(University of Birmingham), D. Gareth Evans(Manchester Academic Health Science Centre), Shirley V. Hodgson(St George's, University of London), V Murday(Woolmanhill Hospital), Shern L. Chew(Sheffield Children's Hospital), John Connell(University of Glasgow), Tom L. Blundell(University of Cambridge), Fiona MacDonald(Birmingham Women's Hospital), Eamonn R. Maher(University of Birmingham)
Human Mutation
October 3, 2009
Cited by 340

Abstract

Succinate dehydrogenase B (SDHB) and D (SDHD) subunit gene mutations predispose to adrenal and extraadrenal pheochromocytomas, head and neck paragangliomas (HNPGL), and other tumor types. We report tumor risks in 358 patients with SDHB (n=295) and SDHD (n=63) mutations. Risks of HNPGL and pheochromocytoma in SDHB mutation carriers were 29% and 52%, respectively, at age 60 years and 71% and 29%, respectively, in SDHD mutation carriers. Risks of malignant pheochromocytoma and renal tumors (14% at age 70 years) were higher in SDHB mutation carriers; 55 different mutations (including a novel recurrent exon 1 deletion) were identified. No clear genotype-phenotype correlations were detected for SDHB mutations. However, SDHD mutations predicted to result in loss of expression or a truncated or unstable protein were associated with a significantly increased risk of pheochromocytoma compared to missense mutations that were not predicted to impair protein stability (most such cases had the common p.Pro81Leu mutation). Analysis of the largest cohort of SDHB/D mutation carriers has enhanced estimates of penetrance and tumor risk and supports in silicon protein structure prediction analysis for functional assessment of mutations. The differing effect of the SDHD p.Pro81Leu on HNPGL and pheochromocytoma risks suggests differing mechanisms of tumorigenesis in SDH-associated HNPGL and pheochromocytoma.


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