ClinVar Miner

Submissions for variant NM_003000.3(SDHB):c.183T>G (p.Tyr61Ter)

dbSNP: rs760169139
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Total submissions: 5
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Submitter RCV SCV Clinical significance Condition Last evaluated Review status Method Comment
Labcorp Genetics (formerly Invitae), Labcorp RCV001389812 SCV001591295 pathogenic Gastrointestinal stromal tumor; Paragangliomas 4; Pheochromocytoma 2024-11-02 criteria provided, single submitter clinical testing This sequence change creates a premature translational stop signal (p.Tyr61*) in the SDHB gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SDHB are known to be pathogenic (PMID: 19454582, 19802898). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with paraganglioma (PMID: 20418362). ClinVar contains an entry for this variant (Variation ID: 438412). For these reasons, this variant has been classified as Pathogenic.
MGZ Medical Genetics Center RCV002289690 SCV002579716 pathogenic Pheochromocytoma 2021-12-01 criteria provided, single submitter clinical testing
Ambry Genetics RCV002413384 SCV002717032 pathogenic Hereditary cancer-predisposing syndrome 2024-12-18 criteria provided, single submitter clinical testing The p.Y61* pathogenic mutation (also known as c.183T>G), located in coding exon 2 of the SDHB gene, results from a T to G substitution at nucleotide position 183. This changes the amino acid from a tyrosine to a stop codon within coding exon 2. This alteration has been detected in multiple individuals diagnosed with a paraganglioma or pheochromocytoma (Lodish MB et al. Endocr Relat Cancer. 2010 Sep;17:581-8; Jochmanova I et al. J Cancer Res Clin Oncol. 2017 Aug;143:1421-1435; Ambry internal data). In addition to the clinical data presented in the literature, this alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation.
GeneDx RCV003320666 SCV004025581 pathogenic not provided 2025-05-28 criteria provided, single submitter clinical testing Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 19958924, 31492822, 22723792, 28374168, 34439168, 20418362)
Section on Medical Neuroendocrinolgy, National Institutes of Health RCV000505331 SCV000599487 pathogenic Hereditary pheochromocytoma-paraganglioma no assertion criteria provided research

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