ClinVar Miner

Submissions for variant NM_000295.5(SERPINA1):c.206C>T (p.Ser69Phe)

gnomAD frequency: 0.00006  dbSNP: rs199687431
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Total submissions: 3
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Submitter RCV SCV Clinical significance Condition Last evaluated Review status Method Comment
Labcorp Genetics (formerly Invitae), Labcorp RCV000353319 SCV005770489 uncertain significance Alpha-1-antitrypsin deficiency 2024-09-11 criteria provided, single submitter clinical testing This sequence change replaces serine, which is neutral and polar, with phenylalanine, which is neutral and non-polar, at codon 69 of the SERPINA1 protein (p.Ser69Phe). This variant is present in population databases (rs199687431, gnomAD 0.01%). This missense change has been observed in individual(s) with lung disease (PMID: 31661293). ClinVar contains an entry for this variant (Variation ID: 315030). Invitae Evidence Modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) has been performed for this missense variant. However, the output from this modeling did not meet the statistical confidence thresholds required to predict the impact of this variant on SERPINA1 protein function. In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance.
Eurofins Ntd Llc (ga) RCV000734913 SCV000863093 uncertain significance not provided 2018-08-22 criteria provided, single submitter clinical testing
Illumina Laboratory Services, Illumina RCV000353319 SCV000389659 uncertain significance Alpha-1-antitrypsin deficiency 2018-01-13 criteria provided, single submitter clinical testing This variant was observed in the ICSL laboratory as part of a predisposition screen in an ostensibly healthy population. It had not been previously curated by ICSL or reported in the Human Gene Mutation Database (HGMD: prior to June 1st, 2018), and was therefore a candidate for classification through an automated scoring system. Utilizing variant allele frequency, disease prevalence and penetrance estimates, and inheritance mode, an automated score was calculated to assess if this variant is too frequent to cause the disease. Based on the score, this variant could not be ruled out of causing disease and therefore its association with disease required further investigation. A literature search was performed for the gene, cDNA change, and amino acid change (if applicable). No publications were found based on this search. This variant was therefore classified as a variant of unknown significance for this disease.

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