Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
CFTR2 | RCV000029526 | SCV000245891 | pathogenic | Cystic fibrosis | 2017-03-17 | reviewed by expert panel | research | |
Labcorp Genetics |
RCV000029526 | SCV002230540 | pathogenic | Cystic fibrosis | 2022-02-27 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ser1231Profs*4) in the CFTR gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CFTR are known to be pathogenic (PMID: 1695717, 7691345, 9725922). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with cystic fibrosis (PMID: 1710600, 27081564, 30548586). This variant is also known as CF3821delT. ClinVar contains an entry for this variant (Variation ID: 35871). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV003473144 | SCV004213572 | pathogenic | Bronchiectasis with or without elevated sweat chloride 1 | 2023-02-01 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000029526 | SCV000052178 | likely pathogenic | Cystic fibrosis | 2015-10-02 | no assertion criteria provided | clinical testing |