Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001040938 | SCV001204530 | pathogenic | Juvenile polyposis syndrome | 2023-12-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln183*) in the SMAD4 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SMAD4 are known to be pathogenic (PMID: 16152648, 16436638, 22810475). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with SMAD4-related conditions. ClinVar contains an entry for this variant (Variation ID: 839230). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV002348352 | SCV002651220 | pathogenic | Familial thoracic aortic aneurysm and aortic dissection; Hereditary cancer-predisposing syndrome | 2018-12-20 | criteria provided, single submitter | clinical testing | The p.Q183* pathogenic mutation (also known as c.547C>T), located in coding exon 4 of the SMAD4 gene, results from a C to T substitution at nucleotide position 547. This changes the amino acid from a glutamine to a stop codon within coding exon 4. 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. |