Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002233154 | SCV000815032 | pathogenic | Juvenile polyposis syndrome | 2018-04-09 | criteria provided, single submitter | clinical testing | This variant has not been reported in the literature in individuals with SMAD4-related disease. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Tyr195*) in the SMAD4 gene. It is expected to result in an absent or disrupted protein product. For these reasons, this variant has been classified as Pathogenic. Loss-of-function variants in SMAD4 are known to be pathogenic (PMID: 16152648, 16436638, 22810475). |
Ambry Genetics | RCV002352125 | SCV002647665 | pathogenic | Familial thoracic aortic aneurysm and aortic dissection; Hereditary cancer-predisposing syndrome | 2018-10-21 | criteria provided, single submitter | clinical testing | The p.Y195* pathogenic mutation (also known as c.585C>G), located in coding exon 4 of the SMAD4 gene, results from a C to G substitution at nucleotide position 585. This changes the amino acid from a tyrosine 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. |