Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002408404 | SCV002720534 | pathogenic | Hereditary cancer-predisposing syndrome; Cardiovascular phenotype | 2020-11-20 | criteria provided, single submitter | clinical testing | The c.1909_1910delCC pathogenic mutation, located in coding exon 16 of the LZTR1 gene, results from a deletion of two nucleotides at nucleotide positions 1909 to 1910, causing a translational frameshift with a predicted alternate stop codon (p.P637Sfs*31). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. Based on the supporting evidence, this variant is expected to be causative of autosomal dominant schwannomatosis and, when found in trans with a second pathogenic mutation, autosomal recessive Noonan syndrome. |
Labcorp Genetics |
RCV003774555 | SCV004664479 | pathogenic | not provided | 2024-01-13 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Pro637Serfs*31) in the LZTR1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LZTR1 are known to be pathogenic (PMID: 24362817, 25335493, 25480913, 25795793, 29469822, 30368668, 30442762, 30442766, 30481304, 30859559). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with LZTR1-related conditions. ClinVar contains an entry for this variant (Variation ID: 1782449). For these reasons, this variant has been classified as Pathogenic. |