Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV001025787 | SCV001188040 | pathogenic | Hereditary cancer-predisposing syndrome | 2023-11-09 | criteria provided, single submitter | clinical testing | The c.68T>G (p.L23*) alteration, located in exon 1 (coding exon 1) of the PTEN gene, consists of a T to G substitution at nucleotide position 68. This changes the amino acid from a leucine (L) to a stop codon at amino acid position 23. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). This alteration was reported in multiple individuals with features consistent with PTEN hamartoma tumor syndrome (Kingston, 2019; Pena-Couso, 2022). Based on the available evidence, this alteration is classified as pathogenic. |
Labcorp Genetics |
RCV003509651 | SCV004295291 | pathogenic | PTEN hamartoma tumor syndrome | 2023-03-27 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu23*) in the PTEN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PTEN are known to be pathogenic (PMID: 9467011, 21194675). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with PTEN-related conditions (PMID: 12938083, 35227301). ClinVar contains an entry for this variant (Variation ID: 826697). For these reasons, this variant has been classified as Pathogenic. |