Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Degerman lab, |
RCV000677348 | SCV000611700 | likely pathogenic | Pulmonary fibrosis and/or bone marrow failure, Telomere-related, 1 | 2017-11-23 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV005056102 | SCV005726890 | uncertain significance | not specified | 2024-11-08 | criteria provided, single submitter | clinical testing | Variant summary: TERT c.3399A>G (p.X1133TrpextX39) changes the termination codon and is predicted to lead to an extended protein with additional amino acids added to the normal C-terminus. The variant was absent in 239294 control chromosomes (gnomAD). c.3399A>G has been reported in the literature in heterozygous state in an individual affected with aplastic anemia, who had shorter telomere length and positive family history for pulmonary fibrosis (Norberg_2018); in this family the variant was also found in a heterozygous unaffected parent, who had telomeres within the lower normal range, however, variable penetrance is known for TERT-Related Disorders. These data do not allow clear conclusions about variant significance. To our knowledge, no experimental evidence demonstrating an impact on protein function has been reported. However, other variants affecting the C-terminal region of the protein (e.g. c.3346_*123del177 / p.Glu1116fsX, p.Phe1127Leu, p.Thr1129Pro, p.Ile1130Val) have been reported in affected individuals (HGMD), indicating the functional importance of this protein region. ClinVar contains an entry for this variant (Variation ID: 446375). Based on the evidence outlined above, the variant was classified as VUS-possibly pathogenic. |