Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory of Molecular Genetics |
RCV001807783 | SCV002056134 | pathogenic | Neurodevelopmental disorder | 2021-12-15 | criteria provided, single submitter | research | |
Revvity Omics, |
RCV002274213 | SCV003819517 | uncertain significance | Neurodevelopmental disorder with speech delay and variable ocular anomalies | 2021-01-27 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004040924 | SCV004965901 | likely pathogenic | Inborn genetic diseases | 2023-12-01 | criteria provided, single submitter | clinical testing | The c.706C>T (p.Q236*) alteration, located in exon 4 (coding exon 4) of the THUMPD1 gene, consists of a C to T substitution at nucleotide position 706. This changes the amino acid from a glutamine (Q) to a stop codon at amino acid position 236. This alteration occurs at the 3' terminus of the THUMPD1 gene, is not expected to trigger nonsense-mediated mRNA decay, and impacts the last 33% of the protein. Premature stop codons are typically deleterious in nature and a significant portion of the protein is affected. Based on data from gnomAD, the T allele has an overall frequency of 0.002% (5/250234) total alleles studied. The highest observed frequency was 0.016% (5/30606) of South Asian alleles. This variant has been reported homozygous in multiple individuals with features consistent with THUMPD1-related neurodevelopmental disorder (Maddirevula, 2019; Broly, 2022). Based on the available evidence, this alteration is classified as likely pathogenic. |
OMIM | RCV002274213 | SCV002559868 | pathogenic | Neurodevelopmental disorder with speech delay and variable ocular anomalies | 2022-08-10 | no assertion criteria provided | literature only |