Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001954597 | SCV002191349 | pathogenic | Fanconi anemia | 2022-05-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln156*) in the FANCM gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FANCM are known to be pathogenic (PMID: 29895858, 30075111). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with ovarian cancer (PMID: 28881617). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004728940 | SCV005338070 | likely pathogenic | FANCM-related disorder | 2024-09-03 | no assertion criteria provided | clinical testing | The FANCM c.466C>T variant is predicted to result in premature protein termination (p.Gln156*). This variant was reported in an individual with high grade serous ovarian cancer as well as in a control (Supplementary Table 6. Dicks et al. 2017. PubMed ID: 28881617). This variant has not been reported in gnomAD, indicating this variant is rare. This variant is classified as pathogenic in ClinVar (https://www.ncbi.nlm.nih.gov/clinvar/variation/1419135/). Nonsense variants in FANCM are expected to be pathogenic. This variant is interpreted as likely pathogenic. |