Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000015217 | SCV002074189 | pathogenic | Congenital amegakaryocytic thrombocytopenia | 2022-01-10 | criteria provided, single submitter | clinical testing | Variant summary: MPL c.556C>T (p.Gln186X) results in a premature termination codon, predicted to cause a truncation of the encoded protein or absence of the protein due to nonsense mediated decay, which are commonly known mechanisms for disease. This variant results in a truncated protein with 71% C-terminal deletion, lacking one of two cytokine receptor domains as well as transmembrane and cytoplasmic domains, leaving the mutational product predicted to have no function as a TPO receptor (Ihara_1999). The variant was absent in 251468 control chromosomes. c.556C>T has been reported in the literature in an individual affected with Congenital Amegakaryocytic Thrombocytopenia (Ihara_1999). No clinical diagnostic laboratories have submitted clinical-significance assessments for this variant to ClinVar after 2014. Based on the evidence outlined above, the variant was classified as pathogenic. |
Fulgent Genetics, |
RCV005025056 | SCV005651186 | pathogenic | Primary myelofibrosis; Thrombocythemia 2; Congenital amegakaryocytic thrombocytopenia 1 | 2024-03-14 | criteria provided, single submitter | clinical testing | |
OMIM | RCV004558254 | SCV000035475 | pathogenic | Congenital amegakaryocytic thrombocytopenia 1 | 1999-03-16 | no assertion criteria provided | literature only |