Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
ARUP Laboratories, |
RCV001811889 | SCV002048612 | likely pathogenic | not provided | 2021-04-02 | criteria provided, single submitter | clinical testing | The HBA2 c.163C>T; p.Gln55Ter, variant (also known as Gln54Ter when numbered from the mature protein, rs281864840) been reported in the heterozygous state in an individual with microcytosis and hypochromia and normal Hb pattern (Eng 2009). This variant is found in the African population with an allele frequency of 0.03% (2/6384 alleles, including 1 homozygote) in the Genome Aggregation Database. This variant induces an early termination codon and is predicted to result in a truncated protein or mRNA subject to nonsense-mediated decay. Based on available information, this variant is considered to be likely pathogenic. References: Eng B et al. Alpha+-thalassemia trait caused by a nonsense mutation in the alpha2-globin gene: codon 54 (CAG>TAG). Hemoglobin. 2009;33(1):72-4. PMID: 19205977. |
Quest Diagnostics Nichols Institute San Juan Capistrano | RCV001811889 | SCV004219824 | pathogenic | not provided | 2023-08-15 | criteria provided, single submitter | clinical testing | The c.163C>T (p.Gln55*) nonsense variant causes the premature termination of HBA2 protein synthesis and is associated with haemolytic anemia (ITHANET (http://www.ithanet.eu/)). In the published literature, this variant has been reported in one affected individual with mild microcytosis and hypochromia (PMID: 19205977 (2009)). Based on this information, the variant is classified as pathogenic. |