Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000672183 | SCV000797263 | likely pathogenic | Hyperinsulinemic hypoglycemia, familial, 1 | 2018-01-18 | criteria provided, single submitter | clinical testing | |
Clinical Genomics, |
RCV002252207 | SCV002522409 | uncertain significance | Maturity onset diabetes mellitus in young | criteria provided, single submitter | research | Mutations in ABCC8 gene are associated with both neonatal diabetes mellitus as well as MODY. Patients with this mutation may have a better response to sulfonylureas. However, no sufficient evidence is found to ascertain the role of this particular variant (rs1554933415) in MODY yet. | |
Clinical Genomics, |
RCV002252208 | SCV002522410 | uncertain significance | Transitory neonatal diabetes mellitus | criteria provided, single submitter | research | Mutations in ABCC8 gene are associated with both neonatal diabetes mellitus as well as MODY. Patients with this mutation may have a better response to sulfonylureas. However, no sufficient evidence is found to ascertain the role of this particular variant (rs1554933415) in neonatal diabetes yet. | |
Department of Medical Genetics, |
RCV000672183 | SCV005187333 | likely pathogenic | Hyperinsulinemic hypoglycemia, familial, 1 | 2024-08-07 | no assertion criteria provided | clinical testing | ABCC8 NM_000352.6: c.1467+1G>T variant, is a splicing variant, changing a canonical nucleotide in splicing donor site. Variant identified in patient diagnose with hyperinsulinemic hypoglycemia [HP_0000825] and Large for gestational age [HP_0001520]. Phenotype classified, according to OMIM, as one of the ABCC8 spectrum disorders; * 600509; Hyperinsulinemic hypoglycemia familial 1; # 256450 Variant classified as Likely Pathogenic due to: lack in the gnomAD population databases [PM2 moderate], loss of function mutation, known mechanism of disease [PS1 strong], variant was reported pathogenic [PP5 supporting], ClinVar RCV000672183.1. The c.1467+1G>T variant was of paternal origin reduced penetrance cannot be excluded according to avaiable data Nessa A et al. Molecular mechanisms of congenital hyperinsulinism due to autosomal dominant mutations in ABCC8, Human Molecular Genetics, Volume 24, Issue 18, September 2015, Pages 5142–5153 |