Total submissions: 11
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000586093 | SCV000698700 | pathogenic | Niemann-Pick disease, type C | 2017-06-26 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV000008998 | SCV000894036 | pathogenic | Niemann-Pick disease, type C2 | 2018-10-31 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000008998 | SCV001211647 | pathogenic | Niemann-Pick disease, type C2 | 2025-01-06 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu20*) in the NPC2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in NPC2 are known to be pathogenic (PMID: 25145893). This variant is present in population databases (rs80358260, gnomAD 0.02%). This premature translational stop signal has been observed in individuals with Niemann-Pick disease type C (PMID: 11125141, 26666848). ClinVar contains an entry for this variant (Variation ID: 8477). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV000008998 | SCV001525184 | pathogenic | Niemann-Pick disease, type C2 | 2020-01-31 | criteria provided, single submitter | clinical testing | This variant was determined to be pathogenic according to ACMG Guidelines, 2015 [PMID:25741868]. |
Laboratorio de Genetica e Diagnostico Molecular, |
RCV000008998 | SCV002512491 | pathogenic | Niemann-Pick disease, type C2 | 2022-01-28 | criteria provided, single submitter | clinical testing | ACMG classification criteria: PVS1 very strong, PS3 supporting, PS4 strong, PM2 moderate, PM3 very strong |
Revvity Omics, |
RCV000008998 | SCV003824143 | pathogenic | Niemann-Pick disease, type C2 | 2022-06-30 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV004018603 | SCV004990701 | pathogenic | Inborn genetic diseases | 2022-05-23 | criteria provided, single submitter | clinical testing | The c.58G>T (p.E20*) alteration, located in exon 1 (coding exon 1) of the NPC2 gene, consists of a G to T substitution at nucleotide position 58. This changes the amino acid from a glutamic acid (E) to a stop codon at amino acid position 20. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This alteration has been detected in the homozygous state, and in conjunction with another NPC2 disease-causing alteration, in multiple individuals with Niemann-Pick disease, type C2 (Millat, 2001; Park, 2003; Imrie, 2015; Sudrié-Arnaud, 2021). Based on the available evidence, this alteration is classified as pathogenic. |
OMIM | RCV000008998 | SCV000029212 | pathogenic | Niemann-Pick disease, type C2 | 2007-04-01 | no assertion criteria provided | literature only | |
Gene |
RCV000008998 | SCV000041174 | not provided | Niemann-Pick disease, type C2 | no assertion provided | literature only | ||
Counsyl | RCV000008998 | SCV000790656 | pathogenic | Niemann-Pick disease, type C2 | 2017-03-31 | no assertion criteria provided | clinical testing | |
Natera, |
RCV000008998 | SCV001464118 | pathogenic | Niemann-Pick disease, type C2 | 2020-09-16 | no assertion criteria provided | clinical testing |