ClinVar Miner

Submissions for variant NM_000142.5(FGFR3):c.1620C>G (p.Asn540Lys)

dbSNP: rs28933068
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Total submissions: 31
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Submitter RCV SCV Clinical significance Condition Last evaluated Review status Method Comment
Hacettepe Pediatric Genetics Laboratory, Hacettepe University RCV000017741 SCV005439182 pathogenic Hypochondroplasia 2024-12-24 criteria provided, single submitter clinical testing The FGFR3 c.1620C>G variant (p.Asn540Lys) was classified as "pathogenic" according to the ACMG criteria 2019. This variant was assessed as deleterious according to the SIFT prediction program (score 0) and the Mutation Taster prediction program (score 1).The Asn540Lys variant in FGFR3 has been reported in a Turkish patient with Hypochondroplasia (https://doi.org/10.4274/jcrpe.787). In summary, the Asn540Lys variant meets our criteria to be classified as pathogenic.
Juno Genomics, Hangzhou Juno Genomics, Inc RCV005411260 SCV005417699 pathogenic Achondroplasia; Camptodactyly-tall stature-scoliosis-hearing loss syndrome; Cervical cancer; Crouzon syndrome-acanthosis nigricans syndrome; Muenke syndrome; Thanatophoric dysplasia type 1; Thanatophoric dysplasia, type 2; Malignant tumor of urinary bladder; Hypochondroplasia; Epidermal nevus; Severe achondroplasia-developmental delay-acanthosis nigricans syndrome; Colorectal cancer; Germ cell tumor of testis; Lacrimoauriculodentodigital syndrome 2 criteria provided, single submitter clinical testing PM2_Supporting+PS4+PS2+PS3_Moderate+PS1
Women's Health and Genetics/Laboratory Corporation of America, LabCorp RCV001332222 SCV005381294 pathogenic Achondroplasia 2024-08-07 criteria provided, single submitter clinical testing Variant summary: FGFR3 c.1620C>G (p.Asn540Lys) results in a non-conservative amino acid change located in the Protein kinase domain (IPR000719) of the encoded protein sequence. Five of five in-silico tools predict a damaging effect of the variant on protein function. The variant was absent in 250610 control chromosomes (gnomAD). c.1620C>G has been reported in the literature in multiple individuals affected with Hypochondroplasia, in some cases as a de novo occurrence (e.g. Maddirevula_2018, Zhu_2022). These data indicate that the variant is very likely to be associated with disease. A different variant affecting the same codon has been classified as pathogenic by our lab (c.1619A>G, p.Asn540Ser), supporting the critical relevance of codon 540 to FGFR3 protein function. The following publications have been ascertained in the context of this evaluation (PMID: 29620724, 35726512). ClinVar contains an entry for this variant (Variation ID: 16338). Based on the evidence outlined above, the variant was classified as pathogenic.
MGZ Medical Genetics Center RCV001332222 SCV002581158 pathogenic Achondroplasia 2022-07-27 criteria provided, single submitter clinical testing
3billion RCV001332222 SCV002572640 pathogenic Achondroplasia 2023-12-19 criteria provided, single submitter clinical testing The variant is not observed in the gnomAD v2.1.1 dataset. Predicted Consequence/Location: Missense changes are a common disease-causing mechanism. In silico tool predictions suggest damaging effect of the variant on gene or gene product [REVEL: 0.69 (>=0.6, sensitivity 0.68 and specificity 0.92); 3Cnet: 0.76 (>=0.6, sensitivity 0.72 and precision 0.9)]. Same nucleotide change resulting in same amino acid change (ClinVar ID: VCV000016338 /PMID: 8589686) and different missense changes at the same codon (p.Asn540Asp, p.Asn540His, p.Asn540Ser, p.Asn540Thr / ClinVar ID: VCV000016344, VCV000016349, VCV000374828, VCV001325830 /PMID: 10777366, 9452043) have been previously reported as pathogenic/likely pathogenic with strong evidence.The variant has been observed in at least two similarly affected unrelated individuals (PMID: 25614871). Therefore, this variant is classified as Pathogenic according to the recommendation of ACMG/AMP guideline.
Genome Diagnostics Laboratory, The Hospital for Sick Children RCV002276553 SCV002566624 pathogenic Connective tissue disorder 2020-07-01 criteria provided, single submitter clinical testing
Laboratorio de Genetica e Diagnostico Molecular, Hospital Israelita Albert Einstein RCV000017741 SCV002512729 pathogenic Hypochondroplasia 2021-12-30 criteria provided, single submitter clinical testing ACMG classification criteria: PS1 strong, PS3 supporting, PS4 strong, PM2 moderate
Kasturba Medical College, Manipal, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, India RCV000017741 SCV002507199 likely pathogenic Hypochondroplasia 2022-05-09 criteria provided, single submitter clinical testing
Kasturba Medical College, Manipal, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, India RCV001804740 SCV002050695 pathogenic Larsen syndrome 2021-12-25 criteria provided, single submitter clinical testing
Blueprint Genetics RCV000255372 SCV001832469 pathogenic not provided 2019-11-30 criteria provided, single submitter clinical testing
Baylor Genetics RCV001332222 SCV001524466 pathogenic Achondroplasia 2020-02-14 criteria provided, single submitter clinical testing This variant was determined to be pathogenic according to ACMG Guidelines, 2015 [PMID:25741868].
CeGaT Center for Human Genetics Tuebingen RCV000255372 SCV001500775 pathogenic not provided 2022-05-01 criteria provided, single submitter clinical testing FGFR3: PS4, PM2, PM6, PP3, PP4
Clinical Genetics and Genomics, Karolinska University Hospital RCV000255372 SCV001449926 pathogenic not provided 2018-05-31 criteria provided, single submitter clinical testing
Fulgent Genetics, Fulgent Genetics RCV000763122 SCV000893667 pathogenic Achondroplasia; Camptodactyly-tall stature-scoliosis-hearing loss syndrome; Cervical cancer; Crouzon syndrome-acanthosis nigricans syndrome; Levy-Hollister syndrome; Muenke syndrome; Thanatophoric dysplasia type 1; Thanatophoric dysplasia, type 2; Malignant tumor of urinary bladder; Hypochondroplasia; Epidermal nevus; Severe achondroplasia-developmental delay-acanthosis nigricans syndrome; Malignant tumor of testis; Carcinoma of colon 2018-10-31 criteria provided, single submitter clinical testing
ARUP Laboratories, Molecular Genetics and Genomics, ARUP Laboratories RCV000255372 SCV000885457 pathogenic not provided 2024-09-23 criteria provided, single submitter clinical testing The FGFR3 c.1620C>G; p.Asn540Lys variant (rs28933068) is a recurrent alteration in patients with hypochondroplasia (Camera 2001, Kannu 2007, Korkmaz 2012, Linnankivi 2012, Xue 2014). Another variant at this position, c.1620C>A, also results in the same amino acid alteration (p.Asn540Lys), and is the most common pathogenic variant in hypochondroplasia patients (Xue 2014). Functional characterization of the variant protein indicates increased phosphorylation of ERK1/2, resulting in an over-activation of the MAPK signaling pathway (Krejci 2008). The c.1620C>G; p.Asn540Lys variant is reported in ClinVar (Variation ID: 16338). It is absent from the Genome Aggregation Database, indicating it is not a common polymorphism. Based on available information, the p.Asn540Lys variant is considered to be pathogenic. References: Camera G et al. Occurrence of thanatophoric dysplasia type I (R248C) and hypochondroplasia (N540K) mutations in two patients with achondroplasia phenotype. Am J Med Genet. 2001; 104(4):277-81. PMID: 11754059. Kannu P et al. FGFR3 mutations and medial temporal lobe dysgenesis. J Child Neurol. 2007; 22(2):211-3. PMID: 17621485. Korkmaz HA et al. Hypochondroplasia in a child with 1620C>G (Asn540Lys) mutation in FGFR3. J Clin Res Pediatr Endocrinol. 2012; 4(4):220-2. PMID: 23149434. Krejci P et al. Analysis of STAT1 activation by six FGFR3 mutants associated with skeletal dysplasia undermines dominant role of STAT1 in FGFR3 signaling in cartilage. PLoS One. 2008; 3(12):e3961. PMID: 19088846. Linnankivi T et al. Neuroimaging and neurological findings in patients with hypochondroplasia and FGFR3 N540K mutation. Am J Med Genet A. 2012; 158A(12):3119-25. PMID: 23165795. Xue Y et al. FGFR3 mutation frequency in 324 cases from the International Skeletal Dysplasia Registry. Mol Genet Genomic Med. 2014; 2(6):497-503. PMID: 25614871.
Ambry Genetics RCV000622950 SCV000741814 pathogenic Inborn genetic diseases 2016-09-19 criteria provided, single submitter clinical testing
Labcorp Genetics (formerly Invitae), Labcorp RCV000255372 SCV000640362 pathogenic not provided 2025-01-18 criteria provided, single submitter clinical testing This sequence change replaces asparagine, which is neutral and polar, with lysine, which is basic and polar, at codon 540 of the FGFR3 protein (p.Asn540Lys). This variant is not present in population databases (gnomAD no frequency). This missense change has been observed in individuals with hypochondroplasia or achondroplasia (PMID: 7670477, 8589686, 9452043, 10360392, 11055896, 11754059, 23149434, 23165795, 25614871). ClinVar contains an entry for this variant (Variation ID: 16338). Invitae Evidence Modeling incorporating data from in vitro experimental studies (internal data) indicates that this missense variant is expected to disrupt FGFR3 function with a positive predictive value of 95%. Experimental studies have shown that this missense change affects FGFR3 function (PMID: 19088846). For these reasons, this variant has been classified as Pathogenic.
Centre for Mendelian Genomics, University Medical Centre Ljubljana RCV000415460 SCV000492852 pathogenic Short stature 2015-06-23 criteria provided, single submitter clinical testing
Eurofins Ntd Llc (ga) RCV000255372 SCV000341534 pathogenic not provided 2018-04-05 criteria provided, single submitter clinical testing
GeneDx RCV000255372 SCV000321637 pathogenic not provided 2022-08-17 criteria provided, single submitter clinical testing Observed in multiple individuals with hypochondroplasia in the published literature (Prinos et al., 1995; Foldynova-Trantirkova et al., 2012); Published functional studies demonstrate this variant results in significantly reduced in vitro expression (Raffioni et al., 1998); Not observed in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 8640234, 29681095, 10360392, 22045636, 23149434, 9857065, 23165795, 11754059, 19088846, 8589686, 28777845, 29478821, 29150894, 17621485, 29620724, 30355600, 26380986, 34567078, 33942288, 32712949, 33389251)
Programa de Pós-Graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília RCV000017741 SCV000223910 pathogenic Hypochondroplasia 2015-04-01 criteria provided, single submitter research
PreventionGenetics, part of Exact Sciences RCV004737156 SCV005344551 pathogenic FGFR3-related disorder 2024-08-26 no assertion criteria provided clinical testing The FGFR3 c.1620C>G variant is predicted to result in the amino acid substitution p.Asn540Lys. This variant has been reported to be the most common cause of hypochondroplasia (Bellus et al. 1995. PubMed ID: 7670477; Prinos et al. 1995. PubMed ID: 8589686). Additionally, functional studies support its pathogenicity (Raffioni et al. 1998. PubMed ID: 9857065). This variant has not been reported in a large population database, indicating it is rare. This variant is interpreted as pathogenic.
Department of Pediatrics, Taizhou Central Hospital, Taizhou University Hospital RCV000017741 SCV005045297 pathogenic Hypochondroplasia 2024-02-01 no assertion criteria provided clinical testing
Clinical Laboratory Sciences Program (CLSP), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS) RCV000017741 SCV003927827 pathogenic Hypochondroplasia 2023-04-01 no assertion criteria provided clinical testing
Laboratory of Diagnostic Genome Analysis, Leiden University Medical Center (LUMC) RCV000255372 SCV002036285 pathogenic not provided no assertion criteria provided clinical testing
Clinical Genetics DNA and cytogenetics Diagnostics Lab, Erasmus MC, Erasmus Medical Center RCV000255372 SCV001964698 pathogenic not provided no assertion criteria provided clinical testing
Joint Genome Diagnostic Labs from Nijmegen and Maastricht, Radboudumc and MUMC+ RCV000255372 SCV001955913 pathogenic not provided no assertion criteria provided clinical testing
Bioscientia Institut fuer Medizinische Diagnostik GmbH, Sonic Healthcare RCV000017741 SCV000746072 pathogenic Hypochondroplasia 2017-09-18 no assertion criteria provided clinical testing
Clinical Molecular Genetics Laboratory, Johns Hopkins All Children's Hospital RCV000017741 SCV000692270 pathogenic Hypochondroplasia 2016-04-06 no assertion criteria provided clinical testing
GeneReviews RCV000017741 SCV000086722 not provided Hypochondroplasia no assertion provided literature only Most common pathogenic variant in hypochondroplasia
OMIM RCV000017741 SCV000038019 pathogenic Hypochondroplasia 1999-04-01 no assertion criteria provided literature only

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