ClinVar Genomic variation as it relates to human health
NM_021870.3(FGG):c.323C>G (p.Ala108Gly)
The aggregate germline classification for this variant, typically for a monogenic or Mendelian disorder as in the ACMG/AMP guidelines, or for response to a drug. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the aggregate classification.
Stars represent the aggregate review status, or the level of review supporting the aggregate germline classification for this VCV record. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the review status. The number of submissions which contribute to this review status is shown in parentheses.
Pathogenic(2); Likely pathogenic(8); Uncertain significance(2); Likely benign(1)
No data submitted for somatic clinical impact
No data submitted for oncogenicity
Variant Details
- Identifiers
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NM_021870.3(FGG):c.323C>G (p.Ala108Gly)
Variation ID: 547969 Accession: VCV000547969.50
- Type and length
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single nucleotide variant, 1 bp
- Location
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Cytogenetic: 4q32.1 4: 154611883 (GRCh38) [ NCBI UCSC ] 4: 155533035 (GRCh37) [ NCBI UCSC ]
- Timeline in ClinVar
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First in ClinVar Help The date this variant first appeared in ClinVar with each type of classification.
Last submission Help The date of the most recent submission for each type of classification for this variant.
Last evaluated Help The most recent date that a submitter evaluated this variant for each type of classification.
Germline Jul 9, 2018 Apr 15, 2024 Nov 17, 2023 - HGVS
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Nucleotide Protein Molecular
consequenceNM_021870.3:c.323C>G MANE Select Help Transcripts from the Matched Annotation from the NCBI and EMBL-EBI (MANE) collaboration.
NP_068656.2:p.Ala108Gly missense NM_000509.6:c.323C>G NP_000500.2:p.Ala108Gly missense NC_000004.12:g.154611883G>C NC_000004.11:g.155533035G>C NG_008834.1:g.5868C>G LRG_585:g.5868C>G LRG_585t1:c.323C>G LRG_585p1:p.Ala108Gly LRG_585t2:c.323C>G LRG_585p2:p.Ala108Gly - Protein change
- A108G
- Other names
- p.Ala108Gly
- Canonical SPDI
- NC_000004.12:154611882:G:C
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Functional
consequence HelpThe effect of the variant on RNA or protein function, based on experimental evidence from submitters.
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Global minor allele
frequency (GMAF) HelpThe global minor allele frequency calculated by the 1000 Genomes Project. The minor allele at this location is indicated in parentheses and may be different from the allele represented by this VCV record.
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0.00160 (C)
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Allele frequency
Help
The frequency of the allele represented by this VCV record.
1000 Genomes Project 0.00160
1000 Genomes Project 30x 0.00187
Trans-Omics for Precision Medicine (TOPMed) 0.00187
The Genome Aggregation Database (gnomAD), exomes 0.00195
Exome Aggregation Consortium (ExAC) 0.00221
The Genome Aggregation Database (gnomAD) 0.00222
NHLBI Exome Sequencing Project (ESP) Exome Variant Server 0.00262
- Links
Genes
Gene | OMIM | ClinGen Gene Dosage Sensitivity Curation |
Variation Viewer
Help
Links to Variation Viewer, a genome browser to view variation data from NCBI databases. |
Related variants | ||
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HI score
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The haploinsufficiency score for the gene, curated by ClinGen’s Dosage Sensitivity Curation task team. |
TS score
Help
The triplosensitivity score for the gene, curated by ClinGen’s Dosage Sensitivity Curation task team. |
Within gene
Help
The number of variants in ClinVar that are contained within this gene, with a link to view the list of variants. |
All
Help
The number of variants in ClinVar for this gene, including smaller variants within the gene and larger CNVs that overlap or fully contain the gene. |
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FGG | - | - |
GRCh38 GRCh37 |
135 | 168 |
Conditions - Germline
Condition
Help
The condition for this variant-condition (RCV) record in ClinVar. |
Classification
Help
The aggregate germline classification for this variant-condition (RCV) record in ClinVar. The number of submissions that contribute to this aggregate classification is shown in parentheses. (# of submissions) |
Review status
Help
The aggregate review status for this variant-condition (RCV) record in ClinVar. This value is calculated by NCBI based on data from submitters. Read our rules for calculating the review status. |
Last evaluated
Help
The most recent date that a submitter evaluated this variant for the condition. |
Variation/condition record
Help
The RCV accession number, with most recent version number, for the variant-condition record, with a link to the RCV web page. |
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Pathogenic/Likely pathogenic (4) |
criteria provided, multiple submitters, no conflicts
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May 4, 2022 | RCV000660564.14 | |
Conflicting interpretations of pathogenicity (3) |
criteria provided, conflicting classifications
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Oct 31, 2023 | RCV000899510.25 | |
Likely pathogenic (1) |
criteria provided, single submitter
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Feb 1, 2019 | RCV000851595.2 | |
Likely pathogenic (1) |
no assertion criteria provided
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May 1, 2020 | RCV001270551.2 | |
Uncertain significance (2) |
criteria provided, multiple submitters, no conflicts
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Nov 17, 2023 | RCV001449762.7 | |
Likely pathogenic (1) |
criteria provided, single submitter
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Mar 10, 2021 | RCV001559328.5 | |
Likely pathogenic (1) |
criteria provided, single submitter
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- | RCV002280883.2 | |
Likely pathogenic (3) |
criteria provided, multiple submitters, no conflicts
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- | RCV003232069.4 |
Submissions - Germline
Classification
Help
The submitted germline classification for each SCV record. (Last evaluated) |
Review status
Help
Stars represent the review status, or the level of review supporting the submitted (SCV) record. This value is calculated by NCBI based on data from the submitter. Read our rules for calculating the review status. This column also includes a link to the submitter’s assertion criteria if provided, and the collection method. (Assertion criteria) |
Condition
Help
The condition for the classification, provided by the submitter for this submitted (SCV) record. This column also includes the affected status and allele origin of individuals observed with this variant. |
Submitter
Help
The submitting organization for this submitted (SCV) record. This column also includes the SCV accession and version number, the date this SCV first appeared in ClinVar, and the date that this SCV was last updated in ClinVar. |
More information
Help
This column includes more information supporting the classification, including citations, the comment on classification, and detailed evidence provided as observations of the variant by the submitter. |
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Likely pathogenic
(Feb 01, 2019)
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criteria provided, single submitter
Method: research
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Abnormal bleeding
Affected status: yes
Allele origin:
unknown
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NIHR Bioresource Rare Diseases, University of Cambridge
Study: ThromboGenomics
Accession: SCV000899329.1 First in ClinVar: Sep 29, 2019 Last updated: Sep 29, 2019 |
Observation 1:
Sex: female
Ethnicity/Population group: European
Observation 2:
Sex: female
Ethnicity/Population group: European
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Uncertain significance
(Jun 04, 2020)
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criteria provided, single submitter
Method: clinical testing
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not specified
Affected status: unknown
Allele origin:
germline
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Laboratory for Molecular Medicine, Mass General Brigham Personalized Medicine
Accession: SCV001653037.1
First in ClinVar: May 29, 2021 Last updated: May 29, 2021 |
Comment:
The p.Ala108Gly variant in FGG has been reported in at least 5 individuals with hypofibrinogenemia, 2 individuals with dysfibrinogenemia, 1 individual with thrombocytopenia, and 1 … (more)
The p.Ala108Gly variant in FGG has been reported in at least 5 individuals with hypofibrinogenemia, 2 individuals with dysfibrinogenemia, 1 individual with thrombocytopenia, and 1 individual with a clotting disorder. It segregated with disease in 3 affected individuals from 1 family, but that family also harbored a variant in FGB that may partially or fully explain the phenotype (Brennan 2000 PMID: 10688828, Bell 2011 PMID: 21228398, Smith 2018 PMID: 30349899, Downes 2019 PMID: 31064749, Guglielmone 2019 PMID: 30632992, Ferrari 2019, Moret 2019 PMID: 31295712, Saes 2019 PMID: 30431218). It has also been identified in 0.36% (462/128216) of European chromosomes by gnomAD (http://gnomad.broadinstitute.org). Computational prediction tools and conservation analyses suggest that this variant may not impact the protein, though this information is not predictive enough to rule out pathogenicity. In summary, while the clinical significance of this variant is uncertain. ACMG/AMP Criteria applied: PS4_Moderate, PP1, BS1, BP4. (less)
Number of individuals with the variant: 1
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Likely pathogenic
(Mar 10, 2021)
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criteria provided, single submitter
Method: clinical testing
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Congenital fibrinogen deficiency
Affected status: unknown
Allele origin:
unknown
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Illumina Laboratory Services, Illumina
Accession: SCV001304620.2
First in ClinVar: May 31, 2020 Last updated: Aug 14, 2021 |
Comment:
The FGG c.323C>G (p.Ala108Gly), also known as p.Ala82Gly based on its location in the mature peptide, and "fibrinogen Dunedin" is a recurrent missense variant. Across … (more)
The FGG c.323C>G (p.Ala108Gly), also known as p.Ala82Gly based on its location in the mature peptide, and "fibrinogen Dunedin" is a recurrent missense variant. Across a selection of the available literature, the p.Ala108Gly has been reported in a heterozygous state in at least 10 individuals, and in a compound heterozygous state in at least one individual, all of whom are reported to have mild-moderate bleeding disorders with or without thromboembolism. This includes four individuals diagnosed with hypofibrinogenemia and one individual diagnosed with hypodysfibrinogenemia (Brennan et al. 2000; Ivaskevicius et al. 2005; Casini et a. 2017; Downes et al. 2019; Wypasek et al. 2019). The p.Ala108Gly variant is reported at a frequency of 0.003603 in the European (non-Finnish) population of the Genome Aggregation Database. This allele frequency is high but is consistent with available disease prevalence and penetrance estimates (Paraboschi et al. 2017). The p.Ala108Gly variant is located in the triple helix region that separates the E and D domains of the protein and it has been suggested that this variant may result in abnormal packing of the helices and defective polymerization, however this has not been confirmed experimentally (Brennan et al. 2000; Casini et a. 2017). Based on the collective evidence and application of the ACMG criteria, the p.Ala108Gly variant is classified as likely pathogenic for congenital fibrinogen deficiency. (less)
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Pathogenic
(May 04, 2022)
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criteria provided, single submitter
Method: clinical testing
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Congenital afibrinogenemia
Affected status: unknown
Allele origin:
germline
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Mendelics
Accession: SCV002516369.1
First in ClinVar: May 28, 2022 Last updated: May 28, 2022 |
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Likely pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Thrombus
Affected status: yes
Allele origin:
germline
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ISTH-SSC Genomics in Thrombosis and Hemostasis, KU Leuven, Center for Molecular and Vascular Biology
Accession: SCV002569321.1
First in ClinVar: Sep 10, 2022 Last updated: Sep 10, 2022 |
Clinical Features:
Deep vein thrombosis (present)
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Likely pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Congenital afibrinogenemia
Affected status: yes
Allele origin:
germline
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ISTH-SSC Genomics in Thrombosis and Hemostasis, KU Leuven, Center for Molecular and Vascular Biology
Accession: SCV002569919.1
First in ClinVar: Sep 10, 2022 Last updated: Sep 10, 2022 |
Observation 1:
Clinical Features:
Low fibrinogen (present)
Observation 2:
Clinical Features:
Variable fibrinogen levels (present)
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Likely pathogenic
(Dec 06, 2021)
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criteria provided, single submitter
Method: clinical testing
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Not provided
Affected status: unknown
Allele origin:
germline
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Mayo Clinic Laboratories, Mayo Clinic
Accession: SCV003929399.1
First in ClinVar: Jun 03, 2023 Last updated: Jun 03, 2023 |
Comment:
PP1, PM2, PM3, PS4_Moderate
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Likely pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Familial dysfibrinogenemia
(Autosomal dominant inheritance)
Affected status: yes
Allele origin:
germline
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Lifecell International Pvt. Ltd
Accession: SCV003929440.1
First in ClinVar: Jun 10, 2023 Last updated: Jun 10, 2023 |
Comment:
A Heterozygous Missense variant c.323C>G in Exon 4 of the FGG gene that results in the amino acid substitution p.Ala108Gly was identified. The observed variant … (more)
A Heterozygous Missense variant c.323C>G in Exon 4 of the FGG gene that results in the amino acid substitution p.Ala108Gly was identified. The observed variant has a maximum allele frequency of 0.00195/0.00229% in gnomAD exomes and genomes, respectively. The severity of the impact of this variant on the protein is medium, based on the effect of the protein and REVEL score . Rare Exome Variant Ensemble Learner (REVEL) is an ensembl method for predicting the pathogenicity of missense variants based on a combination of scores from 13 individual tools: MutPred, FATHMM v2.3, VEST 3.0, PolyPhen-2, SIFT, PROVEAN, MutationAssessor, MutationTaster, LRT, GERP++, SiPhy, phyloP, and phastCons. The REVEL score for an individual missense variant can range from 0 to 1, with higher scores reflecting greater likelihood that the variant is diseasecausing. ClinVar has also classified this variant as ConflictingInterpretations (Variant ID: 547969). This variant is reported in hemizygous for hypofibrinogenemia (Couzen et al., 2022). For these reasons, this variant has been classified as Likely Pathogenic. (less)
Ethnicity/Population group: Asian
Geographic origin: India
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Likely pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Familial dysfibrinogenemia
Affected status: yes
Allele origin:
germline
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ISTH-SSC Genomics in Thrombosis and Hemostasis, KU Leuven, Center for Molecular and Vascular Biology
Accession: SCV004013104.1
First in ClinVar: Jul 22, 2023 Last updated: Jul 22, 2023 |
Clinical Features:
Ischemic colitis (present)
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Likely pathogenic
(-)
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criteria provided, single submitter
Method: clinical testing
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Congenital afibrinogenemia
(Autosomal dominant inheritance)
Affected status: yes
Allele origin:
germline
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Neuberg Centre For Genomic Medicine, NCGM
Accession: SCV004048524.1
First in ClinVar: Oct 28, 2023 Last updated: Oct 28, 2023 |
Comment:
The missense variant c.323C>G (p.Ala108Gly) in FGG gene has been reported in heterozygous state in at least 10 individuals, and in a compound heterozygous state … (more)
The missense variant c.323C>G (p.Ala108Gly) in FGG gene has been reported in heterozygous state in at least 10 individuals, and in a compound heterozygous state in at least one individual, all of whom are reported to have mild-moderate bleeding disorders with or without thromboembolism. This includes four individuals diagnosed with hypofibrinogenemia and one individual diagnosed with hypodysfibrinogenemia (Wypasek et al.,2019) . This variant has been reported to the ClinVar database as Likely Pathogenic. The p.Ala108Gly variant is novel (not in any individuals) in 1000 Genomes and allele frequency of 0.1986% is reported in gnomAD. The amino acid Ala at position 108 is changed to a Gly changing protein sequence and it might alter its composition and physico-chemical properties. In silico tools predict the variant to be tolerated. The residue is conserved across species. The amino acid change p.Ala108Gly in FGG is predicted as conserved by GERP++ and PhyloP across 100 vertebrates. For these reasons, this variant has been classified as Likely Pathogenic. (less)
Clinical Features:
Cerebral venous thrombosis (present)
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Uncertain significance
(Nov 17, 2023)
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criteria provided, single submitter
Method: clinical testing
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not specified
Affected status: unknown
Allele origin:
germline
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Women's Health and Genetics/Laboratory Corporation of America, LabCorp
Accession: SCV003845156.2
First in ClinVar: Mar 26, 2023 Last updated: Jan 06, 2024 |
Comment:
Variant summary: FGG c.323C>G (p.Ala108Gly, aka. Ala82Gly) results in a non-conservative amino acid change located in the coiled-coil domain (IPR012290) of the encoded protein sequence. … (more)
Variant summary: FGG c.323C>G (p.Ala108Gly, aka. Ala82Gly) results in a non-conservative amino acid change located in the coiled-coil domain (IPR012290) of the encoded protein sequence. Four of five in-silico tools predict a benign effect of the variant on protein function. The variant allele was found at a frequency of 0.003 in 1604646 control chromosomes in the gnomAD database, including 12 homozygotes. The observed relatively high frequency together with the homozygous occurrences might indicate a benign nature for the variant. On the other hand, the variant c.323C>G has been reported in the literature in individuals affected with various coagulation disorders, including Hypofibrinogenemia, Dysfibrinogenemia, Thrombocytopenia, Familial multiple coagulation factor deficiencies (FMCFD) with or without a second variant, and also with co-occurring variants in other coagulation genes (e.g. PMIDs: 10688828, 31064749, 33477601, 30431218, 30349899). These occurrences are inconsistent with an established inheritance pattern (i.e., dominant or recessive) and indicate that the variant may be associated with disease. The variant was found to be present at s relatively high frequency in European populations (0.3%-0.4%) and was associated with only a small estimated effect size on plasma fibrinogen (21.1% lower fibrinogen level per copy of the minor allele) in a GWAS (PMID: 26105150), which raises questions about whether it is a causative autosomal dominant variant with variable penetrance and expressivity, an autosomal recessive variant, or a risk-enhancing variant in a possible oligogenic model of inheritance influencing phenotypic heterogeneity (PMID 37583269). To our knowledge, no experimental evidence demonstrating an impact on protein function has been reported. Ten other submitters have cited clinical-significance assessments for this variant to ClinVar after 2014. Multiple submitters reported the variant with conflicting assessments (pathogenic / likely pathogenic [n=8], VUS [n=1], likely benign [n=1]). Based on the evidence outlined above, the variant seems to represent a relatively frequent hypomorphic allele that is subject to interallelic interactions which might result in an incomplete penetrance; therefore, the variant was classified as VUS-possibly pathogenic. (less)
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Likely benign
(Oct 31, 2023)
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criteria provided, single submitter
Method: clinical testing
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not provided
Affected status: unknown
Allele origin:
germline
|
Invitae
Accession: SCV001043785.4
First in ClinVar: Dec 17, 2019 Last updated: Feb 14, 2024 |
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Pathogenic
(May 01, 2022)
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criteria provided, single submitter
Method: clinical testing
|
not provided
Affected status: yes
Allele origin:
germline
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CeGaT Center for Human Genetics Tuebingen
Accession: SCV001249260.20
First in ClinVar: May 12, 2020 Last updated: Apr 15, 2024 |
Comment:
FGG: PP4:Strong, PS4, PP2, PS3:Supporting
Number of individuals with the variant: 5
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Likely pathogenic
(May 01, 2020)
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no assertion criteria provided
Method: research
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Thrombocytopenia
Abnormal bleeding
Affected status: yes
Allele origin:
germline
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Birmingham Platelet Group; University of Birmingham
Accession: SCV001450850.1
First in ClinVar: Dec 19, 2020 Last updated: Dec 19, 2020 |
|
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Pathogenic
(Oct 30, 2023)
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no assertion criteria provided
Method: clinical testing
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Familial dysfibrinogenemia
Affected status: yes
Allele origin:
germline
|
Zotz-Klimas Genetics Lab, MVZ Zotz Klimas
Accession: SCV004099364.1
First in ClinVar: Nov 04, 2023 Last updated: Nov 04, 2023 |
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Pathogenic
(Jun 01, 2017)
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Flagged submission
flagged submission
Method: clinical testing
Reason: This record appears to be redundant with a more recent record from the same submitter.
Notes: SCV000782675 appears to be redundant with SCV003929399.
(less)
Notes: SCV000782675 appears to
(...more)
Source: NCBI
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Congenital afibrinogenemia
Affected status: unknown
Allele origin:
paternal
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Mayo Clinic Laboratories, Mayo Clinic
Accession: SCV000782675.1
First in ClinVar: Jul 09, 2018 Last updated: Jul 09, 2018 |
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Flagged submissions do not contribute to the aggregate classification or review status for the variant. Learn more |
Germline Functional Evidence
There is no functional evidence in ClinVar for this variation. If you have generated functional data for this variation, please consider submitting that data to ClinVar. |
Citations for germline classification of this variant
HelpTitle | Author | Journal | Year | Link |
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Congenital fibrinogen disorders: Strengthening genotype-phenotype correlations through novel genetic diagnostic tools. | Ramanan R | British journal of haematology | 2023 | PMID: 37583269 |
Hemizygous FGG p.Ala108Gly in a hypofibrinogenemic patient with a heterozygous 14.8 Mb deletion encompassing the entire fibrinogen gene cluster. | Couzens A | Haemophilia : the official journal of the World Federation of Hemophilia | 2022 | PMID: 35809055 |
Familial Multiple Coagulation Factor Deficiencies (FMCFDs) in a Large Cohort of Patients-A Single-Center Experience in Genetic Diagnosis. | Preisler B | Journal of clinical medicine | 2021 | PMID: 33477601 |
A rare heterozygous variant in FGB (Fibrinogen Merivale) causing hypofibrinogenemia in a Swedish family. | Fager Ferrari M | Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis | 2020 | PMID: 32852326 |
Genetic and clinical characterization of congenital fibrinogen disorders in Polish patients: Identification of three novel fibrinogen gamma chain mutations. | Wypasek E | Thrombosis research | 2019 | PMID: 31479941 |
Next-Generation Sequencing of 17 Genes Associated with Venous Thromboembolism Reveals a Deficit of Non-Synonymous Variants in Procoagulant Genes. | Manderstedt E | Thrombosis and haemostasis | 2019 | PMID: 31352677 |
Clinical and molecular characterization by next generation sequencing of Spanish patients affected by congenital deficiencies of fibrinogen. | Moret A | Thrombosis research | 2019 | PMID: 31295712 |
Diagnostic high-throughput sequencing of 2396 patients with bleeding, thrombotic, and platelet disorders. | Downes K | Blood | 2019 | PMID: 31064749 |
Recurrent superficial venous thrombophlebitis because of mutations in the protein C and fibrinogen genes in a young Argentinian female. | Guglielmone HA | Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis | 2019 | PMID: 30632992 |
Whole exome sequencing in the diagnostic workup of patients with a bleeding diathesis. | Saes JL | Haemophilia : the official journal of the World Federation of Hemophilia | 2019 | PMID: 30431218 |
High-frequency actionable pathogenic exome variants in an average-risk cohort. | Rego S | Cold Spring Harbor molecular case studies | 2018 | PMID: 30487145 |
Identification and characterization of novel mutations implicated in congenital fibrinogen disorders. | Smith N | Research and practice in thrombosis and haemostasis | 2018 | PMID: 30349899 |
Fibrinogen as a Pleiotropic Protein Causing Human Diseases: The Mutational Burden of Aα, Bβ, and γ Chains. | Paraboschi EM | International journal of molecular sciences | 2017 | PMID: 29240685 |
Genetics, diagnosis and clinical features of congenital hypodysfibrinogenemia: a systematic literature review and report of a novel mutation. | Casini A | Journal of thrombosis and haemostasis : JTH | 2017 | PMID: 28211264 |
Rare and low-frequency variants and their association with plasma levels of fibrinogen, FVII, FVIII, and vWF. | Huffman JE | Blood | 2015 | PMID: 26105150 |
Clinical and laboratory characteristics of children with venous thromboembolism and protein C-deficiency: an observational Israeli-German cohort study. | Limperger V | British journal of haematology | 2014 | PMID: 25039884 |
Carrier testing for severe childhood recessive diseases by next-generation sequencing. | Bell CJ | Science translational medicine | 2011 | PMID: 21228398 |
Severe bleeding and miscarriages in a hypofibrinogenemic woman heterozygous for the gamma Ala82Gly mutation. | Zdziarska J | Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis | 2009 | PMID: 19300242 |
Fibrinogen Leipzig II (gamma351Gly-->Ser and gamma82Ala-->Gly): hypodysfibrinogenaemia due to two independent amino acid substitutions within the same polypeptide chain. | Meyer M | Thrombosis and haemostasis | 2007 | PMID: 17938819 |
gammaAla82Gly represents a common fibrinogen gamma-chain variant in Caucasians. | Ivaskevicius V | Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis | 2005 | PMID: 15795540 |
Hypofibrinogenemia in an individual with 2 coding (gamma82 A-->G and Bbeta235 P-->L) and 2 noncoding mutations. | Brennan SO | Blood | 2000 | PMID: 10688828 |
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Text-mined citations for rs148685782 ...
HelpRecord last updated Apr 15, 2024
This date represents the last time this VCV record was updated. The update may be due to an update to one of the included submitted records (SCVs), or due to an update that ClinVar made to the variant such as adding HGVS expressions or a rs number. So this date may be different from the date of the “most recent submission” reported at the top of this page.