248 Matching Annotations
  1. Last 7 days
    1. GT 40

      Case29: GT40, Female, India, age of onset is 6 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGB3

      Variant: NM_000212.2:c.428T>G (p.Leu143Trp)

      LegacyVariant: N/A

      ClinVar: 13567

      CAiD: CA123252

      gnomAD: MAF in the Other population is 0.0001629 https://gnomad.broadinstitute.org/variant/17-45361875-T-G)

    2. GT 09

      Case18: GT09, Female, India, age of onset is 21 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Patients were recruited as they presented consecutively from 1996 to 1998 for evaluation of a mucocutaneous bleeding disorder

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: All patients examined had defective ADP, epinephrine, and collagen induced aggregation and normal ristocetin induced aggregation

      CasePreviousTesting: Mutations were detected by the method of single strand conformation polymorphism (SSCP) analysis, followed by nucleotide sequencing and confirmation by restriction fragment length polymorphism (RFLP) assays. The sequences of the primers employed and the reaction conditions for PCR amplification of the exons, adjacent intronic regions, and 50 and 30 untranslated regions of the aIIb and b3 gene

      Gene: ITGB3

      Variant: NM_000212.2:c.428T>G (p.Leu143Trp) and NM_000212.2:c.1261G>A (p.Val422Met)

      LegacyVariant: N/A

      ClinVar: 13567

      CAiD: CA123252 and CA400028437

      gnomAD: MAF in the Other population is 0.0001629 https://gnomad.broadinstitute.org/variant/17-45361875-T-G

    1. cases 1

      Case1: Female, 25 years old, Japanese

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A per Table 1

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Prolonged ivy bleeding times, bleeding diathesis since early childhood

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Surface expression of αIIbβ3 was analyzed by flow cytometry which was < 5% of normal

      PlateletAggregation: Aggregation in response to ADP, epinephrine and collagen was absent but normal in response to ristocetin

      CasePreviousTesting: Nucleotide sequences of the αIIb and β3 coding regions were determined by direct sequencing of RT-PCR products from platelet RNA.

      Gene: ITGA2B

      Variant: NM_000419.3:c.959T>C (p.Phe320Ser)

      LegacyVariant: (p.Phe289Ser)

      ClinVar: N/A

      CAiD: CA399804774

      gnomAD: N/A

    1. GTP1

      Case1: GTP1, gender, age, or ethnicity not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: Sequencing of both parental genomic DNA confirmed patient was homozygous for IVS4+1G>A mutation

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Flow cytometry showed <5% αIIbβ3 expression, which was confirmed by western blot analysis

      PlateletAggregation: N/A

      CasePreviousTesting: Sequencing of patient genomic DNA was done on ITGA2B (no mention of ITGB3)

      Gene: ITGA2B

      Variant: NM_000419.3:c.574+1G>A (IVS4+1G>A)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA399805691

      gnomAD: MAF in the European non-Finnish population 0.00001235 http://gnomad.broadinstitute.org/variant/17-42462918-C-T

    1. 17

      Case17: Patient MO (patient found in the GT database as well) gender and age are not specified here

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000978, HP:0000132 (Bruising, menorrhagia)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: N/A

      CasePreviousTesting: N/A

      Gene: ITGA2B

      Variant: NM_000419.3:c.1750C>T (p.Arg584Ter)

      LegacyVariant: N/A

      ClinVar: 2892

      CAiD: CA115834

      gnomAD: MAF in the East Asian population is 0.0002176 https://gnomad.broadinstitute.org/variant/17-42457372-G-A

      PreviouslyPublished: Reference numbers 29 and 30 in this article

    2. LeM

      Case10: Patient LeM (found in the GT database) gender and age are not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000979, HP:0000967 (Purpura/petechiae)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: <5% of normal expression

      PlateletAggregation: N/A

      CasePreviousTesting: N/A

      Gene: ITGA2B

      Variant: NM_000419.3:c.1366_1371del

      LegacyVariant: N/A

      ClinVar: 2898

      CAiD: CA8603160

      gnomAD: MAF in the European (non-Finnish) population is 0.000008791 https://gnomad.broadinstitute.org/variant/17-42458268-TGTCTAC-T

      PreviouslyPublished: Reference number 21 in this article

    3. CG

      Case20: Patient CG (Found in GT database) also gender and age are not specified for this patient

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: Gingival bleeding and menorrhagia HP:0000225, HP:0000132

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: About 5% of normal GPIIIa and GPIIb surface expression

      PlateletAggregation: N/A

      CasePreviousTesting: N/A

      Gene: ITGA2B

      Variant: NM_000419.3:c.1787T>C and M_000419.3:c.3060+2T>C

      LegacyVariant: N/A

      ClinVar: 2900

      CAiD: CA115846 and CA290944108

      gnomAD: MAF in the European (non-Finnish) population is 0.0001325 https://gnomad.broadinstitute.org/variant/17-42457148-A-G and MAF in the European (non-Finnish) population is 0.00003876 https://gnomad.broadinstitute.org/variant/17-42451720-A-G

      PreviouslyPublished: References 34 and 35 in this article

    4. 4LW

      Case4: Patient LW (found in GT database)

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000978, HP:0000421, HP:0006298

      (Bruising, Epistaxis, Prolonged bleeding after tooth extraction)

      CaseHPOFreeText: Blood transfusions were needed

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: 12% of normal GPIIIa and GPIIb surface expression

      PlateletAggregation: N/A

      CasePreviousTesting: N/A

      Gene: ITGA2B

      Variant: NM_000419.3:c.641T>C (p.Lue214Pro)

      LegacyVariant: (p.Leu183Pro)

      ClinVar: 2901

      CAiD: CA115848

      gnomAD: N/A

      PreviouslyPublished: References 14 and 15

  2. www.researchgate.net www.researchgate.net
    1. Patient 4

      Case4: Patient 4, Female, 12 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: Affected sister is Patient 3

      ParentalGenotype: N/A (Not consanguineous Caucasians, showed no increased bleeding tendency)

      CasePresentingHPOs: HP:0000967

      (Petechiae)

      CaseHPOFreeText: Hematomas, prolonged in vitro bleeding time

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Flow cytometry analysis revealed that there was no surface expression of GPIIb/IIIa for Patient 4 and there was approx. 1520 of GPIIb/IIIa expression for Patient 4.

      PlateletAggregation: All patients' platelets showed severely reduced platelet aggregation after stimulation with collagen and ADP in contrast to the normal range (See Table 1). Stimulation with epinephrine and arachidonic acid also demonstrated decreased platelet aggregation. In contrast, ristocetin-induced platelet aggregation was within a normal range.

      CasePreviousTesting: Sequenced ITGA2B and ITGB3 genes from one patient of each family (Patient 2 and 3) and Patient 1 and 4 were screened for the identified mutation in the corresponding family.

      Gene: ITGA2B

      Variant: NM_000419.3:c.1787T>C (p.Ile596Thr)

      LegacyVariant: N/A

      ClinVar: 2900

      CAiD: CA115846

      gnomAD: MAF in the European (non-Finnish) population is 0.0001325 http://gnomad.broadinstitute.org/variant/17-42457148-A-G

    1. A female patient

      Case1: Female, 20 years old, Chinese

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000978, HP:0000421,

      (Easy bruising, epistaxis)

      CaseHPOFreeText: Prolonged bleeding time (more than 20 minutes, absent clot retraction

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Decreased of surface expression of αIIb and β3 in patient's platelets

      PlateletAggregation: Absent in vitro platelet aggregation in response to ADP, epinephrine, and collagen, but relatively normal ristocetin induced platelet aggregation

      CasePreviousTesting: DNA fragments containing exons and flanking intronic regions of ITGA2B and ITGB3 genes were produced by PCR using primers. Amplified fragments were subjected to analysis by direct DNA sequencing

      Gene: ITGA2B

      Variant: NM_000419.3:c.527C>A (p.Pro157His)

      LegacyVariant: (p.Pro126His)

      ClinVar: N/A

      CAiD: CA8603447

      gnomAD: MAF in the African population is 0.00006689 http://gnomad.broadinstitute.org/variant/17-42462966-G-T

    1. GT6

      Case6: (GT6), Male, 82 years old, French

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Mucocutaneous bleeding

      CaseNotHPOs: N/A

      ProteinExpression: 40-55% surface expression levels of αIIbβ3

      Platelet Aggregation: Absent platelet aggregation to all agonists (no mention for which agonists or response to ristocetin)

      CasePreviousTesting: All the information we are given is "mutation screening of the ITGA2B and ITGB3 genes" the method for sequencing etc. was not stated

      Gene: ITGB3

      Variant: NM_000212.2:c.665T>C (p.Leu222Pro) and NM_000212.2:c.1871G>A (p.Cys592Tyr)

      LegacyVariant: (p.Leu196Pro) and (p.Cys624Tyr) (The paper gives legacy and current nomenclature)

      ClinVar: N/A

      CAiD: CA291224887 and CA400032726

      gnomAD MAF in the European (non-Finnish) population is 0.00006482 https://gnomad.broadinstitute.org/variant/17-45363676-T-C

    2. M1

      Case9: (M1) Male, 9 years old, French Gypsy

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Mucocutaneous bleeding

      CaseNotHPOs: N/A

      ProteinExpression: Failed to express alphaIIbbeta3 on the surface of their platelets

      Platelet Aggregation: Absent platelet aggregation to all agonists (no mention for which agonists or response to ristocetin)

      CasePreviousTesting: All the information we are given is "mutation screening of the ITGA2B and ITGB3 genes" the method for sequencing etc. was not stated

      Gene: ITGA2B

      Variant: NM_000419.3:c.1544+1G>A

      LegacyVariant: N/A

      ClinVar: 2895

      CAiD: CA10575473

      gnomAD N/A

    1. FO

      Case7: Patient FO

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs:

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: N/A

      CasePreviousTesting: The amplification of DNA fragments using PCR and their electrophoretic migration through a denaturing gradient was used to scan the entire coding region, splice site junctions and promoter regions of the GPIIb and GPIIIa genes for all 20 patients in this study

      Gene: ITGA2B

      Variant: NM_000419.3:c.2153dup and NM_000419.3:c.1234G>A (p.Gly412Arg)

      LegacyVariant: (p.Gly381Arg)

      ClinVar: 381748

      CAiD: CA913189170 and CA8603182

      gnomAD MAF in the Latino population is 0.0001453 https://gnomad.broadinstitute.org/variant/17-42458406-C-T

    2. StopMB

      Case14: Patient MB

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: N/A

      CasePreviousTesting: The amplification of DNA fragments using PCR and their electrophoretic migration through a denaturing gradient was used to scan the entire coding region, splice site junctions and promoter regions of the GPIIb and GPIIIa genes for all 20 patients in this study

      Gene: ITGA2B

      Variant: NM_000419.3:c.1211-78A>G

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940720

      gnomAD: N/A

    1. 2

      Case2: Male, 3 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0030137 (Prolonged bleeding following circumcision)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.1652G>A (p.Arg551Gln)

      LegacyVariant: (p.Arg520Gln)

      ClinVar: N/A

      CAiD: CA8602986

      gnomAD: MAF in the South Asian population is 0.00006536 https://gnomad.broadinstitute.org/variant/17-42457470-C-T

    2. 10

      Case10: Female, 7 years old, Indian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000421, HP:0000790 (Epistaxis, hematuria)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      ProteinExpression: Diagnosis of GT was made on the basis of quantitive determination of receptor count by flow cytometric analysis of GPIIb-IIIa

      PlateletAggregation: Diagnosis of GT was made on the basis of impaired platelet aggregation (platelet aggregation was tested against ristocetin, ADP, collagen, epinephrine and arachidonic acid)

      CasePreviousTesting: Multiplex PCR by using GPIIb primers and CSGE analysis were performed

      Gene: ITGA2B

      Variant: NM_000419.3:c.2415del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940581

      gnomAD: N/A

    1. Supplementary Tables 1 and 2 combined information:

      Case3: GT3, Female, 12 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: Not available per supplementary table 1

      ParentalGenotype: Parents are not consanguineous, no other genotype information available

      CasePresentingHPOs: HP:0000978, HP:0000979, HP:0031364, HP:0000421, HP:0000225

      (Bruising, purpura, ecchymosis, epistaxis, gingival bleeding)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Showed <5% of αIIbβ3 expression measured by flow cytometry

      PlateletAggregation: Platelet aggregation showed no response to ADP and collagen but normal response to ristocetin

      CasePreviousTesting: All exons from ITGA2B and ITGB3 genes were amplified by PCR using intronic primers. DNA sequencing was determined by Sanger sequencing.

      Gene: ITGA2B

      Variant: NM_000419.3: c.1750C>T (p.Arg584Ter)

      LegacyVariant: N/A

      ClinVar: 2892

      CAiD: CA115834

      gnomAD: MAF in East Asian population: 0.0002176 https://gnomad.broadinstitute.org/variant/17-42457372-G-A

    2. Supplementary Tables 1 and 2 combined information:

      Case6: GT6, Male, 7 years old

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: Not available per supplementary table 1

      ParentalGenotype: Parents are not consanguineous, no other genotype information available

      CasePresentingHPOs: HP:0000978, HP:0000979, HP:0031364, HP:0000421

      (Bruising, purpura, ecchymosis, epistaxis)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Showed 10-20% of αIIbβ3 expression measured by flow cytometry

      PlateletAggregation: Platelet aggregation showed a small amount of response to ADP and collagen but normal response to ristocetin

      CasePreviousTesting: All exons from ITGA2B and ITGB3 genes were amplified by PCR using intronic primers. DNA sequencing was determined by Sanger sequencing.

      Gene: ITGA2B

      Variant: NM_000419.3:c.812C>G (p.Ala271Gly) and NM_000419.3:c.2172G>A (p.Met724Gln)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA399805123 (p.Ala271Gly) and CA399798895 (p.Met724Gln)

      gnomAD: N/A

    1. patient 3

      Case3: Patient 3, Female, 27 years old

      DiseaseAssertion: Glanzmann thrombasthenia type I (Diagnosed at 10 years old)

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Bleeding phenotypes are not specified per patient in this article, rather, it states: "Petechia, epistaxis, and prolonged bleeding after trauma were the most common symptoms among studied patients"

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: This patient has type 1 Glanzmann thrombasthenia; therefore, according to this article, this proband had between 0-5% of normal levels of surface GPIIb/IIIa expression.

      PlateletAggregation: Prolonged bleeding time, abnormal clot retraction, impaired platelet aggregation induced by most physiological agonists (ADP, epinephrine, and collagen) except ristocetin, mucosal bleeding, easy bruising, epistaxis, as well as normal prothrombin/activated partial thromboplastin time, and normal platelet count. (This is among inclusion criteria for this study)

      CasePreviousTesting: To identify the underlying molecular mechanism of GPIIb/IIIa complex abnormalities among probands in this study, all the 30 exons of ITGA2B and the 15 exons of ITGB3 were analyzed using PCR–CSGE and DNA sequencing.

      Gene: ITGA2B

      Variant: NM_000419.3:c.113del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940264

      gnomAD: N/A

    1. 21CabGT-21

      Case21: (ProbandGT-21) Male, age not specified, Caucasian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      ProteinExpression: Flow cytometry showed <5% GPIIIa and GPIIIb surface expression

      Platelet Aggregation: N/A

      CasePreviousTesting: Promoter and exon sequences of aIIb and b3 genes were amplified and directly sequence

      Gene: ITGB3

      Variant: NM_000212.2:c.191G>A (p.Cys64Tyr) the second mutation was not identified

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA291224490

      gnomAD N/A

    2. 12

      Case12: (Proband CabGT-12), Female, age not specified, Caucasian

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      ProteinExpression: Flow cytometry showed 19% GPIIb and 40% GPIIIa surface expression

      Platelet Aggregation: N/A

      CasePreviousTesting: Promoter and exon sequences of aIIb and b3 genes were amplified and directly sequence

      Gene: ITGA2B

      Variant: NM_000419.3:c.2113T>C (p.Cys705Arg) and NM_000419.3:c.3060+2T>C (p.Val982_Lys1020del)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA8602816 and CA290944108

      gnomAD MAF in the European (non-Finnish) population is 0.000008792 https://gnomad.broadinstitute.org/variant/17-42455140-A-G and MAF in the European non Finnish population for (p.Val982_Lys1020del) is 0.00003876 https://gnomad.broadinstitute.org/variant/17-42451720-A-G

    1. 13.

      Case13: Female, African, age not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: N/A

      PlateletAggregation: Minimal information, not specific enough

      CasePreviousTesting: Sanger sequencing identified disease-causing variants in 18 out of 20 patients (Probands 6 and 14 excluded) with istoantibodies to αIIbβ3. The mutations were evenly distributed between ITGB3 and ITGA2B.

      Gene: ITGA2B

      Variant: NM_000419.3:c.1357C>T (p.Arg453Ter)

      LegacyVariant: N/A

      ClinVar: 631773

      CAiD: CA399803529

      gnomAD: N/A

    1. GT-13b

      Case11: (GT-13) Male, carrier, age or ethnicity not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: Probands GT11 -GT14 are related to GT-13 see Table 1

      ParentalGenotype: Parents may be included in Table 1; however, not specified so no information

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Bleeding severity: Not available (See Supplementary Table 3)

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Flow cytometry performed and CD41 and CD61 were observed (See Supplementary Table 3)

      PlateletAggregation: Minimal information (See Supplementary Table 3)

      CasePreviousTesting: DNA was extracted from peripheral blood samples from patients and family members, and Sanger sequencing and PCR was performed. Samples were processed for targeted sequencing using the available SHGp heme panel of 393 genes.

      Gene: ITGB3

      Variant: NM_000212.2:c.727G>C (p.Asp243His)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA400023600

      gnomAD: N/A

    1. Case1: Female, 48 years old, ethnicity not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: HP:0000421, HP:0000225, HP:0000978, HP:0000132, HP:0006298, HP:0005261

      (Epistaxis, gingival bleeding, easy bruising, menorrhagia, bleeding after tooth extraction, hemarthrosis

      CaseHPOFreeText: Hemorrhage after surgery

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Platelet surface glycoprotein analysis by flow cytometry revealed a severe αIIbβ3 deficiency (Table 3 shows specific values)

      PlateletAggregation: There was a failure of ADP, collagen and adrenalin to induce platelet aggregation, but ristocetin-induced platelet aggregation (RIPA) was normal

      CasePreviousTesting: Integrin alphaIIb subunit gene (ITGA2B) sequencing showed that this proband was a compound heterozygote

      Gene: ITGA2B

      Variant: NM_000419.3:c.1214T>C (p.Ile405Thr) and NM_000419.3:c.1234G>A (p.Gly412Arg)

      LegacyVariant: (p.Ile374Thr) (p.Gly381Arg)

      ClinVar: 381748

      CAiD: CA290950815 (p.Ile403Thr) and CA8603182 (p.Gly412Arg)

      gnomAD: MAF in Latino population 0.0001453 http://gnomad.broadinstitute.org/variant/17-42458406-C-T

    1. P4

      Case4: P4, gender, age, ethnicity not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Article mentions all patients have a severe bleeding phenotype

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: αIIbβ3 expression levels were (0.6% in patient 4)

      PlateletAggregation: N/A

      CasePreviousTesting: Acknowledgements section mentions acknowledging the Genoscope team for sequencing both ITGA2B and ITGB3 genes of the GT patients in this article

      Gene: ITGA2B

      Variant: NM_000419.3:c.857T>A (p.Val268Asp)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA399805011

      gnomAD: N/A

    1. Supplementary Table S1:

      Case39: GT45, French, age and gender not specified

      DiseaseAssertion: Glanzmann thrombasthenia type I

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: All patients had a life-long history of mucocutaneous bleeding

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: All patients in this study met the clinical and platelet function requirements for GT-- this includes an absent or strongly reduced expression of alphaIIbBeta3 in platelets

      PlateletAggregation: All patients in this study met the clinical and platelet function requirements for GT-- this includes absent or severely reduced platelet aggregation with at least three physiological agonists

      CasePreviousTesting: Sanger sequencing was performed. Sanger sequencing ensured coverage of all exons and splice sties of the ITGA2B and ITGB3 genes and extended 300-500 bp into the introns as well as including the UTR. They sequenced 416 bp upstream of the ITGA2B promoter and 463 bp upstream of the ITGB3 promoter. In total they sequenced 51.2% of the ITGA2B gene and 19.4% of the larger ITGB3 gene

      Gene: ITGA2B

      Variant: NM_000419.3:c.551_626del (p.Arg184_Gln208del) and the other variant is noted as "LR deletion" and that is all the information we are given so I will note it as an Unknown Variant

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA915940373

      gnomAD: N/A

    1. GT14

      Case35: (GT14) Gender, age and ethnicity are not specified

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: Inclusion criteria were patients with a history of mucocutaneous bleeding (Figure 1 shows a bar diagram of all the clinical manifestations in the patient cohort in this article)

      CaseNotHPOs: N/A

      ProteinExpression: Platelet receptor alphaIIbbeta3 protein was analyzed by flow cytometry followed by western blotting

      Platelet Aggregation: Inclusion criteria for probands was absent or reduced platelet aggregation with agonists such as ADP, adrenaline, arachidonic acid, and collagen (no mention of ristocetin here-- this article does not tell us the specific aggregation for each proband in the paper)

      CasePreviousTesting: For mutation analysis of ITGA2B and ITGB3 genes, DNA extraction from whole blood, PCR, heteroduplex PCR followed by CSGE and DNA sequencing were performed. All 30 exons of ITGA2B and 15 exons of ITGB3, as well as their promoters, were analyzed by CSGE following heteroduplex PCR.

      Gene:

      Variant: NM_000419.3:c.188+8del

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA8603523

      gnomAD MAF in the South Asian population is 0.0002613 https://gnomad.broadinstitute.org/variant/17-42466645-AC-A

    1. A 56-year-old Japanese female

      Case1: Female, 56 years old, Japanese

      DiseaseAssertion: Glanzmann thrombasthenia (Diagnosed at 21 years of age)

      FamilyInfo:

      ParentalGenotype:

      CasePresentingHPOs: HP:0004406, HP:0000225

      (Recurrent epistaxis, gingival bleeding)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: Flow cytometry demonstrated significantly decreased expression of CD41 and CD61 to less than 20% of normal levels (See Figure 2)

      PlateletAggregation: An in vitro assay revealed no platlet aggregation in response to agonists except ristocetin.

      CasePreviousTesting: DNA sequencing analysis revealed compound heterozygous mutations confirming a diagnosis of Glanzmann thrombasthenia

      Gene: ITGA2B

      Variant: NM_000419.3:c.2602-3C>G and NM_000419.3:c.641T>C (p.Leu214Pro)

      LegacyVariant: N/A

      ClinVar: 2893 and 2901

      CAiD: CA10575472 and CA115848

      gnomAD: MAF in East Asian population 0.00006523 http://gnomad.broadinstitute.org/variant/17-42453087-G-C

    1. Case9: Patient MR, gender and age are not specified, all of these patients are Caucasian (either Italian or European)

      DiseaseAssertion: Glanzmann thrombasthenia

      FamilyInfo: N/A

      ParentalGenotype: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: All patients presented with a current or past history of bleeding and a bleeding time >15 min. Bleeding symptoms were evaluated by examining available hospital records. Mild bleeders were defined as those who bled only after trauma or surgery or had minor symptoms, such as epistaxis. Moderate/severe bleeders were defined as those with a history of spontaneous or life threatening hemorrhages, such as gastrointestinal bleeding, or who had repeated episodes requiring platelet transfusions

      CaseNotHPOs: N/A

      CaseNotHPOsFreeText: N/A

      ProteinExpression: See Table 1

      PlateletAggregation: See Table 1

      CasePreviousTesting: To identify point mutations responsible for GT, we have sequenced all coding regions of Ib and 3 genes and intron/exon boundaries.

      Gene: ITGA2B

      Variant: NM_000419.3:c.1214T>C (p.Ile374Thr)

      LegacyVariant: N/A

      ClinVar: N/A

      CAiD: CA290950815

      gnomAD: N/A

    1. KMP 1

      Case#: KMP 1, female, 39 yrs, East Slovakia

      DiseaseAssertion: HCM

      FamilyInfo: n/a

      CasePresentingHPOs: n/a

      CaseHPOFreeText: symptomatic; LVEF 60%; NYHA I.; ECG; echocardiography

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: no LVOTO; no ICD

      CasePreviousTesting: Additional Sanger sequencing of exons 12, 24, 25 of MYBPC3, exon 12 NEBL, exons 12, 20, 21 of SCN5A, exon 7 of TNNI3, and exon 9 of TNNT2 gene

      CaseGenotypingMethod: Sanger sequencing

      Variant: NM_000257.4(MYH7):c.2845G>A (p.Glu949Lys)

      ClinVar: 14093 https://www.ncbi.nlm.nih.gov/clinvar/variation/14093/

      CAID: n/a

      gnomAD: absent

    2. KMP 16

      Case#: KMP 16, female, 60 yrs, East Slovakia

      DiseaseAssertion: HCM

      FamilyInfo: n/a

      CasePresentingHPOs: n/a

      CaseHPOFreeText: symptomatic; LVOTO yes; LVEF 39-40%; NYHA I.; ICD yes; ECG; echocardiography;

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      CasePreviousTesting: Additional Sanger sequencing of exons 12, 24, 25 of MYBPC3, exon 12 NEBL, exons 12, 20, 21 of SCN5A, exon 7 of TNNI3, and exon 9 of TNNT2 gene

      CaseGenotypingMethod: Sanger sequencing;

      Variant: NM_000257.4(MYH7):c.2845G>A (p.Glu949Lys)

      ClinVar: 14093 https://www.ncbi.nlm.nih.gov/clinvar/variation/14093/

      CAID: n/a

      gnomAD: absent

    3. KMP 1

      Case#: KMP 1, female, 39 yrs, East Slovakia

      DiseaseAssertion: HCM

      FamilyInfo: n/a

      CasePresentingHPOs: n/a

      CaseHPOFreeText: symptomatic; LVEF 60%; NYHA I.; ECG; echocardiography

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: no LVOTO; no ICD

      CasePreviousTesting: Additional Sanger sequencing of exons 12, 24, 25 of MYBPC3, exon 12 NEBL, exons 12, 20, 21 of SCN5A, exon 7 of TNNI3, and exon 9 of TNNT2 gene

      CaseGenotypingMethod: Sanger sequencing

      Variant: NM_000257.4(MYH7):c.2845G>A (p.Glu949Lys)

      ClinVar: 14093 https://www.ncbi.nlm.nih.gov/clinvar/variation/14093/

      CAID: n/a

      gnomAD: absent

    4. KMP 16

      Case#: KMP 16, female, 60 yrs, East Slovakia

      DiseaseAssertion: HCM

      FamilyInfo: n/a

      CasePresentingHPOs: n/a

      CaseHPOFreeText: symptomatic; LVOTO yes; LVEF 39-40%; NYHA I.; ICD yes; ECG; echocardiography;

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      CasePreviousTesting: Additional Sanger sequencing of exons 12, 24, 25 of MYBPC3, exon 12 NEBL, exons 12, 20, 21 of SCN5A, exon 7 of TNNI3, and exon 9 of TNNT2 gene

      CaseGenotypingMethod: Sanger sequencing;

      Variant: NM_000257.4(MYH7):c.2845G>A (p.Glu949Lys)

      ClinVar: 14093 https://www.ncbi.nlm.nih.gov/clinvar/variation/14093/

      CAID: n/a

      gnomAD: absent

  3. Sep 2026
    1. -year-old girl without any detectable fundus abnormalities.

      Case#: Patient 8 yo, F, Turkiye, onset at 8yo (early onset)

      DiseaseAssertion:STGD1

      FamilyInfo: no consanguinity between parents, neither parents are affected or show symptoms

      CasePresentingHPOs: HP:0008035, HP:0011504

      CaseHPOFreeText: vision of 6/10

      CaseNotHPOs: HP:0000007, HP:0000608

      CaseNotHPOFreeText: normal movements and mobility, unremarkable slit-lamp, no fundoscopy changes, unremarkable OCT

      Genotyping Method: N/A

      PreviouslyPublished: N/A

      Variant: NM_000350.3a: c.3322C>T,p.(Arg1108Cys)rs61750120

      CAID: CA220683

      SupplementalData: N/A

    1. Case 1

      Case#:1, 44-year-old man

      DiseaseAssertion: Stargardt disease

      FamilyInfo: no known family history of an ocular disease

      CasePresentingHPOs: HP:0007663, HP:0007793, HP:0012045, HP:0000603

      CaseHPOFreeText: gradual, relatively recent decreased visual acuity in the right eye, some pigment mottling in both maculae and ‘fish-tail'-like retinal flecks, central relative scotoma

      CaseNotHPOs:

      CaseNotHPOFreeText:

      Genotyping Method: “Analysis of the entire coding region of the ABCA4 gene”

      PreviouslyPublished: NR

      Variant: NM_000350.3:c.191C>T

      ClinVar:2733951

      CAID:CA341285580

      SupplementalData:

    1. A 25-year-old White man presented with bilateral central vision loss due to foveal lesions consisting of vitelliform fluid.

      Case#: Patient 1, male, Caucasian, onset at 20yo, USA

      DiseaseAssertion: ABCA4

      FamilyInfo: No family history of retinal disease.

      CasePresentingHPOs: HP:0007677, HP:0030603, HP:0030500, HP:0030636, HP:0004328, HP:0012372

      CaseHPOFreeText: Bilateral central vision loss, progressive decline in visual acuity (20/60 both eyes), foveomacular vitelliform lesions with fluid accumulation, optical gap lesions progressing to cavitated appearance after fluid resorption, thinning and abnormal reflectivity of photoreceptor layers, near-infrared autofluorescence abnormalities in lesion-adjacent regions

      CaseNotHPOs: HP:0000510, HP:0000511

      CaseNotHPOFreeText: No generalized rod or cone dysfunction on full-field electroretinogram, EOG findings not consistent with bestrophinopathy (Arden ratio 1.62)

      Genotyping Method: Exome sequencing

      PreviouslyPublished: None

      Variant: NM_000350.3(ABCA4):c.5882G>A (p.Gly1961Glu), NM_000350.3(ABCA4):c.4139C>T (p.Pro1380Leu)

      ClinVar: ClinVarID:7888, ClinVarID:7904

      CAID: N/A

      SupplementalData: N/A

    1. two cases from two additional families (case 3, 11 years and case 4, 11 years).

      Case#:two cases from two additional families (case 3, 11 years and case 4, 11 years).

      DiseaseAssertion: Stargardt’s Disease

      FamilyInfo: NR

      ParentalTesting: NR

      CasePresentingHPOs: HP:0030500, HP:0011507

      CasePhenotypeFreeText: LogMAR visual acuity for the right and left eye of cases 1–4 was 0.3 and 0.2, 0.1 and 0.1, 0.5 and 0.4, and 0.3 and 0.4, respectively. Gross disruption of the outer retinal layers at the macula in all cases; in two (cases 2 and 4), the presumed external limiting membrane (ELM) peak was broadened with the inner segment ellipsoid band (ISe) missing. Subtle white-yellowish fine dots at the macula and numerous white-yellowish flecks extending anterior to the arcade are shown in the colour fundus photograph of case 1. Autofluorescence (AF) imaging of case 1 detected well-defined dots with high signal at the central macula surrounded by a ring of increased signal and numerous foci with high or low signal extending to the peripheral retina. Case 2 also had subtle white-yellowish fine dots at the central macula and numerous white-yellowish flecks extending anterior to the arcade, both associated with high signal on AF imaging. In addition, case 3 had white-yellowish fine dots at the macula and numerous white-yellowish flecks extending to the periphery, both of which had high or low signal on AF imaging. Case 4 showed subtle fine macular dots mainly in a para-foveal location, which are well-defined on AF imaging.

      CaseNotHPOs: HP:0007401, HP:0000505

      CaseNotPhenotypeFreeText: Most cases with STGD have central macular atrophy with numerous more peripheral flecks (Michaelides et al. 2003). Given their relatively good visual acuity, it is likely that the central macular dots observed in our cases may be an early sign of macular dysfunction before the development of macular atrophy. Similar fine macular dots or a ‘mottled macula’ have also been reported in other inherited retinal diseases

      CasePreviousTesting: The age of disease onset in cases 1–4, defined as either the age at which visual loss was first noted by the subject or in the asymptomatic subjects when abnormal retinal appearance was first detected, was 5, 7, 8, and 6 years old, respectively.

      GenotypingMethod: After informed consent was obtained, blood samples were taken from probands of 2/3 families for ABCA4 screening. A full medical history was obtained, and a full ophthalmologic examination was performed in all cases. Mutation screening of ABCA4 was performed in two probands of the three families, and two likely disease-causing variants were identified in each case; c.768G > T, p.V256V (a previously reported splicing-altering synonymous variant) and c.4363T > C, p.C1455R (a missense variant) in case 1, and c.1906C > T, p.Q636* (a non-sense variant) and c.5461-10 T > C (a disease-associated intronic variant with uncertain effect) in case 3. A blood sample was not available in one proband (case 4).

      Variant: NM_000350.3(ABCA4):c.1906C>T (p.Gln636Ter) and NM_000350.3:c.5461-10T>C

      LegacyVariant: c.1906C>T (p.Gln636Ter) and c.5461-10T>C

      ClinVar: 265012 and 92870

      CAID: CA10588302 and CA220687

      gnomeAD: 1:94528164 G / A and 1:94476951 A / G

      MultipleGeneVariants:No

      PreviouslyPublished: No

      AdditionalInfo: Most symptoms/diagnoses are consistent with Stargardt’s Disease 3, however the probands in the study were younger in age, so many of the symptoms hadn’t progressed much. Also, all of the cases had decent visual acuity, which contradicts a symptom of Stargardt’s Disease 3. Similar fine macular dots or a ‘mottled macula’ have also been reported in other inherited retinal diseases, for example, in those caused by mutations in RDH5 or RPE65, both of which encode proteins with known function in the visual cycle. The thickening of the ELM may be an OCT abnormality that precedes atrophy in the early stages of STGD

    2. two siblings were from one consanguineous family (case 1, 11 years and case 2, 9 years)

      Case#: two siblings (female) were from one consanguineous family (case 1, 11 years and case 2, 9 years)

      DiseaseAssertion: Stargardt’s Disease

      FamilyInfo: NR

      ParentalTesting: NR

      CasePresentingHPOs: HP:0030500, HP:0011507

      CasePhenotypeFreeText: LogMAR visual acuity for the right and left eye of cases 1–4 was 0.3 and 0.2, 0.1 and 0.1, 0.5 and 0.4, and 0.3 and 0.4, respectively. Gross disruption of the outer retinal layers at the macula in all cases; in two (cases 2 and 4), the presumed external limiting membrane (ELM) peak was broadened with the inner segment ellipsoid band (ISe) missing. Subtle white-yellowish fine dots at the macula and numerous white-yellowish flecks extending anterior to the arcade are shown in the colour fundus photograph of case 1. Autofluorescence (AF) imaging of case 1 detected well-defined dots with high signal at the central macula surrounded by a ring of increased signal and numerous foci with high or low signal extending to the peripheral retina. Case 2 also had subtle white-yellowish fine dots at the central macula and numerous white-yellowish flecks extending anterior to the arcade, both associated with high signal on AF imaging. In addition, case 3 had white-yellowish fine dots at the macula and numerous white-yellowish flecks extending to the periphery, both of which had high or low signal on AF imaging. Case 4 showed subtle fine macular dots mainly in a para-foveal location, which are well-defined on AF imaging.

      CaseNotHPOs: HP:0007401, HP:0000505

      CaseNotPhenotypeFreeText: Most cases with STGD have central macular atrophy with numerous more peripheral flecks (Michaelides et al. 2003). Given their relatively good visual acuity, it is likely that the central macular dots observed in our cases may be an early sign of macular dysfunction before the development of macular atrophy. Similar fine macular dots or a ‘mottled macula’ have also been reported in other inherited retinal diseases

      CasePreviousTesting: The age of disease onset in cases 1–4, defined as either the age at which visual loss was first noted by the subject or in the asymptomatic subjects when abnormal retinal appearance was first detected, was 5, 7, 8, and 6 years old, respectively.

      GenotypingMethod: After informed consent was obtained, blood samples were taken from probands of 2/3 families for ABCA4 screening. A full medical history was obtained, and a full ophthalmologic examination was performed in all cases. Mutation screening of ABCA4 was performed in two probands of the three families, and two likely disease-causing variants were identified in each case; c.768G > T, p.V256V (a previously reported splicing-altering synonymous variant) and c.4363T > C, p.C1455R (a missense variant) in case 1, and c.1906C > T, p.Q636* (a non-sense variant) and c.5461-10 T > C (a disease-associated intronic variant with uncertain effect) in case 3. A blood sample was not available in one proband (case 4).

      Variant: NM_000350.3(ABCA4):c.768G>T (p.Val256=) and NM_000350.3(ABCA4):c.4363T>C (p.Cys1455Arg)

      LegacyVariant: c.768G>T (p.Val256=) and c.4363T>C (p.Cys1455Arg)

      ClinVar: 99505 and 377404

      CAID: CA227458 and CA957621

      gnomeAD: 1:94564350 C / A and 1:94495177 A / G

      MultipleGeneVariants:No

      PreviouslyPublished: No

      AdditionalInfo: Some symptoms/diagnoses are consistent with Stargardt’s Disease 3, however the probands in the study were younger in age, so many of the symptoms hadn’t progressed much. Also, all of the cases had decent visual acuity, which contradicts a symptom of Stargardt’s Disease 3.

  4. Jul 2026
    1. Patient 1

      Case:Patient 1, Male, 4 y/o, German and Thai

      DiseaseAssertion:FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents. De novo. Patient 1 has maternally inherited duplications at 15q21.12(47292250-47309868)x3 and Xp22.31(6451676-8115124)x3 of unknown clinical significance.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0002197, HP:0005484, HP:0011344, HP:0001252, HP:0020045,HP:0000540, HP:0010808, HP:0002019, HP:0003781, HP:0012741, HP:0002421, HP:0000748, HP:0003763, HP:5200017, HP:0025112, HP:0000957

      CaseHPOFreeText: At 19 months, could not sit independently and no speech development. Stereotypic hand and head movements. High pain tolerance. X-ray at age 2 showed broad ribs. Improved head control by age 4.

      CaseNotHPO:HP:0410263, HP:0002376

      CaseNotHPOFreeText:Dysmorphic features. breathing abnormalities

      CasePreviousTesting:No previous testing

      PreviouslyPublished:Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing

      Gene:FOXG1

      Variant:46,XY,t(9;14)(q22.3;q11.2)dn

      HGVS:Not provided

      ClinVarID:426096

      gnomAD:Not provided

    2. Patient 3

      Case:Patient 3, Male, 1 y/o, Brazilian

      DiseaseAssertion: FOXG1 syndrome

      FamilyInfo: Non-consanguineous parents

      ParentalGenotype: No family testing mentioned.

      CasePresentingHPOs: HP:0000252, HP:0001252, HP:0000486

      CaseHPOFreeText: Developed microcephaly within 1 year. Developmental delay, unable to sit without assistance at 1 year old. Central Nervous System (CNS) MRI showed a volumetric reduction of the cerebral parenchyma, hypomyelination, and hypoplasia of corpus callosum mainly involving the anterior part and prominent lateral ventricles

      CaseNotHPO: HP:0030917

      CaseNotHPOFreeText: Normal length, weight, HC at birth. No retinal abnormalities.

      CasePreviousTesting: Not asserted.

      PreviouslyPublished: Not previously published.

      GenotypingMethod: Sanger sequencing, mate-pair sequencing

      Gene: FOXG1

      Variant: 46,XY,t(2;14)(q37;q11.2)dn

      HGVS: Not provided.

      ClinVarID:426094

      gnomAD:Not provided

    3. Patient 2

      Case:Patient 2, Female, 5 y/o, Brazilian

      DiseaseAssertion:quadriplegic cerebral palsy with axial hypotonia and distal spasticity

      FamilyInfo: Non-consanguineous parents. Parents had normal karyotypes. Older sister was clinically normal.

      ParentalGenotype: Normal karyotypes for both parents.

      CasePresentingHPOs: HP:0002098, HP:0010959, HP:0008755, HP:0002090, HP:0032661, HP:0001274, HP:0011344, HP:0001249, HP:0001344, HP:0000748, HP:0034435, HP:0000486, HP:0000483, HP:0200136

      CaseHPOFreeText: Dilated superficial blood vessels seen on brain MRI.

      CaseNotHPO:N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: Not asserted

      PreviouslyPublished: Not previously published

      GenotypingMethod:Mate-pair sequencing, Sanger sequencing, chromosome analysis

      Gene: FOXG1

      Variant: 46,XX,t(4;14)(q27;q13)dn

      HGVS: Not provided

      ClinVarID: 426095

      gnomAD: Not provided

    1. 52

      Case#:Patient 52, female, 3 years old

      DiseaseAssertion:Neonatal/Infantile Epileptic Encephalopathy (NIEE)

      FamilyInfo:DeNovo. The family is Chinese

      ParentalGenotype:The authors only conducted singleton and not trio-based exome sequencing so the parents' exomes were not sequenced.

      CasePresentingHPOs:HP:0011344, HP:0002069, HP:0007359, HP:0011097, HP:0100704, HP:0001332, HP:0002072, HP:0012171.

      CaseHPOFreeText:Patient 52 presents with severe global developmental delay and epilepsy.

      Patient 52 has generalized tonic/clonic/tonic-clonic seizures, focal seizures and spasms. Patient 52's seizure onset occurred at 3 months old.

      Patient 52 has cortical visual impairment (CVI), dystonia, chorea, and hand-washing sterotypies.

      Patient History

      @ 3 months - Patient 52 had generalized tonic/clonic/tonic-clonic seizures.

      Patient 52 was on 3 antiepileptic drugs at most recent follow-up visit which reduced seizure frequency by >50%.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:The authors selected a cohort of 31 patients with seizure cryptogenic Neonatal/Infantile Epileptic Encephalopathy (NIEE) and seizure onset before 24 months.

      Exclusion criteria included: (1) Patients with a definite history of brain insult, malformation of cortical development, neurocutaneous and syndromal disorders, and confirmed or highly suspected neurometabolic disorders based on clinical and biochemical markers. (2) Patients with Dravet syndrome and epilepsy at infancy with migrating focal seizure were also excluded because the majority of variants are detected in the SCN1A (>85%) and KCNT1 (approximately 50%) genes.

      Formal neuropsychological testing or best clinical assessment was used to classify patient development or intelligence.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Whole Exome Sequencing (WES) variant results were filtered in a panel of 430 epilepsy-associated genes. After selection of variants from the 430-gene panel, the synonymous variants, variants with variant frequency <10%, and variants with allele frequency >1% were removed.

      Gene:CDKL5

      Variant:NM_003159.2 c. 1849delC (p. Arg617Valfs*4)

      The authors state that the variant is a heterozygous frameshift deletion.

      The authors state that this is a novel variant and is pathogenic.

      HGVS:Not provided

      ClinVarID:Not found

      CAID:Not found.

      gnomAD:Not found

      MultipleGeneVariants:Not provided

    1. Case  1

      Case: Patient 1, female, 2 years old

      DiseaseAssertion: Rett Syndrome

      FamilyInfo: DeNovo. Patient 1 was the second child of a nonconsanguineous Chinese couple. Patient 1 was born at full term with a birth weight of 3.83 kg.

      ParentalGenotype(s):Not provided

      CasePresentingHPOs:HP:0011344, HP:0001250, HP:0001252, HP:0000252, HP:0000748, HP:0003763, HP:0005469, HP:0000486, HP:0012171.

      CaseHPOFreeRext:Patient 1 presents with severe global developmental delay, epilepsy, and hypotonia. The Patient History contains all of Patient 1's phenotypes along with the progression of her condition.

      Patient History

      @ 3 months - Patient 1 had microcephaly (head circumference was less than 3rd percentile with a body weight and body height at 75th percentile). Patient 1 had hypotonia.

      Patient 1 was given a metabolic screening, a muscle enzyme, and a brain tomography with normal results.

      @ 6 months - Patient 1 had microcephaly, flat occiput, right divergent squint, and hypotonia. No syndromal diagnosis could be ascertained at that time.

      @ 2 years - Patient 1 had epilepsy.

      Patient 1 had severe global development delay.

      Patient 1 was given an EEG which showed nonspecific background slowing, but no epileptiform abnormalities. Patient 1 was also given a brain MRI which showed mild thinning of corpus callosum without major structural defect. Patient 1 had no developmental regression but she developed stereotypical hand movements, bruxism, and occasional outburst of laughter.

      Based on these phenotypes, Angelman/Rett Syndrome was suspected.

      CaseNOTHPOs: HP:0002353.

      CaseNOTHPOFreeText: Patient 1 was given an EEG which detected no epileptic abnormalites.

      CasePreviousTesting: Genetic investigations (including methylation-specific multiplex ligation-dependent probe amplification (MS-MLLPA)) was conducted for Angelman Syndrome, UBE3A gene, MECP gene, and array CGH. These studies were negative. A FOXG1 related disease was suspected

      PreviouslyPublished:Not previously published

      GenotypingMethod: A FOXG1 gene test showed a de novo frameshift pathogenic mutation FOXG1 {NM_005249.3} c. 396_397ins26; FOXG1{NP_005240.3} :(p. Gly133TRPfs*68) which confirmed the diagnosis of a FOXG1 related congenital variant of Rett Syndrome.

      Gene:FOXG1

      Variant: (NM_005249.3) c. 396_397ins26 (p. Gly133Trpfs*68)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:Not found

      gnomAD:Not found

    2. Case  2

      Case:Patient 2, female, Chinese

      DiseaseAssertion:Global delay

      FamilyInfo:Patient 2 was the first child of nonconsanguineous Chinese couple born at 38-week gestation. The mother had gestational diabetes mellitus that required insulin therapy.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0000365, HP:0020049, HP:0000252, HP:0001263, HP:0012171, HP:0000154, HP:0000708, HP:0003763, HP:0002376, HP:0012433.

      CaseHPOFreeText:

      Patient History

      @ birth - Patient 2 presented with mild grade bilateral hearing impairment and left divergent squint diagnosed at birth.

      @ Follow-up visit - Patient 2 had microbrachycephaly and global developmental delay. Brain MRI, metabolic screening and array CGH were normal.

      @ 1 year - Patient 2 had stereotypical handwashing movement.

      There was no clinical or electrical seizure.

      Patient 2 has craniofacial features like microbrachycephaly, wide mouth, divergent squint, and behavioral phenotype.

      @ 1.5 years - Patient 2 had bruxism and developmental regression. Patient 2 also had loss of some motor and social skills.

      CaseNotHPOs:HP:0001250

      CaseNotHPOFreeText:Patient 2 has no seizures.

      CasePreviousTesting:Not provided

      PreviouslyPublished:Not previously published

      GenotypingMethod:Not provided

      Gene:MECP2 (MN_004992.3) (NP_004983.1)

      Variant:c. 808C>T (p. Arg270*)

      HGVS:Not provided

      ClinVarID:Not found

      CAID:CA172577

      gnomAD:Not found

      MultipleGeneVariants:NA

    1. first patient

      Case:Patient 1, female, 11 years old

      DiseaseAssertion:Rett Syndrome - Atypical Variant

      FamilyInfo:De Novo. Patient 1's parents were healthy. When Patient 1 was clinically examined, the head circumferences of her mother and father were 53 cm (P25) and 59 cm (P90), respectively. The parents had normal weight.

      ParentalGenotype:Both parents were sequenced for Patient 1's mutation, and the deletion was not detected.

      CasePresentingHPOs:HP:0001249, HP:0001513, HP:0001626, HP:0000256, HP:0010465, HP:0012758, HP:0000750, HP:0012433, HP:0002591, HP:0001250, HP:0020174, HP:0000316, HP:0000336, HP:0000431, HP:0000377, HP:0000470, HP:0001156, HP:0001500.

      CaseHPOFreeText:

      Patient history

      @ birth - Patient 1 was born at 38 weeks of gestation after an uncomplicated pregnancy. Her weight was 3,390 g (P69), height 51 cm (P60), and her head circumference was 36 cm (P90).

      @ 6 months - Patient 1 experienced developmental delay.

      @ 9 months - Patient 1 sat without support.

      @ 2 years - Patient 1 began to walk.

      @ later on - Patient 1 presented with speech delay and behavioral disturbances. The behavioral disturbances were reduced by the drug risperidone.

      @ early childhood - Patient 1 has been obese and appeared to display hyperphagia.

      @ 8 years - Patient 1 developed precocious puberty.

      @ 10 years - Patient 1 had her first epileptic seizure. Treatment with lamotrigine prevented further seizures. The seizures later became refractory to this treatment.

      @ 10 years - Patient 1 presented with a height of 160 cm (P>97) and a head circumference of 59 cm (P>97). She had hypertelorism and prominent eyebrows. Her nasal bridge was broad and auricles were fleshy. In addition, Patient 1's neck was short and the fingers were short and wide.

      Patient 1 has an intellectual disability, metabolic syndrome, and macrocephaly.

      CaseNotHPOs:HP:0002540.

      CaseNotHPOFreeText:Patient 1 sat without support at 9 months old. She walked at 2 years.

      CasePreviousTesting:Patient 1 was given a conventional cytogenetic analysis. The chromosomal analyses (46,XX) and array CGH results (BlueGnome CytoChip ISCA 4×180K v1.0; Agilent Human Genome CGH Microarray 180K) were normal. Patient 1 was also given a methylation-specific MLPA to exclude a Temple syndrome, which is also characterized by weight gain and precocious puberty. In addition, Prader-Willi syndrome was ruled out by methylation testing. This syndrome is another imprinting disease causing obesity and intellectual disability.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Whole-exome sequencing analysis of the entire exome was conducted for Patient 1. Whole-genome sequencing showed heterozygosity in Patient 1, which was confirmed by Sanger sequencing. Macrocephalic syndrome genes including PTEN, NSD1, NFIX, SETBP1, RAI1, and PHF6 were analyzed, and no additional variants of interest (pathogenic, likely pathogenic, or variants of uncertain significance) were observed.

      Gene:MECP2

      Variant:c. 1162_1172del (p. Pro388*), heterozygosity, frameshift.

      HGVS:NM_004992.3

      ClinVarID:Not found

      CAID:CA1139667881

      gnomAD:Not found

      MultipleGeneVariants:Not provided

    1. Patient 2

      Case:Patient 2, female, 2.5 years old

      DiseaseAssertion:CDKL5 Disorder

      FamilyInfo:De Novo with an unremarkable family history.

      ParentalGenotype:Not provided

      CasePresentingHPOs:HP:0032792, HP:0007359, HP:0011154, HP:0002194, HP:0010862, HP:0000750, HP:0012434, HP:0000710, HP:0100023, HP:0000252, HP:0009062, HP:0010845, HP:0020174, HP:0010841.

      CaseHPOFreeText:

      Patient history

      @ 2 months to 2.5 years - Patient 2 experienced tonic and focal seizures with autonomic symptoms.

      @ 2 years - Patient 2 was diagnosed with CDKL5 disorder.

      Patient 2 had severe delayed gross motor development, severe delayed fine motor development, severe delayed language development and delayed social development. Patient 2 had hyperoral and hand flapping stereotypies. She also had microcephaly (< 2 SD) and axial hypotonia.

      Patient 2 was given a brain EEG which detected Delta slowing of the background followed by generalized attenuation during seizures and multifocal interictal epileptiform abnormalities.

      @ 2.5 years - Patient 2 experienced seizures in clusters.

      Treatments

      Antiepleptic treatments included:Phenobarbital, Topirimate, Clobazam, Valproate, Keppra, Vitamin B6, Phenytoin, Lamotrigine, Nitrazepam, Oxcarbazepine, Mirtazipine, KCI, Levetiracetam, ant ketogenic diet.

      Patient 2 was also treated with Carnitine. Patient 2's seizures seem to have changed in type over time but continued.

      Other testing

      Tests were conducted on Patient 2 to obtain data in the following areas: NBS, lactate, lipoprotein profile, plasma and urine amino acids, urine organic acids, acylcarnitine profile, total and free serum carnitine levels, plasma ammonia, total plasma homocysteine, serum CK, liver enzymes, urine alpha-AASA, creatine, biotinidase, VLCFA, Batten disease screen, CSF analysis (amino acids, lactate, glucose, protein, cell count, neurotransmitters), MRI-brain with spectroscopy, and karyotype.

      CaseNotHPOs:Not provided

      CaseNotHPOFreeText:Not provided

      CasePreviousTesting:Patient 2 was given a gene sequence test for the genes SCNIA and MECP2. No gene mutation was found for these two genes.

      PreviouslyPublished:Not previously published

      GenotypingMethod:Patient 2 was given a CDKL5 gene sequence test. The test detected a mutation in the CDKL5 gene.

      Gene:CDKL5

      Variant:c. 2480_2486dupCAGATCT. frameshift

      The authors state that CDKL5 gene sequencing detected a de novo duplication in exon 17, c. 2480_2486dupCAGATCT, resulting in a frameshift (Boston University School of Medicine, Center for Human Genetics, Boston, MA). This is a novel change that has not been reported before in ExAC. Only pathogenic point mutations in exon 17 have previously been reported. In a patient with a previously reported frameshift mutation in exon 18, a truncated CDKL5 transcript was detected. A truncated protein would lack the C-terminus and would not localize correctly in the cell, as demonstrated in vitro. Accordingly, any reading frame altering mutations proximal to exon 18 are null-variants. Therefore, this mutation is classified as pathogenic according to ACMG criteria.

      HGVS:Not provided

      ClinVarID:547188

      NM_001323289.2 (CDKL5): c. 2480_2486dup (p. Gln830fs)

      Allele ID: 538303

      CAID:Not found

      gnomAD:Not found

      MultipleGeneVariants:Not provided

  5. Mar 2026
    1. 7-year-old boy

      Case#: 7-year-old boy

      DiseaseAssertion: Atrial flutter (AFL), sick sinus syndrome (SSS), Brugada syndrome (BrS)

      FamilyInfo: Family history of sudden death in maternal grandfather at age 30 years. Family testing identified the same SCN5A variant in the proband's mother and sister. The mother was asymptomatic but had a coved type ST elevation in V1 lead recorded at the 3rd intercostal position (Fig. 1e) and remained free of cardiac events until age 37 years. His sister's ECG was normal, and she remained free of cardiac events for 10 months

      ParentalTesting: Mother was found to have the same LOF variant

      CasePresentingHPOs: HP:0004749, HP:0011712, HP:0011704, HP:0011654

      CaseHPOFreeText: AFL detected on ECG with right bundle branch block but no history of arrhythmia, congenital heart disease, or cardiomyopathy. Post-RFCA, patient had sinus arrest lasting up to 7s, leading to diagnosis of sick sinus syndrome (SSS). Post-ablation ECG following a second RFCA revealed Brugada-type patterns, raising suspicion of Brugada syndrome (BrS) which eventually lead to a diagnosis.

      CaseNotHPOs: HP:0001638, HP:0001279, HP:0011675

      CaseNotHPOFreeText: Cardiomyopathy, syncope, arrhythmia

      CasePreviousTesting: NR

      Genotyping Method: NR

      FunctionalAnalysis: NR

      Variant: c.2678G > A p.Arg893His

      ClinVar: 67749

      CAID: CA016396

      gnomAD: https://gnomad.broadinstitute.org/variant/3-38585800-C-T?dataset=gnomad_r4 (v4.1.0 GrpMax FAF: 0.000003390 (European non-Finnish) )

  6. Aug 2025
    1. A 55-year-old male

      Case#: 55-year-old man

      DiseaseAssertion: single coronary artery (SCA) and presented with dilated cardiomyopathy (DCM)

      FamilyInfo: Unremarkable

      ParentalTesting: NR

      CasePresentingHPOs: HP:0002094, HP:0031352, HP:0001638, HP:0001644, HP:0010741

      CaseHPOFreeText: chest tightness and dyspnoea after activity lasting for 2 months. CTCA showed congenital absence of the right coronary artery. TTE revealed enlargement of the left heart and cardiomyopathy. CMR revealed DCM. oedema of both lower limbs. Laboratory data in Table 1.

      CaseNotHPOs: NR

      CaseNotHPOFreeText: Stenosis

      CasePreviousTesting: See NGS results in Supplementary Table 1

      Genotyping Method: Genetic screening (NGS results in Supplementary Table 1) with confirmation by Sanger

      FunctionalAnalysis: NR

      Variant: c.1858C>T (p.Arg620Cys)

      ClinVar: 67694

      CAID: CA015449

      gnomAD: v4.1.0 GrpMax FAF: 0.00002033 (European non-Finnish)

      AdditionalInfo: The patient also has APOA5:c.990_993delAACA (p. Asp332Valfs*5) (P/LP in ClinVar with 2 stars)