23 Matching Annotations
  1. Last 7 days
    1. PatientID: 23

      KindredID: 7

      Case: M, 31Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 23, had a brother (patient 24) and father (patient 25) who were both genetically confirmed with the mutation. The brother presented with a CNS hemangioblastoma, renal cell carcinoma, and pancreatic cysts/tumors at age 32. The father presented with renal cell carcinoma and pancreatic cysts/tumors at age 58.

      CasePresentingHPOs: HP:0010797 (Hemangioblastoma)

      CaseHPOFreeText: The proband, patient 23, presented with a CNS hemangioblastoma at age 31.

      CaseNotHPOs: HP:0001737; HP:0001732; HP:0002666; HP:0005584; HP:0009711 (Pancreatic cysts, Abnormality of the pancreas, Pheochromocytoma, Renal cell carcinoma, Retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: p.R69Afs*63 (c.204_205insG)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189244; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.204_205insG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant

      CivicName: R69AFS*63 (c.204_205insG)

      MultipleGeneVariants: N/A

    2. PatientID: 25

      KindredID: 7

      Case: M, 58Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: The proband, patient 23, had a brother (patient 24) and father (patient 25) who were both genetically confirmed with the mutation. The brother presented with a CNS hemangioblastoma, renal cell carcinoma, and pancreatic cysts/tumors at age 32. The father presented with renal cell carcinoma and pancreatic cysts/tumors at age 58.

      CasePresentingHPOs: HP:0001737; HP:0001732; HP:0005584 (Pancreatic cysts, Abnormality of the pancreas, Renal cell carcinoma)

      CaseHPOFreeText: The proband's father, patient 25, presented with renal cell carcinoma and multiple pancreatic cysts/tumors.

      CaseNotHPOs: HP:0002666; HP:0009711; HP:0010797 (Pheochromocytoma, Retinal capillary hemangioma, Hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: This cohort was also published in a later paper by Wang et al., 2018 (PMID: 29330336).

      SupplementalData: Patient and family genotype-phenotype information is listed in Supplementary Table 1.

      Variant: p.R69Afs*63 (c.204_205insG)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189244; https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.204_205insG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant

      CivicName: R69AFS*63 (c.204_205insG)

      MultipleGeneVariants: N/A

    1. patients with VHL disease (Figs. 1 and 2, and Table 1)

      PatientID: 3

      KindredID: 2

      Case: F, 69Y0M, Arab

      DiseaseAssertion: VHL

      FamilyInfo: No family history of VHL disease was described for this patient. Immediate family members were recommended to genetically test for the relevant variant or monitor for VHL-related symptoms.

      CasePresentingHPOs: HP:0006770; HP:0006880; HP:0009713; HP:0000107; HP:0001737 (clear cell renal cell carcinoma; cerebellar hemangioblastoma; spinal hemangioblastoma; renal cyst; pancreatic cysts)

      CaseHPOFreeText: At 63Y, Patient 3 had a left radical nephrectomy for renal cell carcinoma. She also had multiple pancreatic and right renal cysts. At 67Y, Patient 3 exhibited cerebellar and spinal hemangioblastomas, renal cell carcinoma, and cysts in kidneys and pancreas. She was diagnosed with VHL disease. Two years later, had a right radical nephrectomy for renal cell carcinoma. Her entire pancreas was covered with cysts (see table 1).

      CaseNotHPOs: HP:0002088; HP:0001392; HP:0005264; HP:0001743 (abnormal lung morphology; abnormality of the liver; abnormality of the gallbladder; abnormality of the spleen)

      CaseNotHPOFreeText: No lesions were observed in the lungs, liver, gallbladder, and spleen.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData:  N/A

      Variant: p.I151T (c.452T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 428803, www.ncbi.nlm.nih.gov/clinvar/variation/428803/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: I151T (c.452T>C)

      MultipleGeneVariants: N/A

    2. Table 1

      PatientID: N/A

      KindredID: 6

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: adrenal pheochromocytoma

      FamilyInfo: Transmission of the variant could not be determined since family history is not available. Patient’s variant reported as germline.

      CasePresentingHPOs: HP:0006748 (adrenal pheochromocytoma)

      CaseHPOFreeText: Patient had Unilateral, Benign, Adrenal PH (see table 1)

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 9663592

      SupplementalData:  N/A

      Variant: p.L63P (c.188T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2227, https://www.ncbi.nlm.nih.gov/clinvar/variation/2227/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transition

      CivicName: L63P (c.188T>C)

      MultipleGeneVariants: N/A

    1. Our series comprised 125 eligible subjects with germlineVHL c.505 T/C mutation, including 64 previously known and 61 newly diagnosed mutation carriers.

      GroupID: None

      DiseaseAssertion: VHL

      GroupSize: 125

      GroupNumberMales: 58

      GroupNumberFemales: 67

      GroupEthnicity: German

      GroupAgeRange: 4-86 Y

      GroupInfo: The subjects included 64 patients belonging to 15 families with a known VHL c.505 T/C mutation. From their test programme, another 10 c.505 T/C mutation carriers were identified. As well, all consenting first degree relatives (at risk subjects) of mutation carriers, irrespective of disease status, were subjected to mutation analysis, resulting in another 51 mutation carriers detected.

      GroupPresentingHPOs: HP:0002666, HP:0009713, HP:0009711, HP:0010797, HP:0006748, HP:0006737, HP:0006770, HP:0002893, HP:0100616, HP:0030357, HP:0002894 (pheochromocytoma, spinal hemangioblastoma, retinal capillary hemangioma, hemangioblastoma, adrenal pheochromocytoma, extraadrenal pheochromocytoma, clear cell renal cell carcinoma, pituitary adenoma, testicular teratoma, small cell lung carcinoma, neoplasm of the pancreas)

      GroupHPOFreeText: 96 patients had clinical manifestations of VHL. 55 subjects (31 males, 24 females) developed pheochromocytoma during their lifetime. Overall penetrance for pheochromocytomas was estimated to be 31% by age 35 and 60% by age 70. Other frequent lesions were retinal angioma (36%), hemangioblastoma of the spine (36%), and, to a lesser extent, hemangioblastoma of the brain (16%). One patient with angiomatosis retinae developed at least 25 retinal angiomas, whereas the remaining patients had an average of two angiomas with no more than five lesions in one patient. 15 patients had bilateral and 25 unilateral involvement of the retinae. Pheochromocytoma was observed as a single tumour with adrenal or extra-adrenal localization in 32 patients, but 23 mutation carriers developed multiple pheochromocytomas. Four patients developed renal clear cell carcinoma (estimated overall penetrance 13% by the age of 70). Two of these patients died of metastases. All renal clear cell carcinomas were unilateral, single tumours, and no kidney showed renal cysts. Three of the patients with renal cell carcinoma were female. The kidney tumours were detected at the ages of 46 (male patient), 48, 63, and 74 years. Two patients with renal cell carcinoma also had multiple spinal hemangioblastomas. Other rare tumours were one pancreatic islet cell tumour and one pituitary adenoma; both neoplasms had been incidentally found in a dead 34 year old woman at necropsy. One 68 year old male patient was noted to have small cell lung cancer, and two other males developed testicular teratocarcinoma both at 39 years of age.

      GroupNotHPOs: N/A

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Y98H (c.292T>C)

      LegacyVariant: p.Y98H (c.505T>C)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2223 https://www.ncbi.nlm.nih.gov/clinvar/variation/2223/

      CAID: N/A

      gnomAD: 0.00001343 https://gnomad.broadinstitute.org/variant/3-10183823-T-C

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: Y98H (c.292T>C)

      MultipleGeneVariants: N/A

  2. Nov 2026
    1. PatientID: 6321

      KindredID: 343

      Case: Sex Unknown, Age Unknown, French

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: Families were recruited from the French VHL Registry. Enrolment in the study required identification of the germline VHL mutation (currently 85% of the families included in the French VHL Registry) and available data regarding renal phenotype. A total of 126 families fulfilled these criteria.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: Severe renal disease (any solid lesion before 25 years of age, five or more solid lesions within one or two kidneys, or metastasis of renal cell carcinoma). Individual RCC phenotype is noted as positive.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Phenotype and genotype information can be found in Supplementary Table S1.

      Variant: p.R69Afs*63 (c.204dup)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189244, https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.204dup

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: duplication; plus_1_frameshift_variant

      CivicName: R69Afs*63 (c.204dup)

      MultipleGeneVariants: N/A

    1. Lung adenocarcinoma has never before been reported to be associated with von Hippel-Lindau (VHL) disease. Here, we report a case of VHL disease in a patient who had metachronous multiple lung adenocarcinomas. The patient is a 64-year-old-woman with VHL disease. She underwent surgical resection of one adenocarcinoma and one atypical adenomatous hyperplasia. A second lung adenocarcinoma developed metachronously. A point mutation in the VHL gene was confirmed in DNA from a blood sample, and loss of heterozygosity at the VHL locus was detected in the lung adenocarcinoma. The VHL dysfunction may have a role in the development of multiple lung adenocarcinomas.

      PatientID: 1

      KindredID: 1

      Case: F, 64Y0M, Japanese

      DiseaseAssertion: VHL

      FamilyInfo: Her father was killed in an accident when she was young. Her older brother died of renal cell carcinoma associated with VHL disease at the age of 58. Her younger sister was also diagnosed with renal cell carcinoma that was associated with VHL disease. No members past the proband had been genetically tested.

      CasePresentingHPOs: HP:0006880; HP:0030078; HP:0005584; HP:0001737 (cerebellar hemangioblastoma; lung adenocarcinoma; renal cell carcinoma; pancreatic cysts)

      CaseHPOFreeText: of a hemangioblastoma of the cerebellum when she was 37 years old. Her right kidney was resected because of renal cell carcinoma at the age of 59. Concurrently, she received a pancreatojejunostomy for a pancreatic cyst. At the age of 63, radiofrequency ablation was performed for renal cell carcinoma of her left kidney. In the same year, computed tomography screening of the patient’s lungs detected nodules in the right middle lobe and left upper division. A computed tomography–guided needle biopsy of the nodule in the right middle lobe resulted in a diagnosis of adenocarcinoma (Fig 1). We concurrently performed a lobectomy of the patient’s right middle lobe and a partial resection of the left upper division.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.S65L (c.194C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 182975, https://www.ncbi.nlm.nih.gov/clinvar/variation/182975/

      CAID: N/A

      gnomAD: https://gnomad.broadinstitute.org/variant/3-10183725-C-T

      VariantEvidence: Loss of heterozygosity (LOH) at the VHL locus was detected in the lung adenocarcinoma. The hepatic adenocarcinoma was found with somatic EGFR mutations and loss of heterozygosity at the VHL locus; authors speculate that dysfunctional pVHL may promote mutations on the EGFR gene.

      MutationType: missense_variant;transition

      CivicName: S65L (c.194C>T)

      MultipleGeneVariants: N/A

  3. Oct 2026
    1. 37 M 26 B A VHL T401C L63P

      PatientID: 37

      KindredID: 37

      Case: M, 26Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: None

      CohortInfo: Patients with apparently sporadic pheochromocytomas.

      CasePresentingHPOs: HP:0006748 (Adrenal pheochromocytoma)

      CaseHPOFreeText: The patient had a benign adrenal pheochromocytoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L63P(c.188T>C)

      LegacyVariant: p.L63P(c.401T>C)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2227 https://www.ncbi.nlm.nih.gov/clinvar/variation/2227/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L63P(c.188T>C)

      MultipleGeneVariants: N/A

    1. same mutation in two out of the three clinically healthy brothers

      PatientID: None (Brother 2)

      KindredID: ASP (L63P)

      Case: M, Age Unknown, Hungarian

      DiseaseAssertion: Asymptomatic

      FamilyInfo: Family screening showed the presence of the L63P mutation in two out of the three clinically healthy brothers, whereas the mutation was absent in a clinically healthy son. Proband of this family presented with an apparently sporadic pheochromocytoma and the L63P germline mutation of the VHL gene.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.L63P (c.188T>C)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2227, https://www.ncbi.nlm.nih.gov/clinvar/variation/2227/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as L63P and cDNA change was mapped to c.188T>C.

      MutationType: missense_variant;transition

      CivicName: L63P (c.188T>C)

      MultipleGeneVariants: N/A

    1. 5-generation Chinese family with VHL

      PatientID: III-9

      KindredID: 1

      Case: M, 63Y0M, Chinese

      DiseaseAssertion: Assumed VHL

      FamilyInfo: Eight affected individuals in the patient’s family were retrospectively identified by reviewing medical records and from the recall of relatives. Three had passed away before 40 years of age because of central nervous system hemangioblastoma. Among the 10 living family members that carried the same NM_000551.3:c.326_339dupTCCACAGCTACCGA the patient carried, 3 had renal cysts and 1 had developed renal cell carcinoma, 2 had central nervous system hemangioblastoma, 1 had retinal hemangioblastomas, 1 was diagnosed with glioblastoma, and 5 were asymptomatic.

      CasePresentingHPOs: HP:0005584; HP:0000107; HP:0010797 (Renal cell carcinoma, renal cyst, CNS hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0009711 (Retinal hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.Gly114Serfs*50(c.326_339dupTCCACAGCTACCGA)

      LegacyVariant: N/A

      ClinVarID: N/A

      CAID: CA2573051018 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2573051018

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: duplication

      CivicName: G114fs (c.326_339dupTCCACAGCTACCGA)

      MultipleGeneVariants: N/A

    1. PatientID: 37

      KindredID: 37

      Case: M, 35Y0M, Ethnicity Unknown

      DiseaseAssertion: Adrenal pheochromocytoma

      FamilyInfo: N/A

      CasePresentingHPOs: HP:0006748 (Adrenal pheochromocytoma)

      CaseHPOFreeText: Unilateral benign adrenal pheochromocytoma that was operated on at age 26.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: 32179488

      SupplementalData: N/A

      Variant: p.L63P (c.188T>C)

      LegacyVariant: L63P (c.401T>C)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 2227, https://www.ncbi.nlm.nih.gov/clinvar/variation/2227/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: Variant reported as L63P (c.401T>C), legacy nomenclature (AF010238.1), and was mapped to p.Leu63Pro (c.188T>C) in accordance with reference sequence NM_000551.3.

      MutationType: missense_variant;transition

      CivicName: L63P (c.188T>C)

      MultipleGeneVariants: N/A

    1. PatientID: 26

      KindredID: N/A

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: N/A

      CohortInfo: The authors evaluated 64 VHL patients (32 women and 32 men) with renal involvement of whom 54/64 had undergone renal surgery or a radiofrequency thermal ablation procedure for RCC. In 10/64 VHL patients, at least one or more RCC were diagnosed, however at the time of diagnosis an indication for treatment was not yet present. For all patients several CT/MRI scans existed for retrospective description of tumour growth kinetics.

      CasePresentingHPOs: HP:0005584 (Renal cell carcinoma)

      CaseHPOFreeText: This is a tumor resolution study (VHL patients were investigated based on the presence of renal tumors.) No other phenotypic information is available.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Supplementary Table S6 describes 3 patients with small insertions, including this patient.

      Variant: p.R69Afs*63 (c.204dup)

      LegacyVariant: c.417insG

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA913189244

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: plus_1_frameshift_variant, duplication

      CivicName: R69Afs*63 (c.204_205insG)

      MultipleGeneVariants: N/A

    1. c.269A>T p.Asn90Ile

      PatientID: I:1

      KindredID: 4

      Case: F, 63Y0M, Chinese

      DiseaseAssertion: VHL

      FamilyInfo: Patient’s one son (II:3) was found with the same mutation and hemangioblastoma at 22Y and retinal capillary hemangioma at 32Y. Her other son (II:1) died before diagnosis; thus no DNA sample available. He presented with hemangioblastoma at 19Y

      CasePresentingHPOs: HP:0005584 (renal cell carcinoma)

      CaseHPOFreeText: patient had RCC at 63Y

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.N90I (c.269A>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 223172 https://www.ncbi.nlm.nih.gov/clinvar/variation/223172/

      CAID: N/A

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: N90I (c.269A>T)

      MultipleGeneVariants: N/A

  4. Apr 2026
    1. Urgent treatment for neoplasm consists of (1) cautious use of intravenous diuretics and (2) mediastinal irradiation, starting within 24 hours, with a treatment plan designed to give a high daily dose of radiation but a short total course of therapy to rapidly shrink the local tumor. Intensive radiation therapy combined with chemotherapy will palliate the process in up to 90% of patients. In patients with a subacute presentation, radiation therapy alone usually suffices. Chemotherapy is added if lymphoma or small-cell carcinoma is diagnosed

      endovascular stenting emerging as first-line therapy for rapid symptom relief, while definitive treatment targets the underlying cause

      Glucocorticoids (dexamethasone 4 mg every 6 hours) are commonly prescribed but lack robust supporting data; they may be more beneficial in lymphoma or thymoma and as prophylaxis against radiation-induced edema. [2-4] Importantly, SVC syndrome is no longer considered a medical emergency except in rare cases with life-threatening cerebral edema, laryngeal edema, or altered mental status. When thrombosis is present, catheter-directed thrombolysis or aspiration thrombectomy should be performed within 2-5 days of symptom onset before thrombus organization occurs. [3] The role of long-term anticoagulation after stenting remains unclear, though it is standard when significant thrombosis is present The American College of Chest Physicians recommends obtaining histologic diagnosis before treatment in suspected lung cancer cases, as stenting does not interfere with tissue diagnosis. [2] For small cell lung cancer (SCLC), chemotherapy alone is recommended as first-line treatment given rapid response rates. [2] For non-small cell lung cancer (NSCLC), radiation therapy and/or stent insertion are recommended, with response rates of 59% for chemotherapy and 63% for radiation therapy. [2] Patients with chemotherapy- or radiation-refractory disease should receive vascular stents For device-related thrombosis (catheters, pacemakers), catheter removal should be considered in conjunction with anticoagulation. [4] Endovascular therapy is first-line for device-related obstruction, while surgical bypass may be preferred for mediastinal fibrosis. [7] Both approaches show good mid-term patency, though secondary interventions are common (approximately 27-28%

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  5. Jan 2025
  6. Mar 2021
    1. Results for individual PALB2 variants were normalized relative to WT-PALB2 and the p.Tyr551ter (p.Y551X) truncating variant on a 1:5 scale with the fold change in GFP-positive cells for WT set at 5.0 and fold change GFP-positive cells for p.Y551X set at 1.0. The p.L24S (c.71T>C), p.L35P (c.104T>C), p.I944N (c.2831T>A), and p.L1070P (c.3209T>C) variants and all protein-truncating frame-shift and deletion variants tested were deficient in HDR activity, with normalized fold change <2.0 (approximately 40% activity) (Fig. 1a).

      AssayResult: 5

      AssayResultAssertion: Normal

      StandardErrorMean: 0.15

    1. Most Suspected Brugada Syndrome Variants Had (Partial) Loss of Function

      AssayResult: 64.8

      AssayResultAssertion: Abnormal

      ReplicateCount: 31

      StandardErrorMean: 11.1

      Comment: This variant had a mild loss of function in peak current (50-75% of wildtype). It also had a very large increase in recovery from inactivation (>10-fold slower). Therefore it was considered to have a partial loss of function (in vitro function consistent with Brugada Syndrome). (Personal communication: A. Glazer)