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  1. Last 7 days
    1. In January 2013, a 74-year-old man was admitted to the Department of Neurosurgery at Yonsei University College of Medicine due to gait disturbance and tingling sensation of both legs. The patient was receiving beta-adrenergic antagonist and calcium channel blocker for arterial hypertension. He had lost his vision in the left eye due to cataract and amblyopia in the right eye due to retinitis which had occurred 30 years ago. The patient’s family history included a mother with a brain tumor of unconfirmed pathology, and both brothers with renal cell carcinoma with VHL gene mutation (Fig. 1). Serum carcinoembryonic antigen (CEA) was elevated to 11.78 ng/mL (normal value, 0.0 to 5.0 ng/mL). Although he had no history of diabetes mellitus, serum glucose level was 462 mg/dL and HbA1c was 11.7%, which led to a new diagnosis of diabetes mellitus, and initiation of insulin therapy. Whole spine magnetic resonance imaging (MRI) showed multiple enhancing nodular lesions of the spinal canal suspected leptomeningeal metastasis of unknown primary malignancy (Fig. 2A). Positron emission tomography whole body scan showed intense fludeoxyglucose uptake in a 3-cm-sized heterogeneous mass in the right kidney and focal mural thickening in the sigmoid colon (Fig. 2B and ​andC).C). Colonoscopy showed a 5-cm-sized ulceroinfiltrative lesion in the sigmoid colon and a polypoid lesion in the rectum. Subsequent histological examination confirmed the diagnosis of adenocarcinoma and high grade tubular adenoma with focal carcinoma in situ transformation, respectively. Incisional biopsy of the spinal mass was performed and the histological examination revealed hemangioblastoma.Open in a separate windowFig. 1.Pedigree presenting VHL gene mutation status and malignancy. Both brothers were diagnosed with renal cell carcinoma (RCC) with VHL gene mutation and one of his sons was confirmed VHL mutation without clinical manifestation.Open in a separate windowFig. 2.(A) Spine magnetic resonance imaging showed multiple enhancing nodular lesions of the spinal canal suspected leptomeningeal metastasis of unknown primary malignancy. Positron emission tomography computed tomography whole body scan showed a 3-cm enhancing heterogenous mass in the right kidney (arrow) (B), focal mural thickening with intense fludeoxyglucose uptake in the sigmoid colon (C).The patient underwent laparoscopic right partial nephrectomy, laparoscopic anterior resection of the sigmoid colon, and transanal endoscopic operation of the rectum. Histologic examination of the kidney revealed renal clear cell carcinoma (size, 1.9×1.7 cm), Fuhrman nuclear grade 3 (pT1aN0M0; stage I). In the sigmoid colon, gross pathology showed an ulcerofungating tumor (size, 4.2×3.6 cm) and 3 of 23 examined regional lymph nodes were metastasis. Subsequent histological examination confirmed typical features of colon adenocarcinoma (pT3N1bM0; stage IIIB). The rectum specimen was confirmed to be a 0.5-cm-sized well differentiated adenocarcinoma (pT1N0M0; stage I). The postoperative CEA level was 4.24 ng/mL.Regarding clinical decision processes, we initially suspected VHL disease. Subsequently, polymerase chain reaction (PCR) sequencing analysis of VHL gene showed p.Glu70Lys (c.208G > A) mutation in exon 1, confirming the diagnosis of VHL disease (Fig. 3). Result of endocrine hormonal evaluation for pheochromocytoma was within normal range.Open in a separate windowFig. 3.Polymerase chain reaction sequencing analysis of von Hippel–Lindau (VHL) gene showed a p.Glu70Lys (c.208G > A) mutation in exon 1, confirming the diagnosis of VHL disease.His two sons were screened for VHL disease using PCR sequencing analysis, and one progenity showed p.Glu70Lys (c.208G > A) mutation in exon 1, identical to his father. He underwent ophthalmic examination, abdomen-pelvic computed tomography scan and blood test for catecholamine metabolites, but there were no abnormal findings.After 3 weeks from discharge, he was admitted to hospital complaining of worsened gait disturbance and numbness of both soles. Brain MRI showed three enhancing lesions in bilateral cerebellar hemispheres and left cerebellar tonsil, suggesting hemangioblastomas (Fig. 4). The patient underwent gamma knife surgery in cerebellar lesions and palliative radiotherapy to T9-S1 spine with a total of 45 Gy in 25 daily fractions.Open in a separate windowFig. 4.Brain magnetic resonance imaging showed three enhancing lesions (arrows) in bilateral cerebellar hemispheres (A,B) and left cerebellar tonsil (C), suggesting hemangioblastomas.nAfter one month, follow-up imaging studies showed stable lesions in the brain and spine, but there was a newly developed hepatic metastasis in S6 and an enlarged aortocaval lymph node (Fig. 5). Concurrent serum CEA level increased to 19.54 ng/mL. The multidisciplinary team decided to perform surgery, laparoscopic wedge resection of liver and excision of aortocaval lymph node. Histologic examination of liver revealed a 1.6×1.2-cm-sized metastatic adenocarcinoma, moderately differentiated, clinically from colon. Pathologic finding indicated that the aortocaval lymph node was metastatic carcinoma, favoring renal clear cell carcinoma. He is on regular follow-up in the outpatient clinic and imaging studies show no evidence of recurrence and CEA level is stabilized within normal range.

      PatientID: None (Proband)

      KindredID: 1

      Case: M, 74Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo:Mother with a brain tumor of unconfirmed pathology, and both brothers (70Y and 79Y) with renal cell carcinoma with the same VHL gene mutation as this patient. One son (44Y) has the same mutation but was asymptomatic. Daughter (40Y) had a brain hemorrhage, niece had hematologic malignancy, nephew has pancreatic cancer; genetic information is unclear or not provided for these family members.

      CasePresentingHPOs: HP:0010797; HP:0000822; HP:0000518; HP:0000572; HP:0000646; HP:0000819; HP:0040276; HP:0006770; HP:0032118, HP:0030439; HP:0009713; HP:0002672; HP:0006880 (Hemangioblastoma, Hypertension, Cataract, Visual loss, Amblyopia, Diabetes mellitus, Adenocarcinoma of the colon, Clear cell renal cell carcinoma, Retinitis, Anal canal adenocarcinoma, Spinal hemangioblastoma, Gastrointestinal carcinoma, Cerebellar hemangioblastoma)

      CaseHPOFreeText: History of arterial hypertension and retinitis causing loss of vision in the left eye due to cataract and amblyopia in the right eye. History of retinal hemangioblastoma was presumed. Diagnosed with diabetes mellitus at the time of the study. MRI showed multiple enhancing nodular lesions of the spinal canal, later confirmed to be a hemangioblastoma. Whole body PET scan showed a heterogeneous mass in the right kidney and focal mural thickening in the sigmoid colon. Colonoscopy showed an ulceroinfiltrative lesion in the sigmoid colon and a polypoid lesion in the rectum subsequently confirmed as a adenocarcinoma and high grade tubular adenoma with focal carcinoma, respectively. Histologic examination of the kidney revealed renal clear cell carcinoma. In the sigmoid colon, gross pathology showed an ulcerofungating tumor and some regional lymph nodes were metastasis. The rectum specimen was confirmed to be a well differentiated adenocarcinoma. Brain MRI showed three enhancing lesions in bilateral cerebellar hemispheres and left cerebellar tonsil, suggesting hemangioblastomas. Histologic examination of liver revealed a metastatic adenocarcinoma. Pathologic finding indicated that the aortocaval lymph node was metastatic carcinoma, favoring renal clear cell carcinoma.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: Figure 1

      Variant: p.E70K (c.208G>A)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 43598, https://www.ncbi.nlm.nih.gov/clinvar/variation/43598/

      CAID: N/A

      gnomAD: 0.000004365, https://gnomad.broadinstitute.org/variant/3-10183739-G-A

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: E70K (c.208G>A)

      MultipleGeneVariants: N/A

    1. 64-year-old man carrying the VHL gene mutation affected by simultaneous colon adenocarcinoma, renal clear cell carcinoma and adrenal pheochromocytoma.

      PatientID: None

      KindredID: 1

      Case: M, 75Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient's brother had hypertension at age 77 and was found to carry the mutation. The patient's niece had breast cancer at age 33. Refer to Figure 4 for Pedigree.

      CasePresentingHPOs: HP:0006770, HP:0040276, HP:0006748, HP:0001407, HP:0002716, HP:0032618, HP:0100526, HP:0100598 (clear cell renal cell carcinoma, adenocarcinoma of the colon, adrenal pheochromocytoma, hepatic cysts, lymphadenopathy, renal necrosis, neoplasm of the lung, pulmonary edema)

      CaseHPOFreeText: Patient admitted at age 64 for intermittent abdominal pain, loss of appetite and constipation. He was found to have a solid tumor with areas of colliquative necrosis in the upper pole of the left kidney. The scans also showed distension of the colon with concomitant wall thickening, indicating possible neoplasia. Colonoscopy revealed a small polyp in the rectum-sigmoid junction, and a subsequent histological exam confirmed a diagnosis of adenocarcinoma. Both tumours were removed via a left hemicolectomy and left radical nephrectomy. A histologic examination of the kidney revealed renal clear cell carcinoma. Five years later, an abdominal CT scan revealed an adrenal pheochromocytoma in the right adrenal gland and multiple hepatic cysts in the right kidney and liver. The patient underwent a right adrenalectomy which found no convincing evidence of malignancy. At age 73 total body positron emission tomography (PET)-CT revealed the presence of several metastatic sites (both lungs, a 12×10 mm right sovraclaveare lymphadenopathy, and a 32×12 mm lesions at the mediastinum). An agobiopsy and cytologic broncholavage showed lymphocytes and epithelial cells with voluminous clear cytoplasm and large nuclei with prominent nucleoli, confirming the presence of metastatic lesions of clear cell renal carcinoma. In the same year, CT imaging revealed progression of pulmonary disease. One year later, a new CT scan revealed hepatic metastases and worsening of the mediastinal adenopathy and pulmonary metastases. At age 75, a new CT scan showed stable disease at various metastatic sites with minimal pleural effusion. Later in the month the patient was hospitalized for severe dyspnea, fatigue, and lower limb edema and died a few days later.

      CaseNotHPOs: HP:0009711 (retinal capillary hemangioma)

      CaseNotHPOFreeText: Fundoscopy revealed no vascular abnormalities of the retina.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. c.74C>T, p.P25L

      PatientID: II-1

      KindredID: Family C

      Case: M, 45Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: Only this one member was studied at have the L198P mutation, however the asymptomatic father of patient C II-1 was also a carrier of the same polymorphism (c.74C>T, p.P25L).

      CasePresentingHPOs: HP:0006748; HP:0030405; HP:0009711 (Adrenal pheochromocytoma; pancreatic neuroendocrine tumour; retinal capillary hemangioma)

      CaseHPOFreeText: At the age of 15, patient had pancreatic tumor (malignant pancreatic neuroendocrine tumor). At the age of 16, MRI revealed suprarenal tumor masses bilaterally (pheochromocytomas in the adrenal glands), as well as optic nerve hemangioblastomas of the right eye. At the age of 25, he shows no signs of metastases or new VHL-associated tumors, but since the age of 23, he has been suffering from HLAB27-positive ankylosing spondylitis.

      CaseNotHPOs: HP:0005584; HP:0010797 (renal cell carcinoma; hemangioblastoma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: L198P (c.593T>C) AND P25L (c.74C>T)

      MultipleGeneVariants: Germline, VHL, c.593T>C (p.Leu198Pro)

    1. PatientID: None

      KindredID: 1

      Case: Sex Unknown, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Adrenal pheochromocytoma

      FamilyInfo: The proband was part of a cohort of apparently sporadic cases of pheochromocytoma/ paraganglioma, implying this individual had no family history of VHL disease or pheochromocytoma.

      CasePresentingHPOs: HP:0006748 (Adrenal Pheochromocytoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0002668 (Paraganglioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET, SDHB, SDHC, and SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330, https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988, https://gnomad.broadinstitute.org/variant/3-10183605-C-T?dataset=gnomad_r2_1

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P25L (c.74C>T)

      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

    1. III/6 (44)-----Pro25Leu

      PatientID: IIII-6

      KindredID: 1

      Case: F, 44Y0M, Hungarian

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient's mother (II-5) carried the Ser80Asn mutation and presented with renal cell carcinoma. The patient's siblings (III-7 and III-8) both carried the Ser80Asn mutation. Patient III-7 presented with hemangioblastoma of the brain and retina hemangioblastoma and her children carried the Ser80Asn mutation with clinical presentation. Patient III-8 presented with brain hemangioblastoma, pheochromocytoma, and retina hemangioma. The patient's maternal aunt (II-1) carried both Ser80Asn and Pro25Leu mutation but was asymptomatic. She passed on the Ser80Asn mutation to her daughter (III-1), the proband and this patient's cousin. Refer to figure 1 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: HP:0005584, HP:0002666, HP:0010797, HP:0009711 (renal cell carcinoma, pheochromocytoma, hemangioblastoma, retinal capillary hemangioma)

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: CA020538 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.74C%3ET

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. frameshift mutations (4/16)

      PatientID: 12

      KindredID: 12

      Case: 32Y0M, Sex Unknown, Argentinian

      DiseaseAssertion: VHL

      FamilyInfo: Family history unremarkable; Patient was confirmed to have a de novo mutation.

      CasePresentingHPOs: HP:0010797; HP:0009711; HP:0000107; HP:0030424 (hemangioblastoma; retinal capillary hemangioma; renal cyst; epididymal cyst)

      CaseHPOFreeText: Aged 32Y at diagnosis (genetic testing); fulfils type 1 VHL clinical diagnosis. Retinal hemangioblastomas and CNS hemangioblastomas diagnosed at 32Y, renal cysts were also diagnosed at 32Y, while epididymal cysts were diagnosed first at 23Y (See Table 1 & 2).

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V74Sfs*53 (c.219_232delGGTCATCTTCTGCA)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA2497423672 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/by_caid?caid=CA2497423672

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: minus_2_frameshift_variant

      CivicName: V74Sfs*53 (c.219_232delGGTCATCTTCTGCA)

      MultipleGeneVariants: N/A

    1. PatientID: 7

      KindredID: 7

      Case: F, 40Y0M, Ethnicity Unknown

      DiseaseAssertion: Cerebellar Hemangioblastoma

      FamilyInfo: N/A

      CohortInfo: The cohort included a series of 20 capillary haemangioblastomas of the central nervous system for mutations of the VHL gene.

      CasePresentingHPOs: HP:0006880 (cerebellar hemangioblastoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: p.P25L (c.287C>T)

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: Refer to Table 1 for abnormal SSCP or heteroduplex patterns.

      MutationType: missense_variant;transition

      CivicName:P25L(c.74C>T)

      MultipleGeneVariants: N/A

    1. No abstract available

      PatientID: IV-3

      KindredID: 1

      Case: M, 77Y0M, Ethnicity Unknown

      DiseaseAssertion: VHL

      FamilyInfo: The patient’s mother and two brothers had died with cerebellar hemangioblastoma, although genetic testing was not performed. One of the patient’s four children, a 46Y male, also presented with a small renal tumour, renal cysts, and pancreatic cysts; he was found to carry the same mutation the patient carried. One of the patient’s grandsons, a 10Y male, was also found to carry the same mutation as the patient but was asymptomatic. Genealogical inquiry also revealed that the patient was distantly related to a known VHL family; one member, a 47Y male, was previously operated on for CNS hemangioblastoma, RCC and symptomatic pheochromocytoma and was found to carry the same mutation as the proband. Another female member had previously presented with retinal hemangioblastoma before becoming deceased at 37Y. The paper also asserted that the patient’s grandmother and two distant relatives carried the mutation, although genotyping was not performed and phenotypic information was not provided.

      CasePresentingHPOs: HP:0006880; HP:0001737; HP:0006770; HP:0006748; HP:0000479 (Cerebellar hemangioblastoma, pancreatic serous cystadenoma, clear cell renal cell carcinoma, adrenal pheochromocytoma, retinal lesions)

      CaseHPOFreeText: The patient was originally diagnosed with metastatic bilateral clear cell renal cell carcinoma at 68Y and underwent chemotherapy for three months. The metastases were later reinterpreted to be a cystic hemangioblastoma and a benign serous cystadenoma. The patient was also found to have a non-secreting adrenal pheochromocytoma at 73Y and a clear cell renal cell carcinoma metastasis in the thyroid at 74Y. The patient had also previously presented with retinal lesions, although detailed records were unavailable.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.R82P(c.245G>C)

      LegacyVariant: N/A

      ClinVarID: 193118, http://www.ncbi.nlm.nih.gov/clinvar/variation/193118

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: R82P(c.245G>C)

      MultipleGeneVariants: N/A

  2. Nov 2026
    1. Of the 13 individuals tested, V:2, IV:4, IV:6, III:2, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. With the exception of family member IV:2, none of these individuals reported any features characteristic of VHL disease.

      PatientID: IV:6

      KindredID: 1

      Case: F, Age Unknown, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient had two siblings both of whom carried the P25L mutation. One was asymptomatic (IV:4) whereas another (IV:2) presented with retinal hemangioma and renal cysts. Her cousin (IV:7) was diagnosed at the age of 47 years with renal cell carcinoma and subsequently died at the age of 48 years. Her great grandmother (I:2) had died of a brain tumor in her late 50s. Her grandfather (II:3) had a brain tumor at the age of 53 years and died aged 78 years. As well, her grandfather's sister (II,1) reportedly died of stomach cancer in her 80s. Of the 13 family members tested, V:2, IV:4, IV:6, III:2, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. Refer to Figure 1 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    2. . Of the 13 individuals tested, V:2, IV:4, IV:6, III:2, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. With the exception of family member IV:2, none of these individuals reported any features characteristic of VHL disease.

      PatientID: III:11

      KindredID: 1

      Case: F, 75, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient's father (II:3) had a brain tumour at age 53 and died at age 78. The patient's paternal aunt (II:1) died of stomach cancer at age 80. The patient's paternal grandfather died at age 50 due to a brain tumour. The patient had seven siblings, five of whom underwent genetic testing. Two were found to carry the mutation but both were asymptomatic (patient III:2 and III:3). The patient's sister (III:2) had three children all of whom carried the P25L mutation and were asymptomatic (IV:4 and IV:6) except patient IV:2 who presented with a retinal hemangioma and renal cyst. Her niece, (IV:2) had three children and one was found to carry the mutation. The patient's brother (III:3) had six children one of whom died due to clear cell renal carcinoma at age 48 but did not carry the P25L mutation (IV:7). The patient had three unaffected children who did not carry the mutation. Of the 13 family members tested, V:2, IV:4, IV:6, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. Refer to Figure 1 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: Ongoing clinical follow up of the individuals with P25L over a period of 5 years has continued to show no evidence of additional clinical involvement of VHL disease.

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    3. Of the 13 individuals tested, V:2, IV:4, IV:6, III:2, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene.

      PatientID: III:2

      KindredID: 1

      Case: F, 62, Ethnicity Unknown

      DiseaseAssertion: Asymptomatic

      FamilyInfo: The patient's father (II:3) had a brain tumour at age 53 and died at age 78. The patient's paternal aunt (II:1) died of stomach cancer at age 80. The patient's paternal grandfather died at age 50 due to a brain tumour. The patient had three children all of whom carried the P25L mutation and were asymptomatic (IV:4 and IV:6) except patient IV:2 who presented with a retinal hemangioma and renal cyst. Her daughter (IV:2) had three children and one was found to carry the mutation. The patient had seven siblings, five of whom underwent genetic testing. Two were found to carry the mutation but both were asymptomatic (patient III:3 and III:11). Patient III:3 had six children one of whom died due to clear cell renal carcinoma at age 48 but did not carry the P25L mutation. Of the 13 family members tested, V:2, IV:4, IV:6, III:3, and III:11 were all found to carry the P25L mutation in the VHL gene. Refer to Figure 1 for pedigree.

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      LegacyVariant: N/A

      CaseProblemVariantFreeText: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName:P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. PatientID: 1

      KindredID: 1

      Case: M, 68Y0M, Ethnicity unknown

      DiseaseAssertion: VHL

      FamilyInfo: None.

      CasePresentingHPOs: HP:0002666; HP:0009711; HP:0000107 (pheochromocytoma, retinal capillary hemangioma, renal cyst)

      CaseHPOFreeText: Patient was found observed to have retinal angioma (retinal capillary hemangioma) and a right kidney cortex cyst (30mm). Patient's pheochromocytoma was found incidentally and he remained asymptomatic with steady weight.

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: RET, SDHB, SDHC and SDHD

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. 12 missenses

      GroupID/ KindredID: 4

      DiseaseAssertion: assumed VHL

      GroupSize: 3

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: Chinese

      GroupAgeRange: N/A

      GroupInfo: With a family history, 3 family members were recorded in this group with the given mutation.

      GroupPresentingHPOs: HP:0010797; HP:0009711; HP:0001732 (hemangioblastoma; retinal capillary hemangioma; pancreatic lesion)

      GroupHPOFreeText: 2 members had CNS hemangioblastomas, 1 member had retinal angiomas, and 1 had pancreatic cysts or tumors (an abnormality of the pancreas)

      GroupNotHPOs: HP:0005584; HP:0002666 (renal cell carcinoma, pheochromocytoma)

      GroupNotHPOFreeText: No family members appeared to have the above manifestation.

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V74G (c.221T>G)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: p.V74G (c.434T>G)

      ClinVarID: N/A

      CAID: CA70042528 http://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.221T%3EG

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V74G (c.221T>G)

      MultipleGeneVariants: N/A

  3. Oct 2026
    1. DNA obtained from peripheral blood was available for all patients but only patient RCC-23, with a p.P25L alteration, showed in the germline the same aminoacidic change detected in tumor tissue.

      PatientID: RCC-23

      KindredID: 1

      Case: Sex and Age unknown, Italian

      DiseaseAssertion: VHL

      FamilyInfo: None

      CasePresentingHPOs: HP:0006770 (Clear cell renal cell carcinoma)

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      CasePreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.P25L (c.74C>T)

      CaseProblemVariantFreeText: N/A

      LegacyVariant: N/A

      ClinVarID: 93330 https://www.ncbi.nlm.nih.gov/clinvar/variation/93330/

      CAID: N/A

      gnomAD: 0.002988 https://gnomad.broadinstitute.org/variant/3-10183605-C-T

      VariantEvidence: N/A

      MutationType: missense_variant;transition

      CivicName: P25L (c.74C>T)

      MultipleGeneVariants: N/A

    1. PatientID: 25

      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 S1 describes 19 patients with missense mutations, including this patient.

      Variant: p.V74G(c.221T>G)

      LegacyVariant: c.434T>G

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA70042528

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant;transversion

      CivicName: V74G (c.221T>G)

      MultipleGeneVariants: N/A

    1. Germline mutations were identified in 300/469 (63%) of the families tested; 137 distinct intragenic germline mutations were detected.

      GroupID/ KindredID: 53CE

      DiseaseAssertion: VHL

      GroupSize: N/A

      GroupNumberMales: N/A

      GroupNumberFemales: N/A

      GroupEthnicity: N/A

      GroupAgeRange: N/A

      GroupInfo: This germline familial VHL mutation was taken from the Munich, university of Freiburg and Institute of Pathology database, with an unknown number of members belonging to Family ID 53CE. Table 3 lists all ID and mutations associated with individuals possessing renal carcinoma, without phechromocytoma.

      GroupPresentingHPOs: HP:0005548 (renal cell carcinoma)

      GroupHPOFreeText: Described as a VHL family with RCC, without pheochromocytoma. Other phenotypes are likely, however not detailed in this publication

      GroupNotHPOs: HP:0002666 (pheochromocytoma)

      GroupNotHPOFreeText: N/A

      GroupPreviousTesting: N/A

      PreviouslyPublished: N/A

      SupplementalData: N/A

      Variant: p.V74G (c.221T>G)

      LegacyVariant: p.V74G (c.434T>G)

      CaseProblemVariantFreeText: N/A

      ClinVarID: N/A

      CAID: CA70042528 https://reg.clinicalgenome.org/redmine/projects/registry/genboree_registry/allele?hgvsOrDescriptor=NM_000551.3%3Ac.221T>G

      gnomAD: N/A

      VariantEvidence: N/A

      MutationType: missense_variant; transversion

      CivicName: V74G (c.221T>G)

      MultipleGeneVariants: N/A

  4. Mar 2025
  5. Jan 2022
    1. it's a tricky thing with Max you can spend weeks and refining a patch and afterwards you're the idea is so much gone for yourself that now you have the perfect tool but 00:02:41 you're not interested in using it anymore

      it's a tricky thing with Max you can spend weeks and refining a patch and afterwards you're the idea is so much gone for yourself that now you have the perfect tool but you're not interested in using it anymore

      Classic!

  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: 0.32

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

      AssayResult: 109.6

      AssayResultAssertion: Normal

      ReplicateCount: 11

      StandardErrorMean: 19.8

      Comment: This variant had normal function (75-125% of wildtype peak current, <1% late current, no large perturbations to other parameters). These in vitro features are consistent with non-disease causing variants. (Personal communication: A. Glazer)

  7. Jan 2019
    1. all signals are interchangeable so any out port can be connected to any in port

      For those of us who’ve had to deal with distinctions between audio and control signals, this is actually pretty major. However, it’s already become something in modular synthesis. People who get started in Eurorack, for instance, may not need to worry nearly as much about different types of signals as those who used Csound or, more importantly for this marketing copy, Cycling ’74 Max.

  8. May 2015