Evidence map›Paper›PMID 20567917›Full record

ArticleFamilial cancer2010

Clinical and molecular characterization of Brazilian families with von Hippel-Lindau disease: a need for delineating genotype-phenotype correlation.

Israel Gomy, Greice Andreotti Molfetta, Ester de Andrade Barreto, Cristiane Ayres Ferreira, Dalila Luciola Zanette, José Cláudio Casali-da-Rocha, Wilson Araujo Silva

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In one paragraph

Article in Familial cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07167329 (The BELIEVE-VHL Trial), which is not on this map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07167329 phase2recruitingnot on this mapstarted 2024, after this paper: background citation

The BELIEVE-VHL Trial: A Real-world Longitudinal Study on Belzutifan's Effectiveness, Pharmacogenetics, and Pharmacoeconomics in Von Hippel-Lindau (VHL) Syndrome Using the HIF2α Inhibitor Belzutifan

TypeinterventionalSponsorJosé Claudio Casali da RochaRan2024 to 2030Enrolled100ConditionsVon Hippel Lindau, Von Hippel Lindau Disease, Von Hippel Lindau-Deficient Clear Cell Renal Cell Carcinoma, Hemangioblastoma (HB) of the Central Nervous System (CNS)ArmsBelzutifan
3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Israel GomyDepartment of Genetics, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil. isgomy@gmail.com
Greice Andreotti Molfetta
Ester de Andrade Barreto
Cristiane Ayres Ferreira
Dalila Luciola Zanette
José Cláudio Casali-da-Rocha
Wilson Araujo Silva
Universidade de São Paulo · BRInstituto Nacional do Câncer · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

von Hippel-Lindau (VHL) disease is an autosomal dominant hereditary cancer syndrome that predisposes to the development of a variety of benign and malignant tumours, especially cerebellar haemangioblastomas, retinal angiomas and clear-cell renal cell carcinomas (RCC). The etiology and manifestations are due to germline and somatic mutations in the VHL tumour suppressor gene. VHL disease is classified into type 1 and type 2, showing a clear genotype-phenotype correlation, as type 2 is associated with phaeochromocytoma and essentially caused by missense mutations. The aim of this study is to characterize the phenotype and genotype of families with VHL disease. Eighteen of twenty patients from ten unrelated families underwent genetic testing, nine of them fulfilled VHL disease criteria and one had an apparently sporadic cerebellar haemangioblastoma. Four different germline mutations in the VHL gene were identified: c.226_228delTTC (p.Phe76del); c.217C > T (p.Gln73X); IVS1-1 G > A and IVS2-1 G > C. The first three mutations were associated with type 1 disease and the last one with type 2B, which had never been identified in the germline. The transcriptional processing of a novel splice-site mutation was characterised. Three type 1 VHL families showed large deletions of the VHL gene, two of them encompassed the FANCD2/C3orf10 genes and were not associated with renal lesions. We also suggest that such families should be subclassified according to the risk of RCC and the extent of the VHL gene deletions. This study highlights the need for a through clinical and molecular characterisation of families with VHL disease to better delineate its genotype-phenotype correlation.

Indexed as

Gene DeletionAdolescentAdultBrazilCarcinoma, Renal CellCase-Control StudiesCerebellar NeoplasmsChildDNA Mutational AnalysisDNA, NeoplasmFamilyFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansDNA, NeoplasmVon Hippel-Lindau Tumor Suppressor Protein

Identifiers

PMID20567917
OpenAlexW2055575961

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.