Evidence map›Paper›PMID 8641695›Full record

ArticleHuman genetics1996

Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation. A combined genetic study, including cytogenetics, PCR/SSCP, FISH, and CGH.

H J Decker, C Neuhaus, A Jauch, M Speicher, T Ried, M Bujard, H Brauch, S Störkel, M Stöckle, B Seliger and 1 more

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Article in Human genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 25 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

H J DeckerDepartment of Haematology and Oncology, Johannes-Gutenberg University of Mainz, Germany.
C Neuhaus
A Jauch
M Speicher
T Ried
M Bujard
H Brauch
S Störkel
M Stöckle
B Seliger
C Huber
Johannes Gutenberg University Mainz · DEHeidelberg University · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reaction/single strand conformation polymorphism (PCR/SSCP) analysis with primers from the VHL gene identified a deletion of a single nucleotide in exon 2 in the patient's germline and in the tumor, but not in the DNA of his parents. This deletion therefore must be a de novo mutation. Comparative genome hybridization (CGH) and fluorescence in situ hybridization (FISH) analysis of the G1 tumor with differentially labelled yeast artifical chromosome (YAC) clones showed loss of 3p and of the 3p26 signals, respectively. In conclusion, we identified a de novo germline mutation in the VHL gene of a young patient and a somatic chromosome 3p loss at the homologous chromosome 3 in his renal tumor. Our results suggest a recessive mode of inactivation of the VHL gene, providing solid evidence for its tumor-suppressor gene characteristics. Our data show the diagnostic potential of genetic testing, especially in patients without VHL family history. Furthermore, the findings of homozygous inactivation of the VHL gene in a G1 tumor support the notion that the inactivation of the VHL gene is an early event in tumorigenesis of renal cell carcinoma.

Indexed as

Chromosome DeletionAdultChromosomes, Human, Pair 3DNA Mutational AnalysisExonsFemaleGenes, Tumor SuppressorGerm-Line MutationHemangioblastomaHomozygoteHumansKaryotypingKidney NeoplasmsMaleMolecular Sequence DataPedigree

Identifiers

PMID8641695
OpenAlexW2945860312

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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.