Evidence map›Paper›PMID 18330718›Full record

ArticleMolecular biology reports2009

Genetic analysis of hereditary multiple exostoses in Tunisian families: a novel frame-shift mutation in the EXT1 gene.

Sana Sfar, Abderrazak Abid, Wijden Mahfoudh, Houyem Ouragini, Farah Ouechtati, Sonia Abdelhak, Lotfi Chouchane

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Article in Molecular biology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Sana SfarDepartment of Molecular Immuno-Oncology, Faculty of Medicine, University of Monastir, Monastir, Tunisia.
Abderrazak Abid
Wijden Mahfoudh
Houyem Ouragini
Farah Ouechtati
Sonia Abdelhak
Lotfi Chouchane
Institut Pasteur de Tunis · TNUniversity of Monastir · TNHospital Fatuma Bourguiba Monastir · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary multiple exostoses (HME) is an autosomal dominant orthopaedic disorder most frequently caused by mutations in the EXT1 gene. The aim of the present study is to determine the underlying molecular defect of HME in two multigenerational Tunisian families with 21 affected members and to examine the degree of intrafamilial variability. Linkage analysis was performed using three microsatellite markers encompassing the EXT1 locus and mutation screening was carried out by direct sequencing. In family 1, evidence for linkage to EXT1 was obtained on the basis of a maximum LOD score of 4.26 at theta = 0.00 with D8S1694 marker. Sequencing of the EXT1 revealed a heterozygous G > T transversion (c.1019G>T) in exon 2, leading to a missense mutation at the codon 340 (p.Arg340Leu). In family 2 we identified a novel heterozygous 1 bp deletion in the exon 1 (c.529_531delA) leading to a premature codon stop and truncated EXT1 protein expression (p.Lys177LysfsX15). This mutation was associated with the evidence of an intrafamilial clinical variability and considered to be a novel disease-causing mutation in the EXT1 gene. These findings provide additional support for the involvement of EXT1 gene in the HME disease.

Indexed as

PedigreeAdolescentAdultBase SequenceChildChild, PreschoolExostoses, Multiple HereditaryExostosin 1FemaleGene Expression RegulationHumansMaleMiddle AgedMutationN-AcetylglucosaminyltransferasesSequence Analysis, DNAExostosin 1N-Acetylglucosaminyltransferases

Identifiers

PMID18330718
OpenAlexW2025898243

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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.