Evidence map›Paper›PMID 17285242›Full record

ArticleJournal of human genetics2007

Genetic heterogeneity of megaloblastic anaemia type 1 in Tunisian patients.

Chiraz Bouchlaka, Chokri Maktouf, Bahri Mahjoub, Abdelkarim Ayadi, M Tahar Sfar, Mahbouba Sioud, Neji Gueddich, Zouheir Belhadjali, Ahmed Rebaï, Sonia Abdelhak and 1 more

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Article in Journal of human genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 21% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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  6. Exome sequencing reveals cubilin mutation as a single-gene cause of proteinuria.Journal of the American Society of Nephrology : JASN · 2011
    Article
  7. Article
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

11 authors at 3 institutions in 1 country.

Chiraz BouchlakaMolecular Investigation of Genetic Orphan Diseases, Institut Pasteur de Tunis, BP 74, 13 Place Pasteur 1002, Tunis Belvédère, Tunisia.
Chokri MaktoufMolecular Investigation of Genetic Orphan Diseases, Institut Pasteur de Tunis, BP 74, 13 Place Pasteur 1002, Tunis Belvédère, Tunisia.
Bahri MahjoubDepartment of Paediatrics, C.H.U. Tahar Sfar, Mahdia, Tunisia.
Abdelkarim AyadiDepartment of Paediatrics, C.H.U. Tahar Sfar, Mahdia, Tunisia.
M Tahar SfarDepartment of Paediatrics, C.H.U. Tahar Sfar, Mahdia, Tunisia.
Mahbouba SioudDepartment of Paediatrics, Hôpital d'Enfants, Tunis, Tunisia.
Neji GueddichDepartment of Paediatrics, C.H.U., Monastir, Tunisia.
Zouheir BelhadjaliDepartment of Haematology, C.H.U., Aziza Othmana, Tunis, Tunisia.
Ahmed RebaïCentre de Biotechnologie de Sfax, Sfax, Tunisia.
Sonia AbdelhakMolecular Investigation of Genetic Orphan Diseases, Institut Pasteur de Tunis, BP 74, 13 Place Pasteur 1002, Tunis Belvédère, Tunisia. sonia.abdelhak@pasteur.rns.tn.
Koussay DellagiDepartment of Haematology and Laboratory of Immunology, Vaccinology and Molecular Genetics, Institut Pasteur de Tunis, Tunis, Tunisia.
Institut Pasteur de Tunis · TNCentre of Biotechnology of Sfax · TNUniversity of Monastir · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Megaloblastic anaemia 1 (MGA1) is a rare autosomal recessive condition characterized by selective intestinal vitamin B12 malabsorption and proteinuria. More than 200 MGA1 patients have been identified worldwide, but the disease is relatively prevalent in Finland, Norway and several Eastern Mediterranean regions. MGA1 is genetically heterogeneous and can be caused by mutations in either the cubilin (CUBN) or the amnionless (AMN) gene. In the present study we investigated the molecular defect underlying MGA1 in nine Tunisian patients belonging to six unrelated consanguineous families. Haplotype and linkage analyses, using microsatellite markers surrounding both CUBN and AMN genes, indicated that four out of the six families were likely to be linked to the CUBN gene. Patients from these families were screened for the Finnish, Mediterranean and Arabian mutations already published. None of the screened mutations could be detected in our population. One family showed a linkage to AMN gene. Direct screening of the AMN gene allowed the identification of the c.208-2A>G mutation, previously described in a Jewish Israeli patient of Tunisian origin and in Turkish patients. This suggests that the c.208-2A>G mutation may derive from a single Mediterranean founder ancestor. For the last family, haplotype analysis excluded both CUBN and AMN genes, suggesting the existence of a third locus that may cause MGA1.

Indexed as

Genetic HeterogeneityAdultAgedAged, 80 and overAnemia, MegaloblasticBase SequenceChildDNA Mutational AnalysisFemaleGenetic MarkersHaplotypesHumansLod ScoreMiddle AgedMolecular Sequence DataPedigreeGenetic Markers

Identifiers

PMID17285242
OpenAlexW2036238095

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Registered trials

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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.