Evidence map›Paper›PMID 38760421›Full record

ArticleEuropean journal of human genetics : EJHG2024

The phenotype of MEGF8-related Carpenter syndrome (CRPT2) is refined through the identification of eight new patients.

Laura M Watts, Marta Bertoli, Tania Attie-Bitach, Natalie Roux, Antonio Rausell, Cate R Paschal, Jessica L Zambonin, Cynthia J Curry, Blanche Martin, Rebecca S Tooze and 4 more

Abstract readCase Reports
In one paragraph

Article in European journal of human genetics : EJHG, 2024. 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
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. "Design principles of a membrane-spanning ubiquitin ligase".bioRxiv : the preprint server for biology · 2025
    Article
  6. Hitting the heights with CiteScore.European journal of human genetics : EJHG · 2024
    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

14 authors.

Laura M WattsOxford Centre for Genomic Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Marta BertoliNorthern Genetics Service, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK.
Tania Attie-BitachService de Médecine Génomique des Maladies Rares, Hôpital Necker-Enfants Malades, Paris, France.ORCID 0000-0002-1155-3626
Natalie RouxService de Médecine Génomique des Maladies Rares, Hôpital Necker-Enfants Malades, Paris, France.
Antonio RausellService de Médecine Génomique des Maladies Rares, Hôpital Necker-Enfants Malades, Paris, France.ORCID 0000-0002-4832-6101
Cate R PaschalSeattle Children's Hospital, Seattle, WA, USA.ORCID 0000-0002-9400-5560
Jessica L ZamboninProvincial Medical Genetics Program, BC Women's Hospital and Health Centre, Vancouver, BC, Canada.
Cynthia J CurryUniversity of California San Francisco/Fresno, Fresno, CA, USA.
Blanche MartinMRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Rebecca S ToozeMRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Lara HawkesOxford Centre for Genomic Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Usha KiniOxford Centre for Genomic Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Stephen R F TwiggMRC Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.ORCID 0000-0001-5024-049X
Andrew O M WilkieOxford Centre for Genomic Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK. andrew.wilkie@imm.ox.ac.uk.ORCID 0000-0002-2972-5481

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carpenter syndrome (CRPTS) is a rare autosomal recessive condition caused by biallelic variants in genes that encode negative regulators of hedgehog signalling (RAB23 [CRPT1] or, more rarely, MEGF8 [CRPT2]), and is characterised by craniosynostosis, polysyndactyly, and other congenital abnormalities. We describe a further six families comprising eight individuals with MEGF8-associated CRPT2, increasing the total number of reported cases to fifteen, and refine the phenotype of CRPT2 compared to CRPT1. The core features of craniosynostosis, polysyndactyly and (in males) cryptorchidism are almost universal in both CRPT1 and CRPT2. However, laterality defects are present in nearly half of those with MEGF8-associated CRPT2, but are rare in RAB23-associated CRPT1. Craniosynostosis in CRPT2 commonly involves a single midline suture in comparison to the multi-suture craniosynostosis characteristic of CRPT1. No patient to date has carried two MEGF8 gene alterations that are both predicted to lead to complete loss-of-function, suggesting that a variable degree of residual MEGF8 activity may be essential for viability and potentially contributing to variable phenotypic severity. These data refine the phenotypic spectrum of CRPT2 in comparison to CRPT1 and more than double the number of likely pathogenic MEGF8 variants in this rare disorder.

Indexed as

AcrocephalosyndactyliaPhenotypeAdolescentChildChild, PreschoolFemaleHumansInfantMaleMembrane ProteinsMutationPedigreerab GTP-Binding ProteinsMEGF8 protein, humanMembrane ProteinsRAB23 protein, humanrab GTP-Binding Proteins

Identifiers

PMID38760421
PMCPMC11220001

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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.