Evidence map›Paper›PMID 36349425›Full record

ArticleAmerican journal of medical genetics. Part A2023

Copy number variants suggest different molecular pathways for the pathogenesis of bladder exstrophy.

Agneta Nordenskjöld, Samara Arkani, Maria Pettersson, Johanna Winberg, Jia Cao, Magdalena Fossum, Magnus Anderberg, Gillian Barker, Gundela Holmdahl, Johanna Lundin

Open access · hybridAbstract read
In one paragraph

Article in American journal of medical genetics. Part A, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 7 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

10 authors at 6 institutions in 2 countries.

Agneta NordenskjöldDepartment of Women's and Children's Health, and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-6638-4631
Samara ArkaniDepartment of Women's and Children's Health, and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Maria PetterssonDepartment of Clinical Genetics, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0003-3120-1625
Johanna WinbergDepartment of Clinical Genetics, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0001-6490-4306
Jia CaoDepartment of Women's and Children's Health, and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Magdalena FossumDepartment of Women's and Children's Health, and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Magnus AnderbergDepartment of Pediatric Surgery, Skåne University Hospital, Lund, Sweden.
Gillian BarkerDepartment of Pediatric Surgery, Uppsala Academic Hospital, Uppsala, Sweden.
Gundela HolmdahlDepartment of Women's and Children's Health, and Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Johanna LundinDepartment of Clinical Genetics, Karolinska University Hospital, Stockholm, Sweden.
Karolinska University Hospital · SECopenhagen University Hospital · DKDanderyds sjukhus · SEKarolinska Institutet · SELund University · SEUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bladder exstrophy is a rare congenital malformation leaving the urinary bladder open in the midline of the abdomen at birth. There is a clear genetic background with chromosome aberrations, but so far, no consistent findings apart from 22q11-duplications detected in about 2%-3% of all patients. Some genes are implicated like the LZTR1, ISL1, CELSR3, and the WNT3 genes, but most are not explained molecularly. We have performed chromosomal microarray analysis on a cohort of 140 persons born with bladder exstrophy to look for submicroscopic chromosomal deletions and duplications. Pathogenic or possibly pathogenic microdeletions or duplications were found in 16 patients (11.4%) and further 9 with unknown significance. Two findings were in regions linked to known syndromes, two findings involved the same gene (MCC), and all other findings were unique. A closer analysis suggests a few gene networks that are involved in the pathogenesis of bladder exstrophy; the WNT-signaling pathway, the chromosome 22q11 region, the RIT2 and POU families, and involvement of the Golgi apparatus. Bladder exstrophy is a rare malformation and is reported to be associated with several chromosome aberrations. Our data suggest involvement of some specific molecular pathways.

Indexed as

Bladder ExstrophyChromosome AberrationsChromosomesDNA Copy Number VariationsHumansInfant, NewbornUrinary Bladderbladder exstrophychromosomeCMAgenetic

Identifiers

PMID36349425
PMCPMC10100507
OpenAlexW4308636210

What OpenQuestion holds

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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.