Evidence map›Paper›PMID 39553472›Full record

ArticleFrontiers in genetics2024

An intragenic duplication in the AFF2 gene associated with Cornelia de Lange syndrome phenotype.

Cristina Lucia-Campos, Ilaria Parenti, Ana Latorre-Pellicer, Marta Gil-Salvador, Ilaria Bestetti, Palma Finelli, Lidia Larizza, María Arnedo, Ariadna Ayerza-Casas, Julia Del Rincón and 14 more

Abstract read
In one paragraph

Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

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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

24 authors.

Cristina Lucia-CamposDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Ilaria ParentiInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Ana Latorre-PellicerDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Marta Gil-SalvadorDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Ilaria BestettiSS Medical Genetics Laboratory, SC Clinical Pathology, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Palma FinelliSS Medical Genetics Laboratory, SC Clinical Pathology, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Lidia LarizzaExperimental Research Laboratory of Medical Cytogenetics and Molecular Genetics, IRCCS Istituto Auxologico Italiano, Milan, Italy.
María ArnedoDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Ariadna Ayerza-CasasDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Julia Del RincónDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Laura TrujillanoDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Beatriz MorteCentre for Biomedical Network Research on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.
Luis A Pérez-JuradoCentre for Biomedical Network Research on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.
Pablo LapunzinaCentre for Biomedical Network Research on Rare Diseases (CIBERER), Instituto de Salud Carlos III, Madrid, Spain.
Elsa LeitãoInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Jasmin BeygoInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Christina LichInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Fabian KilpertInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Sabine KayaInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Christel DepienneInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Frank J KaiserInstitute of Human Genetics, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Feliciano J RamosDepartment of Paediatrics, Unit of Clinical Genetics, Service of Paediatrics, University Hospital "Lozano Blesa", School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Beatriz PuisacDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.
Juan PiéDepartment of Pharmacology and Physiology, Unit of Clinical Genetics and Functional Genomics, School of Medicine, University of Zaragoza, CIBERER-GCV02 and IIS-Aragon, Zaragoza, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cornelia de Lange syndrome (CdLS, OMIM #122470, #300590, #300882, #610759, and #614701) is a rare congenital disorder that affects the development of multiple organs and is characterized by physical abnormalities and cognitive and behavioral disabilities. Its molecular basis is mainly based on alterations in genes encoding structural and regulatory proteins related to the cohesin complex. Moreover, other transcriptional regulatory factors have been linked to this syndrome. However, additional causative genes are still unknown, since many patients still lack a molecular diagnosis. Herein, we describe a case with multiple affected family members presenting with an intragenic duplication in the AFF2 gene. The direct tandem intragenic duplication of exons 10, 11 and 12 was detected through high-resolution array Comparative Genomic Hybridization and next-generation sequencing technologies. Confirming the X-linked inheritance pattern, the duplication was found in the patient, his mother and his maternal aunt affected (dizygotic twins). Targeted sequencing with Oxford Nanopore Technologies revealed an aberrant transcript which is predominantly expressed in the patient and his aunt. Along with these results, a significant reduction in AFF2 gene expression levels was detected in these two individuals. Clinically both subjects exhibit a classic CdLS phenotype, whereas the mother is mostly unaffected. Consistent with the phenotypical differences observed between the mother and the aunt, there is a marked difference in X-inactivation patterns skewing. Given the crucial role of AFF2 in transcriptional regulation, it is not surprising that AFF2 variants can give rise to CdLS phenotypes. Therefore, the AFF2 gene should be considered for the molecular diagnosis of this syndrome.

Indexed as

AFF2CdLSfamilial caseintragenic duplicationOxford Nanopore TechnologiesX-inactivation

Identifiers

PMID39553472
PMCPMC11563810

What Socratic holds

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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 Socratic graph.