Evidence map›Paper›PMID 41964217›Full record

ArticleHGG advances2026

Heterozygous CECR2 variants support a distinct neurodevelopmental syndrome with features overlapping cat eye syndrome.

Anushree Acharya, Irma Järvelä, Andrea Hernandez, Yasmin Rajendran, Thashi Bharadwaj, Dana H Goodloe, Susan M Hiatt, Jennifer Morrison, Patricia G Wheeler, Jesse M Hunter and 10 more

Abstract read
In one paragraph

Article in HGG advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

20 authors.

Anushree AcharyaDepartment of Translational Neurosciences, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA.
Irma JärveläDepartment of Medical Genetics, University of Helsinki, Helsinki, Finland.
Andrea HernandezDepartment of Translational Neurosciences, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA.
Yasmin RajendranDepartment of Translational Neurosciences, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA.
Thashi BharadwajCenter for Statistical Genetics, Gertrude H. Sergievsky Center and the Department of Neurology, Columbia University Medical Center, New York, NY, USA.
Dana H GoodloeDepartment of Genetics, the University of Alabama at Birmingham, Birmingham, AL 35223, USA.
Susan M HiattHudsonAlpha Institute for Biotechnology, Huntsville, AL, USA.
Jennifer MorrisonArnold Palmer Hospital for Children, Orlando Health Orlando Regional Medical Center, Orlando, FL, USA.
Patricia G WheelerArnold Palmer Hospital for Children, Orlando Health Orlando Regional Medical Center, Orlando, FL, USA.
Jesse M HunterNationwide Children's Hospital, Columbus, OH, USA.
Rachel SupingerNationwide Children's Hospital, Columbus, OH, USA.
Scott E HickeyNationwide Children's Hospital, Columbus, OH, USA.
Andrea K PetersenDepartment of Genetics and Metabolism, Randall Children's Hospital at Legacy Emanuel, Portland, OR, USA; Genomic Medicine Program, Veteran's Health Administration, Salt Lake City, UT, USA.
Kari MagnussenDepartment of Genetics and Metabolism, Randall Children's Hospital at Legacy Emanuel, Portland, OR, USA.
Marcello ScalaDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, 16132 Genoa, Italy; Medical Genetics Unit, IRCCS Istituto Giannina Gaslini, 16147 Genoa, Italy.
Pasquale StrianoDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, 16132 Genoa, Italy; Pediatric Neurology and Muscular Diseases Unit, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Federico ZaraDepartment of Neurosciences, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, 16132 Genoa, Italy; Medical Genetics Unit, IRCCS Istituto Giannina Gaslini, 16147 Genoa, Italy.
Juha LeppäläThe Wellbeing Services County of South Ostrobothnia, Seinäjoki, Finland.
Suzanne M LealCenter for Statistical Genetics, Gertrude H. Sergievsky Center and the Department of Neurology, Columbia University Medical Center, New York, NY, USA; Taub Institute for Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York, NY, USA.
Isabelle SchrauwenDepartment of Translational Neurosciences, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, USA. Electronic address: ischrauwen@arizona.edu.

Funding

Elucidating the Genetic Etiology of Intellectual Disability in African, Asian, and European FamiliesR01HD109342 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SUZANNE M LEAL, Isabelle Veerle Suzanne Schrauwen · 2023 to 2026
$2.5M
Long-read genome sequencing for the discovery of highly penetrant variation in rare diseasesR01HD112437 · NICHD · HUDSON-ALPHA INSTITUTE FOR BIOTECHNOLOGY · PI Gregory Michael Cooper, Jane Grimwood · 2024 to 2026
$1.8M
NICHD NIH HHS R01 HD109342NICHD NIH HHS R01 HD112437
6 · The paper itself

Abstract

The CECR2 histone acetyl-lysine reader facilitates chromatin remodeling and plays a significant role in neurodevelopment. It resides within the cat eye syndrome (CES) critical region at 22q11.1q11.21. An increased copy number of this region, often as tetrasomy or a supernumerary chromosome, results in CES. The complex chromosomal arrangements and phenotypic variability have hampered the identification of the true cause(s) of CES. Patients and their clinical data were collected from multiple diagnostic and research laboratories. Exome or genome sequencing was performed in affected individuals and, when available, their relatives. Here, we describe six patients with a heterozygous single-nucleotide or small insertion/deletion variant in CECR2 and their clinical features. Variants were either loss-of-function [c.1734dupC:p.(Thr580Hisfs∗98), c.1819C>T:p.(Arg607∗), and c.2281C>T:p.(Arg761∗)] or missense in an intrinsically disordered and potentially critical region at the C terminus of the protein [c.4153C>G:p.(Gln1385Glu), c.4254C>G:p.(Phe1418Leu), and c.4283A>G:p.(Gln1428Arg)]. The main clinical features were delayed growth, relatively small head circumference, developmental delay, and speech issues/delay. Other clinical findings were variable and included intellectual disability; feeding problems; facial dysmorphism; cleft lip/palate; brain, ear, heart, or other organ abnormalities; behavioral abnormalities; and epilepsy. There was significant overlap with common CES features, including ear, heart, and brain abnormalities, intellectual disability, and growth restriction. In conclusion, we characterize a CECR2-associated neurodevelopmental disorder. The consistent molecular and clinical overlap with CES supports CECR2's role in the CES phenotype. These findings implicate diverse variant types in related neurodevelopmental disorders, underscoring CECR2's dosage sensitivity and essential function in epigenetic regulation during development.

Indexed as

Chromosome DisordersCorneal OpacityMutationNeurodevelopmental DisordersAneuploidyChildChild, PreschoolChromosomes, Human, Pair 22Eye AbnormalitiesFemaleHeterozygoteHumansInfantMalePhenotype22q11.1q11.21cat eye syndromececr2dosage sensitivityneurodevelopmentvariant

Identifiers

PMID41964217
PMCPMC13136700

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.