Evidence map›Paper›PMID 21750575›Full record

ArticleEuropean journal of human genetics : EJHG2011

2p15-p16.1 microdeletion syndrome: molecular characterization and association of the OTX1 and XPO1 genes with autism spectrum disorders.

Xudong Liu, Patrick Malenfant, Chelsea Reesor, Alana Lee, Melissa L Hudson, Chansonette Harvard, Ying Qiao, Antonio M Persico, Ira L Cohen, Albert E Chudley and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in European journal of human genetics : EJHG, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Bio-collections in autism research.Molecular autism · 2017
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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

14 authors at 7 institutions in 3 countries.

Xudong LiuDepartment of Psychiatry, Queen's University, Kingston, Ontario, Canada.
Patrick Malenfant
Chelsea Reesor
Alana Lee
Melissa L Hudson
Chansonette Harvard
Ying Qiao
Antonio M Persico
Ira L Cohen
Albert E Chudley
Cynthia Forster-Gibson
Evica Rajcan-Separovic
M E Suzanne Lewis
Jeanette J A Holden
Autism Research Foundation · USChild and Family Research Institute · CAQueen's University · CAUniversity of British Columbia · CAIstituti di Ricovero e Cura a Carattere Scientifico · ITNew York State Office for People With Developmental Disabilities · USUniversity of Manitoba · CA

Funding

Genomewide Search--Autism Susceptibility Loci-supplementR01MH064547 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GESCHWIND, DANIEL H · 2002 to 2006
$9.6M
Autism Speaks AS2173CIHR 43820CIHR MOP 74502CIHR RT-64217NIMH NIH HHS MH64547NIMH NIH HHS R01 MH064547
6 · The paper itself

Abstract

Reports of unrelated individuals with autism spectrum disorder (ASD) and similar clinical features having overlapping de novo interstitial deletions at 2p15-p16.1 suggest that this region harbors a gene(s) important to the development of autism. We molecularly characterized two such deletions, selecting two genes in this region, exportin 1 (XPO1) and orthodenticle homolog 1 (OTX1) for association studies in three North American cohorts (Autism Spectrum Disorder - Canadian American Research Consortium (ASD-CARC), New York, and Autism Genetic Resource Exchange (AGRE)) and one Italian cohort (Società Italiana per la Ricerca e la Formazione sull'Autismo (SIRFA)) of families with ASD. In XPO1, rs6735330 was associated with autism in all four cohorts (P<0.05), being significant in ASD-CARC cohorts (P-value following false discovery rate correction for multiple testing (P(FDR))=1.29 × 10(-5)), the AGRE cohort (P(FDR)=0.0011) and the combined families (P(FDR)=2.34 × 10(-9)). Similarly, in OTX1, rs2018650 and rs13000344 were associated with autism in ASD-CARC cohorts (P(FDR)=8.65 × 10(-7) and 6.07 × 10(5), respectively), AGRE cohort (P(FDR)=0.0034 and 0.015, respectively) and the combined families (P(FDR)=2.34 × 10(-9) and 0.00017, respectively); associations were marginal or insignificant in the New York and SIRFA cohorts. A significant association (P(FDR)=2.63 × 10(-11)) was found for the rs2018650G-rs13000344C haplotype. The above three SNPs were associated with severity of social interaction and verbal communication deficits and repetitive behaviors (P-values <0.01). No additional deletions were identified following screening of 798 ASD individuals. Our results indicate that deletion 2p15-p16.1 is not commonly associated with idiopathic ASD, but represents a novel contiguous gene syndrome associated with a constellation of phenotypic features (autism, intellectual disability, craniofacial/CNS dysmorphology), and that XPO1 and OXT1 may contribute to ASD in 2p15-p16.1 deletion cases and non-deletion cases of ASD mapping to this chromosome region.

Indexed as

Chromosome DeletionChromosomes, Human, Pair 2AllelesChildChild Development Disorders, PervasiveChild, PreschoolChromosome BreakpointsExportin 1 ProteinGene OrderGenetic Association StudiesGenetic Predisposition to DiseaseHaplotypesHumansKaryopherinsOtx Transcription FactorsPolymorphism, Single NucleotideExportin 1 ProteinKaryopherinsOTX1 protein, humanOtx Transcription FactorsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID21750575
PMCPMC3230356
OpenAlexW1996141957

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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.