Evidence map›Paper›PMID 25329894›Full record

ArticlePloS one2014

Genome-wide expression analysis in fibroblast cell lines from probands with Pallister Killian syndrome.

Maninder Kaur, Kosuke Izumi, Alisha B Wilkens, Kathryn C Chatfield, Nancy B Spinner, Laura K Conlin, Zhe Zhang, Ian D Krantz

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 17 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

8 authors at 4 institutions in 2 countries.

Maninder KaurThe Division of Human Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America.
Kosuke IzumiThe Division of Human Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Alisha B WilkensThe Division of Human Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America.
Kathryn C ChatfieldDepartment of Pediatrics, Section of Pediatric Cardiology, The Children's Hospital of Colorado, Denver, Colorado, United States of America.
Nancy B SpinnerThe Department of Pathology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; The Perelman School of Medicine at The University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Laura K ConlinThe Department of Pathology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; The Perelman School of Medicine at The University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Zhe ZhangCenter for Biomedical Informatics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America.
Ian D KrantzThe Division of Human Genetics, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States of America; The Perelman School of Medicine at The University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Children's Hospital of Philadelphia · USUniversity of Pennsylvania · USChildren's Hospital Colorado · USThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pallister Killian syndrome (OMIM: # 601803) is a rare multisystem disorder typically caused by tissue limited mosaic tetrasomy of chromosome 12p (isochromosome 12p). The clinical manifestations of Pallister Killian syndrome are variable with the most common findings including craniofacial dysmorphia, hypotonia, cognitive impairment, hearing loss, skin pigmentary differences and epilepsy. Isochromosome 12p is identified primarily in skin fibroblast cultures and in chorionic villus and amniotic fluid cell samples and may be identified in blood lymphocytes during the neonatal and early childhood period. We performed genomic expression profiling correlated with interphase fluorescent in situ hybridization and single nucleotide polymorphism array quantification of degree of mosaicism in fibroblasts from 17 Caucasian probands with Pallister Killian syndrome and 9 healthy age, gender and ethnicity matched controls. We identified a characteristic profile of 354 (180 up- and 174 down-regulated) differentially expressed genes in Pallister Killian syndrome probands and supportive evidence for a Pallister Killian syndrome critical region on 12p13.31. The differentially expressed genes were enriched for developmentally important genes such as homeobox genes. Among the differentially expressed genes, we identified several genes whose misexpression may be associated with the clinical phenotype of Pallister Killian syndrome such as downregulation of ZFPM2, GATA6 and SOX9, and overexpression of IGFBP2.

Indexed as

Gene Expression ProfilingGenomicsCell LineChildChild, PreschoolChromosome DisordersChromosomes, Human, Pair 12Cytogenetic AnalysisFemaleFibroblastsHumansInfantInfant, NewbornMale

Identifiers

PMID25329894
PMCPMC4199614
OpenAlexW2158575675

What OpenQuestion holds

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LicenceCC BY
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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.