Evidence map›Paper›PMID 23217014›Full record

ArticleBMC cancer2012

Aberrant methylation of the M-type phospholipase A(2) receptor gene in leukemic cells.

Mario Menschikowski, Uwe Platzbecker, Albert Hagelgans, Margot Vogel, Christian Thiede, Claudia Schönefeldt, Renate Lehnert, Graeme Eisenhofer, Gabriele Siegert

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Epigenetic control of group V phospholipase A2 expression in human malignant cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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  11. Anti-Phospholipase AImmunology, endocrine & metabolic agents in medicinal chemistry · 2016
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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

9 authors at 2 institutions in 1 country.

Mario MenschikowskiInstitut für Klinische Chemie und Laboratoriumsmedizin, Technische Universität Dresden, Fetscherstrasse 74, D-01307, Dresden, Germany. Mario.Menschikowski@uniklinikum-dresden.de
Uwe Platzbecker
Albert Hagelgans
Margot Vogel
Christian Thiede
Claudia Schönefeldt
Renate Lehnert
Graeme Eisenhofer
Gabriele Siegert
TU Dresden · DEKlinik und Poliklinik für Psychotherapie und Psychosomatik · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe M-type phospholipase A2 receptor (PLA2R1) plays a crucial role in several signaling pathways and may act as tumor-suppressor. This study examined the expression and methylation of the PLA2R1 gene in Jurkat and U937 leukemic cell lines and its methylation in patients with myelodysplastic syndrome (MDS) or acute leukemia.

methodsSites of methylation of the PLA2R1 locus were identified by sequencing bisulfite-modified DNA fragments. Methylation specific-high resolution melting (MS-HRM) analysis was then carried out to quantify PLA2R1 methylation at 5'-CpG sites identified with differences in methylation between healthy control subjects and leukemic patients using sequencing of bisulfite-modified genomic DNA.

resultsExpression of PLA2R1 was found to be completely down-regulated in Jurkat and U937 cells, accompanied by complete methylation of PLA2R1 promoter and down-stream regions; PLA2R1 was re-expressed after exposure of cells to 5-aza-2'-deoxycytidine. MS-HRM analysis of the PLA2R1 locus in patients with different types of leukemia indicated an average methylation of 28.9% ± 17.8%, compared to less than 9% in control subjects. In MDS patients the extent of PLA2R1 methylation significantly increased with disease risk. Furthermore, measurements of PLA2R1 methylation appeared useful for predicting responsiveness to the methyltransferase inhibitor, azacitidine, as a pre-emptive treatment to avoid hematological relapse in patients with high-risk MDS or acute myeloid leukemia.

conclusionsThe study shows for the first time that PLA2R1 gene sequences are a target of hypermethylation in leukemia, which may have pathophysiological relevance for disease evolution in MDS and leukemogenesis.

Indexed as

DNA MethylationGenes, Tumor SuppressorAdultAgedAntimetabolites, AntineoplasticAzacitidineDecitabineFemaleGenetic Predisposition to DiseaseHumansJurkat CellsLeukemiaMaleMiddle AgedMyelodysplastic SyndromesReceptors, Phospholipase A2Antimetabolites, AntineoplasticAzacitidineDecitabinePLA2R1 protein, humanReceptors, Phospholipase A2

Identifiers

PMID23217014
PMCPMC3561142
OpenAlexW2010587730

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.