Evidence map›Paper›PMID 24686393›Full record

ArticleEpigenetics2014

microRNA-34b/c on chromosome 11q23 is aberrantly methylated in chronic lymphocytic leukemia.

Stefan Deneberg, Meena Kanduri, Dina Ali, Sofia Bengtzen, Mohsen Karimi, Ying Qu, Eva Kimby, Larry Mansouri, Richard Rosenquist, Andreas Lennartsson and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  10. Role of microRNAs in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2023
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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

11 authors at 5 institutions in 3 countries.

Stefan DenebergDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Meena KanduriInstitute of Biomedicine; Department of Clinical Chemistry and Transfusion Medicine; Sahlgrenska University Hospital; Göteborg, Sweden.
Dina AliDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Sofia BengtzenDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Mohsen KarimiDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Ying QuDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Eva KimbyDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Larry MansouriDepartment of Immunology, Genetics and Pathology; Science for Life Laboratory; Uppsala University; Uppsala, Sweden.
Richard RosenquistDepartment of Immunology, Genetics and Pathology; Science for Life Laboratory; Uppsala University; Uppsala, Sweden.
Andreas LennartssonDepartment of Biomedicine and Nutrition; NOVUM; Karolinska Institutet; Stockholm, Sweden.
Sören LehmannDepartment of Internal Medicine/Hematology; Karolinska Institutet; Karolinska University Hospital Huddinge; Stockholm, Sweden.
Karolinska University Hospital · SEKarolinska Institutet · SEInstitute for Biomedicine · ITPediatrics and Genetics · USScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A commonly deleted region in chronic lymphocytic leukemia (CLL) is the 11q22-23 region, which encompasses the ATM gene. Evidence suggests that tumor suppressor genes other than ATM are likely to be involved in CLL with del(11q). A microRNA (miR) cluster including the miR-34b and miR-34c genes is located, among other genes, within the commonly deleted region (CDR) at 11q. Interestingly, these miRs are part of the TP53 network and have been shown to be epigenetically regulated. In this study, we investigated the expression and methylation status of these miRs in a well-characterized cohort of CLL, including cases with/without 11q-deletion. We show that the miR-34b/c promoter was aberrantly hypermethylated in a large proportion of CLL cases (48%, 25/52 cases). miR-34b/c expression correlated inversely to DNA methylation (P = 0.003), and presence of high H3K37me3 further suppressed expression regardless of methylation status. Furthermore, increased miR-34b/c methylation inversely correlated with the presence of 11q-deletion, indicating that methylation and del(11q) independently silence these miRs. Finally, 5-azacytidine and trichostatin A exposure synergistically increased the expression of miR-34b/c in CLL cells, and transfection of miR-34b or miR-34c into HG3 CLL cells significantly increased apoptosis. Altogether, our novel data suggest that miR-34b/c is a candidate tumor suppressor that is epigenetically silenced in CLL.

Indexed as

Gene DeletionAdultAgedAged, 80 and overAntimetabolites, AntineoplasticApoptosisAzacitidineCell Cycle ProteinsChromosomes, Human, Pair 11Cohort StudiesFemaleHistone Deacetylase InhibitorsHistonesHumansHydroxamic AcidsLeukemia, Lymphocytic, Chronic, B-CellAntimetabolites, AntineoplasticAzacitidineBTG4 protein, humanCell Cycle ProteinsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsMicroRNAsMIRN34 microRNA, humantrichostatin Achronic lymphatic leukemiaDNA methylationepigeneticsmicro-RNA

Identifiers

PMID24686393
PMCPMC4053441
OpenAlexW2080426042

What OpenQuestion holds

Textmetadata
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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.