Evidence map›Paper›PMID 26251039›Full record

ArticleCancer science2015

Potential roles of microRNA-29a in the molecular pathophysiology of T-cell acute lymphoblastic leukemia.

Lucila H Oliveira, Josiane L Schiavinato, Mariane S Fráguas, Antonio R Lucena-Araujo, Rodrigo Haddad, Amélia G Araújo, Leandro F Dalmazzo, Eduardo M Rego, Dimas T Covas, Marco A Zago and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 46 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

11 authors at 3 institutions in 1 country.

Lucila H OliveiraDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Josiane L SchiavinatoDepartment of Genetics, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Mariane S FráguasDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Antonio R Lucena-AraujoDepartment of Genetics, Federal University of Pernambuco, Recife, Brazil.
Rodrigo HaddadSchool of Ceilandia, University of Brasilia, Brasilia, Brazil.
Amélia G AraújoDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Leandro F DalmazzoDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Eduardo M RegoDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Dimas T CovasDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Marco A ZagoDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Rodrigo A PanepucciDepartment of Internal Medicine, Medical School of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Universidade de São Paulo · BRUniversidade de Brasília · BRUniversidade Federal de Pernambuco · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence has shown that deregulated expression of members of the microRNA-29 (miR-29) family may play a critical role in human cancer, including hematological malignancies. However, the roles of miR-29 in the molecular pathophysiology of T-cell acute lymphoblastic leukemia (T-ALL) has not been investigated. Here, we show that lower levels of miR-29a were significantly associated with higher blast counts in the bone marrow and with increased disease-free survival in T-ALL patients. Furthermore, miR-29a levels are extremely reduced in T-ALL cells compared to normal T cells. Microarray analysis following introduction of synthetic miR-29a mimics into Jurkat cells revealed the downregulation of several predicted targets (CDK6, PXDN, MCL1, PIK3R1, and CXXC6), including targets with roles in active and passive DNA demethylation (such as DNMT3a, DNMT3b, and members of the TET family and TDG). Restoring miR-29a levels in Jurkat and Molt-4 T-ALL cells led to the demethylation of many genes commonly methylated in T-ALL. Overall, our results suggest that reduced miR-29a levels may contribute to the altered epigenetic status of T-ALL, highlighting its relevance in the physiopathology of this disease.

Indexed as

Antigens, NeoplasmApoptosisCell Line, TumorCell ProliferationClass Ia Phosphatidylinositol 3-KinaseCyclin-Dependent Kinase 6DaunorubicinDisease-Free SurvivalDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADNA Methyltransferase 3BDrug Resistance, NeoplasmEpigenesis, GeneticGene Expression Regulation, LeukemicAntigens, NeoplasmCDK6 protein, humanClass Ia Phosphatidylinositol 3-KinaseCyclin-Dependent Kinase 6DaunorubicinDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Methyltransferase 3BDNMT3A protein, humanMCL1 protein, humanMicroRNAsMIRN29a microRNA, humanMixed Function OxygenasesMyeloid Cell Leukemia Sequence 1 ProteinPeroxidasesPeroxidasinPhosphatidylinositol 3-KinasesPIK3R1 protein, humanProto-Oncogene ProteinsPXDN protein, humanReceptors, Interleukin-1TET1 protein, humanDNMTepigenetic regulationmiR-29aT-cell acute lymphoblastic leukemiaTET

Identifiers

PMID26251039
PMCPMC4637998
OpenAlexW1834286332

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.