Evidence map›Paper›PMID 34410954›Full record

ArticleIn vivo (Athens, Greece)

Combined Therapy of ATRA and Imatinib Mesylate Decreases BCR-ABL and ABCB1/MDR1 Expression Through Cellular Differentiation in a Chronic Myeloid Leukemia Model.

Camila Albuquerque Pinto, Adrhyann Jullyanne DE Sousa Portilho, Maritza Cavalcante Barbosa, Maria Elisabete Amaral DE Moraes, José Alexandre Rodrigues DE Lemos, Rommel Mαrio Rodriguez Burbano, Caroline Aquino Moreira-Nunes

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Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 12 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

7 authors at 2 institutions in 1 country.

Camila Albuquerque PintoHuman Cytogenetics Laboratory, Biological Science Institute, Federal University of Pará, Belém, Brazil.
Adrhyann Jullyanne DE Sousa PortilhoPharmacogenetics Laboratory, Drug Research and Development Center (NPDM), Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, Brazil.
Maritza Cavalcante BarbosaFaculty of Pharmacy, Federal University of Ceará, Fortaleza, Brazil.
Maria Elisabete Amaral DE MoraesPharmacogenetics Laboratory, Drug Research and Development Center (NPDM), Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, Brazil.
José Alexandre Rodrigues DE LemosBiological Science Institute, Federal University of Pará, Belém, Brazil.
Rommel Mαrio Rodriguez BurbanoHuman Cytogenetics Laboratory, Biological Science Institute, Federal University of Pará, Belém, Brazil.
Caroline Aquino Moreira-NunesPharmacogenetics Laboratory, Drug Research and Development Center (NPDM), Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, Brazil; carolfam@gmail.com.
Universidade Federal do Ceará · BRUniversidade Federal do Pará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimChronic Myeloid Leukemia (CML) is a clonal myeloproliferative disease, and a major challenge for the eradication of CML is to understand the cause of the permanence of minimal residual disease (DRM). This work aimed to induce the maturation of leukemic stem cells with All-trans-retinoic acid (ATRA), making them sensitive to treatment with Imatinib (IM). MATERIALS AND

methodsK562 cells were treated with IM and with the combined therapy of ATRA together with IM for 48 and 72 h. The expression of BCR-ABL gene and multidrug resistance gene ABCB1 were evaluated using RT-qPCR.

resultsThe combined ATRA and IM therapy showed a discreet cell differentiation pattern, evidenced by the panoptic morphology analysis at 48 and 72 h of treatment. The BCR-ABL expression showed no statistical difference when treated alone with IM, however in combination with ATRA, the expression was statistically significant in 48 and 72 h (p≤0.0001) and when the treatment groups were compared to each other (p≤0.001). The ABCB1 gene expression showed a decrease in isolated IM therapy (p≤0.05) and in the combination in 48 and 72 h (p≤0.0001).

conclusionCombined ATRA and IM therapy was shown to be effective in decreasing BCR-ABL and ABCB1 genes, possibly through the differentiation of blast cells, demonstrating that the therapy could be potentially effective in the blast crisis of the disease and for those patients who develop resistance to available CML treatments.

Indexed as

BenzamidesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveApoptosisATP Binding Cassette Transporter, Subfamily BCell DifferentiationDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansImatinib MesylatePiperazinesPyrimidinesTretinoinABCB1 protein, humanATP Binding Cassette Transporter, Subfamily BBenzamidesFusion Proteins, bcr-ablImatinib MesylatePiperazinesPyrimidinesTretinoinATRABCR-ABLChronic Myeloid LeukemiaImatinib MesylateMDR

Identifiers

PMID34410954
PMCPMC8408721
OpenAlexW3196106335

What OpenQuestion holds

Textmetadata
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.