Evidence map›Paper›PMID 29301374›Full record

ReviewInternational journal of molecular sciences2018

Why Differentiation Therapy Sometimes Fails: Molecular Mechanisms of Resistance to Retinoids.

Petr Chlapek, Viera Slavikova, Pavel Mazanek, Jaroslav Sterba, Renata Veselska

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  6. Article
  7. Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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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

5 authors at 3 institutions in 1 country.

Petr ChlapekLaboratory of Tumor Biology, Department of Experimental Biology, Faculty of Science, Masaryk University, 61137 Brno, Czech Republic. chlapek@sci.muni.cz.
Viera SlavikovaLaboratory of Tumor Biology, Department of Experimental Biology, Faculty of Science, Masaryk University, 61137 Brno, Czech Republic. slavikova@sci.muni.cz.
Pavel MazanekDepartment of Pediatric Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, 62500 Brno, Czech Republic. mazanek.pavel@fnbrno.cz.
Jaroslav SterbaInternational Clinical Research Center, St. Anne's University Hospital, 65691 Brno, Czech Republic. sterba.jaroslav@fnbrno.cz.
Renata VeselskaLaboratory of Tumor Biology, Department of Experimental Biology, Faculty of Science, Masaryk University, 61137 Brno, Czech Republic. veselska@sci.muni.cz.
St. Anne's University Hospital Brno · CZMasaryk University · CZUniversity Hospital Brno · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoids represent a popular group of differentiation inducers that are successfully used in oncology for treatment of acute promyelocytic leukemia in adults and of neuroblastoma in children. The therapeutic potential of retinoids is based on their key role in the regulation of cell differentiation, growth, and apoptosis, which provides a basis for their use both in cancer therapy and chemoprevention. Nevertheless, patients treated with retinoids often exhibit or develop resistance to this therapy. Although resistance to retinoids is commonly categorized as either acquired or intrinsic, resistance as a single phenotypic feature is usually based on the same mechanisms that are closely related or combined in both of these types. In this review, we summarize the most common changes in retinoid metabolism and action that may affect the sensitivity of a tumor cell to treatment with retinoids. The availability of retinoids can be regulated by alterations in retinol metabolism or in retinoid intracellular transport, by degradation of retinoids or by their efflux from the cell. Retinoid effects on gene expression can be regulated via retinoid receptors or via other molecules in the transcriptional complex. Finally, the role of small-molecular-weight inhibitors of altered cell signaling pathways in overcoming the resistance to retinoids is also suggested.

Indexed as

AnimalsBiological TransportCell DifferentiationDrug Resistance, NeoplasmHumansReceptors, Retinoic AcidRetinoidsTranscription, GeneticReceptors, Retinoic AcidRetinoidscell differentiationdifferentiation therapymechanisms of resistanceretinoids

Identifiers

PMID29301374
PMCPMC5796081
OpenAlexW2781532209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.