Evidence map›Paper›PMID 24070327›Full record

ReviewBioscience reports2013

Multidrug resistance in chronic myeloid leukaemia: how much can we learn from MDR-CML cell lines?

Vivian M Rumjanek, Raphael S Vidal, Raquel C Maia

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Identification of HRSC advances · 2019
    Article
  12. Article
  13. Article
  14. Tendency of K562 Chronic Myeloid Leukemia Cells Towards Cell ReprogrammingTurkish journal of haematology : official journal of Turkish Society of Haematology · 2018
    Article
  15. Article
  16. Inhibition of Siah2 Ubiquitin Ligase by Vitamin K3 Attenuates Chronic Myeloid Leukemia Chemo-Resistance in Hypoxic Microenvironment.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Encapsulation ofInternational journal of nanomedicine · 2017
    Article
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

3 authors at 2 institutions in 1 country.

Vivian M Rumjanek*Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Raphael S Vidal*Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Raquel C Maia†Programa de Pesquisa em Hemato-Oncologia Molecular, Instituto Nacional de Câncer (INCA), Rio de Janeiro, Brazil.
Universidade Federal do Rio de Janeiro · BRInstituto Nacional do Câncer · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hallmark of CML (chronic myeloid leukaemia) is the BCR (breakpoint cluster region)-ABL fusion gene. CML evolves through three phases, based on both clinical and pathological features: a chronic phase, an accelerated phase and blast crisis. TKI (tyrosine kinase inhibitors) are the treatment modality for patients with chronic phase CML. The therapeutic potential of the TKI imatinib is affected by BCR-ABL dependent an independent mechanisms. Development of MDR (multidrug resistance) contributes to the overall clinical resistance. MDR involves overexpression of ABC -transporters (ATP-binding-cassette transporter) among other features. MDR studies include the analysis of cancer cell lines selected for resistance. CML blast crisis is accompanied by increased resistance to apoptosis. This work reviews the role played by the influx transporter OCT1 (organic cation transporter 1), by efflux ABC transporters, molecules involved in the modulation of apoptosis (p53, Bcl-2 family, CD95, IAPs (inhibitors of apoptosis protein)], Hh and Wnt/β-catenin pathways, cytoskeleton abnormalities and other features described in leukaemic cells of clinical samples and CML cell lines. An MDR cell line, Lucena-1, generated from K562 by stepwise exposure to vincristine, was used as our model and some potential anticancer drugs effective against the MDR cell line and patients' samples are presented.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsATP-Binding Cassette TransportersCalcium SignalingCell Line, TumorCytoskeletonDrug Resistance, MultipleDrug Screening Assays, AntitumorHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsOrganic Cation Transporter 1Wnt Signaling PathwayAntineoplastic AgentsApoptosis Regulatory ProteinsATP-Binding Cassette TransportersOrganic Cation Transporter 1

Identifiers

PMID24070327
PMCPMC3839595
OpenAlexW2012149136

What OpenQuestion holds

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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.