Evidence map›Paper›PMID 31717629›Full record

ReviewInternational journal of molecular sciences2019

Druggable Biochemical Pathways and Potential Therapeutic Alternatives to Target Leukemic Stem Cells and Eliminate the Residual Disease in Chronic Myeloid Leukemia.

Fabien Muselli, Jean-François Peyron, Didier Mary

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Design, Synthesis, and Biological Evaluation ofPharmaceuticals (Basel, Switzerland) · 2026
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  6. Biological evaluation of combinations of tyrosine kinase inhibitors with Inecalcitol as novel treatments for human chronic myeloid leukemia.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
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  7. Review
  8. Article
  9. Article
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  15. Review
  16. Drug Resistance in Hematological Malignancies.International journal of molecular sciences · 2020
    Article
  17. Article
  18. Article
  19. Review
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 1 institution in 1 country.

Fabien MuselliUniversité Côte d'Azur, Institut National de la Santé et de la Recherche Médicale (Inserm) U1065, Centre Méditerranéen de Médecine Moléculaire, CEDEX 3, 06204 Nice, France.ORCID 0000-0002-6654-9472
Jean-François PeyronUniversité Côte d'Azur, Institut National de la Santé et de la Recherche Médicale (Inserm) U1065, Centre Méditerranéen de Médecine Moléculaire, CEDEX 3, 06204 Nice, France.
Didier MaryUniversité Côte d'Azur, Institut National de la Santé et de la Recherche Médicale (Inserm) U1065, Centre Méditerranéen de Médecine Moléculaire, CEDEX 3, 06204 Nice, France.ORCID 0000-0003-4136-3556
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic Myeloid Leukemia (CML) is a disease arising in stem cells expressing the BCR-ABL oncogenic tyrosine kinase that transforms one Hematopoietic stem/progenitor Cell into a Leukemic Stem Cell (LSC) at the origin of differentiated and proliferating leukemic cells in the bone marrow (BM). CML-LSCs are recognized as being responsible for resistances and relapses that occur despite the advent of BCR-ABL-targeting therapies with Tyrosine Kinase Inhibitors (TKIs). LSCs share a lot of functional properties with Hematopoietic Stem Cells (HSCs) although some phenotypical and functional differences have been described during the last two decades. Subverted mechanisms affecting epigenetic processes, apoptosis, autophagy and more recently metabolism and immunology in the bone marrow microenvironment (BMM) have been reported. The aim of this review is to bring together the modifications and molecular mechanisms that are known to account for TKI resistance in primary CML-LSCs and to focus on the potential solutions that can circumvent these resistances, in particular those that have been, or will be tested in clinical trials.

Indexed as

Fusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplasm, ResidualNeoplastic Stem CellsProtein Kinase InhibitorsTumor MicroenvironmentFusion Proteins, bcr-ablProtein Kinase Inhibitorsapoptosisautophagychronic myeloid leukemiaclinical trialsepigeneticleukemic stem cellsmetabolismmicroenvironmentresistancetyrosine kinase inhibitors

Identifiers

PMID31717629
PMCPMC6888542
OpenAlexW2983410423

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.