Evidence map›Paper›PMID 31945226›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Tyrosine kinase inhibitors and interferon-α increase tunneling nanotube (TNT) formation and cell adhesion in chronic myeloid leukemia (CML) cell lines.

Maria Omsland, Vibeke Andresen, Stein-Erik Gullaksen, Pilar Ayuda-Durán, Mihaela Popa, Randi Hovland, Atle Brendehaug, Jorrit Enserink, Emmet McCormack, Bjørn Tore Gjertsen

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Tunneling Nanotubes: A New Target for Nanomedicine?International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. 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

10 authors at 3 institutions in 2 countries.

Maria OmslandCentre for Cancer Biomarkers CCBIO, Department of Clinical Science, University of Bergen, Bergen, Norway.
Vibeke AndresenCentre for Cancer Biomarkers CCBIO, Department of Clinical Science, University of Bergen, Bergen, Norway.
Stein-Erik GullaksenCentre for Cancer Biomarkers CCBIO, Department of Clinical Science, University of Bergen, Bergen, Norway.
Pilar Ayuda-DuránDepartment of Molecular Cell Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Mihaela PopaDepartment of Internal Medicine, Hematology Section, Haukeland University Hospital, Bergen, Norway.
Randi HovlandDepartment of Medical Genetics, Haukeland University Hospital, Bergen, Norway.
Atle BrendehaugDepartment of Medical Genetics, Haukeland University Hospital, Bergen, Norway.
Jorrit EnserinkDepartment of Molecular Cell Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.
Emmet McCormackCentre for Cancer Biomarkers CCBIO, Department of Clinical Science, University of Bergen, Bergen, Norway.
Bjørn Tore GjertsenCentre for Cancer Biomarkers CCBIO, Department of Clinical Science, University of Bergen, Bergen, Norway.
Haukeland University Hospital · NOUniversity of Bergen · NOOslo University Hospital · NO

Funding

NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a stem cell disease of the bone marrow where mechanisms of inter-leukemic communication and cell-to-cell interactions are proposed to be important for optimal therapy response. Tunneling nanotubes (TNTs) are novel intercellular communication structures transporting different cargos with potential implications in therapy resistance. Here, we have investigated TNTs in CML cells and following treatment with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon-α (IFNα). CML cells from chronic phase CML patients as well as the blast crisis phase cell lines, Kcl-22 and K562, formed few or no TNTs. Treatment with imatinib increased TNT formation in both Kcl-22 and K562 cells, while nilotinib or IFNα increased TNTs in Kcl-22 cells only where the TNT increase was associated with adherence to fibronectin-coated surfaces, altered morphology, and reduced movement involving β1integrin. Ex vivo treated cells from chronic phase CML patients showed limited changes in TNT formation similarly to bone marrow cells from healthy individuals. Interestingly, in vivo nilotinib treatment in a Kcl-22 subcutaneous mouse model resulted in morphological changes and TNT-like structures in the tumor-derived Kcl-22 cells. Our results demonstrate that CML cells express low levels of TNTs, but CML therapeutics increase TNT formation in designated cell models indicating TNT functionality in bone marrow derived malignancies and their microenvironment.

Indexed as

AnimalsCell AdhesionCell CommunicationCell Line, TumorCells, CulturedFemaleFluorescent Antibody TechniqueHumansImmunoblottingIntegrin beta1Interferon-alphaK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMicroscopy, Electron, ScanningProtein Kinase InhibitorsIntegrin beta1Interferon-alphaProtein Kinase Inhibitorscell adhesionchronic myeloid leukemiainterferon-αtunneling nanotubestyrosine kinase inhibitors

Identifiers

PMID31945226
PMCPMC10894852
OpenAlexW2998946380

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Registered trials

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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.