Evidence map›Paper›PMID 27355944›Full record

ReviewInternational journal of molecular sciences2016

Mesenchymal Stem and Progenitor Cells in Normal and Dysplastic Hematopoiesis-Masters of Survival and Clonality?

Lisa Pleyer, Peter Valent, Richard Greil

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Epigenetic Silencing ofInternational journal of molecular sciences · 2022
    Article
  6. Article
  7. Review
  8. Differential activation of CaNPJ Regenerative medicine · 2021
    Article
  9. Increasing cytosolic CaStem cell research · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Bone marrow niches in myeloid neoplasms.Pathology international · 2020
    Review
  16. Review
  17. Therapy-related acute myeloid leukemia and its prevention.American journal of blood research · 2020
    Review
  18. Article
  19. Review
  20. 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.

Lisa Pleyer3rd Medical Department with Hematology and Medical Oncology, Hemostaseology, Rheumatology and Infectious Diseases, Laboratory for Immunological and Molecular Cancer Research, Oncologic Center, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria. l.pleyer@salk.at.
Peter ValentDepartment of Internal Medicine I, Division of Hematology and Hemostaseology & Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, 1090 Vienna, Austria. peter.valent@meduniwien.ac.at.
Richard Greil3rd Medical Department with Hematology and Medical Oncology, Hemostaseology, Rheumatology and Infectious Diseases, Laboratory for Immunological and Molecular Cancer Research, Oncologic Center, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria. r.greil@salk.at.
Paracelsus Medical University · ATLudwig Boltzmann Institute for Cardiovascular Research · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic syndromes (MDS) are malignant hematopoietic stem cell disorders that have the capacity to progress to acute myeloid leukemia (AML). Accumulating evidence suggests that the altered bone marrow (BM) microenvironment in general, and in particular the components of the stem cell niche, including mesenchymal stem cells (MSCs) and their progeny, play a pivotal role in the evolution and propagation of MDS. We here present an overview of the role of MSCs in the pathogenesis of MDS, with emphasis on cellular interactions in the BM microenvironment and related stem cell niche concepts. MSCs have potent immunomodulatory capacities and communicate with diverse immune cells, but also interact with various other cellular components of the microenvironment as well as with normal and leukemic stem and progenitor cells. Moreover, compared to normal MSCs, MSCs in MDS and AML often exhibit altered gene expression profiles, an aberrant phenotype, and abnormal functional properties. These alterations supposedly contribute to the "reprogramming" of the stem cell niche into a disease-permissive microenvironment where an altered immune system, abnormal stem cell niche interactions, and an impaired growth control lead to disease progression. The current article also reviews molecular targets that play a role in such cellular interactions and possibilities to interfere with abnormal stem cell niche interactions by using specific targeted drugs.

Indexed as

AnimalsBone Marrow CellsEpithelial-Mesenchymal TransitionHematopoiesisHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteMesenchymal Stem CellsMyelodysplastic SyndromesSignal TransductionStem Cell Nicheacute myeloid leukemia (AML)bone marrow stem cell nicheendothelial-to-mesenchymal transitionepithelial-to-mesenchymal transitionimmunomodulationleukemic nichemesenchymal stem cells (MSC)microenvironmentmyelodysplastic syndromes (MDS)neoplastic stem cells

Identifiers

PMID27355944
PMCPMC4964385
OpenAlexW2471084888

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.