Evidence map›Paper›PMID 25394715›Full record

ReviewLeukemia2015

Myelodysplasia is in the niche: novel concepts and emerging therapies.

E Bulycheva, M Rauner, H Medyouf, I Theurl, M Bornhäuser, L C Hofbauer, U Platzbecker

Open access · bronzeAbstract readReview
In one paragraph

Review in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.4field-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

45 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Iron-Loading Anemias.Advances in experimental medicine and biology · 2025
    Review
  3. Bone Marrow Microenvironment Involvement in t-MN: Focus on Mesenchymal Stem Cells.Mediterranean journal of hematology and infectious diseases · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Role of Iron in Benign and Malignant Hematopoiesis.Antioxidants & redox signaling · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. 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

7 authors at 2 institutions in 2 countries.

E BulychevaMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl-Gustav-Carus, Technische Universität, Dresden, Germany.
M RaunerMedizinische Klinik und Poliklinik III, Universitätsklinikum Carl-Gustav-Carus, Technische Universität, Dresden, Germany.
H MedyoufGeorg-Speyer-Haus, Institut for Tumor Biology and Experimental Therapy, 60596, Frankfurt am Main, Germany.
I TheurlDepartment of Internal Medicine VI, Medical University of Innsbruck, Innsbruck, Austria.
M Bornhäuser1] Medizinische Klinik und Poliklinik I, Universitätsklinikum Carl-Gustav-Carus, Technische Universität, Dresden, Germany [2] Center for Regenerative Therapies Dresden, Technical University, Dresden, Germany.
L C Hofbauer1] Medizinische Klinik und Poliklinik III, Universitätsklinikum Carl-Gustav-Carus, Technische Universität, Dresden, Germany [2] Center for Regenerative Therapies Dresden, Technical University, Dresden, Germany.
U PlatzbeckerMedizinische Klinik und Poliklinik I, Universitätsklinikum Carl-Gustav-Carus, Technische Universität, Dresden, Germany.
TU Dresden · DEUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelodysplastic syndromes (MDSs) represent clonal disorders mainly of the elderly that are characterized by ineffective hematopoiesis and an increased risk of transformation into acute myeloid leukemia. The pathogenesis of MDS is thought to evolve from accumulation and selection of specific genetic or epigenetic events. Emerging evidence indicates that MDS is not solely a hematopoietic disease but rather affects the entire bone marrow microenvironment, including bone metabolism. Many of these cells, in particular mesenchymal stem and progenitor cells (MSPCs) and osteoblasts, express a number of adhesion molecules and secreted factors that regulate blood regeneration throughout life by contributing to hematopoietic stem and progenitor cell (HSPC) maintenance, self-renewal and differentiation. Several endocrine factors, such as erythropoietin, parathyroid hormone and estrogens, as well as deranged iron metabolism modulate these processes. Thus, interactions between MSPC and HSPC contribute to the pathogenesis of MDS and associated pathologies. A detailed understanding of these mechanisms may help to define novel targets for diagnosis and possibly therapy. In this review, we will discuss the scientific rationale of 'osteohematology' as an emerging research field in MDS and outline clinical implications.

Indexed as

AnimalsBone MarrowCytokinesDisease ProgressionEpigenesis, GeneticErythropoietinHematopoietic Stem CellsHumansIronIron OverloadMesenchymal Stem CellsMyelodysplastic SyndromesOsteoblastsParathyroid HormoneSignal TransductionCytokinesErythropoietinIronParathyroid Hormone

Identifiers

PMID25394715
PMCPMC4320287
OpenAlexW2056832420

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.