Evidence map›Paper›PMID 28826860›Full record

ReviewExperimental hematology2017

The microenvironment in myelodysplastic syndromes: Niche-mediated disease initiation and progression.

Allison J Li, Laura M Calvi

Open access · greenAbstract readReview
In one paragraph

Review in Experimental hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Constitutive systemic inflammation in Shwachman-Diamond Syndrome.Molecular medicine (Cambridge, Mass.) · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. The Mesenchymal Niche in Myelodysplastic Syndromes.Diagnostics (Basel, Switzerland) · 2022
    Review
  17. VEXAS Syndrome: A Novelty in MDS Landscape.Diagnostics (Basel, Switzerland) · 2022
    Review
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Allison J LiDepartment of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Laura M CalviDivision of Endocrinology and Metabolism, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY. Electronic address: laura_calvi@urmc.rochester.edu.
University of Rochester · US

Funding

The University of Rochester's Clinical and Translational Science InstituteUL1TR002001 · NCATS · UNIVERSITY OF ROCHESTER · PI WILSON, KAREN M., ZAND, MARTIN S · 2016 to 2024
$34.6M
PGE2 mitigation of acute and late radiation injuryU01AI107276 · NIAID · UNIVERSITY OF ROCHESTER · PI CALVI, LAURA M, PALIS, JAMES · 2013 to 2017
$2.9M
Therapeutic Targeting of Leukemia-Microenvironmental InteractionsR01CA166280 · NCI · UNIVERSITY OF ROCHESTER · PI BECKER, MICHAEL W, CALVI, LAURA M · 2013 to 2017
$1.6M
Modulation of aged hematopoietic stem cell nichesR01AG046293 · NIA · UNIVERSITY OF ROCHESTER · PI BECKER, MICHAEL W, CALVI, LAURA M · 2013 to 2017
$954k
The University of Rochester Clinical and Translational Science InstituteTL1TR000096 · NCATS · UNIVERSITY OF ROCHESTER · PI BENNETT, NANCY M, KIEBURTZ, KARL D. · 2012 to 2015
$930k
Mechanism and mitigation of bone marrow microenvironment dysfunction in myelodysplastic syndrome.F30DK113727 · NIDDK · UNIVERSITY OF ROCHESTER · PI LI, ALLISON JINQUAN · 2017 to 2020
$199k
NCATS NIH HHS TL1 TR000096NCATS NIH HHS UL1 TR002001NCI NIH HHS R01 CA166280NIAID NIH HHS U01 AI107276NIA NIH HHS R01 AG046293NIDDK NIH HHS F30 DK113727
6 · The paper itself

Abstract

Myelodysplastic syndromes (MDSs) are clonal disorders of hematopoietic stem and progenitor cells and represent the most common cause of acquired marrow failure. Hallmarked by ineffective hematopoiesis, dysplastic marrow, and risk of transformation to acute leukemia, MDS remains a poorly treated disease. Although identification of hematopoietic aberrations in human MDS has contributed significantly to our understanding of MDS pathogenesis, evidence now identify the bone marrow microenvironment (BMME) as another key contributor to disease initiation and progression. With improved understanding of the BMME, we are beginning to refine the role of the hematopoietic niche in MDS. Despite genetic diversity in MDS, interaction between MDS and the BMME appears to be a common disease feature and therefore represents an appealing therapeutic target. Further understanding of the interdependent relationship between MDS and its niche is needed to delineate the mechanisms underlying hematopoietic failure and how the microenvironment can be targeted clinically. This review provides an overview of data from human MDS and murine models supporting a role for BMME dysfunction at several steps of disease pathogenesis. Although no models or human studies so far have combined all of these findings, we review current data identifying BMME involvement in each step of MDS pathogenesis organized to reflect the chronology of BMME contribution as the normal hematopoietic system becomes myelodysplastic and MDS progresses to marrow failure and transformation. Although microenvironmental heterogeneity and dysfunction certainly add complexity to this syndrome, data are already demonstrating that targeting microenvironmental signals may represent novel therapeutic strategies for MDS treatment.

Indexed as

Cellular MicroenvironmentStem Cell NicheBone Marrow CellsCell ProliferationClone CellsCytokinesDisease ProgressionHumansModels, BiologicalMyelodysplastic SyndromesCytokines

Identifiers

PMID28826860
PMCPMC5737956
OpenAlexW2749684771

What OpenQuestion holds

Textmetadata
LicenceTDM
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.