Evidence map›Paper›PMID 16990774›Full record

ReviewLeukemia2006

Megakaryocytic dysfunction in myelodysplastic syndromes and idiopathic thrombocytopenic purpura is in part due to different forms of cell death.

E J Houwerzijl, N R Blom, J J L van der Want, E Vellenga, J T M de Wolf

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00961064 (A Pilot Study of a Thrombopoietin-Receptor Agonist), which is not on this map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 18% 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.

NCT00961064 phase2completednot on this mapstarted 2011, after this paper: background citation

A Pilot Study of a Thrombopoietin-Receptor Agonist (TPO-R Agonist), Eltrombopag, in Patients With Low to Int-2 Risk Myelodysplastic Syndrome (MDS)

TypeinterventionalSponsorNational Heart, Lung, and Blood Institute (NHLBI)Ran2011 to 2021Enrolled30ConditionsMyelodysplastic Syndromes, ThrombocytopeniaArmsEltrombopag
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Role of autophagy in megakaryocyte differentiation and platelet formation.International journal of physiology, pathophysiology and pharmacology · 2016
    Review
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

E J HouwerzijlDepartment of Hematology, University Medical Center Groningen, Groningen, The Netherlands. e.j.houwerzijl@int.umcg.nl
N R Blom
J J L van der Want
E Vellenga
J T M de Wolf
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelet production requires compartmentalized caspase activation within megakaryocytes. This eventually results in platelet release in conjunction with apoptosis of the remaining megakaryocyte. Recent studies have indicated that in low-risk myelodysplastic syndromes (MDS) and idiopathic thrombocytopenic purpura (ITP), premature cell death of megakaryocytes may contribute to thrombocytopenia. Different cell death patterns have been identified in megakaryocytes in these disorders. Growing evidence suggests that, besides apoptosis, necrosis and autophagic cell death, may also be programmed. Therefore, programmed cell death (PCD) can be classified in apoptosis, a caspase-dependent process, apoptosis-like, autophagic and necrosis-like PCD, which are predominantly caspase-independent processes. In MDS, megakaryocytes show features of necrosis-like PCD, whereas ITP megakaryocytes demonstrate predominantly characteristics of apoptosis-like PCD (para-apoptosis). Triggers for these death pathways are largely unknown. In MDS, the interaction of Fas/Fas-ligand might be of importance, whereas in ITP antiplatelet autoantibodies recognizing common antigens on megakaryocytes and platelets might be involved. These findings illustrate that cellular death pathways in megakaryocytes are recruited in both physiological and pathological settings, and that different forms of cell death can occur in the same cell depending on the stimulus and the cellular context. Elucidation of the underlying mechanisms might lead to novel therapeutic interventions.

Indexed as

ApoptosisAutophagyHumansMegakaryocytesMyelodysplastic SyndromesNecrosisPurpura, Thrombocytopenic, Idiopathic

Identifiers

PMID16990774
OpenAlexW2145859825

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.