Evidence map›Paper›PMID 16645228›Full record

ReviewMedical oncology (Northwood, London, England)2006

Impact of growth factors in the regulation of apoptosis in low-risk myelodysplastic syndromes.

R Tehranchi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Trial
  2. Trial
  3. 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

1 author at 1 institution in 1 country.

R TehranchiHematopoietic Stem Cell Laboratory, Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, SE-22184 Lund, Sweden. Ramin.Tehranchi@stemcell.lu.se
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased apoptosis of hematopoietic progenitors is a hallmark of myelodysplastic syndromes (MDS) and results in ineffective hematopoiesis. Erythroid apoptosis is thought to be the main mechanism underlying the severe anemia observed in the low-risk subgroups, refractory anemia (RA) and RA with ringed sideroblasts (RARS). Treatment with erythropoietin (Epo) alone or in combination with granulocyte colony-stimulating factor (G-CSF) may significantly improve anemia and reduce bone marrow apoptosis. A synergistic effect between Epo and G-CSF has been observed in the clinic, in particular in RARS. However, the molecular mechanisms beyond the anti-apoptotic effect of these growth factors have not been fully understood. This paper outlines the potential mechanisms underlying the augmented apoptosis during the erythroid differentiation in low-risk MDS as well as the anti-apoptotic effect of the growth factors.

Indexed as

ApoptosisCell DifferentiationDNA, MitochondrialErythropoietinFerritinsGranulocyte Colony-Stimulating FactorHematopoiesisHumansMutationMyelodysplastic SyndromesPrognosisDNA, MitochondrialErythropoietinFerritinsGranulocyte Colony-Stimulating Factor

Identifiers

PMID16645228
OpenAlexW2133016731

What OpenQuestion holds

Textmetadata
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.