Evidence map›Paper›PMID 23932236›Full record

ReviewBlood cells, molecules & diseases2013

The impact of trisomy 21 on foetal haematopoiesis.

Irene Roberts, David O'Connor, Anindita Roy, Gillian Cowan, Paresh Vyas

Open access · greenAbstract readReview
In one paragraph

Review in Blood cells, molecules & diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Evolution of myeloid leukemia in children with Down syndrome.International journal of hematology · 2016
    Review
  6. Article
  7. 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

5 authors at 2 institutions in 1 country.

Irene RobertsCentre for Haematology, Imperial College London, UK. Electronic address: irene.roberts@imperial.ac.uk.
David O'Connor
Anindita Roy
Gillian Cowan
Paresh Vyas
Imperial College London · GBUniversity of Oxford · GB

Funding

Medical Research Council G1000729Medical Research Council MC_U137961146Medical Research Council MC_UU_12009/11
6 · The paper itself

Abstract

The high frequency of a unique neonatal preleukaemic syndrome, transient abnormal myelopoiesis (TAM), and subsequent acute myeloid leukaemia in early childhood in patients with trisomy 21 (Down syndrome) points to a specific role for trisomy 21 in transforming foetal haematopoietic cells. N-terminal truncating mutations in the key haematopoietic transcription factor GATA1 are acquired during foetal life in virtually every case. These mutations are not leukaemogenic in the absence of trisomy 21. In mouse models, deregulated expression of chromosome 21-encoded genes is implicated in leukaemic transformation, but does not recapitulate the effects of trisomy 21 in a human context. Recent work using primary human foetal liver and bone marrow cells, human embryonic stem cells and iPS cells shows that prior to acquisition of GATA1 mutations, trisomy 21 itself alters human foetal haematopoietic stem cell and progenitor cell biology causing multiple abnormalities in myelopoiesis and B-lymphopoiesis. The molecular basis by which trisomy 21 exerts these effects is likely to be extremely complex, to be tissue-specific and lineage-specific and to be dependent on ontogeny-related characteristics of the foetal microenvironment.

Indexed as

Chromosomes, Human, Pair 21Fetal DevelopmentTrisomyAnimalsCellular MicroenvironmentDown SyndromeHematopoiesisHumansLeukemiaMiceAcute megakaryoblastic leukaemiaacute myeloid leukaemia in Down syndromeDown syndromeDSembryonic stemESFoetal liverhaematopoietic stem cellHSCIGFinduced pluripotent steminsulin-like growth factoriPSmegakaryocytemegakaryocyte–erythroid progenitorMEPMKML-DSMPPmultipotential progenitorNeonatal leukaemiaTAMtransient abnormal myelopoiesisTransient abnormal myelopoiesisTrisomy 21

Identifiers

PMID23932236
PMCPMC4727253
OpenAlexW1998822827

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.