Evidence map›Paper›PMID 26835364›Full record

ReviewTranslational pediatrics2015

Down syndrome and leukemia: insights into leukemogenesis and translational targets.

Marion K Mateos, Draga Barbaric, Sally-Anne Byatt, Rosemary Sutton, Glenn M Marshall

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Translational pediatrics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.4field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

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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.

Marion K Mateos1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.
Draga Barbaric1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.
Sally-Anne Byatt1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.
Rosemary Sutton1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.
Glenn M Marshall1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.
Sydney Children's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Children with Down syndrome (DS) have a significantly increased risk of childhood leukemia, in particular acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic leukemia (DS-ALL). A pre-leukemia, called transient myeloproliferative disorder (TMD), characterised by a GATA binding protein 1 (GATA1) mutation, affects up to 30% of newborns with DS. In most cases, the pre-leukemia regresses spontaneously, however one-quarter of these children will go on to develop AMKL or myelodysplastic syndrome (MDS) . AMKL and MDS occurring in young children with DS and a GATA1 somatic mutation are collectively termed myeloid leukemia of Down syndrome (ML-DS). This model represents an important multi-step process of leukemogenesis, and further study is required to identify therapeutic targets to potentially prevent development of leukemia. DS-ALL is a high-risk leukemia and mutations in the JAK-STAT pathway are frequently observed. JAK inhibitors may improve outcome for this type of leukemia. Genetic and epigenetic studies have revealed likely candidate drivers involved in development of ML-DS and DS-ALL. Overall this review aims to identify potential impacts of new research on how we manage children with DS, pre-leukemia and leukemia.

Indexed as

(3-5)-MeSH headingschildrenDown syndrome (DS)leukemiapreleukemiatransient myeloproliferative disorder (TMD) of Down syndrome

Identifiers

PMID26835364
PMCPMC4729084
OpenAlexW2174965652

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.