Evidence map›Paper›PMID 22127311›Full record

ReviewBest practice & research. Clinical haematology2011

Genomic profiling of B-progenitor acute lymphoblastic leukemia.

Charles G Mullighan

Abstract readReview
In one paragraph

Review in Best practice & research. Clinical haematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-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

27 citing papers in PubMed, 56 citations in OpenAlex.

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  12. Long Non-Coding RNA and Acute Leukemia.International journal of molecular sciences · 2019
    Review
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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

1 author at 1 institution in 1 country.

Charles G MullighanDepartment of Pathology, St Jude Children's Research Hospital, Memphis, TN 38105, USA. Charles.mullighan@stjude.org
St. Jude Children's Research Hospital · US

Funding

Identifying the spectrum of genetic alterations in high risk ALLRC4CA156329 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI HUNGER, STEPHEN PATRICK, LOH, MIGNON LEE-CHEUN · 2010 to 2010
$1.6M
NCI NIH HHS RC4 CA156329
6 · The paper itself

Abstract

Childhood acute lymphoblastic leukemia (ALL) is comprised of multiple subtypes defined by recurring chromosomal alterations that are important events in leukemogenesis and are widely used in diagnosis and risk stratification, yet fail to fully explain the biology of this disease. In the last 5 years, genome-wide profiling of gene expression, structural DNA alterations and sequence variations has yielded important insights into the nature of submicroscopic genetic alterations that define novel subgroups of acute lymphoblastic leukemia and cooperate with known cytogenetic alterations in leukemogenesis. Importantly, several of these alterations are important determinants of risk of relapse and are potential targets for therapeutic intervention. Here, these advances and future directions in the genomic analysis of ALL are discussed.

Indexed as

Chromosome AberrationsMutationAnimalsB-LymphocytesChildChild, PreschoolCREB-Binding ProteinFusion Proteins, bcr-ablGene Expression ProfilingGene Expression Regulation, NeoplasticGenomicsHumansIkaros Transcription FactorJanus Kinase 1Janus Kinase 2MiceCREB-Binding ProteinCREBBP protein, humanCRLF2 protein, humanFusion Proteins, bcr-ablIkaros Transcription FactorIKZF1 protein, humanJAK1 protein, humanJAK2 protein, humanJanus Kinase 1Janus Kinase 2PAX5 protein, humanPAX5 Transcription FactorReceptors, Cytokine

Identifiers

PMID22127311
PMCPMC3249426
OpenAlexW2146748994

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.