Evidence map›Paper›PMID 21347161›Full record

ArticleSummit on translational bioinformatics2009

Analysis of AML Genes in Dysregulated Molecular Networks.

Eunjung Lee, Hyunchul Jung, Predrag Radivojac, Jong-Won Kim, Doheon Lee

Abstract read
In one paragraph

Article in Summit on translational bioinformatics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Eunjung LeeDepartment of Bio and Brain Engineering, KAIST, Daejeon 305-701, South Korea.
Hyunchul Jung
Predrag Radivojac
Jong-Won Kim
Doheon Lee

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdentifying disease causing genes and understanding their molecular mechanisms are essential to developing effective therapeutics. Thus, several computational methods have been proposed to prioritize candidate disease genes by integrating different data types, including sequence information, biomedical literature, and pathway information. Recently, molecular interaction networks have been incorporated to predict disease genes, but most of those methods do not utilize invaluable disease-specific information available in mRNA expression profiles of patient samples.

resultsThrough the integration of protein-protein interaction networks and gene expression profiles of acute myeloid leukemia (AML) patients, we identified subnetworks of interacting proteins dysregulated in AML and characterized known mutation genes causally implicated to AML embedded in the subnetworks. The analysis shows that the set of extracted subnetworks is a reservoir rich in AML genes reflecting key leukemogenic processes such as myeloid differentiation,

conclusionWe showed that the integrative approach both utilizing gene expression profiles and molecular networks could identify AML causing genes most of which were not detectable with gene expression analysis alone due to their minor changes in mRNA.

Identifiers

PMID21347161
PMCPMC3041561

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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.