Evidence map›Paper›PMID 22343619›Full record

ArticleBritish journal of cancer2012

A network-based, integrative study to identify core biological pathways that drive breast cancer clinical subtypes.

B Dutta, L Pusztai, Y Qi, F André, V Lazar, G Bianchini, N Ueno, R Agarwal, B Wang, C Y Shiang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  5. The development of tumour vascular networks.Communications biology · 2021
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  15. Empirical inference of circuitry and plasticity in a kinase signaling network.Proceedings of the National Academy of Sciences of the United States of America · 2015
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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

14 authors at 4 institutions in 3 countries.

B DuttaDepartment of Systems Biology - Unit 950, The University of Texas MD Anderson Cancer Center, 7435 Fannin Street, Houston, TX 77054, USA.
L Pusztai
Y Qi
F André
V Lazar
G Bianchini
N Ueno
R Agarwal
B Wang
C Y Shiang
G N Hortobagyi
G B Mills
W F Symmans
G Balázsi
The University of Texas MD Anderson Cancer Center · USInstitut Gustave Roussy · FRCenter for Systems Biology · USImperial College London · GB

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Systems-Based Predictions of Responses to Cancer TherapyU54CA112970 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI GRAY, JOE W. · 2004 to 2014
$27.1M
NCI NIH HHS P30 CA016672NCI NIH HHS U54 CA112970
6 · The paper itself

Abstract

backgroundThe rapid collection of diverse genome-scale data raises the urgent need to integrate and utilise these resources for biological discovery or biomedical applications. For example, diverse transcriptomic and gene copy number variation data are currently collected for various cancers, but relatively few current methods are capable to utilise the emerging information.

methodsWe developed and tested a data-integration method to identify gene networks that drive the biology of breast cancer clinical subtypes. The method simultaneously overlays gene expression and gene copy number data on protein-protein interaction, transcriptional-regulatory and signalling networks by identifying coincident genomic and transcriptional disturbances in local network neighborhoods.

resultsWe identified distinct driver-networks for each of the three common clinical breast cancer subtypes: oestrogen receptor (ER)+, human epidermal growth factor receptor 2 (HER2)+, and triple receptor-negative breast cancers (TNBC) from patient and cell line data sets. Driver-networks inferred from independent datasets were significantly reproducible. We also confirmed the functional relevance of a subset of randomly selected driver-network members for TNBC in gene knockdown experiments in vitro. We found that TNBC driver-network members genes have increased functional specificity to TNBC cell lines and higher functional sensitivity compared with genes selected by differential expression alone.

conclusionClinical subtype-specific driver-networks identified through data integration are reproducible and functionally important.

Indexed as

Computer SimulationGene Regulatory NetworksModels, BiologicalProtein Interaction MapsBreast NeoplasmsCell Line, TumorDNA Copy Number VariationsEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesFemaleGene ExpressionGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenes, NeoplasmHumansERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesReceptors, EstrogenReceptors, Progesterone

Identifiers

PMID22343619
PMCPMC3304402
OpenAlexW2040957831

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.