Evidence map›Paper›PMID 28176176›Full record

ArticleBreast cancer research and treatment2017

Amplification of SOX4 promotes PI3K/Akt signaling in human breast cancer.

Gaurav A Mehta, Joel S Parker, Grace O Silva, Katherine A Hoadley, Charles M Perou, Michael L Gatza

Open access · greenAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

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  16. Multi-Omics Analysis ofJournal of personalized medicine · 2021
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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

6 authors at 3 institutions in 1 country.

Gaurav A MehtaRutgers Cancer Institute of New Jersey, 195 Little Albany Street, CINJ 4558, New Brunswick, NJ, 08903, USA.
Joel S ParkerLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Grace O SilvaLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Katherine A HoadleyLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Charles M PerouLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Michael L GatzaRutgers Cancer Institute of New Jersey, 195 Little Albany Street, CINJ 4558, New Brunswick, NJ, 08903, USA. michael.gatza@cinj.rutgers.edu.
University of North Carolina at Chapel Hill · USRutgers Cancer Institute of New JerseyRutgers, The State University of New Jersey · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KATHERINE A. HOADLEY · 1992 to 2026
$59.3M
Therapeutic Targeting of Breast Cancer Tumor Initiating CellsR01CA148761 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEROU, CHARLES M, ROSEN, JEFFREY MARK · 2010 to 2025
$6.5M
A Pathway-based approach to investigate oncogenic mechanisms in ovarian cancerR00CA166228 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI GATZA, MICHAEL L · 2015 to 2017
$747k
NCI NIH HHS P30 CA016086NCI NIH HHS P50 CA058223NCI NIH HHS R00 CA166228NCI NIH HHS R01 CA148761
6 · The paper itself

Abstract

purposeThe PI3K/Akt signaling axis contributes to the dysregulation of many dominant features in breast cancer including cell proliferation, survival, metabolism, motility, and genomic instability. While multiple studies have demonstrated that basal-like or triple-negative breast tumors have uniformly high PI3K/Akt activity, genomic alterations that mediate dysregulation of this pathway in this subset of highly aggressive breast tumors remain to be determined.

methodsIn this study, we present an integrated genomic analysis based on the use of a PI3K gene expression signature as a framework to analyze orthogonal genomic data from human breast tumors, including RNA expression, DNA copy number alterations, and protein expression. In combination with data from a genome-wide RNA-mediated interference screen in human breast cancer cell lines, we identified essential genetic drivers of PI3K/Akt signaling.

resultsOur in silico analyses identified SOX4 amplification as a novel modulator of PI3K/Akt signaling in breast cancers and in vitro studies confirmed its role in regulating Akt phosphorylation.

conclusionsTaken together, these data establish a role for SOX4-mediated PI3K/Akt signaling in breast cancer and suggest that SOX4 may represent a novel therapeutic target and/or biomarker for current PI3K family therapies.

Indexed as

Gene AmplificationSignal TransductionBreast NeoplasmsCell Line, TumorComputational BiologyDatabases, GeneticDNA Copy Number VariationsFemaleGene Expression ProfilingHumansNeoplasms, Basal CellPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSOXC Transcription FactorsTranscriptomePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSOX4 protein, humanSOXC Transcription FactorsAktBreast cancerGenomicsPI3 kinaseSOX4

Identifiers

PMID28176176
PMCPMC5334195
OpenAlexW2587577423

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.