Evidence map›Paper›PMID 22139081›Full record

ArticleOncogene2012

Modeling invasive breast cancer: growth factors propel progression of HER2-positive premalignant lesions.

C-R Pradeep, A Zeisel, W J Köstler, M Lauriola, J Jacob-Hirsch, B Haibe-Kains, N Amariglio, N Ben-Chetrit, A Emde, I Solomonov and 8 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 15% 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, 42 citations in OpenAlex.

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  16. PKCα Attenuates Jagged-1-Mediated Notch Signaling in ErbB-2-Positive Breast Cancer to Reverse Trastuzumab Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 6 institutions in 3 countries.

C-R PradeepDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
A Zeisel
W J Köstler
M Lauriola
J Jacob-Hirsch
B Haibe-Kains
N Amariglio
N Ben-Chetrit
A Emde
I Solomonov
G Neufeld
M Piccart
I Sagi
C Sotiriou
G Rechavi
E Domany
C Desmedt
Y Yarden
Weizmann Institute of Science · ILInstitut Jules Bordet · BETel Aviv University · ILMedical University of Vienna · ATTechnion – Israel Institute of Technology · ILUniversité Libre de Bruxelles · BE

Funding

Next generation strategies to intercept ErbB signalingR37CA072981 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI YARDEN, YOSEF · 2005 to 2014
$2.3M
LATERAL VERSUS VERTICAL SIGNALING BY ERBB2 ONCOPROTEINR01CA072981 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI YARDEN, YOSEF NONE · 1997 to 2004
$953k
NCI NIH HHS CA72981NCI NIH HHS R01 CA072981NCI NIH HHS R37 CA072981
6 · The paper itself

Abstract

The HER2/neu oncogene encodes a receptor-like tyrosine kinase whose overexpression in breast cancer predicts poor prognosis and resistance to conventional therapies. However, the mechanisms underlying aggressiveness of HER2 (human epidermal growth factor receptor 2)-overexpressing tumors remain incompletely understood. Because it assists epidermal growth factor (EGF) and neuregulin receptors, we overexpressed HER2 in MCF10A mammary cells and applied growth factors. HER2-overexpressing cells grown in extracellular matrix formed filled spheroids, which protruded outgrowths upon growth factor stimulation. Our transcriptome analyses imply a two-hit model for invasive growth: HER2-induced proliferation and evasion from anoikis generate filled structures, which are morphologically and transcriptionally analogous to preinvasive patients' lesions. In the second hit, EGF escalates signaling and transcriptional responses leading to invasive growth. Consistent with clinical relevance, a gene expression signature based on the HER2/EGF-activated transcriptional program can predict poorer prognosis of a subgroup of HER2-overexpressing patients. In conclusion, the integration of a three-dimensional cellular model and clinical data attributes progression of HER2-overexpressing lesions to EGF-like growth factors acting in the context of the tumor's microenvironment.

Indexed as

Models, BiologicalAnoikisBreast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorCell ProliferationCell Transformation, NeoplasticErb-b2 Receptor Tyrosine KinasesExtracellular MatrixFemaleGene Expression ProfilingHumansIntercellular Signaling Peptides and ProteinsMammary Glands, HumanNeoplasm InvasivenessPrecancerous ConditionsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesIntercellular Signaling Peptides and Proteins

Identifiers

PMID22139081
PMCPMC3616212
OpenAlexW2057716292

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.