Evidence map›Paper›PMID 20932292›Full record

ArticleBMC cancer2010

Genome profiling of ERBB2-amplified breast cancers.

Fabrice Sircoulomb, Ismahane Bekhouche, Pascal Finetti, José Adélaïde, Azza Ben Hamida, Julien Bonansea, Stéphane Raynaud, Charlène Innocenti, Emmanuelle Charafe-Jauffret, Carole Tarpin and 6 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 5 pooled it
7.9field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 5 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
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  12. CDK12 and CDK13 in oncology: from RNA regulation to therapeutic targeting.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  13. Article
  14. Dual Modes of Gene Regulation by CDK12.bioRxiv : the preprint server for biology · 2025
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  16. Article
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  18. Machine Learning for Detecting and Analyzing Chromoanagenesis Events.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
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  20. Article

39 more citing papers are in PubMed but not listed here.

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

16 authors at 5 institutions in 2 countries.

Fabrice SircoulombMarseille Cancer Research Center, UMR891 Inserm, Institut Paoli-Calmettes, Department of Molecular Oncology, Marseille, France.
Ismahane Bekhouche
Pascal Finetti
José Adélaïde
Azza Ben Hamida
Julien Bonansea
Stéphane Raynaud
Charlène Innocenti
Emmanuelle Charafe-Jauffret
Carole Tarpin
Farhat Ben Ayed
Patrice Viens
Jocelyne Jacquemier
François Bertucci
Daniel Birnbaum
Max Chaffanet
Institut Paoli-Calmettes · FRInstitut Pprime · FRInserm · FRInstitut de Neurobiologie de la Méditerranée · FRInstitut Salah-Azaïz · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAround 20% of breast cancers (BC) show ERBB2 gene amplification and overexpression of the ERBB2 tyrosine kinase receptor. They are associated with a poor prognosis but can benefit from targeted therapy. A better knowledge of these BCs, genomically and biologically heterogeneous, may help understand their behavior and design new therapeutic strategies.

methodsWe defined the high resolution genome and gene expression profiles of 54 ERBB2-amplified BCs using 244K oligonucleotide array-comparative genomic hybridization and whole-genome DNA microarrays. Expression of ERBB2, phosphorylated ERBB2, EGFR, IGF1R and FOXA1 proteins was assessed by immunohistochemistry to evaluate the functional ERBB2 status and identify co-expressions.

resultsFirst, we identified the ERBB2-C17orf37-GRB7 genomic segment as the minimal common 17q12-q21 amplicon, and CRKRS and IKZF3 as the most frequent centromeric and telomeric amplicon borders, respectively. Second, GISTIC analysis identified 17 other genome regions affected by copy number aberration (CNA) (amplifications, gains, losses). The expression of 37 genes of these regions was deregulated. Third, two types of heterogeneity were observed in ERBB2-amplified BCs. The genomic profiles of estrogen receptor-positive (ER+) and negative (ER-) ERBB2-amplified BCs were different. The WNT/β-catenin signaling pathway was involved in ER- ERBB2-amplified BCs, and PVT1 and TRPS1 were candidate oncogenes associated with ER+ ERBB2-amplified BCs. The size of the ERBB2 amplicon was different in inflammatory (IBC) and non-inflammatory BCs. ERBB2-amplified IBCs were characterized by the downregulated and upregulated mRNA expression of ten and two genes in proportion to CNA, respectively. IHC results showed (i) a linear relationship between ERBB2 gene amplification and its gene and protein expressions with a good correlation between ERBB2 expression and phosphorylation status; (ii) a potential signaling cross-talk between EGFR or IGF1R and ERBB2, which could influence response of ERBB2-positive BCs to inhibitors. FOXA1 was frequently coexpressed with ERBB2 but its expression did not impact on the outcome of patients with ERBB2-amplified tumors.

conclusionWe have shown that ER+ and ER- ERBB2-amplified BCs are different, distinguished ERBB2 amplicons in IBC and non-IBC, and identified genomic features that may be useful in the design of alternative therapeutical strategies.

Indexed as

Gene Expression ProfilingGenome, HumanAdenocarcinomaBreast NeoplasmsCell Line, TumorCohort StudiesErb-b2 Receptor Tyrosine KinasesFemaleHumansImmunohistochemistryIn Situ Hybridization, FluorescenceNucleic Acid HybridizationOligonucleotide Array Sequence AnalysisPhosphorylationTreatment OutcomeERBB2 protein, humanErb-b2 Receptor Tyrosine Kinases

Identifiers

PMID20932292
PMCPMC2958950
OpenAlexW2092224388

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.