Evidence map›Paper›PMID 20628393›Full record

ArticleBritish journal of cancer2010

A gene on the HER2 amplicon, C35, is an oncogene in breast cancer whose actions are prevented by inhibition of Syk.

E Katz, S Dubois-Marshall, A H Sims, D Faratian, J Li, E S Smith, J A Quinn, M Edward, R R Meehan, E E Evans and 2 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

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  13. Molecular biology of the cell · 2019
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  16. Emerging targets in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2019
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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

12 authors at 6 institutions in 2 countries.

E KatzBreakthrough Research Unit and Division of Pathology, Institute of Genetics and Molecular Medicine, University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK. elad.katz@ed.ac.uk
S Dubois-Marshall
A H Sims
D Faratian
J Li
E S Smith
J A Quinn
M Edward
R R Meehan
E E Evans
S P Langdon
D J Harrison
Edinburgh Cancer Research · GBUniversity of Edinburgh · GBUniversity of Glasgow · GBVaccinex (United States) · USMRC Institute of Genetics and Molecular Medicine · GBUniversity of Rochester · US

Funding

Medical Research Council MC_U127574433
6 · The paper itself

Abstract

backgroundC35 is a 12 kDa membrane-anchored protein endogenously over-expressed in many invasive breast cancers. C35 (C17orf37) is located on the HER2 amplicon, between HER2 and GRB7. The function of over-expressed C35 in invasive breast cancer is unknown.

methodsTissue microarrays containing 122 primary human breast cancer specimens were used to examine the association of C35 with HER2 expression. Cell lines over-expressing C35 were generated and tested for evidence of cell transformation in vitro.

resultsIn primary breast cancers high levels of C35 mRNA expression were associated with HER2 gene amplification. High levels of C35 protein expression were associated with hallmarks of transformation, such as, colony growth in soft agar, invasion into collagen matrix and formation of large acinar structures in three-dimensional (3D) cell cultures. The transformed phenotype was also associated with characteristics of epithelial to mesenchymal transition, such as adoption of spindle cell morphology and down-regulation of epithelial markers, such as E-cadherin and keratin-8. Furthermore, C35-induced transformation in 3D cell cultures was dependent on Syk kinase, a downstream mediator of signalling from the immunoreceptor tyrosine-based activation motif, which is present in C35.

conclusionC35 functions as an oncogene in breast cancer cell lines. Drug targeting of C35 or Syk kinase might be helpful in treating a subset of patients with HER2-amplified breast cancers.

Indexed as

Genes, erbB-2Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDBreast NeoplasmsCadherinsCell Line, TumorColony-Forming Units AssayDNA PrimersDown-RegulationErb-b2 Receptor Tyrosine KinasesFemaleGene AmplificationHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDCadherinsCDH1 protein, humanDNA PrimersERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesIntracellular Signaling Peptides and ProteinsMIEN1 protein, humanNeoplasm ProteinsProtein-Tyrosine KinasesRNA, MessengerSyk KinaseSYK protein, humanTrastuzumab

Identifiers

PMID20628393
PMCPMC2920017
OpenAlexW2121811406

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.