Evidence map›Paper›PMID 28388586›Full record

ArticleOncotarget2017

HER2 and EGFR amplification and expression in urothelial carcinoma occurs in distinct biological and molecular contexts.

Pontus Eriksson, Gottfrid Sjödahl, Gunilla Chebil, Fredrik Liedberg, Mattias Höglund

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Article
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  6. Article
  7. Review
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  9. Article
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  11. Novel Tyrosine Kinase Targets in Urothelial Carcinoma.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Overexpression of Epidermal Growth Factor Receptor (EGFR) and HER-2 in Bladder Carcinoma and Its Association with Patients' Clinical Features.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Article
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  19. Review
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

5 authors at 3 institutions in 1 country.

Pontus ErikssonDivision of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden.
Gottfrid SjödahlDivision of Urological Research, Department of Translational Medicine, Lund University, Skåne University Hospital, Malmö, Sweden.
Gunilla ChebilUnilabs, Helsingborg Hospital, Helsingborg, Sweden.
Fredrik LiedbergDivision of Urological Research, Department of Translational Medicine, Lund University, Skåne University Hospital, Malmö, Sweden.
Mattias HöglundDivision of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden.
Lund University · SESkåne University Hospital · SEHelsingborgs lasarett · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We analyzed a cohort of 599 cases of urothelial carcinoma for EGFR, ERBB2, and ERBB3 gene expression and genomic alterations. The cohort consisted of a reference set (n = 292) comprising all stages and grades and one set (n = 307) of advanced tumors. All cases were previously classified into urothelial carcinoma molecular subtypes. Genomic amplifications were established by array-CGH or in-situ hybridization, and gene expression both at mRNA and protein levels. Clinical HER2 status was independently evaluated using standard clinical procedures. EGFR amplifications were observed in 14% and ERBB2 amplifications in 23% of the reference cohort. EGFR gains were enriched in the Basal/SCC-like and ERBB2 gains in the Genomically Unstable subtypes. The expression data suggests that the Genomically Unstable show high ERBB2/ERBB3 but low EGFR expression and that Basal/SCC-like tumors show high EGFR but low ERBB2/ERBB3 expression. Whereas the frequency of ERBB2 genomic amplification were similar for cases of the Genomically Unstable subtype in the two cohorts, the Urothelial-like subtype acquires ERBB2 amplifications and expression during progression. Even though a good correlation between gene amplification and ERBB2 gene expression was observed in the Urothelial-like and Genomically Unstable subtypes less than half of the Basal/SCC-like cases with ERBB2 amplification showed concomitant ERBB2 mRNA and protein expression. We conclude that clinical trials using ERBB2 (HER2) or EGFR as targets have not fully appreciated the molecular heterogeneity in which activated ERBB2 and EGFR systems operate. Proper tumor classification is likely to be critical for arriving at thorough conclusions regarding new HER2 and EGFR based treatment regimes.

Indexed as

Biomarkers, TumorGene AmplificationGenes, erbB-2CarcinomaComputational BiologyDNA Copy Number VariationsErbB ReceptorsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansImmunohistochemistryIn Situ HybridizationNeoplasm StagingReceptor, ErbB-3Urologic NeoplasmsBiomarkers, TumorERBB3 protein, humanErbB ReceptorsReceptor, ErbB-3amplificationEGFRHER2molecular subtypeurothelial carcinoma

Identifiers

PMID28388586
PMCPMC5564734
OpenAlexW2598217298

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.