Evidence map›Paper›PMID 26555375›Full record

ArticlePloS one2015

FGFR1 Amplification Is Often Homogeneous and Strongly Linked to the Squamous Cell Carcinoma Subtype in Esophageal Carcinoma.

Katharina von Loga, Jule Kohlhaussen, Lia Burkhardt, Ronald Simon, Stefan Steurer, Susanne Burdak-Rothkamm, Frank Jacobsen, Guido Sauter, Till Krech

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Targeting p-FGFR1Biomedicines · 2025
    Article
  2. Alterations inContemporary oncology (Poznan, Poland) · 2025
    Article
  3. Review
  4. Next-generation sequencing implicates oncogenic roles for p53 and JAK/STAT signaling in microcystic adnexal carcinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  5. Article
  6. Article
  7. Prognostic and clinicopathological significance ofAnnals of translational medicine · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Prognostic implications ofWorld journal of gastroenterology · 2016
    Article
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

9 authors at 2 institutions in 1 country.

Katharina von LogaDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Jule KohlhaussenDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Lia BurkhardtDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ronald SimonDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Stefan SteurerDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Susanne Burdak-RothkammDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Frank JacobsenDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Guido SauterDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Till KrechDepartment of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
University Medical Center Hamburg-Eppendorf · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsAmplification of the fibroblast growth factor receptor 1 (FGFR1) is believed to predict response to multi-kinase inhibitors targeting FGFR1. Esophageal cancer is an aggressive disease, for which novel targeted therapies are highly warranted.

methodsThis study was designed to investigate the prevalence and clinical significance of FGFR1 amplification in a tissue microarray containing 346 adenocarcinomas and 254 squamous cell carcinomas of the esophagus, using dual-labeling fluorescence in situ hybridization (FISH) analysis.

resultsFGFR1 amplification, defined as a ratio of FGFR1:centromere 8 copy numbers ≥ 2.0, was more frequently seen in squamous cell carcinoma (8.9% of 202 interpretable cases) than in adenocarcinoma (1.6% of 308; p<0.0001). There was no association between FGFR1 amplification and tumor phenotype or clinical outcome. To study potential heterogeneity of FGFR1 amplification, all available tumor blocks from 23 FGFR1 amplified tumors were analyzed on conventional large sections. This analysis revealed complete homogeneity of FGFR1 amplification in 20 (86.9%) primary tumors and in all available lymph node metastases. Remarkably, FGFR1 amplification was also seen in dysplasia adjacent to tumor in 6 of 9 patients with FGFR1 amplified primary cancers.

conclusionsIn conclusion, FGFR1 amplification occurs in a relevant subgroup of carcinomas of the esophagus and may play a particular role for development of squamous cell cancers. The high homogeneity of FGFR1 amplification suggests that patients with FGFR1 amplified esophageal cancers may particularly benefit from anti-FGFR1 therapies and prompt for clinical studies in this tumor type.

Indexed as

AdenocarcinomaAdultAgedAged, 80 and overCarcinoma, Squamous CellEsophageal NeoplasmsFemaleGene AmplificationHumansIn Situ Hybridization, FluorescenceLymphatic MetastasisMaleMiddle AgedPrognosisReceptor, Fibroblast Growth Factor, Type 1FGFR1 protein, humanReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID26555375
PMCPMC4640518
OpenAlexW2109020001

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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.