Evidence map›Paper›PMID 27650548›Full record

ArticleOncotarget2016

Fibroblast growth factor receptor 4 induced resistance to radiation therapy in colorectal cancer.

Mohamed A Ahmed, Edgar Selzer, Wolfgang Dörr, Gerd Jomrich, Felix Harpain, Gerd R Silberhumer, Leonhard Müllauer, Klaus Holzmann, Bettina Grasl-Kraupp, Michael Grusch and 2 more

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. An organic extract from ascidianFrontiers in chemistry · 2024
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  12. CoA Synthase (Cancer research · 2020
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  13. Article
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  15. Article
  16. Article
  17. Review
  18. FGF8 induces therapy resistance in neoadjuvantly radiated rectal cancer.Journal of cancer research and clinical oncology · 2019
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Mohamed A AhmedInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Edgar SelzerDepartment of Radiotherapy and Radiobiology, Medical University of Vienna, Austria.
Wolfgang DörrDepartment of Radiotherapy and Radiobiology, Medical University of Vienna, Austria.
Gerd JomrichDepartment of Surgery, Medical University Vienna, Austria.
Felix HarpainDepartment of Surgery, Medical University Vienna, Austria.
Gerd R SilberhumerDepartment of Surgery, Medical University Vienna, Austria.
Leonhard MüllauerClinical Institute of Pathology, Medical University Vienna, Austria.
Klaus HolzmannInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Bettina Grasl-KrauppInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Michael GruschInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Walter BergerInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Brigitte MarianInstitute of Cancer Research, Department of Medicine I, Medical University of Vienna, Austria.
Medical University of Vienna · ATEgyptian Atomic Energy Authority · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In colorectal cancer (CRC), fibroblast growth factor receptor 4 (FGFR4) is upregulated and acts as an oncogene. This study investigated the impact of this receptor on the response to neoadjuvant radiotherapy by analyzing its levels in rectal tumors of patients with different responses to the therapy. Cellular mechanisms of FGFR4-induced radioresistance were analyzed by silencing or over-expressing FGFR4 in CRC cell line models. Our findings showed that the FGFR4 staining score was significantly higher in pre-treatment biopsies of non-responsive than responsive patients. Similarly, high expression of FGFR4 inhibited radiation response in cell line models. Silencing or inhibition of FGFR4 resulted in a reduction of RAD51 levels and decreased survival in radioresistant HT29 cells. Increased RAD51 expression rescued cells in the siFGFR4-group. In radiosensitive SW480 and DLD1 cells, enforced expression of FGFR4 stabilized RAD51 protein levels resulting in enhanced clearance of γ-H2AX foci and increased cell survival in the mismatch repair (MMR)-proficient SW480 cells. MMR-deficient DLD1 cells are defective in homologous recombination repair and no FGFR4-induced radioresistance was observed. Based on our results, FGFR4 may serve as a predictive marker to select CRC patients with MMR-proficient tumors who may benefit from pre-operative radiotherapy.

Indexed as

AdultAgedAged, 80 and overChemoradiotherapy, AdjuvantColorectal NeoplasmsDNA RepairFemaleHT29 CellsHumansMaleMiddle AgedRad51 RecombinaseRadiation ToleranceReceptor, Fibroblast Growth Factor, Type 4FGFR4 protein, humanRad51 RecombinaseReceptor, Fibroblast Growth Factor, Type 4colorectal cancerFGFR4RAD51radiotherapy

Identifiers

PMID27650548
PMCPMC5342528
OpenAlexW2519903272

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.