Evidence map›Paper›PMID 34830951›Full record

ReviewCancers2021

FGF/FGFR-Dependent Molecular Mechanisms Underlying Anti-Cancer Drug Resistance.

Jakub Szymczyk, Katarzyna Dominika Sluzalska, Izabela Materla, Lukasz Opalinski, Jacek Otlewski, Malgorzata Zakrzewska

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.7field-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

53 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
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  4. RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1.Genes to cells : devoted to molecular & cellular mechanisms · 2026
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  7. Mapping the Hypoxic Fitness Landscape of Retinal Pigment Epithelial Cells.International journal of molecular sciences · 2026
    Article
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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

6 authors at 1 institution in 1 country.

Jakub SzymczykDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.ORCID 0000-0003-2022-8064
Katarzyna Dominika SluzalskaDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.ORCID 0000-0002-6307-0204
Izabela MaterlaDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.
Lukasz OpalinskiDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.
Jacek OtlewskiDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.ORCID 0000-0001-8630-2891
Malgorzata ZakrzewskaDepartment of Protein Engineering, Faculty of Biotechnology, University of Wroclaw, Ul. F. Joliot-Curie 14a, 50-383 Wroclaw, Poland.ORCID 0000-0001-8214-1533
University of Wrocław · PL

Funding

National Science Center Sonata Bis 2015/18/E/NZ3/00501National Science Center Sonata Bis grant 2019/34/E/NZ3/00014
6 · The paper itself

Abstract

Increased expression of both FGF proteins and their receptors observed in many cancers is often associated with the development of chemoresistance, limiting the effectiveness of currently used anti-cancer therapies. Malfunctioning of the FGF/FGFR axis in cancer cells generates a number of molecular mechanisms that may affect the sensitivity of tumors to the applied drugs. Of key importance is the deregulation of cell signaling, which can lead to increased cell proliferation, survival, and motility, and ultimately to malignancy. Signaling pathways activated by FGFRs inhibit apoptosis, reducing the cytotoxic effect of some anti-cancer drugs. FGFRs-dependent signaling may also initiate angiogenesis and EMT, which facilitates metastasis and also correlates with drug resistance. Therefore, treatment strategies based on FGF/FGFR inhibition (using receptor inhibitors, ligand traps, monoclonal antibodies, or microRNAs) appear to be extremely promising. However, this approach may lead to further development of resistance through acquisition of specific mutations, metabolism switching, and molecular cross-talks. This review brings together information on the mechanisms underlying the involvement of the FGF/FGFR axis in the generation of drug resistance in cancer and highlights the need for further research to overcome this serious problem with novel therapeutic strategies.

Indexed as

anti-cancer drugscancercancer treatmentdrug resistanceFGFFGFR

Identifiers

PMID34830951
PMCPMC8616288
OpenAlexW3215792443

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.