Evidence map›Paper›PMID 32466597›Full record

ArticleCancers2020

Erdafitinib Resensitizes ABCB1-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs.

Chung-Pu Wu, Tai-Ho Hung, Sung-Han Hsiao, Yang-Hui Huang, Lang-Cheng Hung, Yi-Jou Yu, Yu-Tzu Chang, Shun-Ping Wang, Yu-Shan Wu

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. The fourth-generation EGFR tyrosine kinase inhibitor BLU-945 resensitizes ABCG2-overexpressing multidrug-resistant non-small cell lung cancer cells to cytotoxic anticancer drugs.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2025
    Article
  3. Review
  4. Article
  5. Targeting FGFR for cancer therapy.Journal of hematology & oncology · 2024
    Review
  6. Review
  7. Frontiers in pharmacology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Drug Discovery in Liver Disease Using Kinome Profiling.International journal of molecular sciences · 2021
    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

9 authors at 2 institutions in 1 country.

Chung-Pu WuGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan.ORCID 0000-0002-2434-3361
Tai-Ho HungDepartment of Obstetrics and Gynecology, Taipei Chang Gung Memorial Hospital, Taipei 10507, Taiwan.
Sung-Han HsiaoGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan.
Yang-Hui HuangGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan.
Lang-Cheng HungDepartment of Chemistry, Tunghai University, Taichung 40704, Taiwan.
Yi-Jou YuGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan.
Yu-Tzu ChangGraduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Tao-Yuan 33302, Taiwan.
Shun-Ping WangDepartment of Orthopedics, Taichung Veterans General Hospital, Taichung 40705, Taiwan.
Yu-Shan WuDepartment of Chemistry, Tunghai University, Taichung 40704, Taiwan.ORCID 0000-0003-4027-0710
Chang Gung University · TWTunghai University · TW

Funding

Chang Gung Medical Research Program BMRPC17Chang Gung Medical Research Program CMRP3G0281Chang Gung Medical Research Program CMRPD1J0281Chang Gung Medical Research Program CMRPG1J0071Ministry of Science and Technology, Taiwan MOST-107-2314-B-182A-099Ministry of Science and Technology, Taiwan MOST-108-2113-M-029-009Ministry of Science and Technology, Taiwan MOST-108-2320-B-182-035Ministry of Science and Technology, Taiwan MOST-108-2320-B-182-038-MY3Taichung Veterans General Hospital TCVGH-T1097802
6 · The paper itself

Abstract

The development of multidrug resistance (MDR) in cancer patients, which is often associated with the overexpression of ABCB1 (MDR1, P-glycoprotein) in cancer cells, remains a significant problem in cancer chemotherapy. ABCB1 is one of the major adenosine triphosphate (ATP)-binding cassette (ABC) transporters that can actively efflux a range of anticancer drugs out of cancer cells, causing MDR. Given the lack of Food and Drug Administration (FDA)-approved treatment for multidrug-resistant cancers, we explored the prospect of repurposing erdafitinib, the first fibroblast growth factor receptor (FGFR) kinase inhibitor approved by the FDA, to reverse MDR mediated by ABCB1. We discovered that by reducing the function of ABCB1, erdafitinib significantly resensitized ABCB1-overexpressing multidrug-resistant cancer cells to therapeutic drugs at sub-toxic concentrations. Results of erdafitinib-stimulated ABCB1 ATPase activity and in silico docking analysis of erdafitinib binding to the substrate-binding pocket of ABCB1 further support the interaction between erdafitinib and ABCB1. Moreover, our data suggest that ABCB1 is not a major mechanism of resistance to erdafitinib in cancer cells. In conclusion, we revealed an additional action of erdafitinib as a potential treatment option for multidrug-resistant cancers, which should be evaluated in future drug combination trials.

Indexed as

chemoresistancecombination chemotherapy with JNJ-42756493drug repositioningmodulatorP-glycoprotein

Identifiers

PMID32466597
PMCPMC7352346
OpenAlexW3029044317

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.