Evidence map›Paper›PMID 25436978›Full record

ArticleOncotarget2014

Afatinib circumvents multidrug resistance via dually inhibiting ATP binding cassette subfamily G member 2 in vitro and in vivo.

Xiao-Kun Wang, Kenneth Kin Wah To, Li-Yan Huang, Jing-Hong Xu, Ke Yang, Fang Wang, Zhen-Cong Huang, Sheng Ye, Li-Wu Fu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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 4 institutions in 1 country.

Xiao-Kun WangState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Kenneth Kin Wah ToSchool of Pharmacy, The Chinese University of Hong Kong, Hong Kong, P.R. China.
Li-Yan HuangState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Jing-Hong XuFirst Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.
Ke YangState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Fang WangState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Zhen-Cong HuangState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Sheng YeFirst Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.
Li-Wu FuState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNThe First Affiliated Hospital, Sun Yat-sen University · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) to chemotherapeutic drugs is a formidable barrier to the success of cancer chemotherapy. Expressions of ATP-binding cassette (ABC) transporters contribute to clinical MDR phenotype. In this study, we found that afatinib, a small molecule tyrosine kinase inhibitor (TKI) targeting EGFR, HER-2 and HER-4, reversed the chemoresistance mediated by ABCG2 in vitro, but had no effect on that mediated by multidrug resistance protein ABCB1 and ABCC1. In addition, afatinib, in combination with topotecan, significantly inhibited the growth of ABCG2- overexpressing cell xenograft tumors in vivo. Mechanistic investigations exhibited that afatinib significantly inhibited ATPase activity of ABCG2 and downregulated expression level of ABCG2, which resulted in the suppression of efflux activity of ABCG2 in parallel to the increase of intracellular accumulation of ABCG2 substrate anticancer agents. Taken together, our findings may provide a new and useful combinational therapeutic strategy of afatinib with chemotherapeutical drug for the patients with ABCG2 overexpressing cancer cells.

Indexed as

AfatinibAnimalsAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Blotting, WesternCell Line, TumorDrug Resistance, MultipleDrug Resistance, NeoplasmFemaleFlow CytometryHumansImmunohistochemistryIn Vitro TechniquesMaleMiceABCG2 protein, humanAfatinibAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Neoplasm ProteinsQuinazolinesTopotecan

Identifiers

PMID25436978
PMCPMC4322967
OpenAlexW2168967690

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.