Evidence map›Paper›PMID 27487128›Full record

ArticleOncotarget2016

Ethacrynic acid improves the antitumor effects of irreversible epidermal growth factor receptor tyrosine kinase inhibitors in breast cancer.

Bing Liu, XinPing Huang, YunLong Hu, TingTing Chen, BoYa Peng, NingNing Gao, ZhenChao Jin, TieLiu Jia, Na Zhang, ZhuLin Wang and 1 more

Open 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. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  11. Review
  12. Resistance and Overcoming Resistance in Breast Cancer.Breast cancer (Dove Medical Press) · 2020
    Review
  13. Article
  14. 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

11 authors at 3 institutions in 1 country.

Bing LiuNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
XinPing HuangNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
YunLong HuNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
TingTing ChenNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
BoYa PengNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
NingNing GaoNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
ZhenChao JinNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
TieLiu JiaNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
Na ZhangDepartment of Pathophysiology, Chongqing Medical University, Chongqing, China.
ZhuLin WangShenzhen Conjugenix Pharma-Tech Co. Ltd, Guangdong, China.
GuangYi JinNational-Regional Key Technology Engineering Laboratory for Synthetic Biology of Medicine, Cancer Research Center, Shenzhen University, Shenzhen, China.
Shenzhen University Health Science Center · CNShenzhen University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolonged treatment of breast cancer with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) often results in acquired resistance and a narrow therapeutic index. One strategy to improve the therapeutic effects of EGFR TKIs is to combine them with drugs used for other clinical indications. Ethacrynic acid (EA) is an FDA approved drug that may have antitumor effects and may enhance the cytotoxicity of chemotherapeutic agents by binding to glutathione and inhibiting WNT signaling. While the α,β-unsaturated-keto structure of EA is similar to that of irreversible TKIs, the mechanism of action of EA when combined with irreversible EGFR TKIs in breast cancer remains unknown. We therefore investigated the combination of irreversible EGFR TKIs and EA. We found that irreversible EGFR TKIs and EA synergistically inhibit breast cancer both in vitro and in vivo. The combination of EGFR TKIs and EA induces necrosis and cell cycle arrest and represses WNT/β-catenin signaling as well as MAPK-ERK1/2 signaling. We conclude that EA synergistically enhances the antitumor effects of irreversible EGFR TKIs in breast cancer.

Indexed as

AfatinibAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBreastBreast NeoplasmsCell Cycle CheckpointsCell ProliferationDrug Resistance, NeoplasmDrug SynergismErbB ReceptorsEthacrynic AcidFemaleHumansMAP Kinase Signaling SystemAfatinibAntineoplastic AgentsEGFR protein, humanErbB ReceptorsEthacrynic AcidneratinibProtein Kinase InhibitorsQuinazolinesQuinolinesbreast cancerEGFRethacrynic acidtyrosine kinases

Identifiers

PMID27487128
PMCPMC5295410
OpenAlexW2486211322

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.