Evidence map›Paper›PMID 27057637›Full record

ReviewOncotarget2016

Cancer drug resistance: redox resetting renders a way.

Yuan Liu, Qifu Li, Li Zhou, Na Xie, Edouard C Nice, Haiyuan Zhang, Canhua Huang, Yunlong Lei

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 174 citations in OpenAlex.

  1. Significance of GSH and HRedox report : communications in free radical research · 2026
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32 more citing papers are in PubMed but not listed here.

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

8 authors at 4 institutions in 2 countries.

Yuan LiuState Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, P. R. China.
Qifu LiDepartment of Neurology, The Affiliated Hospital of Hainan Medical College, Haikou, Hainan, P. R. China.
Li ZhouState Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, P. R. China.
Na XieState Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, P. R. China.
Edouard C NiceDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia.
Haiyuan ZhangDepartment of Neurology, The Affiliated Hospital of Hainan Medical College, Haikou, Hainan, P. R. China.
Canhua HuangState Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, P. R. China.
Yunlong LeiDepartment of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, P. R. China.
Hainan Medical College Hospital · CNSichuan University · CNChongqing Medical University · CNMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of redox homeostasis is a crucial factor in the development of drug resistance, which is a major problem facing current cancer treatment. Compared with normal cells, tumor cells generally exhibit higher levels of reactive oxygen species (ROS), which can promote tumor progression and development. Upon drug treatment, some tumor cells can undergo a process of 'Redox Resetting' to acquire a new redox balance with higher levels of ROS accumulation and stronger antioxidant systems. Evidence has accumulated showing that the 'Redox Resetting' enables cancer cells to become resistant to anticancer drugs by multiple mechanisms, including increased rates of drug efflux, altered drug metabolism and drug targets, activated prosurvival pathways and inefficient induction of cell death. In this article, we provide insight into the role of 'Redox Resetting' on the emergence of drug resistance that may contribute to pharmacological modulation of resistance.

Indexed as

Drug Resistance, NeoplasmOxidation-ReductionAntineoplastic AgentsAntioxidantsApoptosisATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily G, Member 2AutophagyCell DeathCell SurvivalDisease ProgressionFluorouracilGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsABCB1 protein, humanABCG2 protein, humanAntineoplastic AgentsAntioxidantsATP-Binding Cassette, Sub-Family C ProteinsATP Binding Cassette Transporter, Subfamily BATP Binding Cassette Transporter, Subfamily G, Member 2Fluorouracilmultidrug resistance-associated protein 1Neoplasm ProteinsReactive Oxygen Speciescancer therapydrug effluxdrug resistanceoxidative stressredox modifications

Identifiers

PMID27057637
PMCPMC5173169
OpenAlexW2322116467

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.