Evidence map›Paper›PMID 38982494›Full record

ReviewCancer cell international2024

Promoting reactive oxygen species accumulation to overcome tyrosine kinase inhibitor resistance in cancer.

Wei Lin, Xiaojun Wang, Mingxin Diao, Yangwei Wang, Rong Zhao, Jiaping Chen, Yongde Liao, Qinghong Long, Yunchong Meng

Abstract readReview
In one paragraph

Review in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. 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.

Wei LinDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China.
Xiaojun WangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China.
Mingxin DiaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China.
Yangwei WangDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China.
Rong ZhaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China.
Jiaping ChenDepartment of Cardiothoracic Surgery, Third Affiliated Hospital of Kunming Medical University (Yunnan Cancer Hospital), Kunming, Yunnan, China.
Yongde LiaoDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China. liaoyongde@hust.edu.cn.
Qinghong LongDepartment of Internal Medicine, Renmin Hospital, Wuhan University, Wuhan, 430022, China. longqh666@163.com.
Yunchong MengDepartment of Thoracic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, P.R. China. 15613523559@163.com.

Funding

National Natural Science Foundation of China 81572277
6 · The paper itself

Abstract

backgroundIn tumor treatment, protein tyrosine kinase inhibitors (TKIs) have been extensively utilized. However, the efficacy of TKI is significantly compromised by drug resistance. Consequently, finding an effective solution to overcome TKI resistance becomes crucial. Reactive oxygen species (ROS) are a group of highly active molecules that play important roles in targeted cancer therapy including TKI targeted therapy. In this review, we concentrate on the ROS-associated mechanisms of TKI lethality in tumors and strategies for regulating ROS to reverse TKI resistance in cancer. MAIN BODY: Elevated ROS levels often manifest during TKI therapy in cancers, potentially causing organelle damage and cell death, which are critical to the success of TKIs in eradicating cancer cells. However, it is noteworthy that cancer cells might initiate resistance pathways to shield themselves from ROS-induced damage, leading to TKI resistance. Addressing this challenge involves blocking these resistance pathways, for instance, the NRF2-KEAP1 axis and protective autophagy, to promote ROS accumulation in cells, thereby resensitizing drug-resistant cancer cells to TKIs. Additional effective approaches inducing ROS generation within drug-resistant cells and providing exogenous ROS stimulation.

conclusionROS play pivotal roles in the eradication of tumor cells by TKI. Harnessing the accumulation of ROS to overcome TKI resistance is an effective and widely applicable approach.

Indexed as

Antioxidant pathwayCancerDrug resistanceReactive oxygen speciesROS homeostasisTyrosine kinase inhibitor

Identifiers

PMID38982494
PMCPMC11234736

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.