Evidence map›Paper›PMID 36115852›Full record

ReviewSignal transduction and targeted therapy2022

Protein tyrosine kinase inhibitor resistance in malignant tumors: molecular mechanisms and future perspective.

Yang Yang, Shuo Li, Yujiao Wang, Yi Zhao, Qiu Li

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
20.0field-weighted citation impact, top 1% 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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.

  1. Pooled it
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  12. Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  13. Review
  14. Article
  15. Novel Functionalized Pyrrolopyridines to Target Brk.Molecules (Basel, Switzerland) · 2026
    Article
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  19. Review
  20. Role of Troponins in CardioOncology.Current treatment options in oncology · 2026
    Review

117 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

5 authors at 4 institutions in 1 country.

Yang Yang *Cancer Center, West China Hospital, Sichuan University, No. 37, GuoXue Xiang, Chengdu, Sichuan, China.
Shuo Li *Second Clinical Medicine College, Lanzhou University, Lanzhou, Gansu, China.
Yujiao Wang *West China Biomedical Big Data Center, Sichuan University, No. 37, GuoXue Xiang, Chengdu, Sichuan, China.
Yi ZhaoFirst Clinical Medicine College, Lanzhou University, Lanzhou, Gansu, China.
Qiu LiCancer Center, West China Hospital, Sichuan University, No. 37, GuoXue Xiang, Chengdu, Sichuan, China. liqiu@scu.edu.cn.
Sichuan University · CNLanzhou University · CNLanzhou University Second Hospital · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein tyrosine kinases (PTKs) are a class of proteins with tyrosine kinase activity that phosphorylate tyrosine residues of critical molecules in signaling pathways. Their basal function is essential for maintaining normal cell growth and differentiation. However, aberrant activation of PTKs caused by various factors can deviate cell function from the expected trajectory to an abnormal growth state, leading to carcinogenesis. Inhibiting the aberrant PTK function could inhibit tumor growth. Therefore, tyrosine kinase inhibitors (TKIs), target-specific inhibitors of PTKs, have been used in treating malignant tumors and play a significant role in targeted therapy of cancer. Currently, drug resistance is the main reason for limiting TKIs efficacy of cancer. The increasing studies indicated that tumor microenvironment, cell death resistance, tumor metabolism, epigenetic modification and abnormal metabolism of TKIs were deeply involved in tumor development and TKI resistance, besides the abnormal activation of PTK-related signaling pathways involved in gene mutations. Accordingly, it is of great significance to study the underlying mechanisms of TKIs resistance and find solutions to reverse TKIs resistance for improving TKIs efficacy of cancer. Herein, we reviewed the drug resistance mechanisms of TKIs and the potential approaches to overcome TKI resistance, aiming to provide a theoretical basis for improving the efficacy of TKIs.

Indexed as

Antineoplastic AgentsNeoplasmsDrug Resistance, NeoplasmHumansProtein Kinase InhibitorsProtein-Tyrosine KinasesTumor MicroenvironmentTyrosineAntineoplastic AgentsProtein Kinase InhibitorsProtein-Tyrosine KinasesTyrosine

Identifiers

PMID36115852
PMCPMC9482625
OpenAlexW4296129731

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.