Evidence map›Paper›PMID 39441520›Full record

ReviewCurrent treatment options in oncology2024

Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.

Chunxiao He, Zilong Wang, Jiaying Yu, Shuang Mao, Xi Xiang

Abstract readReview
In one paragraph

Review in Current treatment options in oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Ferroptosis in gastrointestinal stromal tumors.Journal of gastrointestinal oncology · 2026
    Article
  3. Article
  4. Review
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  6. Article
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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.

Chunxiao He *Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China. hechx26@mail.sysu.edu.cn.
Zilong Wang *The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Jiaying YuScientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China.
Shuang MaoThe Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Xi XiangScientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China. xiangx25@mail.sysu.edu.cn.

Funding

Shenzhen Science and Technology Innovation Commission JCYJ20220530145014033
6 · The paper itself

Abstract

opinion statementGastrointestinal stromal tumor (GIST) is characterized by well-defined oncogenes. Despite the significant improvement in treatment outcomes with adjuvant imatinib therapy for patients, drug resistance remains a major challenge for GIST therapy. This review focuses on the mechanisms contributing to drug resistance phenotype in GIST, such as primary imatinib-resistant mutants, secondary mutations, non-covalent binding of TKI to its target, tumor heterogeneity, re-activation of pro-survival/proliferation pathways through non-KIT/PDGFRA kinases, and loss of therapeutic targets in wild-type GIST. Corresponding suggestions are proposed to overcome drug-resistance phenotype of GIST. This review also summarizes the suitability of currently approved TKIs on different KIT/PDGFRA mutations and updates related clinical trials. Recent potent drugs and emerging strategies against advanced GISTs in clinical trials are presented. Additionally, metabolic intervention offers a new avenue for clinical management in GIST. A landscape of metabolism in GIST and metabolic changes under imatinib treatment are summarized based on currently published data. The OXPHOS pathway is a promising therapeutic target in combination with TKI against sensitive KIT/PDGFRA mutants. Comprehensive understanding of the above resistance mechanisms, experimental drugs/strategies and metabolic changes is critical to implement the proper therapy strategy and improve the clinical therapy outcomes for GIST.

Indexed as

Drug Resistance, NeoplasmGastrointestinal Stromal TumorsMutationProtein Kinase InhibitorsAntineoplastic AgentsBiomarkers, TumorDisease ManagementGastrointestinal NeoplasmsHumansImatinib MesylateMolecular Targeted TherapyProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor alphaTreatment OutcomeAntineoplastic AgentsBiomarkers, TumorImatinib MesylateKIT protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-kitReceptor, Platelet-Derived Growth Factor alphaDrug resistanceGISTImatinibMetabolismTyrosine kinase inhibitor

Identifiers

PMID39441520
PMCPMC11541409

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Registered trials

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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.