Evidence map›Paper›PMID 39568843›Full record

ReviewHeliyon2024

Research progress of drug resistance mechanism of temozolomide in the treatment of glioblastoma.

Hao Wu, Wenwen Gao, Peng Chen, Yao Wei, Haikang Zhao, Fenglu Wang

Abstract readReview
In one paragraph

Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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  11. Review
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Review
  18. Current Understanding of the Exosomes and Their Associated Biomolecules in the Glioblastoma Biology, Clinical Treatment, and Diagnosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  19. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  20. 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

6 authors.

Hao WuDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.
Wenwen GaoDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.
Peng ChenDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.
Yao WeiDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.
Haikang ZhaoDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.
Fenglu WangDepartment of Neurosurgery, The Second Affiliated Hospital of Xi'an Medical University, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma, the most malignant primary brain tumor among gliomas, is characterized by a low cure rate, high recurrence rate, and invasive growth. Without chemotherapy, the median survival of patients is only 12.1 months. The standard treatment for glioblastoma primarily involves surgical resection, complemented by radiotherapy. Temozolomide (TMZ), a new oral alkylating agent, is currently used as the first-line chemotherapy drug for glioma. However, TMZ treatment only improves median survival by 2 months, largely because of the tumor's ability to develop resistance to the drug. The main mechanism underlying this resistance involves DNA repair processes, such as the action of O6⁃methylguanine DNA methyltransferase (MGMT), which repairs the DNA damage caused by TMZ, and other DNA repair mechanisms including mismatch repair and base excision repair. These mechanisms can effectively repair the DNA damage caused by TMZ, thereby reducing the sensitivity of tumor cells to the drug. This study summarized the recent research progress of TMZ resistance mechanism in glioblastoma, aiming to provide a theoretical basis for the development of new therapies. The mechanisms of glioma resistance to TMZ mainly involves DNA damage repair (as mentioned above), abnormal cell signaling pathways (p53-mediated signaling, reactive oxygen species-mediated signaling, endoplasmic reticulum stress and autophagy-related signaling, receptor tyrosine kinase-related signaling, transforming growth factors, β-mediated signaling pathway, Wnt/β-Catenin signaling pathway), glioma stem cells, tumor microenvironment (hypoxic microenvironment, nano-drug delivery system), epidermal growth factor receptor, and microRNAs.

Indexed as

DNA repair mechanismGliomaResistance mechanismSignal pathwayTemozolomide

Identifiers

PMID39568843
PMCPMC11577240

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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.