ArticleJournal of translational medicine2025
DNA methylation remodeling in temozolomide resistant recurrent glioblastoma: comparing epigenetic dynamics in vitro and in vivo.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed.
- Dynamic ecosystems of tumor drug resistance mechanisms: from molecular heterogeneity to systemic interventions.Apoptosis : an international journal on programmed cell death · 2026Review
- The lysine methyltransferase KMT5a and p53 regulate the expression of the key autophagy adaptor p62/SQSTM1 in glioblastoma.Cell communication and signaling : CCS · 2026Article
- Promoter Methylation-Expression Coupling of Gliogenesis Genes inInternational journal of molecular sciences · 2026Article
- A multi-database pharmacovigilance study reveals distinctive immunosuppressive and opportunistic infection disproportionality signals with bevacizumab and temozolomide combination therapy in glioblastoma.Frontiers in medicine · 2026Article
- Methylation profiling in neuropathological tumors diagnosis: a comprehensive review.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundGlioblastoma is the most aggressive type of brain tumor and is associated with a poor prognosis. First-line treatment is surgical resection followed by radiotherapy and temozolomide-based chemotherapy. However, the duration of treatment with temozolomide is limited due to both its toxicity and the development of drug resistance. The prognostic and predictive factor for response to temozolomide is the methylation status of the MGMT promoter. Indeed, loss of MGMT promoter methylation is a major cause of chemoresistance. However, the development of drug resistance is not only associated with changes in MGMT methylation. The entire epigenome changes and acquires specific properties necessary for tumor progression.
methodsTo study epigenetic alterations associated with temozolomide exposure, we generated a TMZ-resistant cell model. We investigated epigenetic alterations in the cell model and in a cohort of patients with recurrent glioblastoma using genome-wide methylome approaches (Epic Arrays 850 k).
resultsWe investigated the epigenetic changes associated with temozolomide exposure. Therefore, we generated a TMZ-resistant cell model and studied the epigenetic features acquired after selective temozolomide pressure. Our next step was to investigate the epigenomic differences between primary and recurrent tumors in a small cohort of patients. Finally, we performed a cross-analysis between the epigenetic differences found in TMZ-resistant cells and recurrent glioblastomas to identify common signatures that could be used to guide future resistance-overcoming studies.
conclusionsTemozolomide induces significant epigenetic changes in glioblastoma, which may contribute to treatment resistance and increased tumor aggressiveness. The results suggest that further research into DNA methylation changes associated with TMZ resistance is crucial. The use of primary tumor cells in resistance models may help identify strategies to overcome chemoresistance in glioblastoma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.