ReviewNaunyn-Schmiedeberg's archives of pharmacology2025
Unraveling the mechanisms of glioblastoma's resistance: investigating the influence of tumor suppressor p53 and non-coding RNAs.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Natural and Synthetic Compounds, Swords for Glioblastoma Therapy: From Tumor to Its Microenvironment.International journal of molecular sciences · 2026Review
- Association Between Temozolomide Resistance and Long Non-Coding RNA Expression Profiles in Glioblastoma Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Glioblastoma (GB) is one of the most fatal CNS malignancies, and its high resistance to therapy and poor outcomes have made it one of the primary challenges in oncology. Resistance to standard therapy, i.e., radio-chemotherapy with temozolomide, is one of the principal causes of the poor prognostic outcomes of GB. Finding the molecular basis of GB resistance to therapy is key to creating effective solution approaches. The general problem of GB resistance is supervised by cancer suppressive protein, p53, and has become a very special interest in molecular research in recent decades. The principal aim of this manuscript is to perform a comprehensive survey on the complex network of interactions developed by p53 with non-coding RNAs (ncRNA) in the context of GB resistance. The present article details the functional aspects of p53 as a cellular stress response protein, including its roles in apoptosis, cell cycle regulation, and DNA repair in glioblastoma (GB), along with the disruption of p53 and its involvement in chemoresistance (CR). It also highlights several classes of ncRNAs, namely microRNAs, long ncRNAs, and circular RNAs, that manipulate p53 signaling in GB-CR. The article likewise explains how disruption in the expression of these ncRNAs can promote GB-CR and how it interacts with essential cellular functions, such as proliferation, apoptosis, and DNA repair. The manuscript also describes the potential of targeting p53 and ncRNAs with their diagnostic and prognostic potential as novel promising therapeutics for GB. Nevertheless, ncRNA-based biomarkers still present challenges for their suitability in GB resistance. However, modern research continues to discover novel prediction targets, potentially enhancing patient outcomes and therapeutic options. Therefore, the neutralization of this intricate regulatory network of GB resistance might have a primary clinical effect in fighting GB resistance therapy and thus might lead to a substantial increase in patient survival and quality of life.
Indexed as
Identifiers
39476245What 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.