Evidence map›Paper›PMID 41128938›Full record

SynthesisJournal of neuro-oncology2025

Investigating glioblastoma chemoresistance: a meta-analysis of microRNA signatures and gene networks.

Mohammad Hamza Bajwa, Sufiyan Sufiyan, Wajiha Amin, Kiran Aftab, Gao Guo, Amyn A Habib, Nouman Mughal, Syed Ather Enam

Abstract readMeta-AnalysisSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Mohammad Hamza BajwaSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan.
Sufiyan SufiyanSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan.
Wajiha AminSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan.
Kiran AftabSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan.
Gao GuoDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Amyn A HabibDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Nouman MughalSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan.
Syed Ather EnamSection of Neurosurgery and Center of Oncological Research in Surgery, The Aga Khan University, Karachi, Pakistan. ather.enam@aku.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemoresistance is a significant issue in glioblastoma (GBM) treatment due to recurrence, poor survival and limited salvage options. Non-invasive biomarkers can identify early chemoresistance. These cohorts may benefit from initiating early chemotherapy or second-line drugs at an earlier timeline.

methodsMeta-analysis of identified miR through systematic review was conducted through data mining and miR-target interaction compilation in validated miR databases. We curated a list of gene targets that underwent pathway enrichment analysis using the EnrichR tool. Network analysis of pathways and protein-protein interactions was conducted using the Metascape bioinformatics tool with several ontology sources.

resultsSignificantly upregulated miR validated in chemoresistant GBM were miR-221, -222, -132, and - 125b. 33 miR are identified in the high expression category. 18 miR were low expression responders in TMZ-resistant GBM. MiR-21 and miR-10b are the most replicated miR for bevacizumab response assessment with a low expression in Avastin-resistant GBM. 5 miR with high expression and 11 miR with low expression were identified; two combined micro-RNA signatures predicted cohorts likely to respond well to bevacizumab therapy. MiRs upregulated in TMZ resistance showed 400 predicted mRNA targets and 411 genes in downregulated miR. For bevacizumab response, upregulated miR yielded 38 genes and 82 in downregulated miR. An integrated, mechanistic model linking these miR to downstream targets and pathways is presented.

conclusionsmiR evaluation of GBM chemo-resistance requires insights into molecular subtypes and key signatures associated with TMZ/BVZ treatment failure. Evaluating a compiled signature's efficacy in improving progression-free and overall survival can highlight the impact of miR in GBM response evaluation. Our meta-analysis provides a template for understanding the key pathways and targets involved in miR-regulation of chemo-resistant GBM and potential applications of our signature in clinical practice.

Indexed as

Brain NeoplasmsDrug Resistance, NeoplasmGene Regulatory NetworksGlioblastomaMicroRNAsBiomarkers, TumorGene Expression Regulation, NeoplasticHumansBiomarkers, TumorMicroRNAsBevacizumabGlioblastomaMeta-analysisMicro-RNATemozolomide

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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.