Evidence map›Paper›PMID 40375039›Full record

ReviewApoptosis : an international journal on programmed cell death2025

Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.

Nikita Ghosh, Debarpan Chatterjee, Aparna Datta

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. FeBioactive materials · 2026
    Article
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  5. Potential therapeutic targeting of BKMolecular oncology · 2026
    Review
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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

3 authors.

Nikita GhoshDepartment of Neuroscience Technology, School of Allied Health Sciences, Yenepoya, Mangalore, Karnataka, India.
Debarpan ChatterjeeUniversity of Glasgow, Glasgow, G12 8QQ, UK.
Aparna DattaDepartment of Pharmaceutical Technology, NSHM Knowledge Campus, Kolkata, India. adatta75@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is one of the most aggressive and treatment-resistant brain tumor, characterized by its heterogeneity and the presence of glioblastoma stem cells (GSCs). GSCs are a subpopulation of cells within the tumor that possess self-renewal and differentiation capabilities, contributing to tumor initiation, progression, and recurrence. This review explores the unique biological properties of GSCs, including their molecular markers, signalling pathways, and interactions with the tumor microenvironment. We discuss the mechanisms by which GSCs evade conventional therapies, such as enhanced DNA repair and metabolic plasticity, which complicate treatment outcomes. Furthermore, we highlight recent advancements in identifying novel biomarkers and therapeutic targets that may improve the efficacy of treatments aimed at GSCs. The potential of targeted therapies, including immunotherapy and combination strategies, is also examined to overcome the challenges posed by GSCs. Ultimately, a deeper understanding of GSC biology is essential for developing personalized treatment approaches that can enhance patient outcomes in glioblastoma.

Indexed as

Brain NeoplasmsDrug Resistance, NeoplasmGlioblastomaNeoplastic Stem CellsAnimalsHumansSignal TransductionTumor MicroenvironmentBiomarkersCombination strategiesGlioblastoma multiformeGlioblastoma stem cellsImmunotherapyTreatment resistant brain tumor

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.