Evidence map›Paper›PMID 40341226›Full record

ArticleScientific reports2025

A quantitative characterization of the heterogeneous response of glioblastoma U-87 MG cell line to temozolomide.

Pragyesh Dixit, Ilyas Djafer-Cherif, Saumil Shah, Karolina Drabik, Arne Traulsen, Bartlomiej Waclaw

Abstract read
In one paragraph

Article in Scientific reports, 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

6 authors.

Pragyesh DixitDioscuri Centre for Physics and Chemistry of Bacteria, Institute of Physical Chemistry, Polish Academy of Sciences, Kasprzaka 44/52, Warszawa, 01-224, Poland.
Ilyas Djafer-CherifDioscuri Centre for Physics and Chemistry of Bacteria, Institute of Physical Chemistry, Polish Academy of Sciences, Kasprzaka 44/52, Warszawa, 01-224, Poland.
Saumil ShahDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, Plön, Germany.
Karolina DrabikDioscuri Centre for Physics and Chemistry of Bacteria, Institute of Physical Chemistry, Polish Academy of Sciences, Kasprzaka 44/52, Warszawa, 01-224, Poland.
Arne TraulsenDepartment of Theoretical Biology, Max Planck Institute for Evolutionary Biology, Plön, Germany.
Bartlomiej WaclawDioscuri Centre for Physics and Chemistry of Bacteria, Institute of Physical Chemistry, Polish Academy of Sciences, Kasprzaka 44/52, Warszawa, 01-224, Poland. bwaclaw@ichf.edu.pl.

Funding

Narodowe Centrum Nauki 2020/37/K/NZ2/03737
6 · The paper itself

Abstract

Most cancers are genetically and phenotypically heterogeneous. This includes subpopulations of cells with different levels of sensitivity to chemotherapy, which may lead to treatment failure as the more resistant cells can survive drug treatment and continue to proliferate. While the genetic basis of resistance to many drugs is relatively well characterised, non-genetic factors are much less understood. Here we investigate the role of non-genetic, phenotypic heterogeneity in the response of glioblastoma cancer cells to the drug temozolomide (TMZ) often used to treat this type of cancer. Using a combination of live imaging, machine-learning image analysis and agent-based modelling, we show that even if all cells share the same genetic background, individual cells respond differently to TMZ. We quantitatively characterise this response by measuring the doubling time, lifespan, cell cycle phase, area and motility of cells, and determine how these quantities correlate with each other as well as between the mother and daughter cell. We also show that these responses do not correlate with the cellular level of the enzyme MGMT which has been implicated in the response to TMZ.

Indexed as

Antineoplastic Agents, AlkylatingBrain NeoplasmsGlioblastomaTemozolomideCell CycleCell Line, TumorCell MovementCell ProliferationDNA Modification MethylasesDNA Repair EnzymesDrug Resistance, NeoplasmHumansMachine LearningTumor Suppressor ProteinsAntineoplastic Agents, AlkylatingDNA Modification MethylasesDNA Repair EnzymesMGMT protein, humanTemozolomideTumor Suppressor ProteinsCancerGlioblastomaMathematical modellingPhenotypic heterogeneityTemozolomide

Identifiers

PMID40341226
PMCPMC12062353

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.