Evidence map›Paper›PMID 23269274›Full record

ArticleCancer research2013

Acute and fractionated irradiation differentially modulate glioma stem cell division kinetics.

Xuefeng Gao, J Tyson McDonald, Lynn Hlatky, Heiko Enderling

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06551909 (Radioimmunotherapy in Solid Tumors), which is not on this map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
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.

NCT06551909 narecruitingnot on this mapstarted 2024, after this paper: background citation

Radioimmunotherapy in Solid Tumors (Aim 2- Stereotactic Neoadjuvant Radiotherapy for Glioblastoma)

TypeinterventionalSponsorIRCCS San RaffaeleRan2024 to 2027Enrolled30ConditionsGlioblastomaArmsNeoaddjuvant Stereotactic Radiotherapy with Simultaneous Integrated Boost
3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 152 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Profiling Glioma Stem Cell Dynamics via 3D-Based Cell Cycle Reporter Assays.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  5. Phagocytosis Checkpoints in Glioblastoma: CD47 and Beyond.Current issues in molecular biology · 2024
    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

4 authors at 2 institutions in 1 country.

Xuefeng GaoCenter of Cancer Systems Biology, Steward Research Institute, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA.
J Tyson McDonald
Lynn Hlatky
Heiko Enderling
Tufts University · USSt. Elizabeth's Medical Center · US

Funding

Project 5 UC BerkleyU54CA149233 · NCI · STEWARD ST. ELIZABETH'S MEDICAL CENTER · PI HLATKY, LYNN · 2010 to 2014
$7.3M
NCI NIH HHS U54 CA149233NCI NIH HHS U54CA149233
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is one of the most aggressive human malignancies with a poor patient prognosis. Ionizing radiation either alone or adjuvant after surgery is part of standard treatment for GBM but remains primarily noncurative. The mechanisms underlying tumor radioresistance are manifold and, in part, accredited to a special subpopulation of tumorigenic cells. The so-called glioma stem cells (GSC) are bestowed with the exclusive ability to self-renew and repopulate the tumor and have been reported to be less sensitive to radiation-induced damage through preferential activation of DNA damage checkpoint responses and increased capacity for DNA damage repair. During each fraction of radiation, non-stem cancer cells (CC) die and GSCs become enriched and potentially increase in number, which may lead to accelerated repopulation. We propose a cellular Potts model that simulates the kinetics of GSCs and CCs in glioblastoma growth and radiation response. We parameterize and validate this model with experimental data of the U87-MG human glioblastoma cell line. Simulations are conducted to estimate GSC symmetric and asymmetric division rates and explore potential mechanisms for increased GSC fractions after irradiation. Simulations reveal that in addition to their higher radioresistance, a shift from asymmetric to symmetric division or a fast cycle of GSCs following fractionated radiation treatment is required to yield results that match experimental observations. We hypothesize a constitutive activation of stem cell division kinetics signaling pathways during fractionated treatment, which contributes to the frequently observed accelerated repopulation after therapeutic irradiation.

Indexed as

Brain NeoplasmsCell DivisionCell Line, TumorDose Fractionation, RadiationGliomaHumansModels, BiologicalNeoplastic Stem Cells

Identifiers

PMID23269274
PMCPMC3594421
OpenAlexW2165073433

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.