ReviewMolecular cancer2011
Chemoresistance of glioblastoma cancer stem cells--much more complex than expected.
Review in Molecular cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 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
180 citing papers in PubMed, 308 citations in OpenAlex.
- Image-based metric of invasiveness predicts response to adjuvant temozolomide for primary glioblastoma.PloS one · 2020Trial
- Targeting YRDC blocks codon-biased FABP7 translation and lipid droplet formation to overcome chemoresistance in glioblastoma.Oncogene · 2026Article
- Adenosine and 1,NInternational journal of molecular sciences · 2026Article
- NANP targeting radiosensitizes glioblastoma through TNFR1 sialylation-driven mesenchymal shift.Nature communications · 2026Article
- Review
- Loss of CD99L2 Contributed to Temozolomide Resistance and Glioblastoma Tumorigenesis Based on Genome-scale CRISPR/Cas9 Screening.Current pharmaceutical design · 2026Article
- Nano-Based Technology in Glioblastoma.Molecules (Basel, Switzerland) · 2025Review
- Review
- FDFT1 maintains glioblastoma stem cells through activation of the Akt pathway.Stem cell research & therapy · 2024Article
- Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration.Nature communications · 2024Article
- Article
- Stanniocalcin-1 promotes temozolomide resistance of glioblastoma through regulation of MGMT.Scientific reports · 2024Article
- Circulating Liquid Biopsy Biomarkers in Glioblastoma: Advances and Challenges.International journal of molecular sciences · 2024Review
- Selective regulation of chemosensitivity in glioblastoma by phosphatidylinositol 3-kinase beta.iScience · 2024Article
- GINS2 regulates temozolomide chemosensitivity via the EGR1/ECT2 axis in gliomas.Cell death & disease · 2024Article
- Mechanical Constraints in Tumor Guide Emergent Spatial Patterns of Glioblastoma Cancer Stem Cells.Mechanobiology in medicine · 2024Article
- Molecular signature of stem-like glioma cells (SLGCs) from human glioblastoma and gliosarcoma.PloS one · 2024Article
- Revisiting Temozolomide's role in solid tumors: Old is gold?Journal of Cancer · 2024Review
- RAR-Dependent and RAR-Independent RXR Signaling in Stem-like Glioma Cells.International journal of molecular sciences · 2023Article
- Glioblastomas: Hijacking Metabolism to Build a Flexible Shield for Therapy Resistance.Antioxidants & redox signaling · 2023Review
120 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastomas (GBM) are a paradigm for the investigation of cancer stem cells (CSC) in solid malignancies. The susceptibility of GBM CSC to standard chemotherapeutic drugs is controversial as the existing literature presents conflicting experimental data. Here, we summarize the experimental evidence on the resistance of GBM CSC to alkylating chemotherapeutic agents, with a special focus on temozolomide (TMZ). The data suggests that CSC are neither resistant nor susceptible to chemotherapy per se. Detoxifying proteins such as O6-methylguanine-DNA-methyltransferase (MGMT) confer a strong intrinsic resistance to CSC in all studies. Extrinsic factors may also contribute to the resistance of CSC to TMZ. These may include TMZ concentrations in the brain parenchyma, TMZ dosing schemes, hypoxic microenvironments, niche factors, and the re-acquisition of stem cell properties by non-stem cells. Thus, the interaction of CSC and chemotherapy is more complex than may be expected and it is necessary to consider these factors in order to overcome chemoresistance in the patient.
Indexed as
Identifiers
What 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.