ReviewCancers2017
Chemotherapeutic Drugs: DNA Damage and Repair in Glioblastoma.
Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 87 citations in OpenAlex.
- Early metabolic reprogramming and carbonic anhydrase IX-mediated extracellular acidification drive radiotherapy-induced glioblastoma cell dedifferentiation.Acta neuropathologica communications · 2025Article
- Unveiling cell-type-specific microRNA networks through alternative polyadenylation in glioblastoma.BMC biology · 2025Article
- Article
- Targeting senescence-associated secretory phenotypes to remodel the tumour microenvironment and modulate tumour outcomes.Clinical and translational medicine · 2024Review
- Phytocompounds and Nanoformulations for Anticancer Therapy: A Review.Molecules (Basel, Switzerland) · 2024Review
- Chlorpromazine overcomes temozolomide resistance in glioblastoma by inhibiting Cx43 and essential DNA repair pathways.Journal of translational medicine · 2024Article
- Unlocking Glioblastoma Vulnerabilities with CRISPR-Based Genetic Screening.International journal of molecular sciences · 2024Review
- Interaction between lncRNAs and RNA-binding proteins (RBPs) influences DNA damage response in cancer chemoresistance.Molecular biology reports · 2024Review
- HOXD-AS2-STAT3 feedback loop attenuates sensitivity to temozolomide in glioblastoma.CNS neuroscience & therapeutics · 2023Article
- Lysine-specific histone demethylase 1A (KDM1A/LSD1) inhibition attenuates DNA double-strand break repair and augments the efficacy of temozolomide in glioblastoma.Neuro-oncology · 2023Article
- Tumor Treating Fields (TTFields) increase the effectiveness of temozolomide and lomustine in glioblastoma cell lines.Journal of neuro-oncology · 2023Article
- Recent Advances in Nanoparticle-Mediated Co-Delivery System: A Promising Strategy in Medical and Agricultural Field.International journal of molecular sciences · 2023Review
- Sodium Propionate Contributes to Tumor Cell Growth Inhibition through PPAR-γ Signaling.Cancers · 2022Article
- Anti-glioblastoma activity of monensin and its analogs in an organoid model of cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Review
- Characterization of Temozolomide Resistance Using a Novel Acquired Resistance Model in Glioblastoma Cell Lines.Cancers · 2022Article
- Approaching Sites of Action of Temozolomide for Pharmacological and Clinical Studies in Glioblastoma.Biomedicines · 2021Article
- Evidence for age-related contributions of DNA damage and epigenetics in brain tumorigenesis.International journal of experimental pathology · 2021Article
- Genotoxic therapy and resistance mechanism in gliomas.Pharmacology & therapeutics · 2021Review
- Differential gene expression-based connectivity mapping identified novel drug candidate and improved Temozolomide efficacy for Glioblastoma.Journal of experimental & clinical cancer research : CR · 2021Article
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
Despite improvements in therapeutic strategies, glioblastoma (GB) remains one of the most lethal cancers. The presence of the blood-brain barrier, the infiltrative nature of the tumor and several resistance mechanisms account for the failure of current treatments. Distinct DNA repair pathways can neutralize the cytotoxicity of chemo- and radio-therapeutic agents, driving resistance and tumor relapse. It seems that a subpopulation of stem-like cells, indicated as glioma stem cells (GSCs), is responsible for tumor initiation, maintenance and recurrence and they appear to be more resistant owing to their enhanced DNA repair capacity. Recently, attention has been focused on the pivotal role of the DNA damage response (DDR) in tumorigenesis and in the modulation of therapeutic treatment effects. In this review, we try to summarize the knowledge concerning the main molecular mechanisms involved in the removal of genotoxic lesions caused by alkylating agents, emphasizing the role of GSCs. Beside their increased DNA repair capacity in comparison with non-stem tumor cells, GSCs show a constitutive checkpoint expression that enables them to survive to treatments in a quiescent, non-proliferative state. The targeted inhibition of checkpoint/repair factors of DDR can contribute to eradicate the GSC population and can have a great potential therapeutic impact aiming at sensitizing malignant gliomas to treatments, improving the overall survival of patients.
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.