ArticleThe Journal of clinical investigation2021
Tumor genotype dictates radiosensitization after Atm deletion in primary brainstem glioma models.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026Review
- Ataxia telangiectasia mutated (ATM) kinase as a predictive biomarker in clinical oncology: implications for a precision treatment approach.Neoplasia (New York, N.Y.) · 2026Review
- Review
- Berzosertib enhances the sensitivity of pediatric diffuse midline glioma H3K27-altered cells to radiotherapy.Cell death & disease · 2026Article
- Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.Journal of extracellular vesicles · 2025Article
- HER2; p53 Co-mutated Cancers Show Increased Histone Acetylation and are Sensitive to Neratinib plus Trastuzumab Deruxtecan.bioRxiv : the preprint server for biology · 2025Article
- Serum metabolic profiling enables diagnosis, prognosis, and monitoring for brainstem gliomas.Nature communications · 2025Article
- DNA damage response in brain tumors: A Society for Neuro-Oncology consensus review on mechanisms and translational efforts in neuro-oncology.Neuro-oncology · 2024Review
- Potentiating the radiation-induced type I interferon antitumoral immune response by ATM inhibition in pancreatic cancer.JCI insight · 2024Article
- Aberrant ATM signaling and homology-directed DNA repair as a vulnerability of p53-mutant GBM to AZD1390-mediated radiosensitization.Science translational medicine · 2024Article
- Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024Review
- Effects of Ataxia-Telangiectasia Mutated Variants on Radionecrosis and Local Control After Stereotactic Radiation Surgery for Non-Small Cell Lung Cancer Brain Metastases.Advances in radiation oncology · 2024Article
- ATM inhibition enhances the efficacy of radiation across distinct molecular subgroups of pediatric high-grade glioma.Neuro-oncology · 2023Article
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- Therapeutic avenues for targeting treatment challenges of diffuse midline gliomas.Neoplasia (New York, N.Y.) · 2023Review
- Antisense oligonucleotide therapy for H3.3K27M diffuse midline glioma.Science translational medicine · 2023Article
- Triple kill: DDR inhibitors, radiotherapy and immunotherapy leave cancer cells with no escape.Acta biochimica et biophysica Sinica · 2022Review
- Article
- The Effect ofCancers · 2022Article
- Radiosensitizing the Vasculature of Primary Brainstem Gliomas Fails to Improve Tumor Response to Radiation Therapy.International journal of radiation oncology, biology, physics · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Diffuse intrinsic pontine glioma (DIPG) kills more children than any other type of brain tumor. Despite clinical trials testing many chemotherapeutic agents, palliative radiotherapy remains the standard treatment. Here, we utilized Cre/loxP technology to show that deleting Ataxia telangiectasia mutated (Atm) in primary mouse models of DIPG can enhance tumor radiosensitivity. Genetic deletion of Atm improved survival of mice with p53-deficient but not p53 wild-type gliomas after radiotherapy. Similar to patients with DIPG, mice with p53 wild-type tumors had improved survival after radiotherapy independent of Atm deletion. Primary p53 wild-type tumor cell lines induced proapoptotic genes after radiation and repressed the NRF2 target, NAD(P)H quinone dehydrogenase 1 (Nqo1). Tumors lacking p53 and Ink4a/Arf expressed the highest level of Nqo1 and were most resistant to radiation, but deletion of Atm enhanced the radiation response. These results suggest that tumor genotype may determine whether inhibition of ATM during radiotherapy will be an effective clinical approach to treat DIPGs.
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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.