ArticleeLife2016
Inactivation of the ATMIN/ATM pathway protects against glioblastoma formation.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Enhancer RNA-mediated transcriptional regulatory programs reveal the malignant progression of glioma.Science advances · 2025Article
- Transcription factor ATMIN facilitates chemoresistance in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Go-Ichi-Ni-San 2: A potential biomarker and therapeutic target in human cancers.World journal of gastrointestinal oncology · 2022Review
- Targeting Cell Cycle Checkpoint Kinases to Overcome Intrinsic Radioresistance in Brain Tumor Cells.Cancers · 2022Review
- MicroRNA-361-5p slows down gliomas development through regulating UBR5 to elevate ATMIN protein expression.Cell death & disease · 2021Article
- Set-Wise Differential Interaction Between Copy Number Alterations and Gene Expressions of Lower-Grade Glioma Reveals Prognosis-Associated Pathways.Entropy (Basel, Switzerland) · 2020Article
- The genomics of oxidative DNA damage, repair, and resulting mutagenesis.Computational and structural biotechnology journal · 2020Review
- Next generation DNA sequencing of atypical choroid plexus papilloma of brain: Identification of novel mutations in a female patient by Ion Proton.Oncology letters · 2019Article
- Article
- The lncRNA TP73-AS1 is linked to aggressiveness in glioblastoma and promotes temozolomide resistance in glioblastoma cancer stem cells.Cell death & disease · 2019Article
- Loss of GINS2 inhibits cell proliferation and tumorigenesis in human gliomas.CNS neuroscience & therapeutics · 2019Article
- Mistletoe-Based Drugs Work in Synergy with Radio-Chemotherapy in the Treatment of GliomaEvidence-based complementary and alternative medicine : eCAM · 2019Article
- MicroRNA203a suppresses glioma tumorigenesis through an ATM-dependent interferon response pathway.Oncotarget · 2017Article
- Mutational burden, immune checkpoint expression, and mismatch repair in glioma: implications for immune checkpoint immunotherapy.Neuro-oncology · 2017Article
- Article
- The promise of DNA damage response inhibitors for the treatment of glioblastoma.Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Glioblastoma multiforme (GBM) is the most aggressive human primary brain cancer. Using a Trp53-deficient mouse model of GBM, we show that genetic inactivation of the Atm cofactor Atmin, which is dispensable for embryonic and adult neural development, strongly suppresses GBM formation. Mechanistically, expression of several GBM-associated genes, including Pdgfra, was normalized by Atmin deletion in the Trp53-null background. Pharmacological ATM inhibition also reduced Pdgfra expression, and reduced the proliferation of Trp53-deficient primary glioma cells from murine and human tumors, while normal neural stem cells were unaffected. Analysis of GBM datasets showed that PDGFRA expression is also significantly increased in human TP53-mutant compared with TP53-wild-type tumors. Moreover, combined treatment with ATM and PDGFRA inhibitors efficiently killed TP53-mutant primary human GBM cells, but not untransformed neural stem cells. These results reveal a new requirement for ATMIN-dependent ATM signaling in TP53-deficient GBM, indicating a pro-tumorigenic role for ATM in the context of these tumors.
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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.