ArticleCancer cell2018
Disruption of the β1L Isoform of GABP Reverses Glioblastoma Replicative Immortality in a TERT Promoter Mutation-Dependent Manner.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Advancements in Telomerase-Targeted Therapies for Glioblastoma: A Systematic Review.International journal of molecular sciences · 2024Pooled it
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026Review
- An EGFR co-amplified lncRNA HELDR promotes glioblastoma malignancy through KAT7-driven gene programs.Nature cell biology · 2026Article
- Biogenesis and Regulation of Telomerase during Development and Cancer.Cold Spring Harbor perspectives in biology · 2026Review
- Review
- GABPB1 activates transcription of ITPR3 and EMT in OSCC progression.Functional & integrative genomics · 2026Article
- INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model.Nature communications · 2025Article
- Multiplexed epigenetic memory editing using CRISPRoff sensitizes glioblastoma to chemotherapy.Neuro-oncology · 2025Article
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
- Glioma stem cells: drivers of tumor progression and recurrence.Stem cell research & therapy · 2025Review
- GABP Promotes Mesangial Cell Proliferation and Renal Fibrosis Through GLI1 in Diabetic Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- BAIAP2L2 promotes the malignancy of hepatocellular carcinoma via GABPB1-mediated reactive oxygen species imbalance.Cancer gene therapy · 2024Article
- Mechanisms of telomere maintenance and associated therapeutic vulnerabilities in malignant gliomas.Neuro-oncology · 2024Review
- IMPDH Inhibition Decreases TERT Expression and Synergizes the Cytotoxic Effect of Chemotherapeutic Agents in Glioblastoma Cells.International journal of molecular sciences · 2024Article
- Prognostic Impact ofCancers · 2024Article
- Immunotherapy for Brain Tumors: Where We Have Been, and Where Do We Go From Here?Current treatment options in oncology · 2024Review
- A radiomics-based nomogram may be useful for predicting telomerase reverse transcriptase promoter mutation status in adult glioblastoma.Brain and behavior · 2024Article
- Therapeutic targeting of PLK1 in TERT promoter-mutant hepatocellular carcinoma.Clinical and translational medicine · 2024Article
- GABPB1 plays a cancer-promoting role in non-small cell lung cancer.Discover oncology · 2024Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
TERT promoter mutations reactivate telomerase, allowing for indefinite telomere maintenance and enabling cellular immortalization. These mutations specifically recruit the multimeric ETS factor GABP, which can form two functionally independent transcription factor species: a dimer or a tetramer. We show that genetic disruption of GABPβ1L (β1L), a tetramer-forming isoform of GABP that is dispensable for normal development, results in TERT silencing in a TERT promoter mutation-dependent manner. Reducing TERT expression by disrupting β1L culminates in telomere loss and cell death exclusively in TERT promoter mutant cells. Orthotopic xenografting of β1L-reduced, TERT promoter mutant glioblastoma cells rendered lower tumor burden and longer overall survival in mice. These results highlight the critical role of GABPβ1L in enabling immortality in TERT promoter mutant glioblastoma.
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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.