ArticleOncotarget2017
BMI-1 is a potential therapeutic target in diffuse intrinsic pontine glioma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 63 citations in OpenAlex.
- Integrated multi-omics identifies lineage-dependent myeloid cells recruitment and the APP-CD74 axis as an immunoregulatory target in pediatric high-grade glioma.Acta neuropathologica · 2026Article
- BMI-1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma.FEBS open bio · 2026Article
- A new hope: Clinical advances in targeted therapies for pediatric diffuse midline glioma.Neuro-oncology advances · 2026Review
- Navitoclax acts synergistically with irradiation to induce apoptosis in preclinical models of H3K27M-altered diffuse midline glioma.Scientific reports · 2025Article
- Novel modifiers of oncoprotein-mediated Polycomb inhibition in Drosophila melanogaster.Genetics · 2025Article
- A specific form of cPRC1 containing CBX4 is co-opted to mediate oncogenic gene repression in diffuse midline glioma.Molecular cell · 2025Article
- Investigating oncoprotein-mediated chromatin dysregulation inbioRxiv : the preprint server for biology · 2025Article
- Mapping naturally presented T cell antigens in medulloblastoma based on integrative multi-omics.Nature communications · 2025Article
- Insights Into the Role of Bmi-1 Deregulation in Promoting Stemness and Therapy Resistance in Glioblastoma: A Narrative Review.Cancer medicine · 2025Review
- Diffuse intrinsic pontine glioma (DIPG): A review of current and emerging treatment strategies.Cancer letters · 2024Review
- Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201.Neuro-oncology · 2024Article
- Radiotherapy and radio-sensitization in H3CNS neuroscience & therapeutics · 2023Review
- Alternative Lengthening of Telomeres in Pediatric High-Grade Glioma and Therapeutic Implications.Cancers · 2023Article
- Limitations of radiosensitization by direct telomerase inhibition to treat high-risk medulloblastoma.Frontiers in oncology · 2023Article
- BAF Complex Maintains Glioma Stem Cells in Pediatric H3K27M Glioma.Cancer discovery · 2022Article
- Combination of BMI1 and MAPK/ERK inhibitors is effective in medulloblastoma.Neuro-oncology · 2022Article
- Glioma Stem Cells in Pediatric High-Grade Gliomas: From Current Knowledge to Future Perspectives.Cancers · 2022Review
- Oncohistones: Hijacking the histone code.Annual review of cancer biology · 2022Article
- A novel association between Bmi-1 protein expression and the SUVmax obtained byOpen life sciences · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse intrinsic pontine glioma (DIPG) is a poor-prognosis pediatric brain tumor. No effective curative therapy is currently available and no therapeutic advances have been made in several decades. BMI-1 is a member of the multimeric protein complex Polycomb repressor complex 1. It is highly expressed in a number of diseases and malignancies and has been implicated in self-renewal of normal and cancer cells, and in DNA damage signaling. The role of BMI-1 in DIPG is largely unknown. Here, we show that BMI-1 is highly expressed in tumor tissue samples of DIPG patients and in patient-derived cancer stem-like cells. BMI-1 downregulation leads to the inhibition of DIPG patient-derived neurosphere cell proliferation, cell cycle signaling, self-renewal, telomerase expression and activity, and suppresses DIPG cell migration. Moreover, targeted inhibition of BMI-1 sensitizes DIPG cells to radiomimetic drug-induced DNA damage. Together, our data validate BMI-1 as a potential therapeutic target to treat children with DIPG.
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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.