ArticleCell reports2020
Super Elongation Complex as a Targetable Dependency in Diffuse Midline Glioma.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Preclinical evaluation of ixazomib for high-risk pediatric brain tumors.bioRxiv : the preprint server for biology · 2026Article
- Elongin B orchestrates chromatin and transcriptional programs in H3K27M-mutant diffuse midline glioma.bioRxiv : the preprint server for biology · 2026Article
- H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibition.bioRxiv : the preprint server for biology · 2026Article
- Berzosertib enhances the sensitivity of pediatric diffuse midline glioma H3K27-altered cells to radiotherapy.Cell death & disease · 2026Article
- Targeting CDK9-dependent transcriptional addiction: a novel chemoprevention strategy for oral carcinogenesis via adenosine deaminase modulation.Cell death & disease · 2025Article
- Targeting processive transcription for Myc-driven circuitry in medulloblastoma.Neuro-oncology · 2025Article
- Targeting Transcriptional Cyclin-Dependent Kinases in Cancer.Molecular cancer therapeutics · 2025Review
- Development of an Anti-CD99 Antibody Enables Targeting of Diffuse Midline Glioma.Cancer research · 2025Article
- PRMT5 Maintains Tumor Stem Cells to Promote Pediatric High-Grade Glioma Tumorigenesis.Molecular cancer research : MCR · 2025Article
- Rapid P-TEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy.Nature communications · 2024Article
- H3K27M mutant glioma: Disease definition and biological underpinnings.Neuro-oncology · 2024Review
- Transcriptional elongation control in developmental gene expression, aging, and disease.Molecular cell · 2023Review
- Immunocal® limits gliosis in mouse models of repetitive mild-moderate traumatic brain injury.Brain research · 2023Article
- PI3K/ c-Myc/AFF4 axis promotes pancreatic tumorigenesis through fueling nucleotide metabolism.International journal of biological sciences · 2023Article
- Advances on Epigenetic Drugs for Pediatric Brain Tumors.Current neuropharmacology · 2023Review
- A Saccharomyces cerevisiae model and screen to define the functional consequences of oncogenic histone missense mutations.G3 (Bethesda, Md.) · 2022Article
- Oncohistones: Hijacking the histone code.Annual review of cancer biology · 2022Article
- Epigenetic programming of pediatric high-grade glioma: Pushing beyond proof of concept to clinical benefit.Frontiers in cell and developmental biology · 2022Review
- AFF4 Predicts the Prognosis of Colorectal Cancer Patients and Suppresses Colorectal Cancer MetastasisFrontiers in oncology · 2022Article
- Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Histone 3 gene mutations are the eponymous drivers in diffuse midline gliomas (DMGs), aggressive pediatric brain cancers for which no curative therapy currently exists. These recurrent oncohistones induce a global loss of repressive H3K27me3 residues and broad epigenetic dysregulation. In order to identify therapeutically targetable dependencies within this disease context, we performed an RNAi screen targeting epigenetic/chromatin-associated genes in patient-derived DMG cultures. This identified AFF4, the scaffold protein of the super elongation complex (SEC), as a molecular dependency in DMG. Interrogation of SEC function demonstrates a key role for maintaining clonogenic potential while promoting self-renewal of tumor stem cells. Small-molecule inhibition of SEC using clinically relevant CDK9 inhibitors restores regulatory RNA polymerase II pausing, promotes cellular differentiation, and leads to potent anti-tumor effect both in vitro and in patient-derived xenograft models. These studies present a rationale for further exploration of SEC inhibition as a promising therapeutic approach to this intractable disease.
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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.