ArticleNature communications2021
BRD4-mediated repression of p53 is a target for combination therapy in AML.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 76 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Effects of BCL-2 and MCL-1 Inhibition on Apoptotic and Transcriptional Profiles in Acute Myeloid Leukemia.Medicina (Kaunas, Lithuania) · 2026Article
- Activating p53Nature communications · 2026Article
- Systematic interrogation of drug sensitivities in melanoma reveals potent synergistic and antagonistic drug combinations with translational potential.Communications medicine · 2026Article
- Exploiting tumor lineage features for precision cancer therapy.Trends in cancer · 2026Review
- Antecedent enhancer activity predicts future susceptibility to seizures in mice.Nature communications · 2026Article
- A triple-action PROTAC for wild-type p53 cancer therapy.Cell reports. Medicine · 2025Article
- BRD4 inhibition suppresses histone H4 UFMylation to increase ferroptosis sensitivity through TXNIP.Cell death & disease · 2025Article
- Single-cell transcriptome analysis profiles the enlarged subsets of myeloid-biased HSPCs with preleukemic characters in disuse osteoporosis mice.Cell & bioscience · 2025Article
- Super-enhancers in tumors: unraveling recent advances in their role in Oncogenesis and the emergence of targeted therapies.Journal of translational medicine · 2025Review
- Targeting mutant p53: a key player in breast cancer pathogenesis and beyond.Cell communication and signaling : CCS · 2024Review
- Expanded profiling of WD repeat domain 5 inhibitors reveals actionable strategies for the treatment of hematologic malignancies.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Divergent Processing of Cell Stress Signals as the Basis of Cancer Progression: Licensing NFκB on Chromatin.International journal of molecular sciences · 2024Review
- The BET PROTAC inhibitor GNE-987 displays anti-tumor effects by targeting super-enhancers regulated gene in osteosarcoma.BMC cancer · 2024Article
- BET Bromodomain Inhibition Potentiates Ocular Melanoma Therapy by Inducing Cell Cycle Arrest.Investigative ophthalmology & visual science · 2024Article
- Caspase-resistant ROCK1 expression prolongs survival of Eµ-Myc B cell lymphoma mice.Disease models & mechanisms · 2024Article
- A phenotypic screening approach to target p60AmotL2-expressing invasive cancer cells.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
- Exploration of ANKRD27 as an immune-related prognostic factor in pan-cancer and hepatocellular carcinoma.Frontiers in oncology · 2024Article
- FAM222A, Part of the BET-Regulated Basal Endothelial Transcriptome, Is a Novel Determinant of Endothelial Biology and Angiogenesis-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
Corrections and comments
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Authors and funding
31 authors at 7 institutions in 3 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a typically lethal molecularly heterogeneous disease, with few broad-spectrum therapeutic targets. Unusually, most AML retain wild-type TP53, encoding the pro-apoptotic tumor suppressor p53. MDM2 inhibitors (MDM2i), which activate wild-type p53, and BET inhibitors (BETi), targeting the BET-family co-activator BRD4, both show encouraging pre-clinical activity, but limited clinical activity as single agents. Here, we report enhanced toxicity of combined MDM2i and BETi towards AML cell lines, primary human blasts and mouse models, resulting from BETi's ability to evict an unexpected repressive form of BRD4 from p53 target genes, and hence potentiate MDM2i-induced p53 activation. These results indicate that wild-type TP53 and a transcriptional repressor function of BRD4 together represent a potential broad-spectrum synthetic therapeutic vulnerability for AML.
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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.