ReviewCold Spring Harbor symposia on quantitative biology2016
The Essential Transcriptional Function of BRD4 in Acute Myeloid Leukemia.
Review in Cold Spring Harbor symposia on quantitative biology, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 44 citations in OpenAlex.
- Clinical presentation and differential splicing of SRSF2, U2AF1 and SF3B1 mutations in patients with acute myeloid leukemia.Leukemia · 2020Trial
- BRD4 regulation of PIM1 identifies a novel therapeutic vulnerability in acute megakaryoblastic leukemia.Cancer cell international · 2026Article
- Single-cell transcriptome analysis profiles the enlarged subsets of myeloid-biased HSPCs with preleukemic characters in disuse osteoporosis mice.Cell & bioscience · 2025Article
- BRD4 inhibition leads to MDSC apoptosis and enhances checkpoint blockade therapy.The Journal of clinical investigation · 2025Article
- RNA sequestration in P-bodies sustains myeloid leukaemia.Nature cell biology · 2024Article
- Article
- MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024Review
- Human VDAC pseudogenes: an emerging role for VDAC1P8 pseudogene in acute myeloid leukemia.Biological research · 2023Article
- Monocytic differentiation and AHR signaling as Primary Nodes of BET Inhibitor Response in Acute Myeloid Leukemia.Blood cancer discovery · 2021Article
- The Novel Oral BET-CBP/p300 Dual Inhibitor NEO2734 Is Highly Effective in Eradicating Acute Myeloid Leukemia Blasts and Stem/Progenitor Cells.HemaSphere · 2021Article
- Gene Transcription as a Therapeutic Target in Leukemia.International journal of molecular sciences · 2021Review
- Review
- Novel Targeted Therapeutics in Acute Myeloid Leukemia: an Embarrassment of Riches.Current hematologic malignancy reports · 2021Review
- BRD4-mediated repression of p53 is a target for combination therapy in AML.Nature communications · 2021Article
- Review
- Bromodomain inhibitor jq1 induces cell cycle arrest and apoptosis of glioma stem cells through the VEGF/PI3K/AKT signaling pathway.International journal of oncology · 2019Article
- Investigations of Structural Requirements for BRD4 Inhibitors through Ligand- and Structure-Based 3D QSAR Approaches.Molecules (Basel, Switzerland) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) is often initiated by genetic alterations of machineries that regulate chromatin and transcription, thereby blocking cell differentiation. Such mechanisms may also render leukemia cells vulnerable to perturbations of transcriptional regulators, which includes small molecules targeting the coactivator protein BRD4. Numerous studies have validated BRD4 as a therapeutic target in diverse subtypes of AML; however, the vital function of BRD4 in this disease is only beginning to be understood. Here we discuss the recent progress in elucidating the transcriptional function of BRD4 in AML cells, with an emphasis on the desirable attributes, but also the inherent limitations, of targeting general coactivator proteins as cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.