ArticleCancer research2026
Catalytic Inhibition of p300 Preferentially Targets IRF4 Oncogenic Activity and Tumor Growth in Multiple Myeloma.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- A positive feedback loop between YTHDC1 and EP300 drives multiple myeloma tumorigenesis.Oncogene · 2026Article
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- An orally active dual CBP/p300 degrader targets core dependencies of multiple myeloma.Cell reports · 2026Article
- UniversalEPI: robust prediction of cell type-specific and differential chromatin interactions from DNA sequence and chromatin accessibility.Nucleic acids research · 2026Article
- Discovery of a paralog-selective p300 protein degrader with potent anti-cancer activity in hematological malignancies.Nature communications · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors.
Funding
Abstract
The oncogenic transcription factor (TF) IRF4 is a currently undrugged universal multiple myeloma dependency. Using transcriptional regulatory network mapping, an unbiased multiomics target ID approach, we identified the coactivator lysine acetyltransferase (KAT) p300 as a key IRF4 partner. Validation of this preferential relationship through quantitative interactome mapping revealed that IRF4 was the most abundant multiple myeloma-specific dependency and more closely complexed with p300 than other TFs, such as IKZF1/IKZF3. Development of optimized p300 KAT inhibitors enabled inhibition of IRF4 activity and multiple myeloma proliferation ex vivo and in vivo. p300/CBP KAT inhibition preferentially targeted multiple myeloma cells over normal cells, specifically modulating the multiple myeloma transcriptome, and the p300 KAT inhibitors more completely inhibited IRF4 activity at lower levels compared with existing p300/CREB-binding protein (CBP) bromodomain inhibitors. Furthermore, combining p300/CBP KAT inhibition and therapeutics with orthogonal mechanisms targeting transcription in multiple myeloma elicited synergistic antitumor effects. Together, these data motivate the ongoing clinical development of p300/CBP KAT inhibition in multiple myeloma. SIGNIFICANCE: Inhibition of p300 lysine acetyltransferase activity preferentially modulates the IRF4 transcriptional regulatory network and is orthogonal to mechanisms of multiple myeloma standard-of-care treatment, supporting the translational potential of p300 inhibitors.
Indexed as
Identifiers
What Socratic 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 Socratic graph.