Evidence map›Paper›PMID 39929233›Full record

ReviewEpigenomics2025

Dysregulation of the p300/CBP histone acetyltransferases in human cancer.

Longxia Xu, Hongwen Xuan, Xiaobing Shi

Abstract readReview
In one paragraph

Review in Epigenomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Review
  2. Nonlinearities and Switch-Like Behavior in Gene Expression: From Genetics to Biochemistry and Back.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Review
  4. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Longxia XuDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Hongwen XuanDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Xiaobing ShiDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.

Funding

High Throughput Screen for Inhibitors of the YEATS2 Histone Acylation ReaderR01CA268440 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI SHI, XIAOBING · 2022 to 2025
$1.7M
NCI NIH HHS R01 CA268440
6 · The paper itself

Abstract

p300 (E1A binding protein 300) and CBP (CREB-binding protein) are critical regulators of chromatin dynamics and gene expression, playing essential roles in various cellular processes, including proliferation, differentiation, apoptosis, and immune responses. These homologous histone acetyltransferases (HATs) function as transcriptional co-activators by acetylating histones and non-histone proteins. p300/CBP is essential for development, and dysregulation of p300 and CBP has been implicated in several human diseases, particularly cancer. Somatic mutations that inactivate p300/CBP are frequently observed across various cancer types. Additionally, other mutations leading to translocations or truncations of p300/CBP can result in enhanced catalytic activity, potentially representing novel gain-of-function mutations that promote tumor progression. In this review, we discuss the mechanisms underlying the regulation of p300/CBP HAT activity, its dysregulation in cancer, and the development of p300/CBP inhibitors and their potential in cancer therapies.

Indexed as

Histone AcetyltransferasesNeoplasmsp300-CBP Transcription FactorsAcetylationAnimalsCREB-Binding ProteinGene Expression Regulation, NeoplasticHumansMutationCREB-Binding ProteinHistone Acetyltransferasesp300-CBP Transcription FactorscancerCBPhistone acetyltransferaseinhibitorP300somatic mutationTAZ2truncation

Identifiers

PMID39929233
PMCPMC11812348

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.