Evidence map›Paper›PMID 39030358›Full record

ReviewLeukemia2024

Silencing GNAS enhances HDAC3i efficacy in CREBBP wild type B cell lymphoma.

Patrizia Mondello

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Contract to kill: GNAS mutation.Molecular cancer · 2025
    Review
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

1 author.

Patrizia MondelloDivision of Hematology, Mayo Clinic, Rochester, MN, USA. mondello.patrizia@mayo.edu.ORCID 0000-0002-0355-3757

Funding

American Society of Hematology (ASH) Junior Faculty Scholar AwardGerstner Family Foundation Career Development AwardLymphoma Research Foundation (LRF) CDA 1020588
6 · The paper itself

Abstract

The genetic era has opened the opportunity of using personalized therapeutic approaches, in part based on targeting genes with somatic mutations. For example, lymphomas harboring the highly recurrent CREBBP mutation show dependency on HDAC3, thus selective inhibition of HDAC3 reversed the epigenetic effects of CREBBP mutation, halted lymphoma growth, and induced MHC class II expression, enabling the T-cells to recognize and kill lymphoma cells. However, CREBBP wild type (WT) cells are less sensitive to this approach. In this issue of Leukemia, He et al. have executed a genome-wide CRISPR screening that identified GNAS as a target to maximize the therapeutic activity of HDAC3 inhibition in CREBBP WT lymphoma.

Indexed as

ChromograninsCREB-Binding ProteinGTP-Binding Protein alpha Subunits, GsHistone DeacetylasesLymphoma, B-CellGene SilencingHistone Deacetylase 3Histone Deacetylase InhibitorsHumansChromograninsCREB-Binding ProteinCREBBP protein, humanGNAS protein, humanGTP-Binding Protein alpha Subunits, GsHistone Deacetylase 3Histone Deacetylase InhibitorsHistone Deacetylases

Identifiers

PMID39030358

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.