Evidence map›Paper›PMID 38085608›Full record

ArticleBlood cancer discovery2024

Transcriptional Plasticity Drives IMiD and p300 Inhibitor Resistance in Multiple Myeloma.

Seongseok Yun, John L Cleveland

Open access · greenAbstract readComment
In one paragraph

Article in Blood cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 53% of its field
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

3 citing papers in PubMed, 0 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Seongseok YunDepartment of Malignant Hematology, Moffitt Cancer Center & Research Institute, Tampa, Florida.ORCID 0000-0001-7343-1635
John L ClevelandDepartment of Tumor Microenvironment & Meta-stasis, Moffitt Cancer Center & Research Institute, Tampa, Florida.ORCID 0000-0002-7561-9065
Moffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

summaryIn this issue of Blood Cancer Discovery, Neri, Barwick, and colleagues and Welsh, Barwick, and colleagues performed RNA sequencing, chromatin immunoprecipitation sequencing, assay for transposase-accessible chromatin using sequencing, and genetic studies to characterize the underlying mechanisms of immunomodulatory drug (IMiD) resistance in multiple myeloma. They demonstrated that IMiD resistance is driven by sustained expression of MYC and IRF4 via transcriptional plasticity that involves induction of ETV4 and BATF proteins, the binding of these proteins to their super-enhancers, and the recruitment of BRD4 and p300. Finally, these studies suggest IMiD and p300 inhibitor combination as a promising therapeutic strategy in multiple myeloma. See related article by Neri, Barwick, et al., p. 56 (9). See related article by Welsh, Barwick, et al., p. 34 (10).

Indexed as

Multiple MyelomaBromodomain Containing ProteinsCell Cycle ProteinsHumansImmunomodulating AgentsNuclear ProteinsPeptide HydrolasesTranscription FactorsBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsImmunomodulating AgentsNuclear ProteinsPeptide HydrolasesTranscription Factors

Identifiers

PMID38085608
PMCPMC10772544
OpenAlexW4389613232

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.