Evidence map›Paper›PMID 35547739›Full record

ArticleFrontiers in immunology2022

FGFR2-BRD4 Axis Regulates Transcriptional Networks of Histone 3 Modification and Synergy Between Its Inhibitors and PD-1/PD-L1 in a TNBC Mouse Model.

Josh Haipeng Lei, Lei Zhang, Zhenyi Wang, Raoul Peltier, Yusheng Xie, Ganchao Chen, Shiqi Lin, Kai Miao, Chu-Xia Deng, Hongyan Sun

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2022. 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
0.3field-weighted citation impact, top 49% 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, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

10 authors at 4 institutions in 3 countries.

Josh Haipeng LeiCancer Center, Faculty of Health Sciences, University of Macau, Macau, Macau SAR, China.
Lei ZhangCancer Center, Faculty of Health Sciences, University of Macau, Macau, Macau SAR, China.
Zhenyi WangHefei National Laboratory for Physical Sciences at the Microscale and School of Life Sciences, University of Science and Technology of China, Heifei, China.
Raoul PeltierDepartment of Chemistry, City University of Hong Kong, Kowloon, Hong Kong SAR, China.
Yusheng XieDepartment of Chemistry, City University of Hong Kong, Kowloon, Hong Kong SAR, China.
Ganchao ChenDepartment of Chemistry, City University of Hong Kong, Kowloon, Hong Kong SAR, China.
Shiqi LinCancer Center, Faculty of Health Sciences, University of Macau, Macau, Macau SAR, China.
Kai MiaoCancer Center, Faculty of Health Sciences, University of Macau, Macau, Macau SAR, China.
Chu-Xia DengCancer Center, Faculty of Health Sciences, University of Macau, Macau, Macau SAR, China.
Hongyan SunDepartment of Chemistry, City University of Hong Kong, Kowloon, Hong Kong SAR, China.
University of Macau · MOCity University of Hong Kong · HKHefei National Center for Physical Sciences at Nanoscale · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic reprogramming is an independent mode of gene expression that often involves changes in the transcription and chromatin structure due to tumor initiation and development. In this study, we developed a specifically modified peptide array and searched for a recognized epigenetic reader. Our results demonstrated that BRD4 is not only an acetylation reader but of propionylation as well. We also studied the quantitative binding affinities between modified peptides and epigenetic regulators by isothermal titration calorimetry (ITC). Furthermore, we introduced the Fgfr2-S252W transgenic mouse model to confirm that this acetylation is associated with the activation of c-Myc and drives tumor formation. Targeted disruption of BRD4 in Fgfr2-S252W mouse tumor cells also confirmed that BRD4 is a key regulator of histone 3 acetylation. Finally, we developed a tumor slice culture system and demonstrated the synergy between immune checkpoint blockade and targeted therapy in triple-negative breast cancer (TNBC). These data extend our understanding of epigenetic reprogramming and epigenetics-based therapies.

Indexed as

Triple Negative Breast NeoplasmsAnimalsB7-H1 AntigenBromodomain Containing ProteinsCell Cycle ProteinsGene Regulatory NetworksHistonesHumansMiceNuclear ProteinsProgrammed Cell Death 1 ReceptorReceptor, Fibroblast Growth Factor, Type 2Transcription FactorsB7-H1 AntigenBrd4 protein, mouseBromodomain Containing ProteinsCell Cycle ProteinsFgfr2 protein, mouseHistonesNuclear ProteinsProgrammed Cell Death 1 ReceptorReceptor, Fibroblast Growth Factor, Type 2Transcription FactorsBRD4epigeneticFGFR2immunotherapyposttranslational modificationsTNBC

Identifiers

PMID35547739
PMCPMC9084888
OpenAlexW4224325422

What OpenQuestion holds

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LicenceCC BY
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.