Evidence map›Paper›PMID 26804164›Full record

ReviewOncogene2016

Epigenomic regulation of oncogenesis by chromatin remodeling.

R Kumar, D-Q Li, S Müller, S Knapp

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  9. Patents on PARP-1 Inhibitors for the Management of Cancer from 2017-2023.Recent patents on anti-cancer drug discovery · 2025
    Review
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10 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 3 countries.

R KumarDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, George Washington University, Washington, DC, USA.
D-Q LiShanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
S MüllerNuffield Department of Clinical Medicine, Old Road Campus, Oxford University, Oxford, UK.
S KnappNuffield Department of Clinical Medicine, Old Road Campus, Oxford University, Oxford, UK.
University of Oxford · GBGeorge Washington University · USShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of the intricate gene expression program represents one of major driving factors for the development, progression and maintenance of human cancer, and is often associated with acquired therapeutic resistance. At the molecular level, cancerous phenotypes are the outcome of cellular functions of critical genes, regulatory interactions of histones and chromatin remodeling complexes in response to dynamic and persistent upstream signals. A large body of genetic and biochemical evidence suggests that the chromatin remodelers integrate the extracellular and cytoplasmic signals to control gene activity. Consequently, widespread dysregulation of chromatin remodelers and the resulting inappropriate expression of regulatory genes, together, lead to oncogenesis. We summarize the recent developments and current state of the dysregulation of the chromatin remodeling components as the driving mechanism underlying the growth and progression of human tumors. Because chromatin remodelers, modifying enzymes and protein-protein interactions participate in interpreting the epigenetic code, selective chromatin remodelers and bromodomains have emerged as new frontiers for pharmacological intervention to develop future anti-cancer strategies to be used either as single-agent or in combination therapies with chemotherapeutics or radiotherapy.

Indexed as

CarcinogenesisEpigenomicsAdenosine TriphosphatasesAnimalsChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA HelicasesHumansMi-2 Nucleosome Remodeling and Deacetylase ComplexNeoplasmsNuclear ProteinsTranscription FactorsAdenosine TriphosphatasesChromosomal Proteins, Non-HistoneDNA HelicasesISWI proteinMi-2 Nucleosome Remodeling and Deacetylase ComplexNuclear ProteinsSMARCA4 protein, humanSMARCA5 protein, humanTranscription Factors

Identifiers

PMID26804164
OpenAlexW2260715119

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.