Evidence map›Paper›PMID 33051686›Full record

ArticleNucleic acids research2020

MYC as a driver of stochastic chromatin networks: implications for the fitness of cancer cells.

Noriyuki Sumida, Emmanouil G Sifakis, Narsis A Kiani, Anna Lewandowska Ronnegren, Barbara A Scholz, Johanna Vestlund, David Gomez-Cabrero, Jesper Tegner, Anita Göndör, Rolf Ohlsson

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Chromatin Hubs: A biological and computational outlook.Computational and structural biotechnology journal · 2022
    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 1 institution in 3 countries.

Noriyuki SumidaDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Emmanouil G SifakisDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Narsis A KianiDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Anna Lewandowska RonnegrenDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Barbara A ScholzDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Johanna VestlundDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
David Gomez-CabreroUnit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, SE-171 76, Stockholm, Sweden.
Jesper TegnerUnit of Computational Medicine, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, L8:05, SE-171 76, Stockholm, Sweden.
Anita GöndörDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Rolf OhlssonDepartment of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Z1:00, SE-171 76 Stockholm, Sweden.
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relationship between stochastic transcriptional bursts and dynamic 3D chromatin states is not well understood. Using an innovated, ultra-sensitive technique, we address here enigmatic features underlying the communications between MYC and its enhancers in relation to the transcriptional process. MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells. Dynamic encounters with pathologically activated enhancers responsive to a range of environmental cues, involved <10% of active MYC alleles at any given time in colon cancer cells. Being the most central node of the chromatin network, MYC itself likely drives its communications with flanking enhancers, rather than vice versa. We submit that these features underlie an acquired ability of MYC to become dynamically activated in response to a diverse range of environmental cues encountered by the cell during the neoplastic process.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticAnimalsCarcinogenesisDrosophilaGene Regulatory NetworksHCT116 CellsHumansProto-Oncogene Proteins c-mycStochastic ProcessesProto-Oncogene Proteins c-myc

Identifiers

PMID33051686
PMCPMC7641766
OpenAlexW3092440380

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.