Evidence map›Paper›PMID 26383138›Full record

ReviewNature reviews. Cancer2015

MYC: connecting selective transcriptional control to global RNA production.

Theresia R Kress, Arianna Sabò, Bruno Amati

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 321 papers.

0numbers the graph read from it
0cells of the map it votes in
321citing 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

321 citing papers in PubMed.

  1. Article
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  6. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
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  18. International journal of molecular sciences · 2026
    Review
  19. Article
  20. Article

261 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

3 authors.

Theresia R KressCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT) and Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy.
Arianna SabòCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT) and Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy.
Bruno AmatiCenter for Genomic Science of IIT@SEMM, Fondazione Istituto Italiano di Tecnologia (IIT) and Department of Experimental Oncology, European Institute of Oncology (IEO), Via Adamello 16, 20139 Milan, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two opposing models have been proposed to describe the function of the MYC oncoprotein in shaping cellular transcriptomes: one posits that MYC amplifies transcription at all active loci; the other that MYC differentially controls discrete sets of genes, the products of which affect global transcript levels. Here, we argue that differential gene regulation by MYC is the sole unifying model that is consistent with all available data. Among other effects, MYC endows cells with physiological and metabolic changes that have the potential to feed back on global RNA production, processing and turnover. The field is progressing steadily towards a full characterization of the MYC-regulated genes and pathways that mediate these biological effects and - by the same token - endow MYC with its pervasive oncogenic potential.

Indexed as

Gene Expression Regulation, NeoplasticHumansProto-Oncogene Proteins c-mycRNA, MessengerProto-Oncogene Proteins c-mycRNA, Messenger

Identifiers

PMID26383138

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.