Evidence map›Paper›PMID 30054853›Full record

ReviewFrontiers of medicine2018

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.

Patrick A Carroll, Brian W Freie, Haritha Mathsyaraja, Robert N Eisenman

Open access · hybridAbstract readReview
In one paragraph

Review in Frontiers of medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 1% 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

194 citing papers in PubMed, 2 syntheses or guidelines pooled it, 291 citations in OpenAlex.

  1. Multiple Endocrine Neoplasia Type 5 due to Germline MAX Mutations: A Systematic Review of Tumor Spectrum and Clinical Features.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. STK32C promotes colon tumor progression through activating c-MYC signaling.Cellular and molecular life sciences : CMLS · 2025
    Article

134 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 1 institution in 1 country.

Patrick A CarrollDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA, 90109, USA.
Brian W FreieDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA, 90109, USA.
Haritha MathsyarajaDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA, 90109, USA.
Robert N EisenmanDivision of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA, 90109, USA. eisenman@fhcrc.org.
Fred Hutch Cancer Center · US

Funding

Regulation of cell growth and proliferation by MycR01CA020525 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1985 to 2018
$10.7M
MYC ONCOPROTEIN FUNCTIONR01CA057138 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EISENMAN, ROBERT NEIL · 1991 to 2018
$4.9M
NCI NIH HHS R01 CA020525NCI NIH HHS R01 CA057138
6 · The paper itself

Abstract

Transcription factor networks have evolved in order to control, coordinate, and separate, the functions of distinct network modules spatially and temporally. In this review we focus on the MYC network (also known as the MAX-MLX Network), a highly conserved super-family of related basic-helix-loop-helix-zipper (bHLHZ) proteins that functions to integrate extracellular and intracellular signals and modulate global gene expression. Importantly the MYC network has been shown to be deeply involved in a broad spectrum of human and other animal cancers. Here we summarize molecular and biological properties of the network modules with emphasis on functional interactions among network members. We suggest that these network interactions serve to modulate growth and metabolism at the transcriptional level in order to balance nutrient demand with supply, to maintain growth homeostasis, and to influence cell fate. Moreover, oncogenic activation of MYC and/or loss of a MYC antagonist, results in an imbalance in the activity of the network as a whole, leading to tumor initiation, progression and maintenance.

Indexed as

AnimalsCarcinogenesisDisease ProgressionGene Expression RegulationGene Regulatory NetworksHumansProtein Interaction Domains and MotifsProto-Oncogene Proteins c-mycProto-Oncogene Proteins c-myccancerMAXMLXMYCnetworktranscription

Identifiers

PMID30054853
PMCPMC7358075
OpenAlexW2883764945

What OpenQuestion holds

Textmetadata
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.