Evidence map›Paper›PMID 28466200›Full record

ReviewCurrent topics in microbiology and immunology

MYC and RAF: Key Effectors in Cellular Signaling and Major Drivers in Human Cancer.

Eduard Stefan, Klaus Bister

Abstract readReview
In one paragraph

Review in Current topics in microbiology and immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Somatic Lineage Reprogramming.Cold Spring Harbor perspectives in biology · 2022
    Review
  10. Article
  11. Article
  12. Expanding Roles of De Novo Lipogenesis in Breast Cancer.International journal of environmental research and public health · 2021
    Review
  13. Article
  14. MYC Analysis in Cancer and Evolution.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  15. Article
  16. MYC inhibitors in multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Eduard StefanInstitute of Biochemistry and Center for Molecular Biosciences Innsbruck, University of Innsbruck, Innrain 80-82, 6020, Innsbruck, Austria.
Klaus BisterInstitute of Biochemistry and Center for Molecular Biosciences Innsbruck, University of Innsbruck, Innrain 80-82, 6020, Innsbruck, Austria. klaus.bister@uibk.ac.at.
Universität Innsbruck · AT

Funding

Austrian Science Fund FWF P 23652
6 · The paper itself

Abstract

The prototypes of the human MYC and RAF gene families are orthologs of animal proto-oncogenes that were originally identified as transduced alleles in the genomes of highly oncogenic retroviruses. MYC and RAF genes are now established as key regulatory elements in normal cellular physiology, but also as major cancer driver genes. Although the predominantly nuclear MYC proteins and the cytoplasmic RAF proteins have different biochemical functions, they are functionally linked in pivotal signaling cascades and circuits. The MYC protein is a transcription factor and together with its dimerization partner MAX holds a central position in a regulatory network of bHLH-LZ proteins. MYC regulates transcription conducted by all RNA polymerases and controls virtually the entire transcriptome. Fundamental cellular processes including distinct catabolic and anabolic branches of metabolism, cell cycle regulation, cell growth and proliferation, differentiation, stem cell regulation, and apoptosis are under MYC control. Deregulation of MYC expression by rearrangement or amplification of the MYC locus or by defects in kinase-mediated upstream signaling, accompanied by loss of apoptotic checkpoints, leads to tumorigenesis and is a hallmark of most human cancers. The critically controlled serine/threonine RAF kinases are central nodes of the cytoplasmic MAPK signaling cascade transducing converted extracellular signals to the nucleus for reshaping transcription factor controlled gene expression profiles. Specific mutations of RAF kinases, such as the prevalent BRAF(V600E) mutation in melanoma, or defects in upstream signaling or feedback loops cause decoupled kinase activities which lead to tumorigenesis. Different strategies for pharmacological interference with MYC- or RAF-induced tumorigenesis are being developed and several RAF kinase inhibitors are already in clinical use.

Indexed as

CarcinogenesisSignal TransductionAnimalsHumansNeoplasmsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mycProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-mycBinding interfaceCompartmentalized signalingDrug resistanceMetabolic rewiringOff-target effectsOncogene addictionParadoxical kinase activationProtein-protein interactionsSmall-molecule inhibitionSynthetic lethality

Identifiers

PMID28466200
PMCPMC6250427
OpenAlexW2611741979

What OpenQuestion holds

Textmetadata
LicenceTDM
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.