Evidence map›Paper›PMID 38957016›Full record

ReviewMolecular oncology2024

Immune evasion: An imperative and consequence of MYC deregulation.

Bastian Krenz, Jongkuen Lee, Toshitha Kannan, Martin Eilers

Abstract readReview
In one paragraph

Review in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Integrated Multiomic Profiling Enhances Risk Stratification and Prognostication in Canine Osteosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  2. Review
  3. Review
  4. A non-canonical role ofbioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Review
  7. Resistance mechanism to pembrolizumab inInternational cancer conference journal · 2025
    Article
  8. Article
  9. MYC: The Guardian of Its Own Chaos.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  10. Review
  11. Article
  12. LINC02167 stabilizes KSR1 mRNA in an mJournal of experimental & clinical cancer research : CR · 2025
    Article
  13. Article
  14. 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

4 authors.

Bastian KrenzDepartment of Biochemistry and Molecular Biology, Theodor Boveri Institute, Biocenter, University of Würzburg, Würzburg, Germany.ORCID 0000-0003-1889-3022
Jongkuen LeeDepartment of Biochemistry and Molecular Biology, Theodor Boveri Institute, Biocenter, University of Würzburg, Würzburg, Germany.
Toshitha KannanDepartment of Biochemistry and Molecular Biology, Theodor Boveri Institute, Biocenter, University of Würzburg, Würzburg, Germany.
Martin EilersDepartment of Biochemistry and Molecular Biology, Theodor Boveri Institute, Biocenter, University of Würzburg, Würzburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MYC has been implicated in the pathogenesis of a wide range of human tumors and has been described for many years as a transcription factor that regulates genes with pleiotropic functions to promote tumorigenic growth. However, despite extensive efforts to identify specific target genes of MYC that alone could be responsible for promoting tumorigenesis, the field is yet to reach a consensus whether this is the crucial function of MYC. Recent work shifts the view on MYC's function from being a gene-specific transcription factor to an essential stress resilience factor. In highly proliferating cells, MYC preserves cell integrity by promoting DNA repair at core promoters, protecting stalled replication forks, and/or preventing transcription-replication conflicts. Furthermore, an increasing body of evidence demonstrates that MYC not only promotes tumorigenesis by driving cell-autonomous growth, but also enables tumors to evade the host's immune system. In this review, we summarize our current understanding of how MYC impairs antitumor immunity and why this function is evolutionarily hard-wired to the biology of the MYC protein family. We show why the cell-autonomous and immune evasive functions of MYC are mutually dependent and discuss ways to target MYC proteins in cancer therapy.

Indexed as

NeoplasmsProto-Oncogene Proteins c-mycAnimalsGene Expression Regulation, NeoplasticHumansImmune EvasionProto-Oncogene Proteins c-mycimmune checkpointsimmune evasionimmunotherapyMYCMYC inhibitionstress resiliencetumor metabolism

Identifiers

PMID38957016
PMCPMC11459038

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.