Abstract
Ishak and colleagues report that the loss of p53 disrupts constitutive heterochromatin, enabling the transcription of immunogenic repetitive elements. Unlike acute viral mimicry activation, a chronic viral mimicry response mediated by p53 loss during cancer initiation induces tolerance to cytosolic nucleic acids, ultimately diminishing cellular immunogenicity as a strategy for immune evasion. See related article by Ishak et al., p. 793.
| Original language | English |
|---|---|
| Pages (from-to) | 670-672 |
| Number of pages | 3 |
| Journal | Cancer Discovery |
| Volume | 15 |
| Issue number | 4 |
| DOIs | |
| State | Published - Apr 1 2025 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Animals
- Carcinogenesis/immunology
- Humans
- Immune Evasion
- Immune Tolerance
- Molecular Mimicry
- Neoplasms/immunology
- Tumor Escape
- Tumor Suppressor Protein p53/metabolism
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