Cancer memory as a mechanism to establish malignancy
Cancers during oncogenic progression hold information in epigenetic memory which allows flexible encoding of malignant phenotypes and more rapid reaction to the environment when compared to purely mutation-based clonal evolution mechanisms. Cancer memory describes a proposed mechanism by which compl...
Gespeichert in:
| 1. Verfasser: | |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2025
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| In: |
Biosystems
Year: 2025, Jahrgang: 247, Pages: 1-7 |
| DOI: | 10.1016/j.biosystems.2024.105381 |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.1016/j.biosystems.2024.105381 Verlag, kostenfrei, Volltext: https://www.sciencedirect.com/science/article/pii/S0303264724002661 
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| Verfasserangaben: | Thomas Lissek |
MARC
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| 520 | |a Cancers during oncogenic progression hold information in epigenetic memory which allows flexible encoding of malignant phenotypes and more rapid reaction to the environment when compared to purely mutation-based clonal evolution mechanisms. Cancer memory describes a proposed mechanism by which complex information such as metastasis phenotypes, therapy resistance and interaction patterns with the tumor environment might be encoded at multiple levels via mechanisms used in memory formation in the brain and immune system (e.g. single-cell epigenetic changes and distributed state modifications in cellular ensembles). Carcinogenesis might hence be the result of physiological multi-level learning mechanisms unleashed by defined heritable oncogenic changes which lead to tumor-specific loss of goal state integration into the whole organism. The formation of cancer memories would create and bind new levels of individuality within the host organism into the entity we call cancer. Translational implications of cancer memory are that cancers could be engaged at higher organizational levels (e.g. be “trained” for memory extinction) and that compounds that are known to interfere with memory processes could be investigated for their potential to block cancer memory formation or recall. It also suggests that diagnostic measures should extend beyond sequencing approaches to functional diagnosis of cancer physiology. | ||
| 650 | 4 | |a Cancer | |
| 650 | 4 | |a Epigenetics | |
| 650 | 4 | |a Learning | |
| 650 | 4 | |a Maladaptation | |
| 650 | 4 | |a Memory | |
| 650 | 4 | |a Oncogenesis | |
| 650 | 4 | |a Plasticity | |
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