The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.
Non-genetic cancer cell plasticity and therapy-induced stemness in tumour relapse: ‘What does not kill me strengthens me’
Open accessAbstract
Therapy resistance and tumour relapse after drug therapy are commonly explained by Darwinian selection of pre-existing drug-resistant, often stem-like cancer cells resulting from random mutations. However, the ubiquitous non-genetic heterogeneity and plasticity of tumour cell phenotype raises the question: are mutations really necessary and sufficient to promote cell phenotype changes during tumour progression? Cancer therapy inevitably spares some cancer cells, even in the absence of resistant mutants. Accumulating observations suggest that the non-killed, residual tumour cells actively acquire a new phenotype simply by exploiting their developmental potential. These surviving cells are stressed by the cytotoxic treatment, and owing to phenotype plasticity, exhibit a variety of responses. Some are pushed into nearby, latent attractor states of the gene regulatory network which resemble evolutionary ancient or early developmental gene expression programs that confer stemness and resilience. By entering such stem-like, stress-response states, the surviving cells strengthen their capacity to cope with future noxious agents. Considering non-genetic cell state dynamics and the relative ease with which surviving but stressed cells can be tipped into latent attractors provides a foundation for exploring new therapeutic approaches that seek not only to kill cancer cells but also to avoid promoting resistance and relapse that are inherently linked to the attempts to kill them.
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Cites
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A compendium of mutational cancer driver genes
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Rare cell variability and drug-induced reprogramming as a mode of cancer drug resistance
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Intratumor Heterogeneity: The Rosetta Stone of Therapy Resistance
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Toward Minimal Residual Disease-Directed Therapy in Melanoma
Rambow, F., Rogiers, A., Marin-Bejar, O., Aibar, S., Femel, J., Dewaele, M., Karras, P., Brown, D., Chang, Y. H., Debiec-Rychter, M., et al. (2018) · Cell · doi:10.1016/j.cell.2018.06.025 · Cited by 771
Metadata
- Authors
- Pisco, A. O., & Huang, S.
- Venue
- British Journal of Cancer
- Published
- 2015-05
- Volume
- 112
- Issue
- 11
- Pages
- 1725-1732
- ISSN
- 0007-0920 (ISSN-L)
- 1532-1827
- OpenAlex
- W1569513357
- Cited by
- 283
- References
- 93
- FWCI
- 10.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
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