Cellular Plasticity and the Untapped Therapeutic Potential in Cancer
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (1 April 2021) | Viewed by 39942
Special Issue Editors
Interests: TGFB signaling; PI3K signaling; cancer cell plasticity; ubiquitin modifying enzymes
Special Issue Information
Dear Colleagues,
The administration of targeted therapies in cancer patients with well-defined tumour-driving mutations has markedly improved overall survival. Response rates to these therapies, however, remain disappointing, with quantifiable tumour regression limited by the development of acquired resistance. More recent evidence has indicated that targeted therapy can also rapidly induce diverse, genetically-independent, transcriptional programmes resulting in a “drug-tolerant” or “drug persister” cell population. Consequently, during this nongenetic evolutionary phase, cells are able to undergo an adaptive phenotype switch. This cellular or phenotype plasticity exhibited by a subpopulation by tumour cells has been demonstrated to release cells from their dependence on the tumour-driving alteration, resulting in a population of dedifferentiated, slow-cycling cells, capable of surviving continuous drug treatment. The pool of these drug-tolerant cells that survive initial therapy may eventually acquire validated genetic resistance mechanisms, limiting the efficacy of the therapy in the patient. Importantly, phenotype plasticity may be reversible with discontinued drug treatment resulting in resentisation of cells to the original therapy “drug holiday”. The identification of this subpopulation of slow-cycling drug-tolerant cells paves the way for the identification of a number of novel and incredible therapeutic opportunities to target cellular plasticity prior to the development of acquired resistance, with the potential to significantly improve overall survival in patients.
In this Special Issue, we seek to highlight the mechanisms driving cellular plasticity through alterations including chromatin remodelling, activation of reprogramming factors, and development programmes, such as the epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions. In so doing, we aim to gain a greater understanding of the role of cellular plasticity in disease progression, therapy-resistance and metastasis.
Assoc. Prof. Pieter Eichhorn
Dr. Christine Chaffer
Guest Editors
Manuscript Submission Information
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Keywords
- Cellular plasticity
- Phenotype switching
- EMT
- Drug tolerance
- Chemotherapy
- Targeted therapy
- Metastasis
- Therapy-resistance
