Catch Me If You Can: Cellular Plasticity in Tumor Progression and Drug Resistance.

Cellular plasticity is a broad term comprehending all the reversible mechanisms through which cells respond to stress. In human malignancies, cellular plasticity is aberrantly activated at all stages of pre-malignant and malignant evolution in response to microenvironmental stimuli and therapeutic pressure. The microenvironment is also plastic both responding to and being co-opted by the evolving cancer cells. As a consequence, plasticity confers cancer cells the dynamic capability to adapt to unfavorable and changing microenvironments, which eventually promotes invasion, dissemination, immune evasion, and therapeutic resistance.



Thanks to significant advances in understanding the molecular alterations of cancer cells, the last decades have witnessed the rapid development of targeted therapies and, as a consequence, several new compounds have been introduced in the clinic. However, accumulating evidence has demonstrated that these therapies may induce the plasticity of the neoplastic cells and co-opt the microenvironmental components to further enhance cancer cell plasticity. Such tumor alterations deeply influence the response to therapies, possibly leading to drug-resistant phenotypes and disease progression. Therefore, investigating the different aspects of cellular plasticity is crucial to understanding the mechanisms of drug resistance and the therapeutic strategies to overcome it.



This Research Topic welcomes high quality Original Research articles, Systematic Reviews and Mini Reviews that describe different aspects of cancer and tumor microenvironment cellular plasticity (e.g., epithelial-mesenchymal transition, chromatin remodeling, cell cycle plasticity, transcriptional rewiring, phenotypic switching) with particular emphasis on the mechanisms related to cancer progression, therapeutic response and drug resistance.

Please note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases will not be accepted.