Loading
Life sciences · Journal article
Cellular & Molecular Biology Letters · September 22, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Tumor evolution is a dynamic and multifactorial process driven by genetic alterations, epigenetic remodeling, and adaptive responses to environmental pressures. A central concept emerging from recent cancer research is the role of cellular plasticity in shaping tumor heterogeneity and therapeutic resistance. In particular, the dedifferentiation of mature tumor cells into cancer stem cells (CSCs) has been increasingly recognized as a major mechanism contributing to tumor progression and adaptation. Rather than representing a fixed population derived exclusively from normal stem cells, CSCs are now understood as a dynamic cellular state that can be acquired or lost through reversible phenotypic transitions. These transitions are regulated by complex networks involving transcriptional reprogramming, epigenetic modifications, developmental signaling pathways, and microenvironmental signals. Importantly, dedifferentiation allows differentiated tumor cells to regain stem-like properties, thereby replenishing the CSC pool and facilitating tumor evolution. This review integrates the classical clonal evolution model with the cancer stem cell framework, proposing that dedifferentiation represents a key non-genetic engine of tumor evolution. We discuss the molecular mechanisms underlying CSC plasticity, the role of epithelial–mesenchymal transition, epigenetic reprogramming, and microenvironmental signals in driving dedifferentiation. Furthermore, we examine evidence from single-cell transcriptomics and lineage-tracing studies demonstrating dynamic cell state transitions within tumors. Finally, we explore the implications of CSC plasticity for metastasis, therapy resistance, and future therapeutic strategies targeting tumor evolution.