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A review article about correlation between tumour cell plasticity and cancer cell invasion and metastasis in the last years studies.

Abbas Jedariforoughi.




Abstract
Cited by 15 Articles

Despite improvements in protocols of radio-, chemo-, and immunotherapy, distant metastases are still responsible for the great majority of cancer-related deaths. Detailed studies of mechanisms of cancer cell dissemination are of great importance for understanding tumour progression and developing new targeted drugs.
Tumours are ecosystems composed of cancer cells and non-tumour stroma together in a hypoxic environment often described as wounds that do not heal. Accumulating data suggest that solid tumours hijack cellular plasticity possibly to evade detection by the immune system.
Based on extensive study of the cancer research literature, there are proposed four novel hallmarks of cancer, namely, the potency of cells to regress from a specific specialized functional state, epigenetic changes that can affect gene expression, the role of microorganisms and neuronal signalling, to be included in the hallmark conceptualization along with evidence of various means to exploit them therapeutically.
Cell plasticity definition is the ability of a cell to reprogram and change its phenotypic identity, a phenomenon also known as lineage plasticity. Cell plasticity occurs in several fundamental biological processes, such as embryonic development, wound healing, tissue regeneration, or neoplastic transformation.
The cross-talk between cancer and stromal cells and the interactions with the extracellular matrix, hypoxia and acidosis contribute to triggering a new tumour cell identity and enhancing tumour heterogeneity and metastatic spread.

Key words: Tumour, Plasticity, Cell, perivascular niche (PVN), tumour microtubes (TMs), Cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), tumour microenvironment (TME), A cluster of differentiation 73(CD73), mesenchymal stroma/stem-like cells (MSCs), (CSCN) cancer stem cell niche






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