Anastasis: Cell Survival Mechanism.
Cancers result as the disruption and/or the abnormal regulation of the pathways that coordinate cell growth and cell death. An increasing understanding of these pathways shows numerous
ways that cancer cells might be susceptible to therapy. Therapeutic agents, mainly radiation and drugs, are usually potent promoters of cell cycle arrest and programmed cell death (apoptosis). Genetic and epigenetic modifications that are important in tumorigenesis often hinder these pathways and thus alter cancer cells response to therapeutic actions. These modifications usually differ among cancers and occasionally among tumors of the same tissue type. The outgrowth of a clonal population of cells that follows a loss of tissue homeostasis is one of the hallmarks of cancer development. Tissue homeostasis/balance between cell birth and death is regulated by a several processes such as cell cycle arrest and apoptosis. Defects in these pathways clearly cause
a selective growth advantage. Several cancers possess inactivating mutations in the genes that involve the checkpoints that keep the cell cycle events in their appropriate order1 and influence apoptotic pathways,2 meanwhile some cancer-derived cell lines show a resistance to apoptotic stimuli. Recently, experimental evidence supports the suggestion that genetic modifications that inactivate.
Cancer Stud Mol Med Open J. 2020; 6(1): 5-11. doi: 10.17140/CSMMOJ-6-131
