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Cancer therapy procedures such as chemotherapy and radiotherapy work by overwhelming the capacity of the cell to repair DNA damage, resulting in cell death. Cells that are most rapidly dividing – most typically cancer cells – are preferentially affected.
Depending on the extent of injury, the cellular response may be adaptive and where possible, homeostasis is restored. [1] Cell death occurs when the severity of the injury exceeds the cell's ability to repair itself. [2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused. [1]
Such damage will trigger programmed cell death (e.g. apoptosis) in cancer cells. Cisplatin resistance occurs when cancer cells develop an enhanced ability to reverse such damage by removing the cisplatin from DNA and repairing any damage done.
Inflammation-induced ROS that cause DNA damage can trigger apoptosis, [52] [53] but may also cause cancer if repair and apoptotic processes are insufficiently protective. [45] Bile acids, stored in the gall bladder, are released into the small intestine in response to fat in the diet. Higher levels of fat cause greater release. [54]
Cells with a defective G 2-M checkpoint will undergo apoptosis or death after cell division if they enter the M phase before repairing their DNA. [1] The defining biochemical feature of this checkpoint is the activation of M-phase cyclin-CDK complexes, which phosphorylate proteins that promote spindle assembly and bring the cell to metaphase. [2]
The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).