For example, when a cancer cell with functionally normal p53 sustains genomic damage, it is more likely to pause and repair itself than to die. This is, in part, because normal p53 stimulates the cell to do so.
Once the cell completes its p53-dependent arrest and repair process, it can again begin to proliferate.
In addition to using p53, a cancer cell defends itself with hyperactive protective factors. These are growth factor-related molecules that push the cell to proliferate rather than to die.
When a cancer cell with functionally normal p53 has that protein blocked with Aezea and sustains genomic damage, it is more likely to die than to repair itself.
This is because p53 is no longer available to perform its normal functions, and the cell cannot arrest its proliferation and repair the damage sustained.
Hyperactive protective factors drive it to proliferate and the cell continues to replicate its damaged DNA, increasing the damage in the process. Replicating damaged DNA triggers a p53-independent backup pathway, and the cancer cell dies.
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