Because p53 and RB are so crucial to tumor suppression, their failure can be fatal. If either protein sustains a loss of function mutation, then errors in the DNA can make it past checkpoints. These errors can then lead to malfunctioning cells that cannot regulate their processes and become cancerous. Thus, both proteins are tumor suppressors.
For this scenario, a cell would need to receive a signal to divide. Since it is cloning itself for the replacement of a damaged cell, there must be a mechanism that releases division signals into the body. Perhaps this could be a signal released by the damaged cell itself or maybe another companion cell. What's important is that the replacement cell gets a signal to divide.
How does the cell accumulate extra cellular material to prepare for duplication? If it is increasing the rate of protein synthesis and doubling the cellular genome, where does it acquire all of the extra amino acids, nucleic acid, and other various cellular material?
It's interesting that the mechanisms of proteolysis can occur during the process of the cell cycle. This means that the proteins that add ubiquitin to other proteins functions during this period. These ubiquitinated proteins are then directed to the proteasome, meaning that the proteasome also functions during this time. They are lysed in the proteasome and degraded.
Cancerous cells take advantage of the failure of checkpoints and as a result accumulate more and more mutations. This is why cancerous cells are so hard to eradicate. Drugs can target specific players in specific pathways and disable them to prevent propagation of signals for growth, avoidance of cell death, and motility. But due to the mutability, cancer is able to adapt and utilize a different pathway or player to accommodate its needs for growth and spread. This is known as oncogene addiction.
Retinoblastoma (Rb) is an extremely commonly mutated protein in cancerous cells. Since it acts as a controller of a transcription factor for proteins (E2F)involved in the S phase of the cell cycle, when it has loss of function mutation it is not able to inhibit this TF. That is why Rb is considered a tumor suppressor.
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