How does cell cycle regulation relate to cancer?

P-53, also known as the guardian of the genome, stops the cell to proofread the DNA. If there are minor problems it says fix them; if there are major problems it triggers events that kill the cell. A non-cancerous cell will adhere to cues that it's too crowded or something else is amiss. The first checkpoint determines whether the conditions are favorable for replication and whether the cell has multiplied intact.

If P-53 isn't functioning, then it isn't checking for DNA damage and stopping the cell from being cancerous and making more copies of the damaged DNA. Checkpoints stop the cell from behaving as cancer. It's a little more complex than that but that's the general idea. Cancer cells don't listen to cell to cell spacial cues and replicate endlessly until they form masses; tumors.

Cell cycle regulation ensures orderly progression through cell division phases. Mutations disrupting this control can lead to uncontrolled cell growth, a hallmark of cancer. Dysregulated cell cycle allows rapid division, promoting tumor formation and progression. Key regulatory proteins like cyclins and CDKs play crucial roles in governing the cell cycle. Mutations in these genes contribute to cancer by disrupting checkpoints and promoting aberrant cell proliferation. Targeting cell cycle regulators is a strategy in cancer therapy.