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How can uncontrolled cell division lead to cancer?
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Artist's conception of a human neuron.
Cancer arises when the normal regulatory mechanisms governing cell division fail, allowing cells to proliferate uncontrollably at the expense of the organism. This loss of control typically results from multiple genetic or epigenetic "insults" that rewire the cell's internal circuitry.12
Key factors in this process include:
- Oncogenes: These are mutated or altered versions of normal genes (proto-oncogenes) that promote cell growth. When activated, they can act like a stuck accelerator, forcing cells to divide indefinitely or grow without necessary external growth factors.13
- Tumor Suppressor Genes: These genes normally act as "brakes" on cell division. When both copies of these genes are inactivated by mutation or deletion, the cell loses its ability to restrain proliferation.3
- Checkpoint Failure: Cells possess checkpoint signaling systems designed to detect DNA damage and trigger apoptosis (programmed cell death). Cancerous cells often harbor mutations—such as those in the p53 protein—that allow them to bypass these checkpoints, survive despite damage, and continue dividing.4
As these cells continue to divide, they may accumulate further mutations, eventually enabling them to invade surrounding tissues and spread to distant parts of the body, a process known as metastasis.1