Disruptions to the Cell Cycle

The cell cycle has checkpoints, mainly at G1, G2, and metaphase, where the cell checks its own DNA and internal state before moving forward. If DNA is damaged, proteins like p53 normally pause the cycle so repair can happen, or trigger the cell to self-destruct if the damage is too severe. A checkpoint is only useful if something acts on its verdict. If the checkpoint protein itself is mutated and broken, the cell ignores the damage and divides anyway, passing the same broken DNA to two daughter cells. Repeat that enough times and you get a population of cells accumulating more and more mutations, some of which may disable other checkpoints or growth controls.

Apoptosis is the cell's own emergency shutdown, a tightly controlled genetic program. The cell activates enzymes called caspases that chop up its DNA and proteins from the inside, then packages the pieces into membrane-bound blebs that neighboring cells and immune cells quietly clean up. This is different from necrosis, where a cell is injured, swells, and bursts, spilling its contents and triggering inflammation. A cell with irreparable damage is supposed to trigger its own apoptosis, but if that pathway is also mutated, the damaged cell survives and keeps dividing instead of dying.

This is where signaling connects to cancer. Growth factor pathways normally need an external signal to switch on cell division and switch off again. A mutation that locks one of these pathways permanently on, or disables the checkpoint or tumor suppressor that would halt it, removes the brakes entirely. The cell divides continuously without waiting for a go-ahead or passing inspection, and its damaged descendants can eventually form a tumor.