A cancer cell with mutated EGFR (epidermal growth factor receptor) continues to divide despite DNA damage. Which consequence follows from the mutated receptor's effect on cell cycle checkpoints?

💡 Explanation

Mutated EGFR can lead to continuous activation of downstream signaling pathways that suppress cell cycle checkpoints. Because checkpoint proteins like p53 are not activated, cells with DNA damage bypass arrest and continue dividing; therefore, uncontrolled proliferation occurs, rather than regulated repair or apoptosis prompted by checkpoints.

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