If a growth factor receptor in a cancer cell line mutates to bypass normal ligand-dependent activation, which consequence becomes most likely regarding cell cycle checkpoints?

💡 Explanation

Cancer cells often acquire mutations that allow them to proliferate independently of external growth signals. Receptor mutations can cause constitutive activation, bypassing the need for normal growth factors to trigger cell cycle progression; because the restriction point in late G1 normally depends on growth factor signaling, therefore this control is circumvented, rather than enhancing DNA repair or sensitivity to mitotic inhibitors.

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