Why does cancerous cell proliferation sometimes continue despite checkpoint activation at the G1/S transition due to irreparable DNA damage after radiation therapy?

💡 Explanation

A mutated growth factor receptor can constitutively activate downstream signaling pathways, overriding the normal cell cycle checkpoint controls triggered by DNA damage. Because these checkpoints rely on growth factor receptor-mediated signals to halt cell division, a mutated receptor can bypass this arrest, therefore cancer cell division continues despite checkpoint activation, rather than being stopped by it.

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