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Previous episode p53: the gene that tells a damaged cell to destroy itself

How cancer starts: how a normal cell turns into cancer

Why cancer risk rises with age: one cell needs several mutations

By the age of 60, a big share of the cells in normal, sun-exposed skin already carry a mutation in a cancer gene, and the skin works just fine. So why does cancer need so many years, and why does it come mostly late in life?

  1. 1 Here is what broke in Rono's mole. In one of its cells, a new mutation broke one of the brakes that held the mole still. In melanoma, this is often a brake gene called CDKN2A, not p53. That cell started to copy again, and so did all its copies.

    Here is what broke in Rono's mole. In one of its cells, a new mutation broke one of the brakes that held the mole still. In melanoma, this is often a brake gene called CDKN2A, not p53. That cell started to copy again, and so did all its copies.

  2. 2 So far, Rono's mole has collected at least two hits in the same family of cells: a jammed accelerator fifty years ago, and a broken brake now. That is still not enough for cancer.jammedacceleratorbrokenbrakeat 20at 70

    So far, Rono's mole has collected at least two hits in the same family of cells: a jammed accelerator fifty years ago, and a broken brake now. That is still not enough for cancer.

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Next episode Telomeres: how cancer cells learn to divide forever

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