Aging cells share features with cancer

Ars Technica » Scientific Method 2013-12-02

Cancer disproportionately affects the old.

The older we get, the higher our risk of cancer. With age, we accumulate exposure to environments and chemicals that increase the risk of acquiring cancer-causing mutations. But the danger doesn't increase in a linear manner, and we know little about why there is such a dramatic increase with aging.

Accumulated damage isn’t the only thing going on as we age. The body’s cells also go through a process called senescence. Chief among the changes that come with senescence are alterations to the epigenome, the proteins and chemical modifications that are attached to our DNA. These epigenetic changes can influence which genes are active in different tissues.

During the senescent phase of a human cell’s life, the epigenetic changes are an attempt to shutdown the process of cell division. Cell division involves creating copies of chromosomes and distributing them into two identical copies of the parent cell. But cells that go senescent stop multiplying. Cancer cells manage to bypass the mechanisms that stop them multiplying, including those put in place during senescence.

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