Scientists know that all cells, cancerous and normal, have a genetic pathway called programmed cell death. The problem is, cells often ignore this pathway. In the normal prostate, androgens keep androgen-dependent cells alive; these cells become relatively immortal (it’s like pumping air to a deep-sea diver). But when this life-giving supply of hormones is shut off—by physical or chemical castration—the picture changes. The change in hormones triggers a series of events in which certain genes are expressed, and new proteins are made. Some scientists believe these new proteins prompt a buildup of free calcium in the cells. And the prolonged increase in calcium activates what one Johns Hopkins scientist describes as a “suicide enzyme.” This “suicide” enzyme, something called a calcium-magnesium-dependent end nuclease, functions as a sort of wrecking ball. It breaks down the DNA in the nucleus, and wipes out the cell’s genetic memory bank. The cell no longer replicates, but dies. Over time, it begins to fragment; tiny chunks are later recycled as building materials by other cells. “This is an active process,” the scientist explains, “in which the cell that is destined to die is actively involved in its own death.”

This process happens all the time, particularly during fetal development, “or we wouldn’t be able to develop as people who have arms and legs and appendages,” the scientist continues. “When you’re developing, you have limb buds.

And that’s a particularly tricky, coordinated process. You can imagine—you’ve got to make some cells die and other cells have to live, right next to them.”

Androgen-independent cells, while all this is going on, experience no such increase in calcium. Although they possess a similar suicide pathway, it is not activated.

This is an area of intensive work for prostate cancer researchers—figuring out how to kill these cells, or better yet, how to get them to kill themselves.


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