Random Chance: A Primary Driver of Cancer Mutations?

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By Carl Engelking

Whether we like to or not, we’re all gamblers.

Every waking moment, countless stem cells inside our bodies are dividing in order to replace worn out biological machinery. But every time these perfectly healthy cells divide, roughly three mistakes occur in the genetic code—no one’s perfect. These mutations, though unpredictable, are typically benign, but sometimes this molecular game of Roulette takes an unlucky turn.

“Most of the time these mutations don’t do any harm; they’re in junk DNA, or unimportant places,” says Johns Hopkins cancer researcher Bert Vogelstein. “That’s the usual situation, and that’s good luck. But occasionally they occur in a cancer driver gene, and that’s bad luck.”

Today, there’s little doubt that mutations cause cancer, but there’s less consensus regarding the primary instigators of those mutations.

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1 COMMENT

  1. It seems to me, scientists could cure cancer by preserving healthy cells (ideally when very young before mutations have accumulated) and periodically using a modified virus or gene drive similar to CRISPR/Cas9 to swap out the genes of every cell in our body. This would essentially cure all forms of cancers.

    Because these young genes would also have the full compliment of telomeres, it’s also possible it would halt or even reverse aging to some extent. One could even correct genetic errors or add improvements in these gene “updates.”

    Even if one hadn’t preserved the younger version of un-mutated genes early in life, it might be possible through comparing large numbers of an individual’s genes to identify the mutations and create a pristine sample to manufacture in the laboratory and then re-insert.

    The challenge would come during the replacement to make sure each portion of the genes in a particular cell was correctly primed to know the role it played (as a brain cell, as opposed to a liver cell). Possibly the gene drive would have to compare the replacement against the old cell and fix only those things that are different than the un-mutated younger template and leave the rest intact to retain the epigenetic switches or whatever mechanism is used to activate the specialized functionality.

    It would be interesting to learn how the handful of “functionally immortal” organism in nature deal with this problem.

    Since I’m not a scientist, there are probably many things wrong with this idea—or others have already thought of it.

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