I’m curious if anybody knows of other examples of how this mechanism actually works out physiologically.
Consider telomeres. The body’s inability to repair telomeres can be considered as an adaptive mechanism protecting from tumor formation in early life.
A little thought experiment:
When you’re a unicellular organism, you want to make as many copies of yourself as possible to maximize fitness. When you evolve into a multicellular organism, this strategy ain’t working anymore. A multicellular organism with telomerase expressed in every cell of the body will eventually get a mutation in one of the cell division regulatory cascades which causes it to divide infinitely and kill the whole organism.
For this reason, telomere repair should be disabled in non-reproductive cells so that renegade mutant cells would run out of reproductive capacity and stop dividing. The only way large tumors would occur is due to 2 independent mutations: one for cell division and one for telomerase expression. This is vastly more unlikely. The downside is that lack of telomere repair would lead to gene deregulation and eventual aging.
But longer-lived animals get cancer less, not more. I’ve heard this theory before but I don’t quite understand it. It seems to predict that age would be bounded by a trade-off against child cancers. But in fact selection seems to make animals longer-lived pretty easily (e.g. humans vs homo erectus). Naked mole rats barely get cancer at all, afaik. Do baby bats get cancer more than baby mice?
Consider telomeres. The body’s inability to repair telomeres can be considered as an adaptive mechanism protecting from tumor formation in early life.
A little thought experiment:
When you’re a unicellular organism, you want to make as many copies of yourself as possible to maximize fitness. When you evolve into a multicellular organism, this strategy ain’t working anymore. A multicellular organism with telomerase expressed in every cell of the body will eventually get a mutation in one of the cell division regulatory cascades which causes it to divide infinitely and kill the whole organism.
For this reason, telomere repair should be disabled in non-reproductive cells so that renegade mutant cells would run out of reproductive capacity and stop dividing. The only way large tumors would occur is due to 2 independent mutations: one for cell division and one for telomerase expression. This is vastly more unlikely. The downside is that lack of telomere repair would lead to gene deregulation and eventual aging.
But longer-lived animals get cancer less, not more. I’ve heard this theory before but I don’t quite understand it. It seems to predict that age would be bounded by a trade-off against child cancers. But in fact selection seems to make animals longer-lived pretty easily (e.g. humans vs homo erectus). Naked mole rats barely get cancer at all, afaik. Do baby bats get cancer more than baby mice?