What a cool paper. I wonder if there are any active mutator mechanisms involved, analogous to AID in B cells.
Somatic mutations accumulate in “normal” non-cancerous tissues (blood, skin, liver). But why are mutant clones selected? Do they merely proliferate more, selfishly? Or can clones adapt to disease? Could they protect tissues? We shed light on this: https://t.co/Vu1d4U3stc 1/10
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