[C]ancer might arise more easily than previously thought. By doing experiments on both yeast cells and on human cells in culture, my colleagues and I have been able to show that just a single mutated gene suffices to accelerate cancer. The experiments mimic an early event during cancer development—the acquisition of genetic instability—which is characterized by a faster accumulation of mutations, and by genomic changes which can themselves disrupt cancer tumor suppressor genes or activate oncogenes.
So far it has been difficult to identify when and where genetic instability arises, either because tumor samples represent a late stage of cancer development and thus carry many different mutations.
This new work started from a provocative question posed to me by my mentor, Andrew Murray: “If we let cells choose, how do stable cells evolve into cancer cells?”
This contradicts the prevailing thinking in the field, which, as I noted, states that two inactivating mutations are required for cancer onset. And since a heterozygous mutation in a single gene suffices to trigger genetic instability, and we predict that human cells have 300 such genes, it is very probable that cells turn on the ability to mutate faster.
Read full, original post: A New Idea about How Cancer Begins