Offering a new explanation for what drives cancer, recent research has shown that cells with cancerous mutations can suddenly find themselves most fit, allowing their population to expand when the tissue ecosystem changes due to ageing, smoking, or other stressors.
Arguing against the commonly held “accumulation of mutations” model of cancer, the study favours a model that depends on evolutionary pressures acting on populations of cells. It, therefore, contends that the ecosystem of a healthy tissue landscape lets healthy cells outcompete ones with cancerous mutations.
This new thinking about what drives cancer development may have profound implications for cancer therapy and drug design.
“We have been trying to make drugs that target mutations in cancer cells,” said study senior author James DeGregori, associate director for basic science at University of Colorado Cancer Center in the US.
“But if it is the ecosystem of the body, and not only cancer-causing mutations, that allows the growth of cancer, we should also be prioritising interventions and lifestyle choices that promote the fitness of healthy cells in order to suppress the emergence of cancer,” said DeGregori.
The proposed model, presented in the journal PNAS, helps to answer a longstanding question in cancer science known as Peto’s Paradox — if cancer is due to random activating mutation, larger animals with more cells should be at greater risk of developing the disease earlier in their lives.
Well, then why do mammals of vastly different sizes and lifespans all seem to develop cancer mostly late in life? The answer to this proposed by researchers is that in addition to activating mutation, cancer may require age-associated changes to the tissue landscape in order for evolution to favour the survival and growth of cancer cells over the competition from healthy cells.