Attacking the weaknesses of cancer may hold the key to unlocking new treatments, according to scientists whose research into the evolution of early animals has led them to a new theory of how the disease works.
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Australian National University astrobiologist Charley Lineweaver, Professor Paul Davies from Arizona State University and oncologist Mark Vincent from the University of Western Ontario have developed a theory that suggests cancer forms when recently evolved genes are damaged and cells have to revert to using older, inappropriate genetic pathways.
"For the past 15 years, Paul and I have been looking at the big questions such as, 'Are we alone?' And one of the things you do when you study astrobiology is you study the large-scale evolution of life on this planet, and an important part of that is how multicellularity evolved. And that's where we got involved in cancer, because cancer is a disease of multicellular organisms," Dr Lineweaver said. "Essentially, what we're adding to the understanding of cancer is evolution as a central feature."
Their research, which was recently published in BioEssays, looked at cancer from what is known as an atavistic model. Atavism is sometimes called a "genetic throwback" and examples of genetic atavism in humans include cases where people may have a third nipple, toe or finger webbing or a tail, Dr Lineweaver said. "Because these features we know existed in our ancestors, that means the genes to produce these features are still in us. But normally, they're repressed during embryogenesis while you're in the womb and your body is developing.
"But when something goes wrong with that, then these ancient features show up and that's what's called an atavism. That's what we believe cancer is doing."
Dr Lineweaver said the new model would not provide an overnight cure but created the possibility of new ways to treat cancer.
"Our model, in contrast to the standard model, is predictive in the sense that it make predictions about what capabilities cancer can and cannot have, and that's why we're so excited because it tells doctors, 'The cancer will do this but it won't do this', and it makes predictions about its progression," he said.
"Cancer is unregulated cell growth ... it spreads and take over various parts of the body. That's the thing that's mostly targeted by currently strategies.
"Unregulated cell proliferation is a strength of cancer because it is so deeply embedded, deeply entrenched in cancer cells, and it doesn't make sense to attack your enemy's strength. What's important is you figure what the weaknesses of cancer are and that's what we can predict with our model that the standard model cannot do."
To better understand cancer, the team turned to the knowledge found in the genome sequences from a large range of humans' distant relatives, including fish, corals and sponges.
Dr Lineweaver said the adaptive immune system of humans has evolved "relatively recently" and it seemed cancer cells do not have the ability to "talk to and be protected" by it.
"The new therapeutic strategies we are proposing target these weaknesses," he said.
Dr Vincent agrees there is the possibility of "novel therapeutic implications" from their work.
"Our emphasis would be more on the systematic exploitation of signature differences between cancer and normal cells," he said.
"These differences, which conform to primitive cellular life ... suggestive of adaptation to ancient ocean chemistry, potentially allow cancer cells to be selectively destroyed based on 'marker differences' compared to normal cells, rather than by the current focus on inhibiting causative mutations."
