Cancer could be an 'evolutionary throwback' locked within our genes, linked to the time before we became multicellular animals, according to a new study.
Professor Paul Davies of Arizona State University and Dr Charles Lineweaver of the Australian National University in Canberra, outline their hypothesis in the latest issue of the journal Physical Biology.
The astrobiologists say looking at cancer from an evolutionary viewpoint suggests the mechanisms that lead to cancer are locked in an 'ancient toolkit'. This toolkit comprises of genes that evolved more than a billion years ago when simple, single cells began to co-operate in multicellular organisms.
As multicellular organisms evolved, regulatory genes were 'switched on' causing single cells to stop dividing and become more specialised, for example as liver or blood cells.
It could be that cancer reverses this process, causing cells to 'revert' to a loose-knit co-operation that evolved before multicellular life began, the researchers say.
Lineweaver says the model could be tested by sequencing the genomes of the simplest multicellular life to trace the evolution of these genes.
"Our new model should give oncologists new hope," he says.
"We think that the tumours that develop in cancer patients today take the same form as these simple cellular structures did more than a billion years ago.
"It suggests that cancer is a limited and ultimately predictable adversary."
The researchers point out that genome studies indicate that some of the genes that potentially cause cancer, oncogenes, have an ancient origin.
"Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly efficient pre-programmed response to stress, honed by a long period of evolution," says Davies, Director of the BEYOND: Center for Fundamental Concepts in Science at Arizona State University.
Comparative genomics the next step
Lineweaver says the research is a "new conceptualisation" of what cancer is, and has had a positive reception from oncologists. "All of the factors and adaptations that make cancer seem so complex are ones whose genetic basis evolved billions of years ago," he says.
Professor Nick Hayward, head of the oncogenetics laboratory at the Queensland Institute of Medical Research says the research presents a "novel hypothesis", but needs more genetic information from a range of organisms to be testable.
"What they are proposing is consistent with general views of the cancer stem cell hypothesis, which is that cells revert back to a state where they are able to function in a more pluripotent [capable of affecting more than one organism] rather than a differentiated state."
Hayward says by comparing the genomes of single-celled and multicellular organisms, and identifying genes that have radically changed, they could be tested against the number of known cancer-causing genes.
"That would be a direct test of the hypothesis and would give credence to the model."