Is there a cure for cancer? New understanding of the disease's origins could help scientists fight it

Sarah Spickernell
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The atavistic model suggests fast multiplication would have benefited single-celled organisms (Source: Getty)
Before there were complex multicellular organisms like humans, there were single-celled organisms. For these much simpler beings, the uncontrollable multiplication of a cell would have posed no threat to their health.
In fact, a group of scientists at the Arizona State University in the US say it could have provided a form of protection – it gave single-celled organisms an increased chance of survival when faced with an external threat such as radiation.
But when complex organisms developed, they could no longer survive an external threat by rapid proliferation – at this point, immortality was passed through eggs and sperm instead. Yet the genes coding for the fast multiplication that causes cancer did not go away at that point, which is why humans continue to develop the disease.
This controversial new theory for the evolutionary purpose behind cancer is based on an “atavistic model”, which means cancer is the result of the re-expression of an ancient trait lying dormant until the cell faces difficult external circumstances – at that point, it switches on the gene for fast multiplication in order to ensure it survives the threat.
“Cancer is a fail-safe,” Dr Paul Davies, one of the lead researchers involved in the study, told Scientific American. “Once the subroutine is triggered, it implements its program ruthlessly.”
In a paper published in the journal BioEssays, the researchers behind the theory argue that the trait would have evolved hundreds of millions of years ago, when there existed a common, single-celled ancestor for all multicellular organisms alive today.
Davies says that if the model is correct it could help researchers develop new and effective treatments for cancer. Speaking at a medical engineering conference held at Imperial College London last month, Davies suggested that rather than targeting cancer's ability to reproduce, new treatments could be developed based on cancer's newly exposed “Achilles' heel”.
For example, under the atavistic model cancer would have evolved when there was less oxygen on Earth and the environment was more acidic. This means that exposing cancer patients to high levels of oxygen and reducing the acidity of their diets could potentially stop cancer cells proliferating and therefore reduce the size of tumours.
Another possible area of treatment promoted by Davies is that of immunotherapy, which involves infecting patients with bacterial or viral agents. He argues that if the new theory is correct, cancer cells should be more vulnerable than normal cells to being killed by foreign infectious agents – this is because protective functionality is diminished when the cancer cells “reboot into safe mode”.

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