Cancer formation is a process akin to the development of a newly evolved species, rather than a result of mutation, according to a study recently published by researchers at UC Berkeley.

Published in the July 1 issue of the journal Cell Cycle, the study, led by campus professor of molecular and cell biology Peter Duesberg, presents a theory that cancer formation is not the result of genetic mutation, as has long been thought. According to Duesberg, carcinogenesis is the result of speciation — the formation of a new species over the course of evolution.

The study challenges the long-held belief that cancer is the result of genetic mutations which result in uncontrolled cell growth, instead arguing that cancer formation stems from aneuploidy — chromosomal disruption which alters the balance of genes, resulting in cells with new traits.

“(The research) started off maybe 10 to 12 years ago on the idea ‘let’s have a look at the chromosomes as causes of cancer,’” Duesberg said. “That also was an older idea, but it was abandoned because of the mutations theory. What we confirmed here was that there was always aneuploidy.”

Duesberg said that ordinarily humans have 46 chromosomes in the majority of cells, defining the human species. However, he said he could not find a cancer that has 46 chromosomes, stating that many fatal cancers, including lung and colon cancers, have 70 to 80 chromosomes and sometimes even more.

Mark Vincent, a medical oncologist at the London Regional Cancer Program and an associate professor at the University of Western Ontario, said in an email that he agrees with the campus team’s theory that chromosomal disruption is the root cause of cancer.

However, Vincent said in the email that he does not believe cancer formation ends with speciation.

“What worries me is, once transformed, what have cancer cells become?” Vincent said in the email. “It is not enough to consider just speciation, one has to go beyond that; I think cancer represents a different form of life, with a particular evolutionary purpose.”

In terms of implications, Duesberg said he believes that this research could allow for earlier diagnoses of cancer. Vincent said he agreed, although he questioned how much earlier diagnoses could be made.

“Aneuploidy could certainly be looked at for earlier diagnosis of fully transformed cells, but will it be possible to use this with cells that are on the way to cancer but not yet there?” he said in the email.

Looking toward the future, Vincent added that he would like people to try to see cancer as an “evolutionary phenomenon, as having some meaning and connection with the deep history of life on earth.”

Virginia Tech graduate student and co-author of the paper Joshua Nicholson said in email that the research will assist in pointing toward the causes of cancer.

According to Duesberg, while his research may provide answers regarding the origins of cancer that the more commonly held mutation theory cannot provide, there are still issues with finding functional proof of his theory.

“What’s mostly missing is functional proof. Nobody has been able to isolate a gene from a cancer that can be transferred … and shown to cause cancer,” he said. “That’s the ultimate proof for anything in biology or in science anywhere. You need functional proof.”