Challenging the Standard Model of Cancer


Despite decades of research, cancer remains an enigma. Conventional wisdom holds that cancer is driven by random mutations that create aberrant cells that go wild in the body.

In a new article published this week in the journal BioEssays, Researchers in Arizona and Australia challenge this model by proposing that cancer is a type of genetic return, which progresses through a series of reversions to ancestral life forms. Unlike the conventional model, the distinguishing abilities of cancer cells are not primarily generated by mutations, the researchers say, but are pre-existing and latent in normal cells.

Professor Regents, Paul Davies, director of the Beyond Center for Fundamental Concepts in Science at Arizona State University, and Kimberly Bussey, cancer geneticist and bioinformatician in the Precision Medicine program at Midwestern University, Glendale, Arizona, teamed up with Charles Lineweaver and Anneke Blackburn at Australian National University (ANU) in Canberra to refine what they call the Serial Atavism (SAM) model of cancer. This model suggests that cancer occurs through several stages that resuscitate old cellular functions.

These functions are retained by evolution for specific purposes such as embryonic development and wound healing, and are usually disabled in the adult form of complex organisms. But they can be reactivated if something compromises the body’s regulatory controls. It is the resulting resurrection stages, or atavistic inversions, that are primarily responsible for the ability of cancer cells to survive, proliferate, resist treatment, and metastasize, the researchers said.

Davies and Bussey are also members of ASU’s Arizona Cancer Evolution Center (ACE), which seeks to understand cancer, not only in humans, but across complex species, in light of evolutionary processes.

“Cancer research has been transformed in recent years by comparing the genetic sequences of thousands of species to determine the age of genes,” Davies said. Just as geologists can date rock strata, geneticists can date genes, a technique known as phylostratigraphy.

“The atavistic model predicts that the genes needed for cancer to perform are mostly old – in some cases little change over billions of years,” Davies added.

Lineweaver explained, “In biology, nothing makes sense except in the light of evolution, and in the case of cancer, nothing makes sense except in light of the profound evolutionary changes that have occurred when we have become multicellular organisms. “

“The atavistic model of cancer has grown in popularity around the world,” Bussey added. “In part, this is because it makes many predictions that can be tested by phylostratigraphy, contrary to conventional somatic mutation theory.”

Blackburn, a cancer biologist at ANU’s John Curtin School of Medical Research, agreed.

“Oncologists and cancer biologists are increasingly aware of the importance of age in genes,” she said. “We now need to use this knowledge to develop new therapeutic strategies. A better understanding of cancer can lead to better treatment outcomes.”


Skip Derra, ASU Media Relations, (480) 965-4823; [email protected]

For interviews:

Associate Professor Charley Lineweaver

School of Research in Astronomy and Astrophysics and School of Research in Earth Sciences, ANU

T: +61 2 6125 6717 or +61 2 6125 0822

Phone: +61457550577

E: [email protected]

Associate Professor Anneke Blackburn

John Curtin School of Medical Research, ANU

T: +61 405 067 200

[email protected]

Professor Paul Davies

Beyond Center, Arizona State University

Tempe, Arizona T: +61 2 6125 5172

E: [email protected]

Kimberly Bussey

Precision Medicine Program

Midwestern University

Glendale Arizona,

+1 623-537-6598

[email protected]

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