From the source, Davies' argument (for those who don't want to register for Physics World):

Cancers prevalence among multi-cellular organisms indicates it is "deeply embedded in the logic of life". It is found among mammals, birds, fish, reptiles, and other organisms. The human genome is pre-loaded with a "cancer sub-routine" that is triggered by various factors. Once triggered, most cancers follow a similar pattern: reproduce uncontrollably in a specific organ, then spread throughout the host, invading and colonizing other organs and parts of the bodies with the help of tumors.

> The overall impression is of a carefully orchestrated and pre-programmed strategy--its aim to multiply cancer cells and colonize new sites--which is unleashed when neoplastic cells somehow evade the normal regulatory mechanisms of the organism and embark on their own agenda.

Seeing a "highly organized and efficient behaviour in biology" leads Davies and Lineweaver to suspect evolutionary mechanisms at play. Davies finds that orthodox explanations describing cancer as random genetic mutations starting from scratch leave too many unanswered questions--such as why they are fitter than the existing healthy cells in a body, why such random mutation provides "a whole series of mutually supportive survival traits ... in a period of just years of months", why dormant cancer returns in the same organ after a primary tumor is removed, or "why cancer cells deliberately transplanted into certain tissues, or cancer nuclei into healthy cells, often results in normal behaviour", while the reverse process results in cancerous cells.

Thus, from a physics perspective, "there are clues pointing to cancer as a phenomenon influenced by forces and fields--not one that is purely ruled by genetic instruction." Sadly, the article never dives into more on this physics perspective and what kinds of forces and fields may be at play, instead turning to evolutionary biological arguments from embryonic development applied to cancer development.

> Cells are usually regulated by mechanisms that instruct them when to multiply and when to die. What we believe is that when these mechanisms malfunction, the cells revert to the default option, a genetic subroutine programmed into their ancestors long ago, of behaving in a selfish way.

> Lineweaver and I suggest that genes that are active in early-stage embryogenesis and silenced thereafter – which, by our hypothesis, are generally the ancient and highly conserved genes – may be inappropriately reactivated in the adult form as a result of some sort of insult or damage. This trigger serves to kick-start the cascade of maladaptation events we identify as cancer. So the "cancer subroutine" is really just a re-run of an embryonic developmental program. We envisage a collection of ancient conserved genes driving the cancer phenotype, in which the metastatic mobility of cancer cells and the invasion and colonization of other organs merely reflects the dynamically changing nature of embryonic cells and their ability to transform into different types of tissues.

> The big picture is that we attribute cancer's survival traits to deep evolution on a billion-year scale, rather than orthodox explanations that point to evolution from scratch with each case of the disease. In our theory, the latter remains true, but is a small perturbation.

The ASU article covers much of the rest of the original article by Davies. ASU just left out much of the lead-up to how they arrived at their conclusions.

Physics World also has a lot more coverage in the current issue, entitled "Physics of Cancer". The entire issue can be downloaded as PDF here: http://physicsworld.com/cws/download/jul2013