… “To use a computer analogy, cancer is like Windows defaulting to “safe mode” after suffering an insult of some sort,” Davies writes.
The result of this malfunction is the start of a cascade of events that we identify as cancer – a runaway proliferation of cells that form a tumour, which eventually becomes mobile itself, spreading to other parts of the body and invading and colonizing.
Orthodox explanations suppose that cancer results from an accumulation of random genetic mutations, with the cancer starting from scratch each time it manifests; however, Davies and Lineweaver believe it is caused by a set of genes that have been passed on from our very early ancestors and are “switched on” in the very early stages of an organism’s life as cells differentiate into specialist forms.
The pair suggests that the genes that are involved in the early development of the embryo – and that are silenced, or switched off, thereafter – become inappropriately reactivated in the adult as a result of some sort of trigger or damage, such as chemicals, radiation or inflammation.
“Very roughly, the earlier the embryonic stage, the more basic and ancient will be the genes guiding development, and the more carefully conserved and widely distributed they will be among species,” Davies writes.
Several research teams around the world are currently providing experimental evidence that shows the similarities between the expression of genes in a tumour and an embryo, adding weight to Davies and Lineweaver’s theory. …
It may help to think of cancer as what happens when immune system inflammation responses can not get rid of an attack on the body. One Ph.D. student studying evolutionary biology had this perspective:
The fact is that cancer cells have a selective advantage in their host, simply because they multiply rapidly. Within that host, the cancer cells are “winning.” However, this ultimately kills the host – so the advantage stops there. A hereditary tendency to develop cancer would be a selective disadvantage since individuals prone to cancer would tend to die early and be less likely to pass on their genes.
One lesson from this is that you can have opposing selective pressures acting at different scales.
Could cancer have evolved to protect us?
A physics-based, “atavistic” model posits that cancer is a “safe mode” for stressed cells and suggests that oxygen and immunotherapy are the best ways to beat the disease. …
Could cancer be our cells’ way of running in “safe mode,” like a damaged computer operating system trying to preserve itself, when faced with an external threat? That’s the conclusion reached by cosmologist Paul Davies at Arizona State University in Tempe (A.S.U.) and his colleagues, who have devised a controversial new theory for cancer’s origins, based on its evolutionary roots. If correct, their model suggests that a number of alternative therapies, including treatment with oxygen and infection with viral or bacterial agents, could be particularly effective.
At first glance, Davies, who is trained in physics rather than biomedical science, seems an unlikely soldier in the “war on cancer.” But about seven years ago he was invited to set up a new institute at A.S.U.—one of 12 funded by the National Cancer Institute—to bring together physical scientists and oncologists to find a new perspective on the disease. “We were asked to rethink cancer from the bottom up,” Davies says.
Davies teamed up with Charley Lineweaver, an astrobiologist at The Australian National University in Canberra, and Mark Vincent, an oncologist at the London Health Sciences Center in Ontario. Together they have come up with an “atavistic” model positing cancer is the reexpression of an ancient “preprogrammed” trait that has been lying dormant. In a new paper, which appeared in BioEssays in September, they argue that because cancer appears in many animals and plants, as well as humans, then it must have evolved hundreds of millions of years ago when we shared a common single-celled ancestor. At that time, cells benefited from immortality, or the ability to proliferate unchecked, as cancer does. When complex multicellular organisms developed, however, “immortality was outsourced to the eggs and sperm,” Davies says, and somatic cells (those not involved in reproduction) no longer needed this function.
The team’s hypothesis is that when faced with an environmental threat to the health of a cell—radiation, say, or a lifestyle factor—cells can revert to a “preprogrammed safe mode.” In so doing, the cells jettison higher functionality and switch their dormant ability to proliferate back on in a misguided attempt to survive. “Cancer is a fail-safe,” Davies remarks. “Once the subroutine is triggered, it implements its program ruthlessly.”
It makes a lot of sense to me. If true, the first step would be to remove the insult, the thing triggering the cellular safe mode response.