We think of cancer as a disease, a form of runaway cell growth within an organism. But we might not have realized what cancers really are: separate, brand new parasitic species that evolve from and prey upon their human hosts.

That's the theory put forward by UC Berkeley biologist Peter Duesberg, who argues that the very act of carcinogenesis - the formation of cancer - is itself a form of speciation, in which distinct new species evolve. That may seem a little far-fetched, so let's take a look at Duesberg's precise reasoning to see exactly what's going on here.


A key idea for Duesberg and his team is that cancer is the result of chromosome disruption, rather than the current scientific consensus that they are formed by genetic mutations. If the researchers are correct, an actual change in the nature of cancer's chromosomes would be far more drastic than just some simple mutations - basically, if something inside you has a totally different chromosomal makeup than you do, then it kind of has to be its own separate species.

That's part of the argument. Duesberg has more:

"Cancer is comparable to a bacterial level of complexity, but still autonomous, that is, it doesn't depend on other cells for survival; it doesn't follow orders like other cells in the body, and it can grow where, when and how it likes. That's what species are all about.

This isn't just a pedantic argument about what does and does not constitute a new species. If Duesberg is correct, then medical treatments that focus on blocking mutations are on the wrong track. This new theory holds that it isn't simply a few mutated genes that initiate cancerous cell growth; instead, when the chromosomes themselves are disrupted, some of them are deleted, others are broken or truncated, and some are even duplicated.

The end result is a cell that's completely different from those around it. The question then is if it's viable enough to survive inside its host body. In most cases, the chromosomal damage probably destroys the would-be cancer. But every so often, it survives, as Duesberg explains:

"If humans changed their karyotype — the number and arrangement of chromosomes — we would either die or be unable to mate, or in very rare cases become another species...You start with a chromosomal mutation, that is, aneuploidy perhaps from X-rays or cigarettes or radiation, that destabilizes and eventually changes your karyotype or renders it non-viable. The rare viable aneuploidies of cancers are, in effect, the karyotypes of new species."


So if this does replace the established mutation view of cancer, what's the upshot? One intriguing possibility is that these cancerous species may be configured for cellular flexibility and immortality, but they're also still very fragile, and their fundamentally damaged chromosomes means they exist right on the very brink of viability. If that's the case, then all we need to do is figure out a way to force cancer to keep evolving, shredding its chromosomes still further until it's no longer able to survive.

Via Cell Cycle. Image via.


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