Cancer resembles life in the transition between single-celled organisms and complex multicellular organisms.
Sometimes stepping back and looking at the big picture can lend new clarity to an ongoing debate. In this case, it took the distant perspective of astrobiologists to reckon the origins of cancer.
The astrobiologists, working with oncologists in the US, have suggested that cancer resembles ancient forms of life that flourished between 600 million and 1 billion years ago.
Read more about what this discovery means for cancer research.
The genes that controlled the behaviour of these early multicellular organisms still reside within our own cells, managed by more recent genes that keep them in check.
It's when these newer controlling genes fail that the older mechanisms take over, and the cell reverts to its earlier behaviours and grows out of control.
The new theory, published in the journal Physical Biology, has been put forward by two leading figures in the world of cosmology and astrobiology: Paul Davies, director of the Beyond Center for Fundamental Concepts in Science, Arizona State University; and Charles Lineweaver, from the Australian National University.
In the paper, they suggest that a close look at cancer shows similarities with early forms of multicellular life.
"'Advanced' metazoan life of the form we now know, i.e. organisms with cell specialization and organ differentiation, was preceded by colonies of eukaryotic cells in which cellular cooperation was fairly rudimentary, consisting of networks of adhering cells exchanging information chemically, and forming self-organized assemblages with only a moderate division of labor," they write.
According to Lineweaver, this suggests that cancer is an atavism, or an evolutionary throwback.
“Unlike bacteria and viruses, cancer has not developed the capacity to evolve into new forms. In fact, cancer is better understood as the reversion of cells to the way they behaved a little over one billion years ago, when humans were nothing more than loose-knit colonies of only partially differentiated cells.
“We think that the tumours that develop in cancer patients today take the same form as these simple cellular structures did more than a billion years ago,” he said.
In a way, the genes that controlled this early multi-cellular form of life are like a computer operating system's 'safe mode', and when there are failures or mutations in the more recent genes that manage the way cells specialise and interact to form the complex life of today, then the earlier level of programming takes over.
One piece of evidence to support this theory is that cancers appear in virtually all metazoans, with the notable exception of the bizarre naked mole rat.
"This quasi-ubiquity suggests that the mechanisms of cancer are deep-rooted in evolutionary history, a conjecture that receives support from both paleontology and genetics," they write.
Their notion is in contrast to a prevailing theory that cancer cells are 'rogue' cells that evolve rapidly within the body, overcoming the normal slew of cellular defences.
However, Davies and Lineweaver point out that cancer cells are highly cooperative with each other, if competing with the host's cells. This suggests a pre-existing complexity that is reminiscent of early multicellular life.
They also point out that cancers' manifold survival mechanisms are predictable, and unlikely to emerge spontaneously through evolution within each individual in such a consistent way.
The good news is that this means combating cancer is not necessarily as complex as if the cancers were rogue cells evolving new and novel defence mechanisms within the body.
Instead, because cancers fall back on the same evolved mechanisms that were used by early life, we can expect them to remain predictable, thus if they're susceptible to treatment, it's unlikely they'll evolve new ways to get around it.
"Given cancer’s formidable complexity and diversity, how might one make progress toward controlling it? If the atavism hypothesis is correct, there are new reasons for optimism," they write.
"The postulated toolkit of Metazoa 2.0, although admittedly complex, is nevertheless a ﬁxed and ﬁnite feature of multicellular life. The number of tools in the kit is not inﬁnite. What one cancer learns cannot be passed on to the next generation of cancers in other patients.
"Cancer is not going anywhere evolutionarily; it just starts up all over again in the next patient."
They also suggest that new therapies could concentrate on the existing cellular regulation mechanisms that have evolved to keep these ancient genes in check.
The paper is available online at the Physical Biology site.