Cancer resembles life 1 billion years ago, say astrobiologis

Tim Dean (Australian Life Scientist) 08 February, 2011 14:25 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.

Cancer is an evolutionary throwback, resembling early multicellular life, and flourishes when the more evolutionarily recent genes regulate cellular cooperation fail.

The genes that controlled the behaviour of these early multicellular organisms still reside within our own cells, managed by more r 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 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 astrobiology: Paul Davies, director of the Beyond Center for Fundamental Concepts in Science, Arizona State University; and Cha 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 colonies of eukaryotic cells in which cellular cooperation was fairly rudimentary, consisting of networks of adhering cells exchangi 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 a reversion of cells to the way they behaved a little over one billion years ago, when humans were nothing more than loose-knit colo 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 th 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 whe are failures or mutations in the more recent genes that manage the way cells specialise and interact to form the complex life of tod 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 biz naked mole rat.

"This quasi-ubiquity suggests that the mechanisms of cancer are deep-rooted in evolutionary history, a conjecture that receives su 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 th 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 ce 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 ev 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 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 cancers formidable complexity and diversity, how might one make progress toward controlling it? If the atavism hypothesis correct, there are new reasons for optimism," they write.

"The postulated toolkit of Metazoa 2.0, although admittedly complex, is nevertheless a xed and nite feature of multicellular life. T number of tools in the kit is not innite. What one cancer learns cannot be passed on to the next generation of cancers in other pat "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 ancient genes in check. The paper is available online at the Physical Biology site.

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