Evolution, sex and TRACERx: how cancer’s ‘spare tyre’ helps it survive  

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Lung cancer cells

Almost all swine have intercourse. That’s to say, DNA from seman and eggs is exchanged to create offspring with a mixture of both parents’ genes.

It’s the norm in seeds very, where pollen from one weed fertilises another. Even bacteria have a primitive sort of gender, where they provide an extremity, called the pilus, to pass DNA from one cell to another.

In evolutionary periods, this may seem counter-productive. Why would anyone want to pass on only half of their DNA to their offspring, instead of producing a clone asexually?

But for countless species, this exchange of genetic material is essential to survival and has been consistently selected for throughout evolution.

And considering the alternative, it’s easy to see why.

There are some animals that have lost the ability to have sex- such as self-fertile roundworms, a fish called the Amazon molly and particular amoebae. Without the opportunity to reshuffle DNA between unrelated souls, genetic wrongdoings build up.

This phenomenon is known as Muller’s ratchet, and has been observed in many asexual creatures. Any bad mutation that’s picked up by the organism- a turn of the ratchet- will be passed on to its offspring, with no way to revert to the original explanation of the gene.

When the offspring simulates, these mutants are passed away again, along with any added mutations acquired during its lifetime. With each generation, hazardous mutations build up and the ratchet stiffens, until the species is no longer viable.

Cancer cells are asexual

Cancer cadres partition rapidly- picking up lots of DNA errors as they do so- and can be thought of much like an legion of asexual amoebae. And our scientists working on TRACERx, our PS12. 5m project to understand lung cancer evolution, have employed this comparison to explain a inexplicable phenomenon observed in tumour cells.

Looking at a cancer cadre under a microscope, you won’t check the neatly packaged 46 chromosomes found in healthy tissue. Their DNA is in chaos, with divisions of chromosomes exchanged, replicated, or missing all together.

And in some cancer cells, scientists have noticed something even more remarkable, known as entire genome doubling.

“When we look across cancers, and lung cancers in particular, we see that many of them have doubled their genome at some phase in their evolutionary record. Almost every chromosome appears to have been replication, so there is far more DNA than in a normal cell, ” excuses Dr Nicky McGranahan, seam guide for the TRACERx team at University College London.

Until now, the same reasons for this had remained a mystery.

Cancer’s spare tyre

“We envisioned there might actually be a survival advantage to cancer of doubling its genome. Cancer progression is an evolutionary process, and so the principals of Darwinian natural selection apply.”

McGranahan and the team believed it could link to Muller and his ratchet

The team’s theory was that having an extra copy of their genetic code, essentially a genetic save tyre, could benefit cancer cadres. If one copy of the genome gained a dangerous mutant, the cell could continue to survive and segment, thanks to the work of its second copy.

To test this, the researchers established a computer model to recreate the conditions of cancer evolution and determine whether, in theory, natural selection could promote whole genome double-faced. And it turns out it did.

“Our simulations found that, given a sufficiently high rate of pernicious mutants, evolution would advocate genome redoubling, ” clarifies McGranahan.

The causes included heavines to their theory, evidence that in the right circumstances, a second copy of the genome could benefit cancer cadres by antagonizing the the negative consequences of the DNA inaccuracies that build up as cancer cells divide.

But to really positioned the theory to the test, they needed more than simulates. For this, the team turned to lung cancer tests from parties enrolled in the TRACERx study. And almost immediately ran into a problem.

Looking for missile pits

“What’s slippery about studying cancer evolution is that where reference is analyse a cancer, we’re exclusively looking at the cancer cadres that are alive. This is in contrast to studying evolutionary biology, when we can look at the fossil record, which provides a property of information about the evolutionary dead-ends that didn’t go anywhere.”

According to McGranahan, it’s similar to a problem faced by technologists and statisticians analysing airliners coming back from the second world war.

“Many aircrafts came back with lots of bullet punctures in the fuselage, but instead of applying extra protection to these damaged places, the statistician reasoned that the segments that were undamaged, such as the engine, needed to be reinforced. Planes that took a collision to the engine never constituted it back”.

The team took a same approach- looking at how many genetic bullet depressions, or mutants, cancer cadres could survive.

The investigates found evidence of more genetic missile flaws after cancer cadres had double-faced their genome. This provided the evidence they were looking for that whole genome doubling does allow cadres tolerate more DNA missteps and is favoured by natural selection.

The progression of medications

Using conjectures and methods developed by evolutionary biologists, such research has shed light on the complex development of cancer. But these feels don’t merely help us to understand the disease, they could also lead to new treatments.

The opportunity is two-fold, as McGranahan justifies: “Whole genome doubling is a way for cancers to escape the harmful effects of Muller’s ratchet. But this in itself is something we haven’t genuinely explored before, whether mutations in cancer cells could be harmful to the tumour. We hope to identify more of these penchants that could be exploited by new cancer drugs”.

“And what’s more, the fact that cancer cadres so frequently doubled their genome is a key difference between cancer cells and healthy cells. A dope that specifically targets cells with doubled genomes, while leaving health cadres unharmed, could lead to a brand-new medication for many different types of cancer”.

Cancer has find a method to spurn evolution and overcome the issues that afflict asexual amoebae as genetic faults build up. But with assistance from the TRACERx team, let’s hope this could become its downfall.

Thomas Bullen is a science media man at Cancer Research UK

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Robert F
Author: Robert F


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