Human pancreatic cancer cell

Cancer: the selfish cell?

The emergence of cancers in the body is a form of natural selection

Most of the time, the body’s cells work together harmoniously, each contributing to the greater good. Cancer cells, which divide and colonise the body, are an exception to this rule. They prosper at the expense of other cells, but also seal their own fate by eventually killing the host.

A process of selection is seen as cancers develop. Normally, when cells begin to go wrong – for example, if their genes are damaged – they receive signals that tell them to self-destruct. But a cell may acquire mutations (or it might have inherited them) that cause it to resist these signals. Once other changes encourage it to start dividing, it is becoming a cancer cell.

A mass of cancer cells – a tumour – may build up. Eventually it will stop growing because oxygen cannot get to the cells in the centre of the tumour. But if another mutation causes cells to release chemicals that attract new blood vessels, it can start multiplying again. Often, many tiny tumours form in the body, but only one or a few go on to cause problems.

Even with a blood supply, a population of cancer cells is stuck where it originated. But some cells may acquire a new ability – motility. They may detach from the original tumour mass and travel around the body. They may acquire the ability to digest tissue and invade other organs, setting up metastases (secondary cancers).

So, by accumulating genetic changes, cancer cells acquire properties that enable them to overcome the body’s defences. They gain a selective advantage, increase in number and spread. Selection within tumours also leads to resistance to anticancer drugs, such as tamoxifen, much as selection favours antibiotic resistance in bacteria.

But there is a big difference between this process and evolution in the outside world. A cancer cell growing out of control kills its host, so it’s soon ‘extinct’. Natural selection is not so crude. ‘Survival of the fittest’ does not mean short-term survival of the strongest and the elimination of all other forms of life.

Dog days

Interestingly, though, there are cancers that have extended their existence beyond their original host. Some cancers are infectious: they can be spread from one animal to another and set up a new tumour. (Cancers caused by viruses are infectious in a sense, but it is the virus rather than the cancer itself that is transmitted.)

An infectious tumour is currently ravaging the wild Tasmanian devil population. Devil facial tumour disease, which is spread by bites, has more than halved the devil population. First seen in 1996, it probably arose in a female devil in the 1990s before being spread across Tasmania.

An infectious dog tumour, which is spread through sex, also exists. Sequencing two cases from Australia and Brazil has suggested that they shared a common ancestor around 500 years ago, although the tumour may have been around for as long as 11,000 years. During its existence, it has accumulated a staggering 2 million mutations.

A family tree of cancers

As cancer cells in the body accumulate mutations, different populations of mutated cells emerge – creating an ecosystem of variants, just as in populations of organisms in external environments. The most ‘fit’ of these cells divide most extensively, but other populations will also be present. Family trees can be drawn up to show how they are related to one another and to an ancestral initiating cancer cell.

A new mutation may arise in one of the ‘minor’ populations and proliferate more vigorously, coming to predominate. Treating cancer can also affect this cancer ecosystem. Leukaemia treatment may eliminate some cancer cell populations, but some not affected may then proliferate to take their place, leading to relapse.

Lead image:

Human pancreatic cancer cell.

Anne Weston, LRI, CRUK/Wellcome Images CC BY NC ND


About this resource

This resource was first published in ‘Evolution’ in January 2007 and reviewed and updated in December 2014.

Genetics and genomics, Microbiology, Health, infection and disease
Education levels:
16–19, Continuing professional development