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Cells, Microbes & Viruses / Re: Have cancers evolved processes to protect themselves?
« on: 10/04/2013 12:34:52 »Listening to one of the podcasts this week I was struck by the suggestion that some cancers recruit other cells/proteins (I forget what) in order to minimise their exposure to the bodies immune response.
When I also reflected on the transmittable cancers afflicting the Tasmanian Devil population then I wonder if these cancers aren't acting more like an organism that has arisen via evolutionary processes rather than as errors in the cells.
Top say it another way, if whole classes of cancers act in this way, such that they have 'evolved' processes to protect themselves, in which case they are acting rather like an organism such as a bacteria or a virus.
This seems strange and I struggle to see how this sits with my current understanding of cancers.
Does anyone want to shed some light on it?
Hi Simon
Cancers are fantastically interesting in this respect, self cells that become aberrant and faulty to the extent that they sometimes seem like a whole different organism! What it's important to note is that cancers arise from what is termed as a 'microevolutionary process', as they are exposed to specific environments or processes, they are able to survive for longer in these environments (due to previous mutations), and so they have more of a chance to overcome these factors. As was stated before, cancers almost always have a dysfunctional apoptotic pathways, I believe something like 50% of all cancers have a mutation in the crucial apoptosis gene loci for p53 [1]. Therefore, apoptotic signals induced by other cells do not work, and the cell is then protected by these societal constraints, and is able to become more and more mutated to avoid other factors (such as evading the immune system, propogating a constant growth signal, inducing angiogenesis for example). As the cell breaks its normal characteristics and begins to become deaf to the local society of cells and the social rules, and begins to grow and proliferate and refuse to die, one can begin to see these cells as self-serving. Indeed, cancer cells are termed as 'selfish cells' by many experts, because they prioritise their own survival over the health of the local environment, and the overall organism as a whole.
The use of evolution via selection is true of organisms too, and I can certainly see why you saw their behaviour as organism-esque. If I were to describe a cell that acts to preserve itself with not much care for the overall health of the local environment, that consantly attempts to capitalise on nutrients from the local environment and overcomes factors that may work to destroy it, you could easily think I was talking about a bacteria, or a fungi.
The microevolutionary process in cancers is, typically, driven my internal mutations to its own genetic material, or by epigenetic modulation of gene products. Certain environments can aid in quickening this process, which is why cancers sometimes recruit other cells to do its bidding by establishing these environments. Chronic illnesses in people that have conditions where these environments are always in place often have an increased chance of developing cancer, and therefore have a predisposition. Inflammation is now beginning to be considered an essential part of cancer, for example (it also requires that cancers can become resistant to the deadly immune response, of course), and research has suggested that chronic inflammatory illnesses can increase the risk of cancer in patients, Crohns patients in one study were found to have a 2.64x increased risk of developing colon cancer in their lifetime, for example, or colitis sufferers have a 2.75x increased risk [2], or that dermamyositis sufferers are more likely to develop cancer than non sufferers by a factor of 2.4x and 3.4x in men and women, respectively[3]. So basically, when a selective pressure is applied, cancerous cells can evolve to overcome them!
[1] HOLLSTEIN, M., SIDRANSKY, D., VOGELSTEIN, B. and HARRIS, C., 1991. P53 Mutations in Human Cancers. Science, 253(5015), pp. 49-53.
[2] BERNSTEIN, C., BLANCHARD, J., KLIEWER, E. and WAJDA, A., 2001. Cancer risk in patients with inflammatory bowel disease - A population-based study. Cancer, 91(4), pp. 854-862.
[3] SIGURGEIRSSON, B., LINDELOF, B., EDHAG, O. and ALLANDER, E., 1992. Risk of Cancer in Patients with Dermatomyositis Or Polymyositis - a Population-Based Study. New England Journal of Medicine, 326(6), pp. 363-367.