Cancer and Evolution: A Biological Link?

[TheSkyKing]

Hey everyone. For my Biology II AP class we were assigned a project in which we have to basically write a term paper on a subject relating to evolution. I asked my teacher whether cancer was tied to evolution in any way and he said there is a possibility. I just have no clue where to start. If anyone could answer that question in a little more detail it would be greatly appreciated. Thank you.

 

[Moonbear]

Sounds like your teacher gave you a disguised, "I don't know" answer. It's probably going to depend how you want to approach the topic.

If this is a topic you want to write on, why don't you first tell us why you think it could be tied to evolution. I think it will be difficult to find references linking the two ideas, but if you're allowed to be speculative, I think there's an argument that can be made.

 

[Phobos]

Not sure about any direct relation between cancer and evolution; however, DNA mutation can lead to evolution (if carried through a population's gene pool) or cancer (in an unfortunate individual). The underlying point may be that DNA is mutable.

 

[Averagesupernova]

EVERYTHING is tied to evolution in one form or another. Cancer has been shown to be hereditary. Although that doesn't prevent someone with no cancer in the family from getting cancer. It just means you are less prone than families with a history of cancer. I can think of several women I know who have had reproductive organ related cancer in their early 20s. They won't be having kids. Contrary to what a lot of people believe, we are still evolving in certain ways.

 

[loseyourname]

It's important to remember that any given form of cancer requires many different factors of causation, some of which are environmental and some of which are genetic. What you might want to look into is whether or not there have been any studies into the possible utility of the mutations alone in the absence of the environmental triggers necessary for actual cancer. There may very well be some advantage to some of these mutations. I'm entirely guessing on that, but there are so many different mutations that can serve as a precursor, it seems likely prima facie that at least one or two can have potentially beneficial effects. I really have no idea whether or not this has ever been looked into, though.

 

[nautica]

Cancer is the greatest form of evolution known to man kind. Consider individual cells. Cancerous cells are mutated in a way that they are unable to die. They do not recognize signals to die, they protect themselves from apoptosis, they replicate and there offspring do not have the ability to die.

This brief paragraph can in NO way do justice to the evolutionary implications of cancer when considering the cell and molecular level, its only problem is that it has not found a way for its host to survive.

Nautica

 

[TheSkyKing]

Thank you so much guys. Your replies have led me in the right direction in which to approach this. I owe you all one.

 

[TheSkyKing]

Cancer and Evolution Part II-Cyclin Dependent Kinases and the RB protein.

For the past weeks I have been speculating on the causes of cancer by reading up on cell division, DNA replication, and genetics and I have come to find that there is no easy way of approaching a way to write a paper on the evolution of cancer. I remember reading that the one cause of cancer, which specific type I do not know, that resulted in defective protein, p52. p52 is responsible for the production of p21 which binds to the cyclin depentent kinase complexes to inhibit their actions which are described below. In the cells cyclin D cdk 4 as well as Cyclin E cdk 2 control the G1 phases of the cell cycles. Controlling the S phase is the cyclin complex Cyclin A cdk 2 and Cyclin B cdk 1 which controls the cells enterance from the G2-M phase. When Cyclins Cdk 4 and 2 are not inhibited by p21, the RB protein (retinoblastoma) is phosphorlyated by the cyclins therefore inhibiting the inhibitor. In other words the phosphorylation of the RB protein actually keeps the cell cycle going. When p52 stops functioning then no p21 is produced and therefore the actions of the inhibiting of RB by the cyclin dependent kinases continues freely and thus leads to unexpected cell growth. From reading this I began to think that maybe there is a possible way that a protein or component within the cell may have evolved over time which led to the evolution of more complex cancers. How is my aim? Am I even on the right track?

 

[iansmith]

A small correction. it is not p52 but p53.

I also merge both thread.

 

[gamze]

I think cells evolved ways to protect their damaged DNA from replicating and harming the individual they belong to (protooncogenes, for example). It may be a relationship between cancer and evolution. The cancer cells cannot survive although they are 'immortalized', and additionally they lead to the death of the organism they belong to. At last, evolution of many ways to protect from cancer took place. However, there is still cancer, which may be because cells also want to have some mutations to introduce some variation tool for evolution. There seems to be an equilibrium of two opposing forces.

 

[Monique]

From reading this I began to think that maybe there is a possible way that a protein or component within the cell may have evolved over time which led to the evolution of more complex cancers. How is my aim? Am I even on the right track?

Well, you described the detailed story but you are not seeing the concepts.

Do you know the function of p53? It is mutated in approximately 50% of cancers, the pathway is probably mutated in almost all cancers. p53 is involved in recognizing DNA damage, its normal function is to halt replication when damage is detected. A cell with mutated p53 won't stop dividing in a crisis and will thus accumulate more errors.

If you want to know more about the biology of cancers, you also need to read up on apoptotic pathways, mainly cytC/mitochondrial pathway and the deathreceptor pathway (p53 is involved in these pathways too): these will also be mutated in cancerous cells.

And I want to clear up one thing:

Are you talking about cellular evolution or organism evolution? Cancer is not directly involved in the evolution of an organism: only when it involves germ cells can it be passed down to the next generation.

 

[Sho'Nuff]

How is my aim? Am I even on the right track?

Yep, well on your way, this is how mouse cells acquire the ability to divide constantly, for human cells you'll need to inactivate the retinoblastoma/E2F pathway separately (mutations in p16 or pRb itself) since its only weakly regulated by p53. Many more steps are needed to become a full blown cancer cell and each step can be considered an evolutionary selection process where for instance preasure can be death by shortening of telomeres. Only the cells that are able to mutate in a way that they can maintain telomere length will survive, thus cancer can be viewed as a survival of the fittest cell struggle to overcome the fail safe mechanisms imposed by the evolution of the organism to keep the cell in check.
It was shown nicely by the lab of Weinberg that a minimum of 5 genetic lesions (mutations/interventions) is needed to turn a perfectly healthy human cell into a transformed cancerous cell.