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  Topic: Measels and Cancer< Next Oldest | Next Newest >  

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(Permalink) Posted: Jan. 02 2007,14:47   

As a layman, I have read about the evolutionary benefits of sickle cells as an anti-malaria weapon. Can someone please tell me whether there are similar evolutionary benefits of measels and cancer and where I might read a layman’s explanation of these phenomenona?

Is this the right forum for this level of question?


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(Permalink) Posted: Jan. 02 2007,15:00   

Measles, maybe?


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(Permalink) Posted: Jan. 02 2007,15:08   

Assuming this is a serious question (though my troll alarm is going off), the benefit of measles is to the infecting virus, not to the human (the symptoms probably make it easier for the virus to transmit itself to a new host - I could look this up if you're up for a serious discussion).

Can't think of any particular benefit of cancer to the host.

"Why waste time learning, when ignorance is instantaneous?" -Calvin


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(Permalink) Posted: Jan. 02 2007,15:32

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(Permalink) Posted: Jan. 02 2007,16:11   

Again, on the off chance this is a serious inquiry, cancers are driven by some of the very factors that drive multicellular "lifestyles."  It's very hard to be a multicellular animal--with lineages of generalized cell-types that divide and divide and specialize and specialize, requiring controls on what aspect of each cell's "total" genetic instructions to deploy, and when to deploy them--and then to turn around and turn off the division and say, "Okay, boys, that's enough now.  Just sit there on idle, doing nothing but what you've been told--or, better yet, just die!--until you hear different!"

Cancers "take advantage" (by means of mutation and other errors) of the machinery of multicellularity that allows cells to live in concert, multiplying, specializing, mutually signalling and communicating, exporting and importing products of cellular metabolism, etc.  

Because multicellularity is the result of an evolutionary process (that is, not designed with an eventual goal in mind, but a product of adaptation, exaptation, jury-rigging, trade-offs, and compromise among competing propulations of cells and cellular control mechanisms), it doesn't always work perfectly.  Some of the balances between growth and termination of growth, supplying nutrition to "healthy" cells and denying nutrition to "unhealthy" cells, etc., can gang aft aglay.  Usually it takes several different mutations or insults to derail the cellular maintenance "machinery," and then further mutations within the population of "unhealthy" cells (growing where and when they're not supposed to) to avoid the body's anti-cancer responses.

Just as the mother and embryo can be usefully looked at as in a state of evolutionary competition (at the same time as, and as well as, they should be looked at as cooperating) for scarce resources, healthy cells and cancer cells are also wrapped up in an evolutionary "arm's race."  Those cancer cells that escape the body's control mechanisms--refusing to die, shut off, or express themselves in whatever limited fashion they are "supposed" to--no longer have the "interests" of the overall animal in mind.  As the group of cancer cells grows and divides and further mutations within the cancerous lineage of cells generates still more variation--the cancer itself can evolve to evade the body's various defensive techniques.

If a population of unwanted rabbits (in Australia, let's say, where they are pests without adequate natural controls on their growth) is exposed to an effective poison, there will almost always be a few rabbits who happen to be somewhat or entirely resistant to the effects of the poison.  Widespread application of the poison will initially reduce the rabbit population dramatically but--unless the poison is utterly effective--the population is all too likely to rebound.  And the rabbits within the rebounding population, being descended from resistant or immune survivors, will be less affected by the next round of poison application.

So it goes for antibiotic resistance.

And so it goes for lines of cancerous cells.  The body's controls work well, most of the time, to ward off cancers until the animal or human is mature enough to reproduce.  Most--not all, but most--cancers are diseases of advanced age: because any given animal's ancestors have survived long enough to reproduce and support their offspring toward maturity (but have not necessarily survived much longer), cancers are fairly rare in the young.  (Another way of phrasing this is, that the young who do contract cancer, and fail to fend it off, mostly do not survive to reproduce.)  Because cancers that attack the body late in life do not face the same selection pressures (that is, the failure of an animal to survive a late-developing cancer will have little impact on the relative survival of that animal's offspring, which may already be grown and having its own offspring), many late-developing cancers have eluded the pruning shears of natural selection.

Remember, there is no "goal" of evolution where only the nice, disease-free, cute, warn'n'fluffy animals get to survive.  Predators survive too, if they gobble enough prey.  Bacteria and viruses survive too, if they are successful enough at colonizing and infecting their hosts.

And cancers survive too, because--if the "right" sequence of mutations and other propitious (for them) events occur, they can successfully out-compete the cells of their host body.

While cancerous cell lineages mostly do not survive the death of their "host," and so do not propogate in the usual evolutionary manner past that cut-off (though, up until that time, their growth and reproduction within the body can be analyzed from an evolutionary perspective), the body's anticancer mechanisms cannot be "perfect" (nothing in nature is perfect--everything comes with a metabolic "cost" or trade-off; absolute perfection of those mechanisms might well, for example, seriously inhibit the very processes that enable multicellularity; bodies tend to do a reasonably-good job defeating cancers of youth, but cannot, for the reasons previously suggested, easily "inherit" the ability to stave off cancers of later life), the same general types of mutations, break-downs, and failures tend to arise again and again in each new generation of animals, allowing a new cycle of cancers to get growing.

There are, of course, as one would expect from an evolutionary perspective, a few cancers which can "jump" or be transmitted from host to host--see a couple of interesting posts on Carl Zimmer's blog "The Loom," in this regard.

The last issue or so of "Scientific American" also has a good round-up article on the general topic of "Why we get cancer."  That might be a good place to go next...

That should make for a start.  Beyond that, others may be able to share some specifics, or you could take those suggestions and run with them (i.e., independent study--something that the internet enables with incredible facility).


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(Permalink) Posted: Jan. 06 2007,16:59   

I guess we're still unclear whether the questioner was a one-time drive-by, or a sincerely interested person who's just away thinking or researching.

Sticking with the charitable interpretation, however, I'll add this tidbit from PZ Myers' roundup of one of the sessions at the Phoenix conferece he's been attending.  As you'll see, there's a tie-in with cancer/multicellular animals (the bolding is mine):
N.W. Blackstone: Foods-eye view of the transition from basal metazoans to bilaterians. This was another weird talk that came from a completely different perspective and made me think. It might actually be a little too weird, but it's still provocative and interesting. Blackstone is looking at everything from the perspective of metabolic signaling—he's clearly one of those crazy people coming out of the bacterial tradition. Cells communicate with one another with the byproducts of metabolism, where the redox state of membrane proteins are read as indicators of the internal state of the cells (he later calls this "honest signaling", because there aren't any intermediates between the cell and the expression of its metabolic state). The big innovation in the eukaryotes was to escape volume constraints by folding their chemiosmotic membranes into the interior of the organism, and the major animal innovation was the evolution of the mouth, which allowed specialized acquisition and processing of food patches. Subsequent evolution was to allow the animal to sense and seek out and exploit food patches in an environment where they were dispersed in a non-uniform manner. Another interesting tangent was the question of cancer: long-lived sponges and cnidarians don't get cancer. His explanation was that it was because their cells use that "honest" metabolic signaling, so that rogue cells don't have a way to trick the organism into allowing them to use more resources than they actually need; the only way to signal is to exhibit genuine metabolic distress, and cells with metabolic problems will die. Our cells have these indirect, multi-layered signaling mechanisms that allow cancer cells to "lie" to the organism as a whole.

More, uh, food for thought...


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(Permalink) Posted: Jan. 10 2007,16:15   

Still more info on the topic of evolution and cancer, this time from Carl Zimmer's science blog, "The Loom."  Provocatively titled, um, "Cancer: An Evolutionary Disease."  Lots o' links and other info:

But is our drive-by poster ever gonna return?

Will Nick survive another week of marriage to Nora?

Stay tuned!

  6 replies since Jan. 02 2007,14:47 < Next Oldest | Next Newest >  


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