It seems that you mostly hear about varouis cancers in people and different mammals, domestic and wild. But you never hear about it in birds, fish, reptiles, amphibians or insects.
I know chickens get ovarian cancer and can be infected by a virus that causes sarcomas.
Are chickens just an aberration and cancer is mostly non-existent in the other classes?
We hear a lot about it in humans and other mammals because we’re particularly interested in those, but it’s false that we never hear about cancers in other animals, with or without skeletons. As already shown once in this thread.
Another example is this debunking of the previously(?) persistent myth that sharks don’t get cancer: Sharks Do Get Cancer: Tumor Found in Great White - Seeker
Some more examples to prove the point:
A vet discusses reptiles and cancer:
Tumors of Fishes, Amphibians, and Reptiles (full article is pdf, but the first page appears on the web page in non-pdf form)
http://cancerres.aacrjournals.org/content/8/12/657
Cancer in snakes:
http://reptile-parrots.com/forums/showthread.php/535-Cancer-in-Snakes
Cancers and Tumors in Birds (petMD):
Poking around on google, I couldn’t find any references to insects getting cancer in the wild. However, insects under laboratory conditions have developed tumors and cancers. Generally speaking, insects live very short lives. They just don’t live long enough for cancer-causing mutations to occur at a significant rate. Theoretically though, cancers and tumors should be occurring, even in the wild, just at a very low rate due to their short lifespans.
Cancer, or at least the dysregulated proliferation of cells in some manner, is the natural fate of all multicellular organisms if they live long enough. Even plants get a form of cancer.
The remarkable thing is that multicellular life exists at all. For billions of years, all of life was single-celled organisms, and most of it still is. This is a more natural evolutionary state, since every cell may have descendants. As cells compete for survival, every cell has a potential evolutionary future. The most successful single-celled organisms are usually those that follow a straightforward strategy something like scarf up as many nutrients as possible from the environment, metabolize those nutrients as efficiently as possible, then make as many copies of myself as possible as quickly as possible.
By contrast, from an evolutionary perspective, multicellular life seems an odd strategy. In complex multicellular organisms, the billions or trillions of somatic cells have no descendants at all, they have no direct evolutionary future. The vast majority of cells in the organism sacrifice their individual procreative potential for the sake of a tiny number of germline cells (eggs or sperm in humans). This only makes sense because all cells in an organisms share the same DNA. The self-sacrificing somatic cells do have an indirect evolutionary future, because the successful passage of germline cells into the next generation means that identical copies of their own DNA proliferate.
In order for multicellular life to be feasible, the DNA incorporates complex regulatory mechanisms to control the growth of somatic cells to specific limited quantities in specific places for the benefit of the organism as a whole. Make a liver so big, then stop proliferating. Make a certain thickness of skin, then stop proliferating. Make are many leukocytes as necessary to protect the organism, then stop. And, from an evolutionary perspective, all of this is dedicated to increase the chance of the organism’s sperm or eggs making it into the next generation.
The problem is that the body of a multicellular organism is itself an evolutionary environment where cells are constantly replicating and acquiring new DNA mutations, either by routine copying errors or exacerbated by carcinogens and the bombardment of radiation. There are many redundant checks and balances to regulate the growth of cells for the good of the organism as a whole, but sooner or later some cells will acquire enough DNA mutations in key places (usually at least 6 mutations) to override all of the checks and balances. When this happens, the organism reverts to the “wild west” of evolutionary competition among selfish single cells. And the most “successful” cells in that environment are those that follow the ancestral evolutionary strategy: scarf up as many nutrients as possible from the environment, metabolize the nutrients as efficiently as possible, then make as many copies of myself as possible as quickly as possible. This is cancer.
Riemann: Thanks - very useful post.
Article on the topic. Once you get tree cancer pointed out to you, you see it everywhere – it is really quite common.
Riemann, that is one of the most interesting posts I have ever read on TSD. Thinking about led me to the following question. One can think of a beehive as a multicellular organism with the individual bees as cells. Since they are genetically identical, this would explain why they can give up their reproductive imperative, except for the queen and the drones who function much like the ovary and testes in us. So does a beehive (or, for that matter, an ant nest) ever suffer from cancer. This would involve a worker bee suddenly acquiring the ability to reproduce and do so repeatedly with the daughters inheriting the same capability and eventually, perhaps, destroying the hive. One problem with this is the necessity of feeding the wild offspring. Something analogous to angiogenesis would have to take place, new comb where they are fed and raised to adulthood. Has such behavior ever taken place?
That’s a really interesting question. I don’t know the answer, but I’ll offer a little background for others who may not be familiar with the genetics of Hymenoptera:
https://en.wikipedia.org/wiki/Haplodiploidy
https://en.wikipedia.org/wiki/Eusociality
It would be overstating the case to say that sterile workers are exactly equivalent to the somatic cells in multicellular organisms, but there is clearly a parallel. Colonies operate in some respects as though they were a single organism, with the queen and rare daughter-queens as the germline.
Fascinating question indeed. I spitballing here, but I’m gonna bet the answer is no.
Human liver cells already know how to reproduce. That’s how you grew from having one liver cell as an early proto-fetus to having several pounds of them now. That’s also how you maintain your liver now in the face of continuous ongoing low-rate cell death. Ditto most of the other cell lines in your body. Self-cloning reproduction is part of their workaday behavior repertoire. Subject to very tight organism-level limits on actually doing that behavior.
By contrast, worker bees/ants are thoroughly lacking the capability to self-clone at any stage in their life cycle.
Starting from proper function, the mutations/malfunctions needed to have a liver cell slip its properly regulated reproductive limits and go into unregulated reproduction mode are tiny compared to the mutations/malfunctions necessary for a worker bee/ant to spontaneously develop the ability to self-clone.
So while a bee/ant colony could in principle develop the analog of cancer, the statistical obstacles to it happening in fact are far more formidable than those preventing ordinary cancer.
Interesting post. So what incentive were there to form multicellular life? To my knowledge reasons such as:
Energy requirements go down as size increases (six tons of mice have a higher energy requirement than one 6 ton elephant).
Cells can specialize in a multicellular organism.
Are why some life forms made the switch, but for 80% of our history I think life was all single celled.
Also as far as cancer, isn’t it more an issue of the immune system than mutations? Humans generally do not start to get cancer until old age. But so do other mammals like dogs, cats or horses. However for a dog old age could be 12 years old, for a horse old age is 20.
http://www.nature.com/nrc/journal/v3/n12/images/nrc1235-f1.jpg
A mouse has the same odds of cancer at 2 years that a human does at 80 years. Cancer doesn’t seem to strike after X years, cancer seems more to strike after a life form is X% completed with a normal life expectancy. If a mouse lives 2 years, at 75% of its life expectancy (18 months) cancer rates are 20%. For humans who live 80 years, cancer rates are 20% at 60 years.
There are many checks and balances and surveillance mechanisms (yes, including in part the immune system) to prevent mutations from leading to uncontrolled cell proliferation and cancer. The fact that mammals of different species tend to succumb to cancer at a similar point fairly late in their lifespan (but after different absolute times) is simply because there was no selection pressure to evolve checks and balances and surveillance mechanisms to prevent cancer past a point when our ancestors were mostly dead from other causes anyway. A human that is less likely to develop cancer at 10 years old has a substantial fitness advantage; a mouse has none, because there are no 10-year-old mice.
There was a recent article about why elephants don’t get cancer more often, since bigger animals mean more cells (and more cell divisions to create those cells) which mean more chances for things to go wrong. It turns out they have many more copies of a tumor-suppressing gene that kills off cells with DNA damage at a higher rate.
It’s in the nature of animal cells to go cancerous eventually, and the body has ways to prune pre-cancerous cells quickly. I guess that there is some cost to having tumor-suppression active, so that animals that don’t have lifespans long enough to benefit from it quickly lose it.
I’d venture to guess either improved locomotion or size. Both offer you the ability to capture and defeat, then devour, your competitors.
Most random mutations are harmful, not beneficial.
Mammals, at least, have mechanisms in place to try and detect and repair damage done to DNA. (I assume that non-mammalian creatures do as well, but I don’t know so for sure.) And yes, the concentrations in your body of those factors decrease with age. Though, whether that’s a factor of your body deteriorating, and thus doing a worse job of making the things that could help it, or the body being designed to deteriorate by reducing those factors, is currently an area of research. (I’m voting for the latter.)
As to why multicellularism:
In one sense, it’s simply flocking behavior writ very large. Doesn’t matter if it’s birds, bison, or fish. If we all stick together we collectively benefit X% versus not. Even though individual survival to reproduce is always binary: you’re either eaten first or you’re not.
Flocking behavior is itself an outgrowth of predator flooding behavior. e.g. Cicadas or mayflies that all emerge at once so they possibly can’t all be eaten.
To be sure, my examples of both flocks and cicadas are already multicellular life. But many species of algae form dense mats and IIRC some of the motile single-celled critters actively swim to clump, rather than swimming at random or towards open water.
Once some single-celled species lives and dies in a clump, you’ve got the preconditions for specialization to take root if any happens to emerge. e.g. crunchier cell membranes around the outside, better waste processing in the center, etc.
Lather, rinse, repeat a few billion billion times and here we are.
As Riemann indirectly pointed out near the top, there’s a lot of scale invariance in behavioral biology. The same tactics appear in molecules, cells, animals, small groups, and large societies.
I believe that the more difficult leap was from prokaryote to eukaryote. Once you have a nucleus capable of storing enough DNA to program for multiple cell types, pretty much everybody starts experimenting with the communal thing.
But note that there’s an important qualitative difference between communal strategies and multicellularity. In the communities that you describe (assuming that we’re not talking about the exceptional genetics of Hymenoptera), the individual organisms may be related, but the relatedness will be less than 0.5, often much less. Thus, cooperative strategies are rather complex and subtle, based on mutual benefit or reciprocity; a willingness to take true self-sacrificial risk will operate under the principles of kin selection, based on relatedness <0.5. No individual organisms in these communities will easily give up the prospect of prospect of passing their own DNA into the next generation.
In a multicellular organism, all cells share the exact same DNA, i.e. the relatedness is 1. So, from an evolutionary perspective, specialization of cell type and complete subjugation of “self-interest” to the good of the organism as a whole makes sense. Individual cells are “indifferent” to whether their own genomic DNA or the identical copy that resides in a germ cell gets into the next generation.
Bees is an interesting question. The manner in which a hive gets a queen, or replaces her is remarkable, and part of the really interesting bit is that it isn’t just queens that can be fertile.
Normally a queen will prepare for her departure by laying female eggs (the queen can control the sex of the egg - if she allows an egg to be fertilised by stored sperm it is female, unfertilised it is male) into specially prepared queen cells. Often the queen later slims down and leads a swarm of older bees out of the hive, to establish a new hive. Later a new queen hatches in the hive, and typically immediately proceeds to kill her sister queens whilst they are still in their cells. She then leads a mating flight, mates with a goodly number of drones, and returns to the hive to start life as the new laying queen.
However, all worker bees are female. But they remain in a state of suppressed development, mediated by pheromones secreted by the developing larvae and by the queen. If a queen dies, or becomes so frail that she ceases to lay, before the workers have built queen cells and she has laid into them, the hive will run out of eggs and brood. This is dire, and without any new eggs, there is no way to make a new queen. But the brood recognition pheromone level will drop, and the weak or absent queen will mean no queen mandibular pheromone suppressing ovary development. So some worker bees will begin to develop mature characteristics, and become fertile. This maturation also includes the secretion of the queen mandibular pheromone develops - so further maturation by other workers will be suppressed - so a hive will only gain a small number of maturing workers.
A matured worker, although technically fertile, has not been inseminated, and cannot lay eggs that will develop into females. Not having been raised as a queen she has not physically developed enough to be able to mate. So she can only ever lay male eggs. A queenless hive is in a desperate position, there will be a number of laying workers, but only drones produced. So the hive is unable to replace its workers, and will die in a few weeks.
The above applies to the European honeybee. Other insects and especially bees have slightly different behaviours. Many include laying workers. It seems a common tactic is for eggs laid by the queen to be recognised as such (more appropriate pheromones) and eggs laid by workers get eaten by other workers.
One could imagine that there is scope for things to go wrong on many levels. A queenless hive turning out only drones has some curious parallels to some diseases.