I\’ve no idea whether it\’s a good theory of cancer but it\’s certainly an interesting one:
Together we developed the theory that cancer tumours are a type of atavism that appears in the adult form when something disrupts the silencing of ancestral genes. The reason that cancer deploys so many formidable survival traits in succession, is, we think, because the ancient genetic toolkit active in the earliest stages of embryogenesis gets switched back on, re-activating the Proterozoic developmental plan for building cell colonies. If you travelled in a time machine back one billion years, you would see many clumps of cells resembling modern cancer tumours.
The implications of our theory, if correct, are profound. Rather than cancers being rogue cells degenerating randomly into genetic chaos, they are better regarded as organised footsoldiers marching to the beat of an ancient drum, recapitulating a billion-year-old lifestyle. As cancer progresses in the body, so more and more of the ancestral core within the genetic toolkit is activated, replaying evolution\’s story in reverse sequence. And each step confers a more malignant trait, making the oncologist\’s job harder.
Do we have any doctorly types here who could give us a view?
Is this compatible with the view that cancer is a thousand diseases with one symptom in common i.e. uncontrolled cell growth?
dearieme @ 1: Yes, that looks like a valid inference to me.
I see the basis of an argument. Since cancer cells are so successful, how come they were suppressed in the first place , those billions of years agao?
I see two problems.
First, cancer is rather adequately explained by genes being turned on or off – tumour suppressors, cell cycle checkpoints, constitutive activation of signaling pathways that say “go forth increase and multiply” to the cell. Secondly, genes that have fallen into disuse (and he gives the timeline of ~1 billion years) will by now be mutated beyond function. There is not going to be any plausible way of “reactivating” these. We’d also have to wonder how plants managed to evolve along an essentially cancer-free pathway but vertebrates did not (bear in mind that going back the 1 billion years he talks about takes us to an ancestor that you and the grass in your back garden have in common).
So cancer has enough to work on with the machinery for controlling and directing cell division without resorting to long-forgotten genes.
I dunno but I do know this certain forms of tumour actually secrete stuff that causes angiogenesis to the tumour – diverting capillaries towards it to further it’s growth. I learned this at an applied math seminar and to be honest I found it very spooky. At the cost of anthropomorphism it seemed the tumours had almost a will to live.
@dearieme:
Well put.
@ Ben: thank you. As you probably guessed, the “view” isn’t original – I saw it somewhere on the web.
PZ Myers is unimpressed
http://scienceblogs.com/pharyngula/2011/0 4/aaargh_physicists.php
Nick:
Nothing particularly anthropomorphic about it other than the word “will,” and that for lack of any other, more descriptive word. If it’s alive, it’s got it; if it ain’t, it don’t.
Another factor in cancerous cells is that the property of contact inhibition is also lost. Normally a cell will stop dividing after a certain number of previous divisions after it comes into contact with other cells. Cancer cells have lost this ability, which is one of the reasons why they are so naughty.
Cancer involves cells doing things they have always done (grow, divide, move, invade) at inappropriate times and places. It the complex regulatory mechanisms which malfunction. An excellent (if v.technical) overview is the seminal paper in the field: The Hallmarks of Cancer
by: Douglas Hanahan, Robert A. Weinberg
Cell, Vol. 100, No. 1. (7 January 2000), pp. 57-70. doi:10.1016/S0092-8674(00)81683-9 Key: citeulike:710800
This has been updated (Cell 2011, sorry dont have full ref)
It’s a mix of things. Contact inhibition is present in some of the nastiest cancer cell lines you can lay your hands on, and absent in others. It depends what genes are damaged and how – in short whether it’s doing too much of what it should do or not enough of it. But we already know that a lot of these aberrant properties are down to bog standard gene stuff, even down to knowing which genes are turned up, or down, or screwed in some other way. Invoking long-dead genes is simply not necessary.
‘Cell’ paper is Vol 144 No 5, Mar 4 2011. The pdf is free to download.
Gene – Intelligent comment as usual.
This isn’t necessarily a bad idea at all, in fact if PZ dislikes it then it may have merit ! All they are saying though is that cancer cells become “like” stem cells and the “ancient genes” they are expressing are expressed even now in stem cells, it just that they are normally not expressed after that stage.
I believe that some of these ideas have come from the stem cell research community where one major road block in the research is that although they can now reasonably successfully take an ordinary cell and under certain conditions turn it “back” to a stem-like cell, such cells are alarmingly likely to have many traits in common with malignant cancer cells.
I think what they mean is that once a cell differentiates certain “ancient genes” are suppressed basically for the rest of that cell’s (and it’s progenies) life; and that one way of looking at cancer is that this gene suppression fails.
My own take is that this may well be a reasonable approach and possibly even lead to significant advances. However i would suggest that it needs to be better presented since almost all accounts I have seen seem to not quite understand it.
Isn’t this a yes and a no? Cancers use the same methods to multiply as ancient cells and as modern cells, but the brakes have failed. That is, a normal modern body cell is using those “ancient genes” too, but restrained.
One interesting thing is HPV; wart viruses. Which produce colonies of cells, of course. They are already implicated in some cancers, but I am suspicious that they may be a primary cause of many cancers, since a virus that transfers genes that cause cell division (to produce warts) is just asking for trouble.
The most famous cancer cell line, HeLa, which at one time was found to be so virulent that it had colonised and replaced every other supposed cancer research cell line, worldwide, has been genetically analysed and found to have arisen from gene transfer from an HPV. It is so good at living that it can live outside the body, cells can live on lab benches, drift from petri dish to petri dish and, it has been argued should thus be considered not a cancer but a new species.
We may want to ask why we’re only immunising young women against one HPV. It may be wise to try to eradicate them all, in all the population. How many of us haven’t had a wart somewhere?
That is, maybe plants don’t get cancer because they don’t get warts.