Fighting Cancer with Math
zoloback writes "A group of scientists have developed a mathematical method to fight certain forms of cancer. The study has taken the team several years, but the first trial on a human has been successful. You can read the actual paper. It looks like a huge advancement in science, because there's a possibility to extrapolate the method to other types of cancer" From the article: "The researchers have evidence to show that all tumors grow in the same way, irrespective of the tissue or species in which they develop. In a previous paper, these researchers reported that tumor growth, rather than being exponential as commonly believed, is a much slower "linear" process similar to the growth of certain crystals and other natural phenomena."
Im very Impressed Im sure. But its not really fighting cancer with math, just creating a good model on how to repond with the treatments we have.
Go Away! Not for Sale
The breakthrough lies in the connection between the variables that allow a tumor to grow and the control that can be put over those variables, a lot of these were never considered before (such as barometric pressure inside the mass, and blood vessel proliferation).
This are easily controllable factors, so instead of treating the tumor by trying to kill the cells via radio or chemical therapy, they attack the factors that (in a mathematical model) determine the growth of the tumor, turning them into negative variables and therefore extinguishing the mass
The future will take care of itself.. It has in the past
I thought I'd send a quick response to this. You can't get a nobel prize in Mathematics. I'm not sure if they could get one with this research for medicine though. I'm guessing it's that possible. Peace.
how much are we tempting Nature to change the formula
Cancer is an anomaly of mitosis; it is not an organism and therefore does not evolve. The body regularly squashes cells which go into a sort-of mitotic infinite loop, and that's the end of that. It's the ones that the immune system does not recognize that grow into tumors.
There is a follow-up article criticizing the original article: abstract
And a response by the original authors: abstract
In any event, it's a little premature to celebrate. Their follow-up work in mice (abstract) used implanted tumours. It is already known that tumours have the capacity to evade immune response, and we should not be surprised that implanting a foreign tumour mass into a host and stimulating the immune system will provoke a favourable response. The situation is more complicated when trying to raise the immune system to attack a tumour comprised of one's own cells. It seems to me that, at this point, they are trying to prove their particular growth model, not developing a de facto cure.
That their devised strategy worked on a single human subject is cause for optimism, and nothing more. That work has not been published (that I could find), so there is no way to properly assess the result. At this point, they are more than likely drumming up press to ensure continued funding for their research... not that there's anything wrong with that ;).
Link
And some detail on how it works...
I'm too much of a damn pessimist to believe it's true after reading something similar to this just about every week followed by "could lead to treatments"... Here's hoping I'm wrong.
What if Digg added local news and a Slashdot inspired comment karma system? ---
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At the risk of trolling beyond my bounds...
It irks me to hear a good joke all the way to the end, only to find someone botched the punchline. Thank you fellow mathematician for enlightening us to the real deal.
Just so this isn't a pure fluff-post, here's a link to the abstract of the original paper from clinical studies in mice, published in Physical Review Letters, June 7, 2004. Mind you this has only been tested in one human case study and they make no claims to generalize this to other forms of cancer.
http://scitation.aip.org/getabs/servlet/GetabsSer
I will most likely download the full report tomorrow from the university.
Actually, unregulated mitosis is just one of the mutations that contributes to cancer. Some of the others include: genetic instability, resistance to apoptosis signaling (i.e. no cell suicide,) ability to recruit vasculature, ability to migrate (i.e. reduce cell-cell bonding and increased motility,) ability to survive in novel body environments. These are loosely related to the "stages" of cancer.
Each of these mutations is selected for by very stringent competition for nutrients both among cancer cells themselves and the body's normal cells. There is a very real type of evolution occuring, and as the cancer cells begin to ignore the signals coming from nearby cells and their behavior represents their own individual interests rather than the interests of the body as a whole--they have in a very literal sense become an independent organism. It is not exactly analogous to a speciation event, but it is related.
A literature search for "evolution" and "cancer" would return a number of papers that borrow models from evolutionary biology to model cancer.
The excitement over this paper, or "treatment" is perhaps a bit premature. Scaling treatment is a common and quite popular approach in many growth phenomena, and has been investigated to death in the context of crystal growth (MBE, molecular beam epitaxy), but ironically, the equation that bears the name "MBE equation" does not actually describe MBE growth correctly (in my view). Therefore, saying that equation (2) in the original paper describes the physical process of "surface diffusion" in the case of MBE or surface cancer cells is highly suspect. The growth of the cancer cells might be well approximated by the growth MBE equation (2), but this is mere curve fitting, and a closer look at the underlying physical mechanisms is more important than getting good fits.
If I've read your post correctly, you've misunderstood the article. They're arguing -- convincingly -- that the Gompertz model should be thrown out in favor of an MBE (Molecular Beam Epitaxy) model. The MBE model differs from the Gompertz model in that it has most of the growth occurring at the tumor surface, rather than uniformly throughout. It's this phenomenon that they're targeting their therapies at.