http://www.genomebiology.com/2001/3/1/comment/1001
With the great quote:
"...If a hundred years of cancer research has taught us anything, it is that if you must get cancer, you want to be a mouse, because we can cure cancer in mice."
Actually as far as I know we can’t cure mice of cancer - by cancer I mean natural cancers that mice get as they age just like human cancers. I have looked through the literature in great detail and I can’t find a single recent paper where anyone has even tried curing mice of cancer. If anyone know of one I would love to read it.
The way we go about trying to cure cancer is insane. We basically take inbred mice, inject them with a cancer cell line to give them cancer, and then treat them with experimental drug X. This process is nothing like how real human cancers arise. On top of this we only test new drugs in people that have failed all other treatments and have very high tumour burdens. We then demand that the new drug have a significant effect in these patients despite us needing drugs that work in newly diagnosed patients. If we get a drug that works it is more by chance than design.
It's interesting how your perspective will change after reading the literature. It is the same thing with the various mutations claimed to cause cancer. For example, in this thread someone claims mutations to BRAF cause cancer. I am nearly certain that inspecting the literature will not result in any studies where that gene in a normal cell was mutated, and then it took on the properties of a cancer cell.
Maybe we will see some data on many cell generations later and in conjunction with various other treatments, but not the direct experiment of "non-cancer cell + BRAF mutation = cancer cell" while "non-cancer ell + control treatment = non-cancer cell".
Actually do you have a ref for this? I can't easily think of how they would date the mutation.
The bigger problem is these 5 mutations can be drawn from hundreds of possible genes so the combinations are almost endless.
This is all based on the Armitage and Doll 1954 theory, they write: "This result will be valid for large values of t (of the order of a human lifetime) provided that p_l x t, P_2 x t, ..., p_r x t are all sufficiently small (as could be assumed in an application of this theory to human cancer)" http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2007940/
Here, the "the probability of occurrence of the r-th change, in that line of descent, is p, per unit time [t]". So obviously if p or t is large enough, the probability of dying from cancer goes above 1, which is non-physical. There is a simplification being made here that was reasonable in the pre-computer age. What happens if you implement the same theory without that simplification?
The reason why this is done is it is much easier to do than the experiments that should be done. It is like the old joke about the drunk looking for his keys under the street light because the light is better despite have lost them in dark alley behind.
The best suggestion I have seen is to make better use of all the millions of pets we have. Dogs and cats get cancer that is very similar to human cancer (much more so than mice) and these are all natural cancers. We need to encourage people to sign up their pets for cancer treatment and conduct many more trials in pets. The fact that we don’t do this at any scale is a sign that we are not too serious about curing cancer.
And research funding is probably conservative, since mice is the 'less bad' idea, money flow this way. Some competition may help changing habits.
More importantly this question has already been asked by researchers and most people are happy for their pets to participate in such trials especially when they know they are really helping cure cancer.
Maybe it is cheaper to keep trying and there is less oversight so more BS gets through...