yeah but P53 redundancies are a pretty big deal in answering that question. We have one P53 gene and if it gets damaged the cell gets to run amok. Those other animals have like 12 p53 genes, and don't get cancer.
The evidence that p53 duplication is an important mechanism is very interesting, but we know p53 is not the sole answer. A good example of this is both humans and mice have one copy of the p53 gene yet humans are vastly more resistant to developing cancer than mice.
It is because we have been selected for a much longer lifespan than mice. Basically during human evolution there has been a selection process for greater resistance to developing cancer - if we got cancer at the rate mice get it almost nobody would make it to be a teenager.
Humans are by animal standards very long lived and naturally quite resistant to developing cancer. We have many more anti-cancer biochemical and genetic systems (antioncogenes) that work much better than the same systems in mice.
Please, your statement is so ambiguous that it makes almost no sense.
1. Which mouse? An inbred laboratory possibly immunodeficient strain, a genetically engineered mouse to GET cancer at a high rate, or maybe a wild type free-range mouse?
2. Which cancer? Do you realize that it is almost impossible to get realistic models of prostate cancer or that mice simply live to short to get colorectal cancer - even when the relevant mutations are introduced?
Sorry if I was being ambiguous. All mice are less resistant to cancer than humans, even wild type mice. Mice in nature rarely live long enough to get cancer, but if you put them up in a mouse retirement home (lab), a large percentage of wild mice will get spontaneous cancers.
Yes mouse cancer in not a great model for human cancer and we probably should not be using mice - about the only good thing they have going for them as a model is they are small and cheap.
Personally I would like to see us using pets (dogs and cats) much more as their cancers are a much better match to human cancers in both how they develop and how they progress. That we are not taking better advantage of this resource to develop new treatments is a tragedy.
I suspect one reason could be that mice have much faster metabolisms than humans. Also, typically the speed of metabolism is typically inversely correlated with size, although there definitely are some outliers too.
Mice have far few cells than humans so they should be much less likely to get cancer (all things being equal). Peto’s paradox is all about this effect [1].
Foremost the number of times a gene is found does not directly relate to its expression, and mutant proteins are often significantly more reactive than their counterparts. Also having more genes means the risk of getting a damaged gene goes up.
Most importantly people for the last 20 years have tried to genetically integrate working p53 into cancer cells, and it has little effect on most types of cancer.
Some cancers (testicular if I recall), are the result of a p53 mutation. Crucially, fixing the mutated gene did not fix the cancer. The community I work with has a lot of skepticism about claims that simply increasing the quantity of tumor suppressor gene will fix cancer.
Most likely having more genes means that there was a higher chance of receiving a viable beneficial mutation somewhere early in the animals evolutionary history, although it does little for the individual animal in the present day.
Correlation, meet causation.
What is the valid counterpoint?