Fight Aging!

My attention was drawn to a Spanish article on one of the many research groups investigating the role of p53 in aging and cancer. There has been a great deal of interest in finding ways around the "cancer or aging, choose one" limitation to this set of biochemical mechanisms, thought to apply until recently. This Spanish article is somewhat in advance of the scientific publication; I'm not sure why that is the case.

The translation via Google is fair (suggestions taken on a better translation automaton):

In this line, Serrano said that the genomes of a chimpanzee and humans are virtually identical at 99.8%. However, the maximum life of a chimpanzee is 60 years and the human rarely exceeds 110. The average of a chimpanzee is 40 years and that of a human, 80. There must be something in our genes very subtle changes made to live 50 years to live 100. Then, along with the team of Mary Blasco, we are going to make some genetic manipulation to see if we can increase longevity in mice much more. That is our challenge If we get a mouse in the privileged environment of a laboratory comes to live three years to live six passes, it would be proof that longevity is flexible and would know how to enlarge it.

So it seems compelled to ask the molecular biologist in this battle if they have undertaken together against cancer and aging, it is just a matter of putting telomerase a mouse to make it immortal. The answer is no, because telomerase makes more cancer. To ensure a tumor, which has activated telomerase, and if a mouse has more telomerase than normal, for example, on transgenic mice, we know that you have more tumors. What we have done is to use the superratones Manuel, because p53 protects cancer and a 18% lengthens the life of mice, and if we add to this the gene of immortality, telomerase, which got these mice [to] live an average of 50% more, without cancer, which are words older. That is what we have discovered now.

Because this extension of life, 50% in superratones is the longest that has been described in mammals.

You get the gist, despite the breakdown of translation in the last few sentences: there are combinations of metabolic and genetic states in mammals not selected for by evolution that nonetheless lead to a clearly superior beast, from our perspective at least. Well, more or less. If you head over to the Methuselah Foundation forums, you'll find that Michael Rae wrote a long piece on this research back in mid-2007, before the life span studies were complete:

The standard reading is that the "Super p53" mice are getting less cancer, but are having their [life spans] restrained by lack of tissue replenishment due to stem cell loss, while the telomerase transgenics are on the opposite horn of the same dilemma. It seems at least possible that if one overlaid the strong cancer resistance conferred by the former, with the increase in stem cell mobilization and proliferative capacity of the latter, you'd wind up with a long-lived, slow-aging mouse.

There are a lot of caveats and details both prior and after that statement, many of which still apply even with these final life span study results. It's not all completely clear-cut, as is often the case, but I can see this impressive work garnering a great deal of attention in the popular press once it jumps the language gap for the English-speaking world.