Wednesday, August 22, 2007

No longer a cancer/youth tradeoff

This paper recently rolled off the presses touting p53 - that notable universal tumor suppressor gene that must be neutralized for cancer to proceed - actually has not only its usual cancer-resistance abilities, but potentially have youth-preserving ability when paired with a stabilizing protein, Arf.

This is pretty much counterintuitive to conventional wisdom; It's generally been accepted that getting old is a controlled mechanism to fight off the perpetual tumor generation going on in all of our bodies (you and I are likely killing a dozen or so tumor sites every day). In essence, you trade off maintaining your youthful looks and facility in order to live a long time. Not so, says this new paper!

Now, the sample sizes of some of the groups, especially in the somewhat dubious biomarker and biochemical studies seem quite small, and the fact they had to stoop to using a p value of 0.1 makes me veeeery leery. Still, I know keeping a dumb mouse alive for two years is no small feat, and direct comparisons are probably the only way to go here, so the t test suffers from the unpaired choices. Perhaps more worrying is their handwaving to dismiss the effect of the Ink genes, also known to have cancer-resistance properties. They seem to pull a 'Look over there!' moment towards the end of the paper.

All that said, there's some reasonable physiological evidence to make a story here, just probably not enough to topple the current hypothesis.

Finally, while this gene model keeps the mice youthful, still crossing that tightrope as if they were a spring whelp, it did not increase their life span. But ah, to die young after living a full life - doesn't seem so bad, eh?

2 comments:

Bobbi said...

I can't get to the article itself, but if they're getting a huge effect size (a d of .8 is considered "large," at least in psych), I can almost forgive the p < .1. Alpha cutoffs are more-or-less arbitrary and strongly influenced by sample size, after all.

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