AKR1B10? It turns out to be something that's "rapidly reversible upon smoking cessation." [Reversible and permanent effects of tobacco smoke exposure on airway epithelial gene expression. Beane J, Sebastiani P, Liu G, Brody JS, Lenburg ME, Spira A. Genome Biol. 2007;8(9]:R201.)
And who are Spira et al.? Why, they're the very same ones who cranked out the propaganda, which deceived the public to think that activation of the PI3K system, which is actually a sign of virus infection, is associated with smoking - by using the word "smokers" 76 times, while admitting at the bottom of (another) article that "this increased activity is independent of smoking status or other smoking-related disease." HPV is an example of an infection that's directly implicated in lung cancer.
Evidently Spira et al turned up their noses at AKR1B10, because unlike PI3K, it had no use for predicting lung cancer. There's even a study here that implicates DOWNregulation of AKR1B10 gene expression in colorectal cancer.
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Replied on Thursday, November 11, 2010 7:57 AM
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