Absolutely nothing about the data collected related to different human populations just different types of tissue.
Further, I don't see anything that relates to % of biomass of the tissue just total cell divisions. Presumably the skin, lungs, a digestive track tissues are at high risks because they compromise a lot of tissue, it divides rapidly, and it's not protected from environmental factors ex: sunlight/smoking/spicy food. However, I suspect the paper digs into things a little further to account for such factors.
Yeah, I'm talking about the different populations thing to illustrate an extreme example about the 'luck' concept. It's not directly related to the study.
Not sure I understand the % biomass issue. The tissues you're referring to - epithelial - are the ones doing the bulk of the cell division in adults, and the ones where you'd typically get the (early stage) cancers. Something like smoking increases your risk in two ways. You get a higher mutation rate (chemicals enter your cells and mess with DNA replication). You also increase the number of 'lung cells' you need to clean out and replace, causing more cell division. Obesity (and size in general) has a direct theoretical effect: more cells = more opportunities to divide = more risk events. Caloric restriction presumably is the opposite of that: do nothing and eat nothing, don't have your cells get replaced, and you reduce the number of risk events.
I think the deeper question in cancer math, if you get the single-gene level biologists and population level statisticians to talk to each other, is how much of the cancer is due to mechanics (number of cells, division counts) that are out of our control, mechanics that we can affect, genetics that are out of our control, and how much is genetics that are fragile but susceptible to prevention and early treatment. That's the sweetspot; that's what we ultimately want to find - genetic markers of things that are going to break but can be patched or protected or fixed.
That's why we want accurate models of risk - in different kinds of tissues - in the first place.
It seems like more cells = more risks of mutation = more risk of cancer. So, I would presume it's something that needs to be accounted for in their model.
However, based on the wording that seems to be total cell divisions and I don't know enough about rates of cell division or cancer to tell from that chart. In the end a gall bladder weighs less than 1/4th of a pound where the small intestine is ~3.5 pounds so it hardly seems like they can just ignore it.
Though, if it's really just cell divisions and not organ weight that matters then that's a much stronger finding IMO.
PS: And no I am not paying 20$ to read the actual article. Though if it's free somewhere I would like to read it.
The fact that species with more cells don't get more cancer is known as Peto's paradox. Perhaps it is also true at the tissue level. See http://en.wikipedia.org/wiki/Peto%27s_paradox
Absolutely nothing about the data collected related to different human populations just different types of tissue.
Further, I don't see anything that relates to % of biomass of the tissue just total cell divisions. Presumably the skin, lungs, a digestive track tissues are at high risks because they compromise a lot of tissue, it divides rapidly, and it's not protected from environmental factors ex: sunlight/smoking/spicy food. However, I suspect the paper digs into things a little further to account for such factors.