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.