Hi, pathology resident here, studying prostate cancer, and apoptosis in particular. This is an interesting study, and I'm glad to have seen it. I submit that growing a line of cells in culture has relatively little the natural progression of those cells in vivo. Indeed, any cell line that can be propogated in definitely ex vivo surely has some funky stuff going on inside. So, if you're inclined to say that we should be skeptical of mouse models, we should be really skeptical of cell lines. For example, the modal number of chromosomes in these cells is something like 85 (normal is 46).
That said, interesting idea. I noted in the methods that the cells were not grown in low-oxygen conditions, and I'm wondering, if the authors are listening, why they didn't do that.
Well said. I find it disappointing how many cancer researchers delight in their arcane knowledge of cell line characteristics and will debate heartily about which is the right model for an experiment, so at the end of the day other cancer researchers can review their work and nod approvingly about their choice of cell lines, etc. These cells are exceedingly unnatural, even by the standards of cancer cells, and their extensive use in research now far exceeds their ability to tell us things that are meaningful about cancer in the body (IMO). I understand science requires reproducibility, and (in principle at least) cell line work is more reproducible... but I'm worried were chasing red herrings. If you are using cell lines to do basic research on a very specific subsystems, that is likely OK, but so much research these days is "translational" and involves observing cell-wide changes and reactions.
If you're referring to the results about VO2max, please bear in mind that growing cells in culture has nothing to do with that. The issue is that cells generally accumulate far less oxidative damage when grown at 3% oxygen, as compared to atmospheric (21%). So, perhaps they did grow them at low oxygen tension, but it doesn't seem like that's the case from their methods.
May I ask you what you think about organ generation. As testbed I mean, is it naive to believe it could be a better substrate than ex-vivo, and than in-vivo in other animals ?
> Long-term exercise is known to reduce serum levels of growth stimulating hormones. In contrast, the endocrine effects of acute endurance exercise include increased levels of mitogenic factors such as GH and IGF-1.
Two points:
1. how to best understand "long-term exercise" vs "acute endurance exercise" in lay terms here roughly?
2. how mitogenic is growth hormone vs IGF-1? Raised GH seems to raise IGF-1 "usually", but for example during fasts for more than a day or couple of days, GH weirdly seems to go up very drastically while of course IGF-1, insulin, mTOR, leptin all trend ever-lower
Always wondered whether the bodybuilders tried to raise GH for its own sake primarily or just in order to initiate the cascade of other "growth & proliferation" pathways..
So they can partially block some effects of the exercise serum with rEGF, but I hope they (or someone else) figures out what all of the other active components are.
It might be interesting to make an exercise cocktail.
I work in a pharma company and it comes up every time a marketing person comes to a science meeting in a particular department. The short version is that it's very very hard, even if we can profile all of the changes during exercise (which we can't), you can't just use that to know what to administer to someone.
At that point it sounds like it would be easier to jab an electrode in your neck matrix-style and have your body go through a programmed exercise while you watch a movie or something.
Physical activity is associated with reduced risk of several cancers, including aggressive prostate cancer. The mechanisms mediating the effects are not yet understood; among the candidates are modifications of endogenous hormone levels. Long-term exercise is known to reduce serum levels of growth stimulating hormones. In contrast, the endocrine effects of acute endurance exercise include increased levels of mitogenic factors such as GH and IGF-1. It can be speculated that the elevation of serum growth factors may be detrimental to prostate cancer progression into malignancy. The incentive of the current study is to evaluate the effect of acute exercise serum on prostate cancer cell growth. We designed an exercise intervention where 10 male individuals performed 60 minutes of bicycle exercise at increasing intensity. Serum samples were obtained before (rest serum) and after completed exercise (exercise serum). The established prostate cancer cell line LNCaP was exposed to exercise or rest serum. Exercise serum from 9 out of 10 individuals had a growth inhibitory effect on LNCaP cells. Incubation with pooled exercise serum resulted in a 31% inhibition of LNCaP growth and pre-incubation before subcutaneous injection into SCID mice caused a delay in tumor formation. Serum analyses indicated two possible candidates for the effect; increased levels of IGFBP-1 and reduced levels of EGF. In conclusion, despite the fear of possible detrimental effects of acute exercise serum on tumor cell growth, we show that even the short-term effects seem to add to the overall beneficial influence of exercise on neoplasia.
That said, interesting idea. I noted in the methods that the cells were not grown in low-oxygen conditions, and I'm wondering, if the authors are listening, why they didn't do that.