Norman Sharpless, Managing Director at Jupiter Bioventures and Professor of Cancer Policy and Innovation at UNC School of Medicine, shared a post on LinkedIn:
“As someone who spent a lot of time trying to figure out how the CDKN2a (INK4a/ARF) locus works, it makes me really happy to see this work. The consistent finding has been that inactivation of exon 2 of this archetypal tumor suppressor locus in many species augments the in vitro (and in vivo) growth of certain differentiated cell types (think fibroblasts, glia, melanocytes, cartilage, etc).
Here, the authors show greatly increased growth of porcine muscle progenitor cells lacking p16INK4a and ARF.
I am not sure we were thinking about lab-grown pork chops when we did all those studies, but you have to go where the science takes you…”
More posts featuring Norman Sharpless.