Commentary: From epidemiology to molecular biology—vitamin D and colorectal cancer prevention

Abstract

In 1987 I commenced a post-doctoral position at Cornell University, Ithaca, NY. My prior ‘exposure’ to vitamin D was connected with studies of intestinal transport systems that were regulated by 1,25-dihydroxyvitamin D. This investigation had been initiated by the director of my institute, Prof. Dr Meinrad Peterlik, who himself had been a post doctoral fellow at Cornell University with the well-known investigator of intestinal calcium transport and vitamin D, Prof. Robert H. Wasserman. At Cornell University I first became interested in the magical properties that 1,25-dihydroxyvitamin D had on growth, differentiation, and survival of cancer cells. My growing interest was further stimulated by some controversial papers published by the group of Garland et al. from the University of California San Diego (UCSD) in La Jolla, CA. 1 These papers for the first time connected enhanced incidence of colon cancer to lack of sunlight and reduced serum vitamin D. This was a daring thought and, from knowledge existing on vitamin D renal synthesis in 1980, downright heretical. While I was incredulous and wished I could join this group for their studies (I had previously been an undergraduate and graduate student at UCSD and had much enjoyed the California sunshine!) this obviously had implications for my subsequent work. In 1991, after rejoining the Department of Pathophysiology at the University of Vienna, Austria, we showed that only in nanomolar concentrations the active vitamin D metabolite inhibited growth of human colon cancer cells. Intriguingly, the picomolar concentrations that are normally found in serum rather enhanced growth of these cells. The relevance of nutritional calcium together with vitamin D in colorectal cancer prevention postulated by the Garland group 2