Fred Brewer of the Albert Einstein College of Medicine continues the discussion on the differences between basic and translational research. (Titled "Basic versus Translational Research" in print version.)
In your May President’s Message, discussion continues on the apparent lack of support of “basic research” versus “translational research” by the National Institutes of Health. I’m concerned because this affects our research into the molecular basis of lectin-carbohydrate interactions in cellular recognition (glycobiology), which, until recently, was supported by the National Cancer Institute for 30 years.
So, let’s examine the linguistic claims that basic and translational research are separate efforts. In the present context, let’s define “basic research” as studies of biological processes and the molecules involved. “Translational research” can be defined as studies that target the molecular basis of disease, with the hopeful goal of a “cure.” However, finding cures for diseases such as cancer requires understanding the alteration of normal cellular processes to the transformed state and then changing the latter to the former. Thus, both the disease state and normal state need molecular definition, which requires research into both. In other words, you can’t fix something unless you understand what the differences are. (Automobile mechanics know this well.) Thus, both basic and translational research need NIH support because they are interlocked scientifically.
It follows that care needs to be given in defining basic research as something without evident translational components. This is the base line required for translational research. We need much more data on the molecular mechanisms associated with normal homeostasis in human biology, as well as the change involved in the disease process. In this regard, our “basic research” has led to new models of the interactions of lectins with cell surface glycans of pathogens in innate immunity (1) and cellular homeostasis in metazoans (ground state for health) (2). These findings are a result of more than 30 years of basic research!
For future discussion, you may consider the effects on NIH funding of having predominantly one sector of science define equilibrium and nonequilibrium chemical interactions in humans.
Albert Einstein College of Medicine
1. Dam, T. K., and Brewer, C. F. (2010) Lectins as Pattern Recognition Molecules: The Effects of Epitope Density in Innate Immunity. Glycobiology 20, 270 – 278.
2. Dam, T. K., and Brewer, C. F. (2010) Maintenance of Cell Surface Glycan Density by Lectin-Glycan Interactions: A Homeostatic and Innate Immune Regulatory Mechanism. Glycobiology, in press.