NOTE: Since these FOAs were released, NIH has restricted applications to one per institution (one for R01, one for R21). If you are interested in applying to either of these announcements, contact Steve Wasserman by February 14. We may need to perform an internal pre-review to determine UVa nominees.
The following description was taken from the R01 version of this FOA.
Since its establishment in 2002, the NIDDK IBDGC, in collaboration with the International IBD Genetics Consortium (IIBDGC), has identified about 200 previously unknown susceptibility loci for IBD. These newly identified loci have helped to elaborate a wealth of new detail in our understanding of the roles of the innate and acquired immune systems in the pathophysiology of IBD. The IBDGC has also identified a previously unsuspected role for the autophagy pathway in IBD pathophysiology. However, the vast majority of the newly identified loci contain multiple genes, and for about 90% of these loci, causal genes and genetic variants have yet to be identified. The mechanisms by which most of the newly discovered susceptibility loci affect IBD pathophysiology thus remain unknown. The IBDGC has recently been awarded renewed funding to elucidate these mechanisms. However, the IBDGC’s current resources permit them to explore the functions of only a limited number of genes within a limited set of physiological domains. This FOA invites investigators from outside the IBDGC to establish collaborations with the IBDGC to exploit more fully the great wealth of well-characterized patients, biological samples, and data already amassed by the IBDGC to elucidate the mechanisms by which IBD susceptibility genetic variants influence the pathophysiology of IBD. Investigators from a wide range of disciplines with possible relevance to IBD (e.g., immunology, cell biology, microbiology, bioinformatics, systems biology) are encouraged to respond to this FOA. Applications must not duplicate studies already completed or ongoing within the IBDGC. Multi-site clinical trials will not be considered responsive to this FOA.
Activities appropriate for ancillary studies include the following, as well as many others not mentioned in this list:
- Genetic analysis of IBD-related clinical and biological phenotypes in domains not previously investigated (e.g., intestinal remodeling and healing, enteric nervous system),
- Epigenomic, transcriptomic, proteomic, and metabolomic analyses of relevant tissue samples from recruited subjects, and systems biology analyses of the resulting data,
- Analyses of the composition and activities of the intestinal microbiome of recruited subjects,
- Screening of candidate genes and genetic variants in gut barrier, mucosal immune, and other physiological domains, using cultured cells, organoids, Drosophila, zebrafish, mice, and other assay platforms,
- Analyses of the relationships among host genetic variation, intestinal microbiome composition and activity, and variation in the presentation, severity, natural history, and response to treatment of IBD,
- Elucidation of regulatory interactions between DNA sites within the known IBD susceptibility loci and other genes, regardless of their genomic location, or
- Reanalysis of existing data with novel analytic approaches to identify previously unknown susceptibility loci.
Deadline: March 20, 2018; February 21, 2019; February 21, 2020 (letters of intent due 30 days prior to deadline)
- R01 – https://grants.nih.gov/grants/guide/rfa-files/RFA-DK-17-017.html
- R21 – https://grants.nih.gov/grants/guide/rfa-files/RFA-DK-17-018.html
Filed Under: Funding Opportunities