The overall objective of the Mayo Clinic Center for Cell Signaling in Gastroenterology (C-SiG) is to exploit signaling pathways in gastrointestinal cells to improve the health of patients with digestive diseases. To do this, C-SiG provides a robust infrastructure, thematic platforms, and career development opportunities to integrate and amplify impactful investigation along the discovery-translation-application paradigm. Our Research Base now consists of 68 scientists (15% growth) involving 18 departments and $23.7 million (direct costs, 2.5% growth) in digestive disease-related funding. Responding to members' evolving interests and scientific advances, we've re-aligned members into three interconnected Mechanistic Research Themes (intracellular signaling, cell-to-cell communication, and genetics/epigenetics), each intersecting with three Disease Focus Groups (liver pathobiology, enteric neurosciences, inflammation/transformation), a matrix that fosters both discovery and disease relevant investigation. Our ongoing CENTRAL HYPOTHESIS is that advances in care of patients with digestive diseases requires a facilitative infrastructure supporting meaningful interactions among multidisciplinary scientists investigating cellular mechanisms, pathways, and therapeutic targets to enhance rapid translation of basic discoveries into clinical trials. Our OVERALL SPECIFIC AIMS are to: i) Foster multidisciplinary research by expanding technical and collaborative capabilities of established GI scientists and attracting investigators from other disciplines; ii) Identify and nurture new GI investigators via a peer-reviewed Pilot and Feasibility (P/F) Program including career development workshops, curricula, and structured mentorship (19/26, 73% of P/F recipients achieving federal funding); iii) Offer core-based specialized equipment, technologies, methodologies, reagents, and expertise (Optical Microscopy, Clinical, and Gene Editing and Epigenomics Cores), with continuous core menu updates, quality assurance and assessments, and project management oversight in response to member feedback; iv) Support a robust Enrichment Program; and v) Promote interactions between C-SiG with other NIDDK centers at Mayo (e.g., PKD Center) and existing DDRCCs, especially in the Midwest (i.e., Midwest DDRCC Alliance). Our global efforts have resulted in 215 manuscripts, with 56% percent intra- and 44% inter-thematic publications (70% involving two or more members). Importantly, we've made critical advances in understanding disease pathogenesis relevant to signal transduction, cell-to-cell communication and genetics/epigenetics, thereby identifying potential disease modifying targets.

Public Health Relevance

Gastrointestinal diseases and their complications have a significant negative effect on public health and incur considerable health care utilization costs. Research supported by this Center grant is critically important to advance our understanding of the mechanisms that underlie digestive diseases. This new knowledge can lead to practical applications for the diagnosis, prevention, monitoring, and treatment of digestive diseases.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
2P30DK084567-11
Application #
9709920
Study Section
Special Emphasis Panel (ZDK1)
Program Officer
Perrin, Peter J
Project Start
2009-09-01
Project End
2024-06-30
Budget Start
2019-09-01
Budget End
2020-06-30
Support Year
11
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Mayo Clinic, Rochester
Department
Type
DUNS #
006471700
City
Rochester
State
MN
Country
United States
Zip Code
55905
Mouchli, Mohamad A; Ouk, Lidia; Scheitel, Marianne R et al. (2018) Colonoscopy surveillance for high risk polyps does not always prevent colorectal cancer. World J Gastroenterol 24:905-916
Rizvi, Sumera; Khan, Shahid A; Hallemeier, Christopher L et al. (2018) Cholangiocarcinoma - evolving concepts and therapeutic strategies. Nat Rev Clin Oncol 15:95-111
Hale, Vanessa L; Jeraldo, Patricio; Chen, Jun et al. (2018) Distinct microbes, metabolites, and ecologies define the microbiome in deficient and proficient mismatch repair colorectal cancers. Genome Med 10:78
Allen, Alina M; Therneau, Terry M; Larson, Joseph J et al. (2018) Nonalcoholic fatty liver disease incidence and impact on metabolic burden and death: A 20 year-community study. Hepatology 67:1726-1736
Rizvi, Sumera; Eaton, John; Yang, Ju Dong et al. (2018) Emerging Technologies for the Diagnosis of Perihilar Cholangiocarcinoma. Semin Liver Dis 38:160-169
Strege, Peter R; Mazzone, Amelia; Bernard, Cheryl E et al. (2018) Irritable bowel syndrome patients have SCN5A channelopathies that lead to decreased NaV1.5 current and mechanosensitivity. Am J Physiol Gastrointest Liver Physiol 314:G494-G503
Bianco, F; Eisenman, S T; Colmenares Aguilar, M G et al. (2018) Expression of RAD21 immunoreactivity in myenteric neurons of the human and mouse small intestine. Neurogastroenterol Motil 30:e13429
Druliner, Brooke R; Ruan, Xiaoyang; Sicotte, Hugues et al. (2018) Early genetic aberrations in patients with sporadic colorectal cancer. Mol Carcinog 57:114-124
Masyuk, Tatyana V; Masyuk, Anatoliy I; LaRusso, Nicholas F (2018) Polycystic liver disease: The interplay of genes causative for hepatic and renal cystogenesis. Hepatology 67:2462-2464
Smoot, Rory L; Werneburg, Nathan W; Sugihara, Takaaki et al. (2018) Platelet-derived growth factor regulates YAP transcriptional activity via Src family kinase dependent tyrosine phosphorylation. J Cell Biochem 119:824-836

Showing the most recent 10 out of 537 publications