GENETIC EPIDEMIOLOGY AND RISK ASSESSMENT PROGRAM PROJECT SUMMARY The unifying goal of the Genetic Epidemiology and Risk Assessment (GERA) Program is the application of genetic and molecular epidemiology methods to the study of critical questions addressing the etiology, prognosis, and survivorship of cancer in human populations. More specifically, GERA members leverage the combination of epidemiologic methods with high-resolution molecular techniques in order to identify risk and prognostic factors; improve risk stratification; and provide an evidence base for primary, secondary, and tertiary prevention strategies. This goal is further accelerated by applying novel and innovative methods from statistics and informatics. To address these fundamental questions, 3 scientific aims have been developed: 1) To use the tremendous advances in genetics and molecular biology to understand genetic, environmental, and gene?environment interactions in the etiology of cancer in human populations; 2) To use these same advances to understand the molecular epidemiology of cancer prognosis and survivorship; and 3) To develop and apply novel statistical and informatics methods for the design and analysis of genetic and molecular epidemiology studies. The GERA Program's cancer etiology studies use family-based, case-control, and cohort study designs and focus on the genetic epidemiology of cancer, premalignant conditions, and intermediate phenotypes, as well as nongenetic risk factors and descriptive epidemiology. Etiologic heterogeneity based on tumor phenotype is also being addressed. Cancer prognosis research focuses on host factors, including genetic and serum biomarkers as well as lifestyle factors that influence prognosis; tumor biomarkers; and survivorship. Novel methods for the design and analysis of genetic and molecular epidemiologic studies are being developed, building on our expertise in biostatistics, medical informatics, and bioinformatics. To achieve these goals we have assembled a team of 29 multidisciplinary members from 4 departments from all 3 campuses. Total direct peer-reviewed funding is $3.6M (79% from the NCI), with total direct funding of $5.4M. Since 2013, the program has generated 744 publications, 36% reflecting intraprogrammatic collaborations and 59% reflecting interprogrammatic collaborations. Notable contributions have been made in the epidemiology of pancreatic, lung, ovarian, breast, colon, prostate, and lymphoproliferative malignancies as well as to the statistical genetics and medical and bioinformatics literature. Leadership of the program is provided by Drs. Cerhan, Parker, and Yang. The Program makes extensive use of Shared Resources. In the next 5 years, we will facilitate innovative research in cancer etiology and prognosis with a focus on genomics and related omics fields, development and application of novel technologies and methods, and translation to the clinic and population as well as back to the lab to inform biology.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA015083-47
Application #
10113620
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
1997-04-25
Project End
2024-02-29
Budget Start
2021-03-01
Budget End
2022-02-28
Support Year
47
Fiscal Year
2021
Total Cost
Indirect Cost
Name
Mayo Clinic, Rochester
Department
Type
DUNS #
006471700
City
Rochester
State
MN
Country
United States
Zip Code
55905
Lu, Yingchang; Beeghly-Fadiel, Alicia; Wu, Lang et al. (2018) A Transcriptome-Wide Association Study Among 97,898 Women to Identify Candidate Susceptibility Genes for Epithelial Ovarian Cancer Risk. Cancer Res 78:5419-5430
Dasari, Surendra; Newsom, Sean A; Ehrlicher, Sarah E et al. (2018) Remodeling of skeletal muscle mitochondrial proteome with high-fat diet involves greater changes to ?-oxidation than electron transfer proteins in mice. Am J Physiol Endocrinol Metab 315:E425-E434
Nowsheen, Somaira; Aziz, Khaled; Aziz, Asef et al. (2018) L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage. Nat Cell Biol 20:455-464
Razidlo, Gina L; Burton, Kevin M; McNiven, Mark A (2018) Interleukin-6 promotes pancreatic cancer cell migration by rapidly activating the small GTPase CDC42. J Biol Chem 293:11143-11153
Wu, Dongyan; Yang, Haitao; Winham, Stacey J et al. (2018) Mediation analysis of alcohol consumption, DNA methylation, and epithelial ovarian cancer. J Hum Genet 63:339-348
Leon-Ferre, Roberto A; Polley, Mei-Yin; Liu, Heshan et al. (2018) Impact of histopathology, tumor-infiltrating lymphocytes, and adjuvant chemotherapy on prognosis of triple-negative breast cancer. Breast Cancer Res Treat 167:89-99
Jahanseir, Khadijeh; Xing, Deyin; Greipp, Patricia T et al. (2018) PDGFB Rearrangements in Dermatofibrosarcoma Protuberans of the Vulva: A Study of 11 Cases Including Myxoid and Fibrosarcomatous Variants. Int J Gynecol Pathol 37:537-546
Painter, Jodie N; O'Mara, Tracy A; Morris, Andrew P et al. (2018) Genetic overlap between endometriosis and endometrial cancer: evidence from cross-disease genetic correlation and GWAS meta-analyses. Cancer Med 7:1978-1987
Yu, Jia; Qin, Bo; Moyer, Ann M et al. (2018) DNA methyltransferase expression in triple-negative breast cancer predicts sensitivity to decitabine. J Clin Invest 128:2376-2388
Sugihara, Takaaki; Werneburg, Nathan W; Hernandez, Matthew C et al. (2018) YAP Tyrosine Phosphorylation and Nuclear Localization in Cholangiocarcinoma Cells Are Regulated by LCK and Independent of LATS Activity. Mol Cancer Res 16:1556-1567

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