Genome-wide Association Study and Mendelian Randomization Analysis of Early-onset Cancers
Approved Research ID: 51539
Approval date: November 28th 2019
It has been reported that early-onset cancers have distinct molecular genetic mechanisms. Thus, unraveling the pathogenesis of early-onset cancer and identifying biomarkers of it is of great importance. The contribution of genetics and genomics research has identified many risk factors of various diseases, especially cancers. However, the study of germline variants related to the early-onset of cancer is still limited. It has been reported that molecular genetic mechanisms of early-onset cancers are different from elder ones and remain largely unexplained. In addition to genetic susceptibility, environmental factors such as virus infection, diet and smoking are likely to increase the risk of cancer and whether they also contribute to the early-onset cancers are unknown. In this study, we plan to perform genome-wide association studies (GWAS) of all kinds of early-onset cancers and identify germline variants that specifically associated with early-onset cancers. We also plan to perform Mendelian randomization studies to identify potential environmental factors associated with early-onset cancers. The project is scheduled to begin in June 2019 and be completed in December 2021. The research plan is as follows: 1) June 2019 - December 2019: Genome-wide association analysis for early-onset cancers. 2) January 2020 - June 2020: (1) Validation of the early-onset cancer GWAS result using the data of our own. (2) Mendelian randomization studies of potential environmental factors and early-onset cancers. 3) July 2020 - December 2021: summarizing research results, writing research papers.
In this study, we plan to perform genome-wide association studies (GWAS) of early-onset cancers to identify germline variants that are specifically associated with early-onset cancers. We also plan to perform Mendelian randomization studies to identify potential environmental factors associated with early-onset cancers.
Cancer is a complex disease which can be driven by genetic predisposition, environmental factors, and the long-term interactions of predisposing genetic variants and environmental factors. Our extending project aimed to identify cancer associated environmental exposures, genetic germline polymorphisms, and gene-by-environment interactions which can help us to understand the etiology and progression of cancer. We also hypothesize that genetic factors may modify the association of environmental exposures with cancer incidence and mortality, which can provide insight into effects of environmental exposures on the tumorigenic process and inform strategies to develop personalized cancer prevention and treatment.