Clinical OMICS

SEP-OCT 2018

Healthcare magazine for research scientists, labs, pathologists, hospitals, cancer centers, physicians and biopharma companies providing news articles, expert interviews and videos about molecular diagnostics in precision medicine

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www.clinicalomics.com September/October 2018 Clinical OMICs 33 biological basis of AF. We should also be able to generate a much more informative polygenic risk score for identifying individuals at high risk of AF. How well that risk score per- forms in the clinic will need to be verified in randomized clinical trials." Ultimately, the ability to identify who is most at risk of developing AF should allow the development of preven- tive approaches that improve patient outcomes and qual- ity of life. "Discovery of novel genetic variants and genes important for atrial fibrillation was only pos- sible because we combined information from multiple biobanks from around the world in a large collabora- tive effort," concluded first author Jonas Bille Nielsen, M.D., Ph.D., a cardiovas- cular researcher at UM. "Combining the advan- tages of each of the data sources helped us to better understand the biology underlying atrial fibrillation." These findings need confirmation but provide a foundation for directing future functional experiments to better under- stand the biology underlying AF. Besides leading to palpitations and reduced fitness, AF is a major risk factor for stroke, heart failure, and death, Nielsen said. "If you just once have seen a person disabled, bound to a wheel chair, and unable to speak as a result of a major stroke, likely caused by atrial fibrillation, you know it is an important disease to treat and prevent. However, cur- rent treatment options are limited, can cause serious side effects, and are very rarely curative." A better understanding of the biological processes under- lying AF could lead to better treatment and prevention, he noted. The team's identification of more than 150 genes that are likely to be involved in the initiation and progression of AF should prove valuable in the search for novel therapies. "An ongoing, randomized trial is currently testing whether continuous monitoring of the heart rhythm using a small implantable device can led to earlier detection of atrial fibril- lation and prevent strokes," Nielsen continued. "If this or similar studies come out positive, it is likely that high-risk persons, such as those with a very high genetic burden or risk score for developing atrial fibrillation, will benefit the most from a device and the implantation could eventually be guided by genetics in combination with other risk factors. This or similar approaches of personalized medicine using genetic information from hundreds or even thousands of variants still needs to be proven to be effective in randomized trials, but is more likely to be successful as our understanding of the genetic mechanisms underlying atrial fibrillation and other common diseases is expanding rapidly due to large col- laborative efforts like the ones we just presented." Jonas Bille Nielsen, M.D., Ph.D., University of Michigan This figure illustrates a network of the most signif- icant biological pathways underlying atrial fibrillation (each represented by a circle, colored according to significance) and the overlap between them (grey lines) measured as similarity of genes across the different pathways. The results are obtained by combining the genetic findings from >1 million people with other biological information from thousands of measurements, including gene expression data from animal and cell studies.

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