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Denny, Joshua C.

https://orcid.org/0000-0002-3049-7332

Mayo Clinic

National Institutes of Health

Citations 27

Probing the Virtual Proteome to Identify Novel Disease Biomarkers
Smith, J. G. , Melander, Olle , Ngo, Debby , Shaffer, Christian M., Ferguson, Jane F. , Herzig, Matthew , McCarty, Catherine A. , Jarvik, Gail P. , Gordon, Allan , Palmer, Melody R. , Crosslin, David R. , Larson, Eric B. , Pacheco, Jennifer A. , Peissig, Peggy , Brilliant, Murray H. , Kitchner, Terrie, Linneman, James G., Namjou, Bahram , Ritchie, Marylyn D. , Borthwick, Kenneth M., Kiryluk, Krzysztof , Mentch, Frank , Sleiman, Patrick , Karlson, Elizabeth W. , Zhu, Yineng, Denny, Joshua C. , Roden, Dan M. , Gerszten, Robert E. , Wang, Thomas J. , Denny, Joshua C , Jarvik, Gail P , Gordon, Adam S , Pacheco, Jennifer A , Kiryluk, Krzysztof , Ferguson, Jane F , Mosley, Jonathan D , Benson, Mark D. , Chute, Christopher G. , Carrell, David , Kullo, Iftikhar J. , Williams, Marc S , Verma, Shefali S. , Vasan, Ramachandran S. , Yang, Qiong , Roden, Dan M. , Smith, J Gustav

Circulation | January 7, 2019 | Volume: 138 | Issue: 22 | Pages: 2469-2481

10.1161/circulationaha.118.036063 Get It

Background: Proteomic approaches allow measurement of thousands of proteins in a single specimen, which can accelerate biomarker discovery. However, applying these technologies to massive biobanks is not currently feasible because of the practical barriers and costs of implementing such assays at scale. To overcome these challenges, we used a “virtual proteomic” approach, linking genetically predicted protein levels to clinical diagnoses in >40 000 individuals. Methods: We used genome-wide association data from the Framingham Heart Study (n=759) to construct genetic predictors for 1129 plasma protein levels. We validated the genetic predictors for 268 proteins and used them to compute predicted protein levels in 41 288 genotyped individuals in the Electronic Medical Records and Genomics (eMERGE) cohort. We tested associations for each predicted protein with 1128 clinical phenotypes. Lead associations were validated with directly measured protein levels and either low-density lipoprotein cholesterol or subclinical atherosclerosis in the MDCS (Malmö Diet and Cancer Study; n=651). Results: In the virtual proteomic analysis in eMERGE, 55 proteins were associated with 89 distinct diagnoses at a false discovery rate q<0.1. Among these, 13 associations involved lipid (n=7) or atherosclerosis (n=6) phenotypes. We tested each association for validation in MDCS using directly measured protein levels. At Bonferroni-adjusted significance thresholds, levels of apolipoprotein E isoforms were associated with hyperlipidemia, and circulating C-type lectin domain family 1 member B and platelet-derived growth factor receptor-β predicted subclinical atherosclerosis. Odds ratios for carotid atherosclerosis were 1.31 (95% CI, 1.08–1.58; P =0.006) per 1-SD increment in C-type lectin domain family 1 member B and 0.79 (0.66–0.94; P =0.008) per 1-SD increment in platelet-derived growth factor receptor-β. Conclusions: We demonstrate a biomarker discovery paradigm to identify candidate biomarkers of cardiovascular and other diseases.
Detecting potential pleiotropy across cardiovascular and neurological diseases using univariate, bivariate, and multivariate methods on 43,870 individuals from the eMERGE network
Zhang, Xinyuan , Veturi, Yogasudha , Bone, William P. , Lucas, Anastasia, Hebbring, Scott J. , Stanaway, Ian B. , Jarvik, Gail P. , Crosslin, David R. , Larson, Eric B. , Sleiman, Patrick , Fasel, David , Wei, Wei‐Qi, Schaid, Daniel J. , Ritchie, Marylyn D. , Jarvik, Gail P , Wei, Wei-Qi , Verma, Shefali S. , Verma, Anurag , Denny, Joshua C. , Rasmussen‐Torvik, Laura J. , Pendergrass, Sarah A. , Smoller, Jordan W. , Håkonarson, Håkon , Weng, Chunhua , Kullo, Iftikhar J. , Chung, Wendy K.

Biocomputing 2019 | November 28, 2018 | Volume: No volume available | Issue: No issue available | Pages: 272-283

10.1142/9789813279827_0025 Get It

A case study evaluating the portability of an executable computable phenotype algorithm across multiple institutions and electronic health record environments
Pacheco, Jennifer A. , Rasmussen, Luke V. , Kiefer, Richard C. , Speltz, Peter, Carroll, Robert J. , Stallings, Sarah , Mo, Huan , Ahuja, Monika, Jiang, Guoqian , LaRose, Eric , Peissig, Peggy , Shang, Ning , Benoit, Barbara, Gainer, Vivian S., Borthwick, Kenneth M., Jackson, Kathryn , Sharma, Ambrish Kumar, Wu, Andy , Roden, Dan M. , Pathak, Jyotishman , Denny, Joshua C. , Thompson, William K. , Denny, Joshua C , Rasmussen, Luke V , Pacheco, Jennifer A , Campion, Thomas R , Wu, Andy Yizhou, Kho, Abel , Roden, Dan M.

Journal of the American Medical Informatics Association | July 14, 2018 | Volume: 25 | Issue: 11 | Pages: 1540-1546

10.1093/jamia/ocy101 Get It

Abstract Electronic health record (EHR) algorithms for defining patient cohorts are commonly shared as free-text descriptions that require human intervention both to interpret and implement. We developed the Phenotype Execution and Modeling Architecture (PhEMA, http://projectphema.org) to author and execute standardized computable phenotype algorithms. With PhEMA, we converted an algorithm for benign prostatic hyperplasia, developed for the electronic Medical Records and Genomics network (eMERGE), into a standards-based computable format. Eight sites (7 within eMERGE) received the computable algorithm, and 6 successfully executed it against local data warehouses and/or i2b2 instances. Blinded random chart review of cases selected by the computable algorithm shows PPV ≥90%, and 3 out of 5 sites had &gt;90% overlap of selected cases when comparing the computable algorithm to their original eMERGE implementation. This case study demonstrates potential use of PhEMA computable representations to automate phenotyping across different EHR systems, but also highlights some ongoing challenges.
LPA Variants Are Associated With Residual Cardiovascular Risk in Patients Receiving Statins
Wei, Wei‐Qi, Li, Xiaohui , Feng, QiPing , Kubo, Michiaki , Peissig, Peggy , Karlson, Elizabeth W. , Jarvik, Gail P. , Shang, Ning , Larson, Eric , Shaffer, Christian M., Maeda, Shiro , Horikoshi, Momoko , Ritchie, Marylyn D. , Larson, Eric B. , Crosslin, David R. , Bland, Harris T. , Pacheco, Jennifer A. , Rasmussen‐Torvik, Laura J. , Cox, Nancy J. , Wilke, Russell A. , Rotter, Jerome I. , Momozawa, Yukihide , Roden, Dan M. , Krauss, Ronald M. , Denny, Joshua C. , Denny, Joshua C , Bland, Sarah T , Jarvik, Gail P , Wei, Wei-Qi , Rotter, Jerome I , Pacheco, Jennifer A , Kullo, Iftikhar J. , Lee, Ming Ta Michael , Edwards, Todd L. , Mosley, Jonathan D , Williams, Marc S , Cronkite, David , Hripcsak, George , Stein, Christoph , Roden, Dan M. , Feng, Qiping , Rasmussen-Torvik, Laura J

Circulation | April 27, 2018 | Volume: 138 | Issue: 17 | Pages: 1839-1849

10.1161/circulationaha.117.031356 Get It

Background: Coronary heart disease (CHD) is a leading cause of death globally. Although therapy with statins decreases circulating levels of low-density lipoprotein cholesterol and the incidence of CHD, additional events occur despite statin therapy in some individuals. The genetic determinants of this residual cardiovascular risk remain unknown. Methods: We performed a 2-stage genome-wide association study of CHD events during statin therapy. We first identified 3099 cases who experienced CHD events (defined as acute myocardial infarction or the need for coronary revascularization) during statin therapy and 7681 controls without CHD events during comparable intensity and duration of statin therapy from 4 sites in the Electronic Medical Records and Genomics Network. We then sought replication of candidate variants in another 160 cases and 1112 controls from a fifth Electronic Medical Records and Genomics site, which joined the network after the initial genome-wide association study. Finally, we performed a phenome-wide association study for other traits linked to the most significant locus. Results: The meta-analysis identified 7 single nucleotide polymorphisms at a genome-wide level of significance within the LPA/PLG locus associated with CHD events on statin treatment. The most significant association was for an intronic single nucleotide polymorphism within LPA/PLG (rs10455872; minor allele frequency, 0.069; odds ratio, 1.58; 95% confidence interval, 1.35–1.86; P =2.6×10 − 10 ). In the replication cohort, rs10455872 was also associated with CHD events (odds ratio, 1.71; 95% confidence interval, 1.14–2.57; P =0.009). The association of this single nucleotide polymorphism with CHD events was independent of statin-induced change in low-density lipoprotein cholesterol (odds ratio, 1.62; 95% confidence interval, 1.17–2.24; P =0.004) and persisted in individuals with low-density lipoprotein cholesterol ≤70 mg/dL (odds ratio, 2.43; 95% confidence interval, 1.18–4.75; P =0.015). A phenome-wide association study supported the effect of this region on coronary heart disease and did not identify noncardiovascular phenotypes. Conclusions: Genetic variations at the LPA locus are associated with CHD events during statin therapy independently of the extent of low-density lipoprotein cholesterol lowering. This finding provides support for exploring strategies targeting circulating concentrations of lipoprotein(a) to reduce CHD events in patients receiving statins.
Research Directions in the Clinical Implementation of Pharmacogenomics: An Overview of US Programs and Projects
Volpi, Simona , Bult, Carol J. , Chisholm, Rex L. , Deverka, Patricia A. , Jacob, Howard J., Kasapi, Melpomeni , McLeod, Howard L. , Roden, Dan M. , Green, Eric D. , Rodriguez, Laura Lyman , Aronson, Samuel , Cavallari, Larisa H. , Denny, Joshua C. , Dressler, Lynn G., Johnson, Julie A. , Leeder, J. Steven , Piquette‐Miller, Micheline , Rasmussen‐Torvik, Laura J. , Ritchie, Marylyn D. , Skaar, Todd C. , Wagle, Nikhil , Weinshilboum, Richard M. , Weitzel, Kristin, Wildin, Robert S. , Manolio, Teri A. , Relling, Mary V. , Weinshilboum, Richard, Denny, Joshua C , Ginsburg, Geoffrey S. , Roden, Dan M. , Williams, Marc S , Klein, Teri E. , Perera, Minoli A. , Rehm, Heidi L. , Weinshilboum, Richard M. , Wilson, John T. , Cavallari, Larisa H , Rasmussen-Torvik, Laura J

Clinical Pharmacology & Therapeutics | February 21, 2018 | Volume: 103 | Issue: 5 | Pages: 778-786

10.1002/cpt.1048 Get It

Response to a drug often differs widely among individual patients. This variability is frequently observed not only with respect to effective responses but also with adverse drug reactions. Matching patients to the drugs that are most likely to be effective and least likely to cause harm is the goal of effective therapeutics. Pharmacogenomics (PGx) holds the promise of precision medicine through elucidating the genetic determinants responsible for pharmacological outcomes and using them to guide drug selection and dosing. Here we survey the US landscape of research programs in PGx implementation, review current advances and clinical applications of PGx, summarize the obstacles that have hindered PGx implementation, and identify the critical knowledge gaps and possible studies needed to help to address them.
SOS2 and ACP1 Loci Identified through Large-Scale Exome Chip Analysis Regulate Kidney Development and Function
Li, Man , Weeks, Olivia , Mijatovic, Vladan, Teumer, Alexander , Tromp, Gerard , Fuchsberger, Christian , Gorski, Mathias , Nutile, Teresa , Sedaghat, Sanaz , Sorice, Rossella , Arking, Dan E. , Bihlmeyer, Nathan A. , Böger, Carsten A., Carroll, Robert J. , Cornelis, Marilyn C., Faul, Jessica D. , Feitosa, Mary F. , Gambaro, Giovanni , Gasparini, Paolo , Giulianini, Franco, Heid, Iris M. , Huang, Jinyan , Imboden, Medea , Jeff, Janina M., Jhun, Min A., Katz, Ronit , Kifley, Annette , Kilpeläinen, Tuomas O. , Laakso, Markku , Li‐Gao, Ruifang , Lohman, Kurt, Lu, Yingchang , Mägi, Reedik , Mihailov, Evelin, Mohlke, Karen L. , Mook‐Kanamori, Dennis O. , Robino, Antonietta , Salvi, Erika , Schick, Ursula M., Schulz, Christina‐Alexandra , Smith, Albert V. , Traglia, Michela , Yerges-Armstrong, Laura M. , Goodarzi, Mark O. , Kraja, Aldi T., Wessel, Jennifer , Group,, CHARGE Glycemic-T2D Working, Group,, CHARGE Blood Pressure Working, Boerwinkle, Eric , Borecki, Ingrid B. , Bork‐Jensen, Jette , Böttinger, Erwin P. , Braga, Daniele , Brandslund, Ivan , Brody, Jennifer A. , Carey, David J. , Christensen, Cramer, Crook, Errol D., Boer, Ian H. de , Vries, Aiko P. J. de , Devuyst, Olivier , Dreisbach, Albert W. , Endlich, Karlhans , Franco, Oscar H. , Glümer, Charlotte , Gottesman, Omri, Grarup, Niels , Guðnason, Vilmundur , Harris, Tamara B., Hofman, Albert , Husemoen, Lise Lotte N. , Jackson, Rebecca D. , Jørgensen, Marit E. , Kähönen, Mika , Kardia, Sharon L. R., König, Wolfgang , Kriebel, Jennifer , Lauritzen, Torsten , Lehtimäki, Terho , Levy, Daniel , Linksted, Pamela , Loos, Ruth J. F. , Lupo, Antonio , Meisinger, Christine, Melander, Olle , Mitchell, Paul, Nauck, Matthias, Orho‐Melander, Marju , Parsa, Afshin, Pedersen, Oluf , Peters, Annette , Peters, Ulrike , Polašek, Ozren , Qi, Lu , Reiner, Alex P. , Rettig, Rainer, Ridker, Paul M., Rivadeneira, Fernando , Rossouw, Jacques E. , Schmidt, Frank , Soranzo, Nicole , Strauch, Konstantin , Toniolo, Daniela , Uitterlinden, André G. , Ulivi, Sheila , Velayutham, Dinesh , Völker, Uwe , Völzke, Henry , Waldenberger, Mélanie , Wang, Jie Jin , Weir, David R. , Witte, Daniel R. , Kuivaniemi, Helena , Fox, Caroline S., Franceschini, Nora , Goessling, Wolfram , Köttgen, Anna , Chu, Audrey Y., Rudan, Igor , Vasan, Ramachandran S. , Duijn, Cornelia M. van , Zhao, Wei , Padmanabhan, Sandosh , Lindgren, Cecilia M. , Franks, Paul W. , Weiß, Stefan , Langenberg, Claudia , Hattersley, Andrew T. , Turner, Stephen T. , Li, Yong , Huffman, Jennifer E. , Lyytikäinen, Leo‐Pekka , Tin, Adrienne , Yang, Qiong , Ahluwalia, Tarunveer S. , Chasman, Daniel I. , Dehghan, Abbas , Jackson, Anne , Kumar, Ashish , Malerba, Giovanni , Ruderfer, Douglas , Smith, Jennifer A. , Zhao, Wei , Liu, Chunyu , Group,, CHARGE Glycemic-T2D Working, Group,, CHARGE Blood Pressure Working, Campbell, Archie I , Coresh, Josef , Curhan, Gary C. , Cusi, Daniele , Denny, Joshua C. , Esko, Tõnu , Fülöp, Tibor , Gerhard, Glenn S. , Hansen, Torben , Hayward, Caroline , Hocking, Lynne J. , Hu, Frank B. , Jørgensen, Torben , Kooperberg, Charles , Launer, Lenore J. , Linneberg, Allan , Liu, Ching‐Ti , Meisinger, Christine, Metspalu, Andres , Nürnberg, Peter , Porteous, David John , Probst-Hensch, Nicole M , Psaty, Bruce M. , Raitakari, Olli Tuomas , Siscovick, David S. , Weiss, Stefan , Völker, Uwe , Teumer, Alexander , van Duijn, Cornelia M , Vasan, Ramachandran S , Smith, Albert V , Loos, Ruth J F , Li-Gao, Ruifang , Brody, Jennifer A , Padmanabhan, Sandosh , Levy, Daniel , de Vries, Aiko P J , Devuyst, Olivier; https://orcid.org/0000-0003-3744-4767

Journal of the American Society of Nephrology | December 5, 2016 | Volume: 28 | Issue: 3 | Pages: 981-994

10.1681/asn.2016020131 Get It

Genome-wide association studies have identified >50 common variants associated with kidney function, but these variants do not fully explain the variation in eGFR. We performed a two-stage meta-analysis of associations between genotypes from the Illumina exome array and eGFR on the basis of serum creatinine (eGFRcrea) among participants of European ancestry from the CKDGen Consortium ( n Stage1 : 111,666; n Stage2 : 48,343). In single-variant analyses, we identified single nucleotide polymorphisms at seven new loci associated with eGFRcrea ( PPM1J , EDEM3, ACP1, SPEG, EYA4, CYP1A1 , and ATXN2L ; P Stage1 <3.7×10 −7 ), of which most were common and annotated as nonsynonymous variants. Gene-based analysis identified associations of functional rare variants in three genes with eGFRcrea, including a novel association with the SOS Ras/Rho guanine nucleotide exchange factor 2 gene, SOS2 ( P =5.4×10 −8 by sequence kernel association test). Experimental follow-up in zebrafish embryos revealed changes in glomerular gene expression and renal tubule morphology in the embryonic kidney of acp1- and sos2 -knockdowns. These developmental abnormalities associated with altered blood clearance rate and heightened prevalence of edema. This study expands the number of loci associated with kidney function and identifies novel genes with potential roles in kidney formation.
PheKB: a catalog and workflow for creating electronic phenotype algorithms for transportability
Kirby, Jacqueline, Speltz, Peter, Rasmussen, Luke V. , Gottesman, Omri, Peissig, Peggy , Pacheco, Jennifer A. , Tromp, Gerard , Pathak, Jyotishman , Ellis, Stephen B. , Thompson, Will K, Savova, Guergana , Haines, Jonathan L. , Roden, Dan M. , Denny, Joshua C. , Basford, Melissa , Carrell, David , Lingren, Todd , Roden, Dan M. , Harris, Paul A. , Denny, Joshua C , Rasmussen, Luke V , Pacheco, Jennifer A

Journal of the American Medical Informatics Association | March 30, 2016 | Volume: 23 | Issue: 6 | Pages: 1046-1052

10.1093/jamia/ocv202 Get It

Abstract Objective Health care generated data have become an important source for clinical and genomic research. Often, investigators create and iteratively refine phenotype algorithms to achieve high positive predictive values (PPVs) or sensitivity, thereby identifying valid cases and controls. These algorithms achieve the greatest utility when validated and shared by multiple health care systems. Materials and Methods We report the current status and impact of the Phenotype KnowledgeBase (PheKB, http://phekb.org ), an online environment supporting the workflow of building, sharing, and validating electronic phenotype algorithms. We analyze the most frequent components used in algorithms and their performance at authoring institutions and secondary implementation sites. Results As of June 2015, PheKB contained 30 finalized phenotype algorithms and 62 algorithms in development spanning a range of traits and diseases. Phenotypes have had over 3500 unique views in a 6-month period and have been reused by other institutions. International Classification of Disease codes were the most frequently used component, followed by medications and natural language processing. Among algorithms with published performance data, the median PPV was nearly identical when evaluated at the authoring institutions (n = 44; case 96.0%, control 100%) compared to implementation sites (n = 40; case 97.5%, control 100%). Discussion These results demonstrate that a broad range of algorithms to mine electronic health record data from different health systems can be developed with high PPV, and algorithms developed at one site are generally transportable to others. Conclusion By providing a central repository, PheKB enables improved development, transportability, and validity of algorithms for research-grade phenotypes using health care generated data.
The phenotypic legacy of admixture between modern humans and Neandertals
Simonti, Corinne , Vernot, Benjamin , Bastarache, Lisa , Böttinger, Erwin P. , Chisholm, Rex L. , Crosslin, David R. , Hebbring, Scott J. , Jarvik, Gail P. , Li, Rongling, Pathak, Jyotishman , Ritchie, Marylyn D. , Roden, Dan M. , Tromp, Gerard , Prato, Jeffrey D., Bush, William S. , Akey, Joshua M. , Denny, Joshua C. , Capra, John A. , Carrell, David , Kullo, Iftikhar J. , Roden, Dan M. , Verma, Shefali S. , Denny, Joshua C , Jarvik, Gail P , Bush, William S

Science | February 12, 2016 | Volume: 351 | Issue: 6274 | Pages: 737-741

10.1126/science.aad2149 Get It

The legacy of human-Neandertal interbreeding Non-African humans are estimated to have inherited on average 1.5 to 4% of their genomes from Neandertals. However, how this genetic legacy affects human traits is unknown. Simonti et al. combined genotyping data with electronic health records. Individual Neandertal alleles were correlated with clinically relevant phenotypes in individuals of European descent. These archaic genetic variants were associated with medical conditions affecting the skin, the blood, and the risk of depression. Science , this issue p. 737
Genetic variation among 82 pharmacogenes: The PGRNseq data from the eMERGE network
Crosslin, DR, Owusu‐Obeng, Aniwaa, Wallace, John R. , Almoguera, Berta , Basford, MA, Bielinski, Suzette J. , Carrell, DS, Connolly, John J. , Doheny, KF, Gallego, CJ, Gordon, Allan , Kirby, Jacqueline, Kitchner, Terrie, Manzi, Shannon , Mejia, A R, Pan, Vivian , Perry, Cassandra, Peterson, JF, Prows, CA, Ralston, James D. , Scott, Stuart A. , Scrol, Aaron, Smith, Maureen E. , Stallings, SC, Veldhuizen, Tamra L., Wolf, W.A., Volpi, Simona , Wiley, Kenneth L , Manolio, Teri A. , Böttinger, Erwin P. , Brilliant, MH, Carey, David J. , Chisholm, Rex L. , Chute, CG, Jl, Haines, Håkonarson, Håkon , Harley, JB, Holm, Ingrid A. , Kullo, IJ, Jarvik, GP, Larson, EB, McCarty, Catherine A. , Williams, MS, Denny, Joshua C. , Rasmussen‐Torvik, LJ, Roden, DM, Ritchie, MD, Rasmussen‐Torvik, Laura J. , Jarvik, Gail P. , Peterson, Josh F. , Bush, William S. , Wallace, J, Crawford, Dana C. , Keating, Brendan J. , Perry, CL, Peterson, JF, Stallings, SC, Li, R, Roden, DM, Ritchie, M.D., Holm, Ingrid A , Hakonarson, Hakon , Denny, Joshua C , Jarvik, Gail P , Bielinski, Suzette , Gordon, Adam S , Connolly, John J , Peterson, Josh F , Scott, Stuart A , Rasmussen-Torvik, Laura J

Clinical Pharmacology & Therapeutics | February 9, 2016 | Volume: 100 | Issue: 2 | Pages: 160-169

10.1002/cpt.350 Get It

Genetic variation can affect drug response in multiple ways, although it remains unclear how rare genetic variants affect drug response. The electronic Medical Records and Genomics (eMERGE) Network, collaborating with the Pharmacogenomics Research Network, began eMERGE‐PGx, a targeted sequencing study to assess genetic variation in 82 pharmacogenes critical for implementation of “precision medicine.” The February 2015 eMERGE‐PGx data release includes sequence‐derived data from ∼5,000 clinical subjects. We present the variant frequency spectrum categorized by variant type, ancestry, and predicted function. We found 95.12% of genes have variants with a scaled Combined Annotation‐Dependent Depletion score above 20, and 96.19% of all samples had one or more Clinical Pharmacogenetics Implementation Consortium Level A actionable variants. These data highlight the distribution and scope of genetic variation in relevant pharmacogenes, identifying challenges associated with implementing clinical sequencing for drug treatment at a broader level, underscoring the importance for multifaceted research in the execution of precision medicine.
Harnessing next-generation informatics for personalizing medicine: a report from AMIA’s 2014 Health Policy Invitational Meeting
Wiley, Laura K. , Tarczy‐Hornoch, Peter , Denny, Joshua C. , Freimuth, Robert R. , Overby, Casey Lynnette, Martin, Ross D., Taylor, Casey Overby , Shah, Nigam H. , Sarkar, Indra Neil , Denny, Joshua C , Freimuth, Robert R , Wiley, Laura K

Journal of the American Medical Informatics Association | February 6, 2016 | Volume: 23 | Issue: 2 | Pages: 413-419

10.1093/jamia/ocv111 Get It

Abstract The American Medical Informatics Association convened the 2014 Health Policy Invitational Meeting to develop recommendations for updates to current policies and to establish an informatics research agenda for personalizing medicine. In particular, the meeting focused on discussing informatics challenges related to personalizing care through the integration of genomic or other high-volume biomolecular data with data from clinical systems to make health care more efficient and effective. This report summarizes the findings ( n = 6) and recommendations ( n = 15) from the policy meeting, which were clustered into 3 broad areas: (1) policies governing data access for research and personalization of care; (2) policy and research needs for evolving data interpretation and knowledge representation; and (3) policy and research needs to ensure data integrity and preservation. The meeting outcome underscored the need to address a number of important policy and technical considerations in order to realize the potential of personalized or precision medicine in actual clinical contexts.