A multi-trait approach identified 7 novel genes for back pain.

Introduction: Back pain (BP) is a complex heritable trait with an estimated heritability of 40% to 60%. Less than half of this can be explained by known genetic variants identified in genome-wide association studies.

Objectives: We applied a powerful multi-trait and gene-based approach to association analysis of BP to identify novel genes associated with BP.

Open Targets Platform: facilitating therapeutic hypotheses building in drug discovery.

The Open Targets Platform (https://platform.opentargets.org) is a unique, open-source, publicly-available knowledge base providing data and tooling for systematic drug target identification, annotation, and prioritisation.

A Mendelian randomization study finds no evidence for causal effects of C-reactive protein (CRP) on chronic pain conditions.

This two-sample Mendelian randomization study examined causal associations of C-reactive protein (CRP) with spinal pain, the extent of multisite chronic pain, and chronic widespread musculoskeletal pain. No causal associations were found between CRP and these pain conditions.

Genotype imputation in human genomic studies.

Imputation is a method that supplies missing information about genetic variants that could not be directly genotyped with DNA microarrays or low-coverage sequencing. Imputation plays a critical role in genome-wide association studies (GWAS). It leads to a significant increase in the number of studied variants, which improves the resolution of the method and enhances the comparability of data obtained in different cohorts and/or by using different technologies, which is important for conducting meta-analyses.

A New Method for Conditional Gene-Based Analysis Effectively Accounts for the Regional Polygenic Background.

Gene-based association analysis is a powerful tool for identifying genes that explain trait variability. An essential step of this analysis is a conditional analysis. It aims to eliminate the influence of SNPs outside the gene, which are in linkage disequilibrium with intragenic SNPs.