bioRxiv Science⌕ Search

Biology subjects

Krebs, K.

Publications and source records attributed to Krebs, K..

4 recordsLinked to original sources

Detecting CYP2C19 deletions from genotyping array signals using neural networks

Since copy number variations (CNVs) in pharmacogenes can cause significant alterations in drug metabolism, their reliable detection is of high importance both for large-scale studies and personalized medicine. Whole-genome sequencing, and specifically long-read sequencing, is the gold standard for CNV detection. Despite increasing availability of these technologies, genotyping arrays are still widely used as cost-effective alternatives in biobank and clinical settings, yet calling CNVs based on array intensity signals is challenging due to low base pair resolution. In this work, we developed a neural network model, nnCNV, to predict deletions in the CYP2C19 pharmacogene region from array intensity signals. We compared our method to the most widely used algorithm, PennCNV, and demonstrated better performance reaching 100% accuracy in the test dataset. Furthermore, we predicted probe-by-probe CYP2C19 deletion coordinates for all Estonian Biobank samples using nnCNV and PennCNV, and validated these predictions using an identity-by-descent (IBD) sharing method, which also demonstrated superior nnCNV performance. For the deletion samples with conflicting PennCNV and nnCNV predictions, we performed PCR analysis for validation, which showed 97% precision for nnCNV compared to 23% for PennCNV. Finally, we assessed the gradient-based feature importance maps and showed that nnCNV utilizes signal intensity information not only from deletion probes, but also from probes in flanking regions. Our results demonstrate that long-range information, which cannot be utilized by hidden Markov models, can improve CNV calling.

bioinformatics↗

Genome-wide study identifies association between HLA-B*55:01 and penicillin allergy

BackgroundHypersensitivity reactions to drugs are often unpredictable and can be life-threatening, underscoring a need for understanding their underlying mechanisms and risk factors. The extent to which germline genetic variation influences the risk of commonly reported drug allergies such as penicillin allergy remains largely unknown. MethodsWe extracted data from the electronic health records of 52,000 Estonian and 500,000 UK biobank participants to study the role of genetic variation in the occurrence of penicillin hypersensitivity reactions. We used imputed SNP to HLA typing data from up to 22,554 and 488,377 individuals from the Estonian and UK cohorts, respectively, to further fine-map the human leukocyte antigen (HLA) association and replicated our results in two additional cohorts involving a total of 1.14 million individuals. ResultsGenome-wide meta-analysis of penicillin allergy revealed a significant association located in the HLA region on chromosome 6. The signal was further fine-mapped to the HLA-B*55:01 allele (OR 1.47 95% CI 1.37-1.58, P-value 4.63x10-26) and confirmed by independent replication in two cohorts. The meta-analysis of all four cohorts in the study revealed a strong association of HLA-B*55:01 allele with penicillin allergy (OR 1.33 95% CI 1.29-1.37, P-value 2.23x10-72). In silico follow-up suggests a potential effect on T lymphocytes at HLA-B*55:01. ConclusionWe present the first robust evidence for the role of an allele of the major histocompatibility complex (MHC) I gene HLA-B in the occurrence of penicillin allergy.

genetics↗

Lifelong genetically lowered sclerostin and risk of cardiovascular disease.

BackgroundInhibition of sclerostin is a novel therapeutic approach to lowering fracture risk. However, phase III randomised controlled trials (RCTs) of romosozumab, a monoclonal antibody that inhibits sclerostin, suggest an imbalance of serious cardiovascular events. MethodsWe used two independent genetic variants (rs7209826 and rs188810925) in SOST (encoding sclerostin) associated with bone mineral density (BMD) as proxies for therapeutic inhibition of sclerostin. We estimated the effects on risk of osteoporosis, fracture, coronary heart disease (CHD) and a further 22 cardiometabolic risk factors and diseases, by combining data from up to 478,967 participants of European ancestry from three prospective cohorts and up to 1,030,836 participants from nine GWAS consortia. In addition, we performed meta-analyses of cardiovascular outcome data from phase III RCTs of romosozumab. ResultsMeta-analysis of RCTs identified a higher risk of cardiac ischemic events in patients randomised to romosozumab (25 events among 4,298 individuals; odds ratio [OR] 2{middle dot}98; 95% confidence interval [CI], 1{middle dot}18 to 7{middle dot}55; P=0{middle dot}017). Scaled to the equivalent dose of romosozumab (210mg/month; 0{middle dot}09 g/cm2 higher BMD), the SOST variants associated with lower risk of fracture (OR, 0{middle dot}59; 95% CI, 0{middle dot}54-0{middle dot}66; P= 1{middle dot}4x10-24), and osteoporosis (OR, 0{middle dot}43; 95% CI, 0{middle dot}36-0{middle dot}52; P=2{middle dot}4x10-18). The SOST variants associated with higher risk of myocardial infarction and/or coronary revascularisation (69,649 cases; OR, 1{middle dot}18; 95% CI, 1{middle dot}06-1{middle dot}32; P=0{middle dot}003) and type 2 diabetes (OR 1{middle dot}15; 95% CI, 1{middle dot}05-1{middle dot}27; P=0{middle dot}003), higher systolic blood pressure (1{middle dot}3mmHg; 95% CI 0{middle dot}8-1{middle dot}9; P=5{middle dot}9x10-6) and waist-to-hip-ratio adjusted for BMI (0{middle dot}05 SDs; 95% CI, 0{middle dot}02 to 0{middle dot}08; P=8{middle dot}5x10-4). ConclusionsGenetically and therapeutically lowered sclerostin leads to higher risk of cardiovascular events. Rigorous evaluation of the cardiovascular safety of romosozumab and other sclerostin inhibitors is warranted.

genetics↗

Translating genotype data of 44,000 biobank participants into clinical pharmacogenetic recommendations: challenges and solutions

PurposeBiomedical databases combining electronic medical records, phenotypic and genomic data constitute a powerful resource for the personalization of treatment. To leverage the wealth of information provided, algorithms are required that systematically translate the contained information into treatment recommendations based on existing genotype-phenotype associations.\n\nMethodsWe developed and tested algorithms for translation of pre-existing genotype data of over 44,000 participants of the Estonian biobank into pharmacogenetic recommendations. We compared the results obtained by whole genome sequencing, whole exome sequencing and genotyping using microarrays, and evaluated the impact of pharmacogenetic reporting based on drug prescription statistics in the Nordic countries and Estonia.\n\nResultsOur most striking result was that the performance of genotyping arrays is similar to that of whole genome sequencing, whereas exome sequencing is not suitable for pharmacogenetic predictions. Interestingly, 99.8% of all assessed individuals had a genotype associated with increased risks to at least one medication, and thereby the implementation of pharmacogenetic recommendations based on genotyping affects at least 50 daily drug doses per 1000 inhabitants.\n\nConclusionWe find that microarrays are a cost-effective solution for creating pre-emptive pharmacogenetic reports, and with slight modifications, existing databases can be applied for automated pharmacogenetic decision support for clinicians.

pharmacology and toxicology↗