Kerri L. Wiggins

This study identifies genetic loci associated with residual pulmonary vascular obstruction and links inflammation to its risk, while showing limited role of impaired fibrinolysis.

The paper identifies genetic loci and proteins associated with venous thromboembolism recurrence risk using GWAS and subgroup analyses across different thrombotic subtypes.

This paper conducts a multi-ancestry time-to-event GWAS to identify genetic variants associated with incident cardiovascular disease in people with type 2 diabetes, finding three novel loci and confirming known CAD variants.

The paper develops PACER to infer clonal expansion rates from single timepoint data and identifies TCL1A activation as a mediator of clonal hematopoiesis fitness.

This study identifies 135 genomic loci associated with venous thromboembolism risk through cross-ancestry GWAS and provides insights into biological pathways and potential therapeutic targets.

This paper constructs a multi-ethnic polygenic risk score for hypertension and shows it is associated with hypertension prevalence, progression, and related clinical outcomes.

The paper uses bidirectional Mendelian randomization to show LTL lengthening increases CHIP risk, while CHIP accelerates LTL shortening, with modest mediation between CHIP and CAD via LTL.

This study identifies DNA methylation sites associated with coffee and tea consumption using EWAS, finding potential links to fatty liver disease through PHGDH expression.

The paper describes a system for harmonizing phenotype data across multiple studies in the TOPMed program, enabling reproducible and shared phenotype data for over 80 studies.

This study identifies 59 sentinel variants and two novel genes associated with telomere length using whole genome sequences from 109,122 trans-ethnic individuals.

This study uses TOPMed whole genome sequences to improve imputation quality and detect rare variant associations in admixed African and Hispanic/Latino populations, identifying two novel associations with hematological traits.

This paper evaluates the causal effect of fibrinogen on coronary heart disease using Mendelian randomization, finding a small effect with multi-variant methods but not with single variant approaches.