Alexander G. Bick

This study links clonal hematopoiesis to accelerated frailty and functional decline across multiple organ systems in humans.

This paper shows that rhodopsin's light protection mechanism evolved to sequester toxic retinal and protect retinal cells, with implications for human disease.

The paper identifies mutation-specific impairments in TET2 and DNMT3A enzymatic activity as predictors of clonal hematopoiesis disease risk using methylation-based activity scores.

This study examines associations between leukocyte telomere length and genomic, phenomic, and geographic factors in diverse U.S. populations, identifying novel loci and genes.

This study investigates the association between mosaic loss of Y chromosome (mLOY) and lung function, emphysema, and epigenetic aging in men across multiple cohorts.

The paper shows genome or exome sequencing underestimates CHIP-disease associations due to low sensitivity and positive predictive value, requiring deep sequencing for accurate results.

The paper identifies a genetic variant that protects against clonal hematopoiesis by regulating RNA-binding protein MSI2 in hematopoietic stem cells.

The paper identifies plasma proteins associated with clonal hematopoiesis and links them to cardiovascular disease through proteomic and genetic analyses.

This study sequenced 35,024 individuals with predominantly African ancestry to address gaps in genomics and healthcare, finding under-documented disease variants and novel associations with drug adverse events and glycemic control.

This study finds that clonal hematopoiesis (CHIP) increases stroke risk across multiple cohorts, with specific gene mutations and inflammatory markers like IL-1RAP modifying this risk.

The paper introduces a closed-loop framework for single-cell foundation models that incorporates perturbation data to improve prediction accuracy, identifying therapeutic targets and pathways in RUNX1-familial platelet disorder.

The paper optimizes a reduced representation DNA methylation sequencing protocol for cost-effective, population-scale studies across species.

The paper identifies genetic drivers and clinical consequences of mosaic chromosomal alterations in 1 million individuals, linking specific aut-mCAs to disease risk and therapeutic targets.

The paper investigates how mutation timing, fitness, and clonal structure influence the clinical progression of clonal hematopoiesis using longitudinal cohort data.

The paper identifies genetic and phenotypic correlates of mosaic loss of chromosome Y in blood using whole genome sequencing data from the TOPMed program.

The paper develops a clinical algorithm to identify individuals with G6PD p.Val68Met variant at risk for diabetes undertreatment using routine lab measurements.

The paper analyzes sequencing data from three cohorts to quantify cytopenia incidence and identify risk factors in clonal hematopoiesis, finding higher cytopenia rates and progression to myeloid neoplasms.

The paper identifies gene-gene interactions affecting blood traits and disease risk using variance QTL approaches in large human cohorts.

The paper develops a method to quantify somatic mutation burden in whole-genome sequencing data without paired-tissue samples and identifies genetic and phenotypic correlates of clonal hematopoiesis without known driver mutations.

Population-stratified GWAS of 2,068 traits in 635,969 Million Veteran Program participants, 29% genetically non-European, yields 98,485 associations and 57,601 fine-mapped signals with largely shared cross-population architecture.

The paper estimates mCA fitness in the NHLBI TOPMed cohort and identifies genetic variants associated with clonal expansion rates.

This study identifies 240 novel genetic loci associated with mosaic loss of chromosome Y through a multi-ancestry GWAS of the Million Veteran Program and UK Biobank.

The paper introduces a cost-effective CHIP assay, identifies 101 CHIP cases in a cohort, and finds heterogeneity in clonal expansion rates by driver gene and individual.

This study profiles single-cell multiomic data from clonal hematopoiesis patients and controls, revealing pro-inflammatory profiles in monocytes and T cell dysfunction.

The paper identifies monocyte-endothelial interaction alterations in TET2 CHIP and shows that targeting CXCR2 and ICAM1 can restore normal interactions.

This study finds that clonal hematopoiesis of indeterminate potential (CHIP) doubles non-small cell lung cancer (NSCLC) risk in non-smokers, and this risk is further increased by exposure to high levels of PM2.5 air pollution.

This study analyzes 4,187 participants over 21 years to identify factors influencing the development of clonal hematopoiesis, finding age, sex, and dyslipidemia as significant predictors.

The paper identifies IL1RAP and AIM2 as key modifiers of CHIP-associated cardiovascular risk using UK Biobank data and CRISPR experiments in mice.

The paper finds that somatic mutations in diseased lung tissue correlate with reduced lung function and cell type proportions in COPD and IPF.

This study identifies genetic drivers and cellular selection signatures of mosaic X chromosome loss in women using large-scale population data and polygenic scores.