Melinda C. Aldrich

The paper identifies lung cancer susceptibility copy number variants (CNVs) and shows their potential role in genomic instability through association analyses and functional validation.

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 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.

The paper introduces CoRE-BED, a framework that identifies novel regulatory elements and shows their association with SNP heritability in complex traits.

This study examines how sex influences the genetic risk of PCOS on metabolic traits using polygenic risk scores and EHR data.

The paper assesses how the performance of an African-ancestry-specific polygenic hazard score varies with local ancestry in 8q24 using genetic data from 6,253 men with African ancestry.

This study analyzes the genetic structure of Gullah African Americans, finding higher African ancestry and lower European admixture compared to non-Gullah African Americans.

The paper improves a polygenic hazard score for prostate cancer age at diagnosis by adding SNPs specific to African ancestry, enhancing performance in this population.

The paper identifies genetic links between impaired pulmonary function and increased lung cancer risk, showing causal relationships through Mendelian randomization and highlighting immune-related pathways.

This paper develops a clinical phenotyping algorithm to identify COPD cases in EHRs using ICD codes, achieving high sensitivity and negative predictive value.

This study identifies three novel genomic regions associated with lung cancer risk in African Americans, showing pleiotropic effects across multiple cancers.

This study quantifies genetic correlations between six solid cancers and other diseases using GWAS data, finding shared heritability and functional enrichment in regulatory regions.