James Yarmolinsky

This paper identifies shared genetic loci between inflammation and cancer risk using non-causal associations, revealing potential therapeutic targets.

This study identifies 40 circulating proteins associated with cancer risk using MR and colocalization, highlighting potential therapeutic targets and adverse effects of protein-altering interventions.

This paper uses Mendelian randomization and electronic health records to show SGLT2 inhibitors reduce prostate cancer risk, with additional evidence from differential expression analysis.

This paper reviews statistical methods to detect and adjust for collider bias in genetic and Mendelian randomization studies of disease progression using individual and summary-level data.

The paper uses a genetic variant to assess cancer risk associated with TYK2 inhibition, finding increased risks for lung cancer and non-Hodgkin lymphoma.

This paper uses Mendelian randomization and colocalization to identify causal relationships between plasma proteins and disease phenotypes, finding 111 putatively causal effects.

This study uses Mendelian randomization to assess the causal effects of adipokines and CRP on breast cancer risk, finding a significant link for hepatocyte growth factor but not others.

This study uses bidirectional Mendelian randomization to investigate causal relationships between inflammatory markers and depression, finding a causal effect of IL-6 on major depressive disorder.