Alex Cagan

The paper investigates how mutation timing, accumulation, and selection in the male germline influence the risk of developmental disorders through de novo mutations.

This study shows that HSC dormancy, not apoptosis, limits mutagenesis in aging, with dormancy disruption accelerating mutation rates.

This study uses sperm sequencing to show that positive selection in the male germline leads to a higher risk of disease-causing mutations in offspring.

This study examines the long-term effects of chemotherapy on normal blood cells by analyzing mutation burdens and cell population structure in treated individuals.

This study examines clonal dynamics and somatic evolution in mouse haematopoiesis, finding that stem cells accrue mutations at a rate similar to human progenitors and exhibit distinct age-related patterns.

This study compares mutational landscapes in somatic and germline cells across 29 anatomical structures, identifying key mutational signatures and their contributions to different cell types.

This study tracks clonal dynamics in human haematopoiesis across age, finding that clonal diversity sharply declines after 70, driven by positive selection on many genes and loss of Y chromosome in males.

This study finds that somatic mutation rates per year decrease with species lifespan across mammals, suggesting evolutionary constraints on mutagenesis and its role in ageing.

The paper analyzes the mutational landscape of normal lymphocytes, revealing off-target effects of programmed genome engineering and the impact of differentiation and microenvironment exposure.

The paper reconstructs phylogenies of human development using whole-genome sequencing to show variable embryonic patterns and lineage asymmetries across individuals and tissues.