Irreversible differentiation into somatic cells is evolutionarily optimal if changing cell phenotype is costly, a few somatic cells already improve the organism's performance, and the organism is large enough.

Measurement of the distribution of fitness effects of new mutations arising in human oesophagus and skin, via new mathematical theory linking dn/ds values and fitness coefficients.

The multi-stage model of carcinogenesis requires the incorporation of aging-dependent somatic selection and life history-dependent evolution of species-specific tumor suppressor mechanisms in order to generalize carcinogenesis across tissues and species.

Influenza vaccination in humans stimulates novel B cell evolution that is detectable in germinal centers, but not the peripheral blood.

Single-cell and bulk sequencing data are combined through theoretical modeling to reveal the number of tissue-specific stem cells, mutation, and proliferation rates under sampling.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

High mutational load tumors mitigate effects from protein-damaging mutations by up-regulating complexes that buffer against misfolding stress, revealing therapeutic vulnerabilities and suggesting disrupted proteostasis is a hallmark of somatic evolution.

Extended somatic hypermutation and clonal evolution associated with antibody neutralization breath in HIV controllers with low plasma viral loads provide promise for HIV vaccine development.

HILARy is a new algorithm for grouping B-cell receptor sequences into distinct lineages, a crucial task to analyze immune response and memory through repertoire sequencing.

Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.