Benjamin Werner

Inferring ecDNA Evolution from Allele Frequency Spectra

This paper introduces ecEvol, a method to infer ecDNA emergence time and other parameters from bulk whole-genome sequencing data, finding that ecDNA typically emerges early and is associated with poorer survival.

Comparative somatic genomics reveals divergent development of cell lineages across scleractinian corals

The paper compares somatic mutation accumulation in two coral species, finding distinct patterns suggesting different cell lineage development mechanisms.

The dynamic fitness landscape of ageing haematopoiesis through clonal competition

This study models clonal competition in ageing haematopoiesis, showing that fitness landscapes evolve with age and predict high-risk clones for patient stratification.

Dynamic optimization of extrachromosomal DNA copy number drives tumour evolution

This study shows ecDNA copy number plasticity drives tumour evolution by generating functional heterogeneity and promoting drug resistance.

Extrachromosomal DNA driven oncogene spatial heterogeneity and evolution in glioblastoma

This study investigates the spatial-temporal evolution of extrachromosomal DNA (ecDNA) in glioblastoma, showing that EGFR ecDNA drives tumor evolution and identifies a potential therapeutic window for early intervention.

On the patterns of genetic intra-tumour heterogeneity before and after treatment

This study uses stochastic models to analyze how genetic intra-tumour heterogeneity changes during and after treatment, finding distinct patterns in mutation frequencies and resistant clone sizes.

Extrachromosomal DNA micronucleation constrains tumour fitness andimproves patient survival

This study shows that ecDNA mis-segregation leads to micronuclei formation, reduced oncogene transcription, and improved patient survival in neuroblastoma.

Mosaic accumulation of somatic genetic variation and estimates of age in the long-lived reef-building coral Acropora palmata

The paper quantifies somatic genetic variation in corals and estimates their age using mutation rates, finding no positive selection and a neutral framework for studying genetic diversity.

The maintenance and de-mixing of extrachromosomal DNA variants in single cells

This study develops computational models to show that mixed ecDNA subpopulations in tumour cells require variant switching and a positive fitness of ecDNA+ cells, not direct co-selection.

Accumulating waves of random mutations before fixation

The paper quantifies joint fixation events of neutral mutations in constant populations, introducing the concept of mutation waves and deriving the Wave Frequency Distribution.

Mutational landscapes of normal breast during age and pregnancy determine cancer risk

This study analyzes mutational landscapes in normal breast tissue across age and pregnancy to understand cancer risk differences.

Model-based tumor subclonal reconstruction

This paper introduces a model-based subclonal reconstruction method that integrates evolutionary theory with machine learning to improve accuracy in tumor subclonal analysis.

dN/dS dynamics quantify tumour immunogenicity and predict response to immunotherapy

The paper quantifies tumor immunogenicity using dN/dS ratios in the immunopeptidome and shows it predicts immunotherapy response by distinguishing adaptation from escape mechanisms.

Measuring the distribution of fitness effects in somatic evolution by combining clonal dynamics with dN/dS ratios

This study links dN/dS ratios to selective coefficients in somatic evolution, revealing the distribution of fitness effects for mutations in human tissues.

Spatially constrained tumour growth affects the patterns of clonal selection and neutral drift in cancer genomic data

This paper shows that spatial tumour structure affects mutation patterns in sequencing data and introduces a framework to account for these effects in cancer genomic analysis.

Reply: Neutral tumor evolution?

The paper responds to criticism of a method used to infer neutral cancer evolution from variant allele frequency distributions, arguing that neutral evolution explains intra-tumour heterogeneity in some cancers.

Should tissue structure suppress or amplify selection to minimize cancer risk?

The paper examines whether tissue structure suppresses or amplifies selection to minimize cancer risk, finding that the distribution of mutant fitness effects determines the optimal tissue architecture.

Estimating stem cell fractions in hierarchically organized tumors

The paper develops a mathematical model to estimate cancer stem cell fractions in tumors using tumor size measurements and linear regression, without requiring detailed microscopic data.