Jamie R. Blundell

The paper distinguishes germline and somatic TP53 variants using whole-exome data from UK Biobank participants, showing somatic variants dominate cancer risk in middle-aged adults.

The paper uses methylation patterns in the protocadherin gene cluster to track clonal dynamics across human tissues over time, revealing subclonal architectures and cryptic expansions not detectable by standard mutation sequencing.

The paper tracks DNA methylation changes in blood samples up to 15 years before AML diagnosis, identifying DMRs linked to clonal expansions and epigenetic reprogramming.

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.

The paper introduces a high-accuracy sequencing method to detect somatic mutations in tissues, revealing extensive selection and driver mutations in oral epithelium and blood samples.

The paper investigates whether immunosurveillance affects clonal haematopoiesis by analyzing MHC binding to mutation hotspots in UK Biobank data, finding no evidence of such influence.

This study uses serial blood samples to analyze pre-cancerous evolutionary dynamics in acute myeloid leukaemia, showing how driver mutations accumulate and drive clonal expansion over decades.

The paper analyzes age-related changes in clonal haematopoiesis (CH) using whole exome data from 420,000 UK Biobank participants, finding a deceleration of clonal expansion with age.

The paper estimates mutation rates and fitness consequences of mosaic chromosomal alterations in blood using UK Biobank data, finding most mCAs have moderate to high fitness effects but occur less frequently than SNVs.

The paper quantifies fitness advantages of pathogenic variants in clonal haematopoiesis using blood sequencing data from ~50,000 individuals.