Charles Swanton

The paper shows ecDNA localizes to the nuclear periphery in cancer, resisting silencing and enhancing transcriptional output through interactions with the nuclear lamina.

The paper identifies genomically unstable secretory cells in fallopian tubes of BRCA1/2 carriers using single-cell transcriptomics, linking them to replication stress and early cancer transformation.

This study uses single-cell and spatial multi-omics to analyze a malignant peripheral nerve sheath tumor, revealing chromosomal instability drives phenotypic diversity and spatial-temporal evolution.

This study links oncogenic RAS activity to immune priming and adenosine-driven immune evasion in lung adenocarcinoma, showing both pro-immunogenic and immunosuppressive effects.

This study shows that cell migration and stromal fibroblasts influence subclone competition in lung cancer, promoting therapy resistance through increased cell mixing.

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.

This study identifies RAS-PI3K signaling as a key regulator of myofibroblastic CAF identity and matrix competence in lung cancer, showing its role in restraining immunomodulatory stromal programs.

The paper identifies regulatory T cells as mediators of resistance to KRAS-G12C inhibitors and anti-PD-1 therapy through spatial proteomic analysis of lung cancer models.

This paper introduces GRITIC, a method to time genomic gains in tumors, finding that copy number gains often accumulate after genome duplication.

Genesis is a modular protein language model that improves immunogenicity prediction for CD8+ epitopes by integrating pMHC and TCR context, outperforming existing models in precision.

The paper uses single-cell imaging to show that drug-tolerant cells in EGFR-mutant lung cancer rewired ERK signaling through endocytic pathways and adhesion complexes, driven by YAP and PTPRS.

The paper evaluates neutralising antibody titres against SARS-CoV-2 variant JN.1 using live-virus microneutralisation assays in vaccinated individuals, finding higher titres in monovalent vaccine recipients.

Refphase uses multi-sample reference phasing to infer haplotype-specific copy numbers and reveal intra-tumour heterogeneity in cancer samples.

MEDICC2 infers cancer phylogenies from copy-number data, accounting for whole-genome doubling and parallel evolution, and performs well on simulated and real datasets.

cloneMap visualizes clonal heterogeneity in genomic data by representing clone size and phylogenetic relationships, applied to cancer datasets.

This paper introduces CAMDAC, a method to deconvolve tumor-normal DNA methylation profiles while accounting for copy number changes, revealing epigenetic instability and distinct patterns in lung cancer.

This study compares the mutagenicity of cisplatin, carboplatin, and oxaliplatin at equitoxic concentrations using whole genome sequencing and phenotypic assays, finding cisplatin induces more mutations and DNA damage.

The paper investigates how whole genome doubling (WGD) in cancer may mitigate Muller’s Ratchet by reducing negative selection on mutations in essential genes after duplication.

The paper investigates genetic epistasis in EGFR-mutant lung cancers using over 2,000 cases, showing that genetic combinations, not single drivers, dominate tumor progression and clinical outcomes.