Charles Swanton
查尔斯·斯旺顿
PhD, FRCP, FMedSci, FRS
Chief Clinician, Cancer Research UK; Group Leader, Cancer Evolution and Genome Instability英国癌症研究首席临床医生;癌症进化与基因组不稳定性组长
👥Biography 个人简介
Charles Swanton FRS FMedSci FRCP PhD is Chief Clinician at Cancer Research UK, Group Leader of the Cancer Evolution and Genome Instability Laboratory at the Francis Crick Institute, and Professor at University College London. He is among the most celebrated cancer biologists of his generation, best known for leading the TRACERx (Tracking Non-Small-Cell Lung Cancer Evolution Through Therapy) study — a landmark multi-regional sequencing programme that has fundamentally reshaped understanding of intratumour heterogeneity, cancer evolution, and the determinants of metastasis and immune evasion. TRACERx demonstrated that most somatic mutations in lung cancer are subclonal and unique to individual tumour regions, explaining treatment failure and immune editing. Swanton's group characterised the role of APOBEC3A/B cytidine deaminases as major mutational processes driving subclonal diversification in multiple cancer types and showed that chromosomal instability (CIN) generates kataegis and complex rearrangements that fuel tumour evolution. He pioneered the use of multiregion WES and circulating tumour DNA (ctDNA) to track cancer evolution non-invasively, enabling early detection and monitoring of treatment resistance. Swanton was elected Fellow of the Royal Society in 2018 and has received numerous major honours including the Brupbacher Prize, the Helmholtz International Fellow Award, and a knighthood (Sir Charles Swanton as of 2023).
🧪Research Fields 研究领域
🎓Key Contributions 主要贡献
TRACERx: Intratumour Heterogeneity in Lung Cancer
Designed and led TRACERx, the most comprehensive prospective multiregion sequencing study of lung cancer evolution, establishing that branched evolution and subclonal heterogeneity drive immune evasion, metastasis, and treatment failure, and redefining how cancer staging and treatment are conceptualised.
APOBEC Mutagenesis and Subclonal Evolution
Demonstrated that APOBEC3A/B-mediated cytosine deamination is a major driver of subclonal diversification across multiple cancer types, linking replication stress and cytidine deaminase activity to the generation of mutational heterogeneity that fuels Darwinian selection.
Chromosomal Instability and Cancer Evolution
Showed that chromosomal instability (CIN) generates structural rearrangements, kataegis, and immune-stimulatory cGAS-STING signalling, establishing CIN as a dual driver of cancer evolution and an inflammatory cancer phenotype, with implications for immunotherapy response.
ctDNA-Based Early Detection and Monitoring
Developed and validated ctDNA sequencing approaches within TRACERx to non-invasively track clonal evolution, detect minimal residual disease, and predict relapse, advancing ctDNA toward clinical implementation for lung and other cancers.
Representative Works 代表性著作
Intratumor heterogeneity and branched evolution revealed by multiregion sequencing
New England Journal of Medicine (2012)
First major multiregion sequencing study demonstrating pervasive branched evolution and intratumour heterogeneity in renal cell carcinoma, with direct implications for cancer staging, biopsy strategies, and targeted therapy.
TRACERx: Tracking non-small-cell lung cancer evolution through therapy
New England Journal of Medicine (2017)
Landmark TRACERx inaugural publication presenting multiregional sequencing of 100 NSCLC patients, revealing the evolutionary trajectories that drive relapse and linking clonal neoantigen burden to immune surveillance.
Chromosomal instability drives metastasis through a cytosolic DNA response
Nature (2018)
Mechanistic study showing that chromosomal instability activates cGAS-STING innate immune signalling, driving a metastatic programme that paradoxically depends on inflammatory signalling, with implications for CIN targeting in cancer therapy.
🏆Awards & Recognition 奖项与荣誉
📄Data Sources 数据来源
Last updated: 2026-01-15 | All information from publicly available academic sources
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