Owen J. Sansom

Medicine · Health Sciences

113h-index50.9kcitations1.2kworks2.22yr avg
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Research Topics

Pancreatic and Hepatic Oncology Research(194), Cancer Cells and Metastasis(130), Cancer Immunotherapy and Biomarkers(118), Cancer Genomics and Diagnostics(110), Cancer-related Molecular Pathways(100)

Publications1.2k total

SOX2 confers tumour permissiveness in a specific skin progenitor population
Nature Communications·2026Open Access
Nucleophosmin supports WNT-driven hyperproliferation and tumor initiation
Nature Genetics·2025Open Access
Inhibiting translation elongation by reducing eIF5A activity induces feedback inhibition of initiation, limiting tumour cell proliferation
Nature Communications·2025· 1 citedOpen Access
Corrigendum to Mutant p53–associated myosin-X upregulation promotes breast cancer invasion and metastasis
Journal of Clinical Investigation·2025Open Access
Figure S7 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S2 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S1 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S5 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S6 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Supplementary Figure Legends from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S3 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Table S1 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure S4 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer
2025Open Access
Figure 6 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Figure 4 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Figure 1 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Figure 2 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Figure 3 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Figure 5 from Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data
2025Open Access
Supplementry Table 3: REACTOME Gene Set Enrichment Analysis results from Spatially Resolved Transcriptomics Deconvolutes Prognostic Histological Subgroups in Patients with Colorectal Cancer and Synchronous Liver Metastases
2025Open Access
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Frequent Co-authors

Jennifer P. Morton(16), Rachel A. Ridgway(16), Hans Clevers(10), Colin Nixon(10), Saadia A. Karim(9), Alan R. Clarke(8), Simon T. Barry(8), Andrew D. Campbell(7), Nigel B. Jamieson(6), Dimitris Athineos(6), Kurt I. Anderson(6), Paul Timpson(6), Thomas Jamieson(6), William Clark(6), Peter J. Bailey(5), Karin A. Oien(5), Nick Barker(5), T.R. Jeffry Evans(5), Andrew V. Biankin(5), Ewan J. McGhee(5)