Publications

Mixed-model and transcriptome-wide association analyses identify transcription factors and genes associated with colorectal cancer susceptibility.

Chen Z. et al, (2026), Nat Commun

Promises under pressure: the modest predictive power of polygenic risk scores.

Horton R. et al, (2026), Eur J Hum Genet

Comparison between germline and somatic loss-of-function RNF43 mutations reveals different genotype-phenotype associations and provides insights into the genetic mechanisms of colorectal tumourigenesis.

Palles C. et al, (2025), Gut

Mathematical Modeling Quantifies "Just-Right" APC Inactivation for Colorectal Cancer Initiation.

Brunet Guasch M. et al, (2025), Cancer Res, 85, 5113 - 5127

Loss of IDH1 and IDH2 mutations during the evolution of metastatic chondrosarcoma.

Cross W. et al, (2025), Genome Biol, 26

Large-scale meta-analysis and precision functional assays identify FANCM regions in which PTVs confer different risks for ER-negative and triple-negative breast cancer.

Billaud A. et al, (2025), Breast, 85

Analysis of IDH1 and IDH2 mutations as causes of the hypermethylator phenotype in colorectal cancer.

Ward JC. et al, (2025), J Pathol, 267, 40 - 55

Replication-associated mechanisms contribute to an increased CpG > TpG mutation burden in mismatch repair-deficient cancers.

Ward JC. et al, (2025), Genome Med, 17

GWAS meta-analysis identifies five susceptibility loci for endometrial cancer.

Ramachandran D. et al, (2025), EBioMedicine, 118

Epithelial GREMLIN1 disrupts intestinal epithelial-mesenchymal crosstalk to induce a wnt-dependent ectopic stem cell niche through stromal remodelling.

Mulholland EJ. et al, (2025), Nat Commun, 16

The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda.

Wismayer R. et al, (2025), BMC Cancer, 25

Genetic variation at 11q23.1 confers colorectal cancer risk by dysregulation of colonic tuft cell transcriptional activator POU2AF2.

Rajasekaran V. et al, (2025), Gut, 74, 787 - 803

Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis.

Woolley CE. et al, (2025), Mol Cancer Res, 23, 300 - 312

Data from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Figure 3 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Figure 4 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Figure 5 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Supplementary Data 1 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Supplementary Figure 1 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Supplementary Figure 2 from Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis

Woolley CE. et al, (2025)

Publications

Mixed-model and transcriptome-wide association analyses identify transcription factors and genes associated with colorectal cancer susceptibility.

Promises under pressure: the modest predictive power of polygenic risk scores.

Comparison between germline and somatic loss-of-function RNF43 mutations reveals different genotype-phenotype associations and provides insights into the genetic mechanisms of colorectal tumourigenesis.

Mathematical Modeling Quantifies "Just-Right" APC Inactivation for Colorectal Cancer Initiation.

Loss of IDH1 and IDH2 mutations during the evolution of metastatic chondrosarcoma.

Large-scale meta-analysis and precision functional assays identify FANCM regions in which PTVs confer different risks for ER-negative and triple-negative breast cancer.

Analysis of IDH1 and IDH2 mutations as causes of the hypermethylator phenotype in colorectal cancer.

Replication-associated mechanisms contribute to an increased CpG > TpG mutation burden in mismatch repair-deficient cancers.

GWAS meta-analysis identifies five susceptibility loci for endometrial cancer.

Epithelial GREMLIN1 disrupts intestinal epithelial-mesenchymal crosstalk to induce a wnt-dependent ectopic stem cell niche through stromal remodelling.

The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda.

Genetic variation at 11q23.1 confers colorectal cancer risk by dysregulation of colonic tuft cell transcriptional activator POU2AF2.

Coevolution of Atypical BRAF and KRAS Mutations in Colorectal Tumorigenesis.

Data from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Figure 3 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Figure 4 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Figure 5 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Supplementary Data 1 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Supplementary Figure 1 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

Supplementary Figure 2 from Coevolution of Atypical <i>BRAF</i> and <i>KRAS</i> Mutations in Colorectal Tumorigenesis

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Publications