Data from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Data from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Data from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Data from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S1 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S1 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S2 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S2 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S3 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S4 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S4 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S5 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S5 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S6 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S6 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Figure S7 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Supplementary Appendix S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S1 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S1 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S2 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S2 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S2 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S3 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S4 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S4 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S4 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Figure S5 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S5 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Figure S6 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Material S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Material S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Methods S1 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Table S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Table S1 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Table S2 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Table S3 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Table S4 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Table S4 from Tissue-Free Liquid Biopsies Combining Genomic and Methylation Signals for Minimal Residual Disease Detection in Patients with Early Colorectal Cancer from the UK TRACC Part B Study

Supplementary Tables S1-S19 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Video S1 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Video S2 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Supplementary Video S2 from Circulating microRNA Analysis in a Prospective Co-clinical Trial Identifies MIR652–3p as a Response Biomarker and Driver of Regorafenib Resistance Mechanisms in Colorectal Cancer

Table S1 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Table S2 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Table S2 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Table S3 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Table S3 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer

Table S4 from Inactivation of <i>NF1</i> Promotes Resistance to EGFR Inhibition in <i>KRAS/NRAS/BRAF<sup>V600</sup></i>-Wild-Type Colorectal Cancer