A targetable PREX2/RAC1/PI3Kβ signalling axis confers resistance to clinically relevant therapeutic approaches in melanoma

Author response: RAS-p110a signalling in macrophages is required for effective inflammatory response and resolution of inflammation

Author response: RAS-p110α signalling in macrophages is required for effective inflammatory response and resolution of inflammation

Characterisation of tumour microenvironment remodelling following oncogene inhibition in preclinical studies with imaging mass cytometry

Combining RASG12C(ON) inhibitor with SHP2 inhibition sensitises immune excluded lung tumours to immune checkpoint blockade: a strategy for turning cold tumours hot

Data from <i>ATMIN</i> Is a Tumor Suppressor Gene in Lung Adenocarcinoma

Data from Facts and Hopes on RAS Inhibitors and Cancer Immunotherapy

Data from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 1 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Figure 1 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 2 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Figure 2 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Figure 2 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 3 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 4 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 5 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Figure 5 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 5 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Figure 6 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Leveraging death of drug-sensitive cancer cells to promote immune-mediated bystander killing of subclones of drug-resistant tumour cells

RAS-p110a signalling in macrophages is required for effective inflammatory response and resolution of inflammation

RAS-p110α signalling in macrophages is required for effective inflammatory response and resolution of inflammation

RAS-p110α signalling in macrophages is required for effective inflammatory response and resolution of inflammation

Supplementary Data from An Immunogenic Model of KRAS-Mutant Lung Cancer Enables Evaluation of Targeted Therapy and Immunotherapy Combinations

Supplementary Figure 1 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Figure 2 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Figure 5 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Figure 7 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Figure 9 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Figures 1-22 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma

Supplementary Figures S1-S10 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma

Supplementary Figures S1-S7 from <i>ATMIN</i> Is a Tumor Suppressor Gene in Lung Adenocarcinoma

Supplementary Table 1 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Table 2 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Table 3 from CRISPR–Cas9 Screening Identifies KRAS-Induced COX2 as a Driver of Immunotherapy Resistance in Lung Cancer

Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma

Supplementary Table S1 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma

Supplementary Table S2 from Targeting the PREX2/RAC1/PI3Kβ Signaling Axis Confers Sensitivity to Clinically Relevant Therapeutic Approaches in Melanoma

Supplementary Table from An Immunogenic Model of KRAS-Mutant Lung Cancer Enables Evaluation of Targeted Therapy and Immunotherapy Combinations

Supplementary Table from An Immunogenic Model of KRAS-Mutant Lung Cancer Enables Evaluation of Targeted Therapy and Immunotherapy Combinations

Supplementary Table from An Immunogenic Model of KRAS-Mutant Lung Cancer Enables Evaluation of Targeted Therapy and Immunotherapy Combinations

Supplementary Tables 1-5 from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

TRACERx Consortium Members from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

TRACERx Consortium Members from Spatial Architecture of Myeloid and T Cells Orchestrates Immune Evasion and Clinical Outcome in Lung Cancer

Table 1 from Facts and Hopes on RAS Inhibitors and Cancer Immunotherapy

Targeted cancer therapy induces APOBEC fuelling the evolution of drug resistance