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2. JAK/STAT3 represents a therapeutic target for colorectal cancer patients with stromal-rich tumors

3. Corrigendum

4. Ensuring accurate stain reproduction in deep generative networks for virtual immunohistochemistry

6. Single-cell AI-based detection and prognostic and predictive value of DNA mismatch repair deficiency in colorectal cancer

7. Metabolic profiling stratifies colorectal cancer and reveals adenosylhomocysteinase as a therapeutic target

11. Multiplex analysis of intratumoural immune infiltrate and prognosis in patients with stage II–III colorectal cancer from the SCOT and QUASAR 2 trials: a retrospective analysis

13. Improving radiotherapy in immunosuppressive microenvironments by targeting complement receptor C5aR1

14. Transformer-based biomarker prediction from colorectal cancer histology: A large-scale multicentric study

20. Histopathological tumour microenvironment score independently predicts outcome in primary operable colorectal cancer

24. MIR21-induced loss of junctional adhesion molecule A promotes activation of oncogenic pathways, progression and metastasis in colorectal cancer

28. The Glasgow Microenvironment Score associates with prognosis and adjuvant chemotherapy response in colorectal cancer

29. The combined tumour-based Fascin/Snail and stromal periostin reveals the effective prognosis prediction in colorectal cancer patients.

30. Prognostic and Predictive Value of Immunoscore in Stage III Colorectal Cancer: Pooled Analysis of Cases From the SCOT and IDEA-HORG Studies.

33. eIF4A1 is essential for reprogramming the translational landscape of Wnt-driven colorectal cancers

35. Correction to: Durvalumab (MEDI 4736) in combination with extended neoadjuvant regimens in rectal cancer: a study protocol of a randomised phase II trial (PRIME-RT)

36. Durvalumab (MEDI 4736) in combination with extended neoadjuvant regimens in rectal cancer: a study protocol of a randomised phase II trial (PRIME-RT)

37. BRF1 accelerates prostate tumourigenesis and perturbs immune infiltration

41. Figure S3 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

42. Figure 4 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

43. Figure 5 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

44. Figure 6 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

45. Supplementary Figure Legends from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

46. Table S1 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

47. Macrophage reprogramming—rather than depletion—is efficacious in a specific subset of colorectal tumor models

48. Figure 3 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

49. Data from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

50. Figure 1 from β-Catenin Drives Butyrophilin-like Molecule Loss and γδ T-cell Exclusion in Colon Cancer

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