Recent advances and challenges in colorectal cancer: From molecular research to treatment

Figure 1 Four distinct pathways of progression from polyps to colorectal cancer, each characterized by specific molecular alterations. Created with MedPeer (medpeer.cn). Copyright permission has been obtained in the Supplementary material. These pathways include the adenoma-carcinoma-metastasis sequence, the traditional serrated pathway, the sessile serrated pathway, and cancers associated with colitis. DCC: Deleted in colorectal cancer; BRAF: B-raf proto-oncogene; SMAD4: Sma and mad homolog; DPC4: Sma and mad homolog family member 4; MGMT: O-6-methylguanine-DNA methyltransferase; MLH1: MutL homolog 1; AKT: Protein kinase B; PI3K: Phosphatidylinositol 3-kinase; TGF-β: Transforming growth factor beta; MSI: Microsatellite instability; TGF: Transforming growth factor; CRC: Colorectal cancer; CIMP-H: CpG island methylator phenotype-high; CIMP-L: CpG island methylator phenotype-low; MSS: Microsatellite stability; MSI-H: High microsatellite instability; MSI-L: Low microsatellite instability; TSA: Traditional serrated adenomas; TSG: Tumor suppressor genes; TSA-HGD: Traditional serrated adenomas with high-grade dysplasia; SSL: Sessile serrated lesions; SSL-HGD: Sessile serrated lesions with high-grade dysplasia; CAC: Colitis-associated cancer; Adenomas-LGD: Adenomas with low-grade dysplasia; Adenomas-HGD: Adenomas with high-grade dysplasia; SAC: Spindle assembly checkpoint; TNF-α: Tumor necrosis factor-α; IL: Interleukin; NF-Κb: Nuclear factor kappa B; APC: Adenomatous polyposis col; KRAS: Kirsten rat sarcoma viral oncogene homolog; STAT3: Signal transducer and activator of transcription 3.