Colorectal premalignant lesions

Precancerous and cancerous colonic lesions encompass a spectrum of colorectal polyps, including conventional adenomatous polyps and serrated lesions like hyperplastic polyps and sessile serrated adenomas, which progress to colorectal cancer through distinct molecular pathways. Adenomatous polyps, predominant in sporadic and hereditary cases (e.g., FAP, Lynch syndrome), exhibit a CMS2-like transcriptomic profile characterized by WNT and MYC pathway activation, chromosomal instability, and early APC mutations, driving epithelial proliferation.[1][2] Serrated polyps, often in the right colon, show CMS1-like features with immune activation, BRAF V600E mutations, CpG island methylator phenotype (CIMP), and potential microsatellite instability from MLH1 silencing.[1][2][3] These lesions represent early carcinogenesis stages, with transcriptomic subtyping (CMS1/CMS2 dominant in premalignancy) aiding risk prediction for progression to invasive CRC subtypes.[1] No drugs directly target these lesions as a molecular entity; management focuses on endoscopic removal and surveillance, with molecular profiling informing personalized prevention strategies.[1][3]

Other names

colorectal polypsadenomatous polypsserrated polypshyperplastic polypssessile serrated adenomas/polyps (SSA/P)traditional serrated adenomas (TSA)