AIM:To investigate the expression of C/EBP homologous protein (CHOP) and its correlation with proliferative/apoptotic ratio (PAR) in colorectal adenoma-carcinoma sequence under the same genetic background .ME-THODS:Four kinds of tissue samples under the same genetic background from 23 patients, including normal colorectal tissue, adenoma with low-grade intraepithelial neoplasia , adenoma with high-grade intraepithelial neoplasia and colorectal adenocarcinoma samples , were collected .TUNEL method and Ki-67 immunohistochemistry were applied to determine the PAR.The expression of CHOP was detected by immunohistochemistry SABC method .RESULTS: ( 1 ) Under the same genetic background , the level of CHOP expression is significantly higher in colorectal adenocarcinoma than that in the ade -noma with high-grade intraepithelial neoplasia , the adenoma with low-grade intraepithelial neoplasia and the normal muco-sa.The level of CHOP expression was significantly higher in the adenoma with high -grade intraepithelial neoplasia than that in the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .The level of CHOP expression was signifi-cantly higher in the adenoma with low-grade intraepithelial neoplasia than that in normal mucosa .(2) Under the same ge-netic background , PAR was significantly higher in the colorectal adenocarcinoma than that in the adenoma with high -grade intraepithelial neoplasia , the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .PAR was significant-ly higher in the adenoma with high-grade intraepithelial neoplasia than that in the adenoma with low-grade intraepithelial neoplasia and the normal mucosa .PAR was significantly higher in the adenoma with low-grade intraepithelial neoplasia than that in the normal mucosa.(3) CHOP levels were positively correlated with PAR in the adenoma with low-grade intraepi-thelial neoplasia , adenoma with high-grade intraepithelial neoplasia and colorectal adenocarcinoma .CONCLUSION:CHOP expression and PAR continuously increased and positively correlated along the adenoma -carcinoma sequence , indica-ting that endoplasmic reticulum stress mediates the carcinogenesis of colorectal adenomas .

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.