Objective:To evaluate the predictive value of secreted phosphoprotein 1(SPP1)gene expression for postoperative survival in patients with advanced liver cancer undergoing hepatic artery interventional chemoembolization...Objective:To evaluate the predictive value of secreted phosphoprotein 1(SPP1)gene expression for postoperative survival in patients with advanced liver cancer undergoing hepatic artery interventional chemoembolization treatment.Method:Bioinformatics methods,including gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis,were used to identify genes related to survival prognosis in hepatocellular carcinoma(HCC)patients.A retrospective analysis of 115 advanced liver cancer patients treated between January 2016 and October 2017 was conducted.Patients were categorized into SPP1 high-expression(n=89)and low-expression groups(n=26).Additionally,115 healthy individuals served as the control group.The relationship between SPP1 expression and clinical pathological features was analyzed.A 60-month follow-up and logistic regression analysis identified risk factors affecting survival.Results:SPP1 mRNA expression was significantly higher in liver cancer patients compared to healthy controls(P<0.05).SPP1 expression levels were significantly associated with tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging(P<0.05).High SPP1 expression,along with tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging,were independent risk factors for survival(P<0.05).The 60-month survival rate was 17.39%,with a median survival of 40 months in the low-expression group versus 18 months in the high-expression group(P<0.05).Conclusion:SPP1 expression is significantly upregulated in advanced liver cancer patients and has predictive value for postoperative survival following hepatic artery chemoembolization treatment.SPP1,combined with clinical indicators such as tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging,may serve as a prognostic biomarker for interventional treatment outcomes.展开更多
Chronic hepatitis B is a global health problem. The clinical outcomes of chronic hepatitis B infection include asymptomatic carrier state, chronic hepatitis(CH), liver cirrhosis(LC), and hepatocellular carcinoma(HCC)....Chronic hepatitis B is a global health problem. The clinical outcomes of chronic hepatitis B infection include asymptomatic carrier state, chronic hepatitis(CH), liver cirrhosis(LC), and hepatocellular carcinoma(HCC). Because of the spontaneous error rate inherent to viral reverse transcriptase, the hepatitis B virus(HBV) genome evolves during the course of infection under the antiviral pressure of host immunity. The clinical significance of pre-S/S variants has become increasingly recognized in patients with chronic HBV infection. Pre-S/S variants are often identified in hepatitis B carriers with CH, LC, and HCC, which suggests that these naturally occurring pre-S/S variants may contribute to the development of progressive liver damage and hepatocarcinogenesis. This paper reviews the function of the pre-S/S region along with recent findings related to the role of pre-S/S variants in liver diseases. According to the mutation type, five pre-S/S variants have been identified: pre-S deletion, pre-S point mutation, pre-S1 splice variant, C-terminus S point mutation, and pre-S/S nonsense mutation. Their associations with HBV genotype and the possible pathogenesis of pre-S/S variants are discussed. Different pre-S/S variants cause liver diseases through different mechanisms. Most cause the intracellular retention of HBV envelope proteins and induction of endoplasmic reticulum stress, which results in liver diseases. Pre-S/S variants should be routinely determined in HBV carriers to help identify individuals who may be at a high risk of less favorable liver disease progression. Additional investigations are required to explore the molecular mechanisms of the pre-S/S variants involved in the pathogenesis of each stage of liver disease.展开更多
基金Medical Research Project of Xi’an Science and Technology Bureau“Molecular Mechanism of miR-1305 Competitive Endogenous circRNA in the Development of Liver Cancer”(Project No.22YXYJ0134)General Project of Key Research and Development Program of Shaanxi Provincial Department of Science and Technology“Mechanism Study on the Inhibition of Liver Cancer Invasion and Metastasis by Downregulating METTL3 and Reducing the m6A Modification Level of MMP3 with Honokiol”(Project No.2023-YBSF-631)。
文摘Objective:To evaluate the predictive value of secreted phosphoprotein 1(SPP1)gene expression for postoperative survival in patients with advanced liver cancer undergoing hepatic artery interventional chemoembolization treatment.Method:Bioinformatics methods,including gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis,were used to identify genes related to survival prognosis in hepatocellular carcinoma(HCC)patients.A retrospective analysis of 115 advanced liver cancer patients treated between January 2016 and October 2017 was conducted.Patients were categorized into SPP1 high-expression(n=89)and low-expression groups(n=26).Additionally,115 healthy individuals served as the control group.The relationship between SPP1 expression and clinical pathological features was analyzed.A 60-month follow-up and logistic regression analysis identified risk factors affecting survival.Results:SPP1 mRNA expression was significantly higher in liver cancer patients compared to healthy controls(P<0.05).SPP1 expression levels were significantly associated with tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging(P<0.05).High SPP1 expression,along with tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging,were independent risk factors for survival(P<0.05).The 60-month survival rate was 17.39%,with a median survival of 40 months in the low-expression group versus 18 months in the high-expression group(P<0.05).Conclusion:SPP1 expression is significantly upregulated in advanced liver cancer patients and has predictive value for postoperative survival following hepatic artery chemoembolization treatment.SPP1,combined with clinical indicators such as tumor size,Child-Pugh grading,lymph node metastasis,and BCLC staging,may serve as a prognostic biomarker for interventional treatment outcomes.
基金Supported by the grant from the National Science Council(NSC 96-2320-B-030-004-MY3),Executive Yuan,Taiwan
文摘Chronic hepatitis B is a global health problem. The clinical outcomes of chronic hepatitis B infection include asymptomatic carrier state, chronic hepatitis(CH), liver cirrhosis(LC), and hepatocellular carcinoma(HCC). Because of the spontaneous error rate inherent to viral reverse transcriptase, the hepatitis B virus(HBV) genome evolves during the course of infection under the antiviral pressure of host immunity. The clinical significance of pre-S/S variants has become increasingly recognized in patients with chronic HBV infection. Pre-S/S variants are often identified in hepatitis B carriers with CH, LC, and HCC, which suggests that these naturally occurring pre-S/S variants may contribute to the development of progressive liver damage and hepatocarcinogenesis. This paper reviews the function of the pre-S/S region along with recent findings related to the role of pre-S/S variants in liver diseases. According to the mutation type, five pre-S/S variants have been identified: pre-S deletion, pre-S point mutation, pre-S1 splice variant, C-terminus S point mutation, and pre-S/S nonsense mutation. Their associations with HBV genotype and the possible pathogenesis of pre-S/S variants are discussed. Different pre-S/S variants cause liver diseases through different mechanisms. Most cause the intracellular retention of HBV envelope proteins and induction of endoplasmic reticulum stress, which results in liver diseases. Pre-S/S variants should be routinely determined in HBV carriers to help identify individuals who may be at a high risk of less favorable liver disease progression. Additional investigations are required to explore the molecular mechanisms of the pre-S/S variants involved in the pathogenesis of each stage of liver disease.
