Individuals having variant genotypes of cytochrome P450 2C19 are at increased risk of developing primary liver cancer in Han populations, without infection with the hepatitis virus

Tumor Biology ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. 9023-9026 ◽  
Author(s):  
Qiao-Yan Li ◽  
Ning-Min Zhao ◽  
Lian-Cai Wang ◽  
Hong-Fei Duan ◽  
Yong-Cheng Ma ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Liver Cancer ◽  
Hepatitis Virus ◽  
Primary Liver Cancer ◽  
Increased Risk ◽  
Cytochrome P450 2C19

scholarly journals Total Cholesterol, Alanine Aminotransferase And the Risk of Primary Liver Cancer: A Population-based prospective study

2020 ◽  
Author(s):  
Miaomiao Sun ◽  
Wanchao Wang ◽  
Xining Liu ◽  
Yiming Wang ◽  
Haozhe Cui ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Total Cholesterol ◽  
Alanine Aminotransferase ◽  
Proportional Hazards ◽  
Primary Liver Cancer ◽  
Joint Effect ◽  
Cox Proportional Hazards ◽  
Additive Models ◽  
Low Level ◽  
Increased Risk

Abstract Background: Previous studies have shown that serum total cholesterol(TC) and serum alanine aminotransferase(ALT) were associated with liver cancer risk, respectively. However, the common contribution of TC and normal-high ALT to primary liver cancer(PLC) has not been reported to date. We aim to assess the separate and joint effect of low TC level and normal-high ALT level on the risk of PLC, a large prospective cohort was conducted in our study.Methods: The participants were divided into 4 groups via cross-matching method according to TC[low level(-)/ non-low level(+)] and ALT[normal level(-)/ normal-high level(+)] status, and using the lower quartile(P25) value(4.24 mmol/L) of TC and the upper quartile(P75) value(22 U/L) of ALT as a threshold, respectively. Incident PLC was confirmed by review of medical records. Cox proportional hazards regression models and interactive additive models were used to evaluate whether the joint effect of low TC level and normal-high ALT level is associated with the risk of PLC.Results: During 1,248,895 person-years follow-up, 298 participants were diagnosed with PLC among 114,972 subjects. TC＜4.24 mmol/L for the “TC(-)” group; TC≥4.24 mmol/L for the “TC(+)” group; ALT＜22U/L for the “ALT(-)” group; ALT≥22U/L for the “ALT(+)”. Compared with the “TC(+)” group, “ALT(-)” group, respectively, the adjusted hazard ratio(HR) and 95% confidence interval(95%CI) for PLC risk was 1.71 (1.34-2.19) in “TC(-)” group and for PLC risk was 1.52 (1.18-1.95) in “ALT(+)” group. In combinatorial analysis, compared with “TC(+) and ALT(-)” group, the significant increased risk of PLC were observed in “TC(+) and ALT(+)” group (HR=1.45; 95%CI: 1.07-1.97), “TC(-) and ALT(-)” group(HR=1.64; 95%CI: 1.21-2.22) and “TC(-) and ALT(+)” group(HR=2.70; 95%CI: 1.84-3.96), respectively. The interaction between “TC(-)” and “ALT (+)” on the risk of PLC was not significant(Pinteraction=0.26). Conclusions: Both low TC level and normal-high ALT level were risk factors of PLC. There is the separate and joint effect of low TC level and normal-high ALT level on the risk of PLC.Trial registration: ChiCTR-TNRC-11001489. Registered August 24, 2011 (retrospectively registered)

Chronic viral hepatitis and its association with liver cancer

2017 ◽  
Vol 398 (8) ◽  
pp. 817-837 ◽  
Author(s):  
Thomas Tu ◽  
Sandra Bühler ◽  
Ralf Bartenschlager
Keyword(s):  
Liver Cancer ◽  
Molecular Mechanisms ◽  
Hepatitis Virus ◽  
Primary Liver Cancer ◽  
Causative Factor ◽  
Metabolic Reprogramming ◽  
Model Systems ◽  
Cellular Stress Response ◽  
Viral Gene ◽  
Hepatitis Viruses

AbstractChronic infection with hepatitis viruses represents the major causative factor for end-stage liver diseases, including liver cirrhosis and primary liver cancer (hepatocellular carcinoma, HCC). In this review, we highlight the current understanding of the molecular mechanisms that drive the hepatocarcinogenesis associated with chronic hepatitis virus infections. While chronic inflammation (associated with a persistent, but impaired anti-viral immune response) plays a major role in HCC initiation and progression, hepatitis viruses can also directly drive liver cancer. The mechanisms by which hepatitis viruses induce HCC include: hepatitis B virus DNA integration into the host cell genome; metabolic reprogramming by virus infection; induction of the cellular stress response pathway by viral gene products; and interference with tumour suppressors. Finally, we summarise the limitations of hepatitis virus-associated HCC model systems and the development of new techniques to circumvent these shortcomings.

scholarly journals Increased risk for primary liver cancer among women exposed to solvents.

1988 ◽  
Vol 14 (6) ◽  
pp. 356-365 ◽  
Author(s):  
Sven Hernberg ◽  
Timo Kauppinen ◽  
Riitta Riala ◽  
M L Korkala ◽  
U Asikainen
Keyword(s):  
Liver Cancer ◽  
Primary Liver Cancer ◽  
Increased Risk

scholarly journals Total cholesterol, alanine aminotransferase and the risk of primary liver cancer: A population-based prospective study in China

2020 ◽  
Author(s):  
Miaomiao Sun ◽  
Wanchao Wang ◽  
Yiming Wang ◽  
Haozhe Cui ◽  
Xining Liu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Total Cholesterol ◽  
Alanine Aminotransferase ◽  
Proportional Hazards ◽  
Primary Liver Cancer ◽  
Joint Effect ◽  
Cox Proportional Hazards ◽  
Additive Models ◽  
Low Level ◽  
Increased Risk

Abstract Background: Previous studies have shown that serum total cholesterol(TC) and serum alanine aminotransferase(ALT) were associated with liver cancer risk, respectively. However, the common contribution of TC and normal-high ALT to primary liver cancer(PLC) has not been reported to date. We aim to assess the separate and joint effect of low TC level and normal-high ALT level on the risk of PLC, a large prospective cohort was conducted in our study. Method: The participants were divided into 4 groups via mismarch method according to TC[low level(-)/ non-low level(+)] and ALT[normal level(-)/ normal-high level(+)] status, and using the lower quartile(P25) value(4.24 mmol/L) of TC and the upper quartile(P75) value(22 U/L) of ALT as a cut point, respectively. Incident PLC was confirmed by review of medical records. Cox proportional hazards regression models and interactive additive models were used to evaluate whether the joint effect of low TC level and normal-high ALT level is associated with the risk of PLC. Results: During 1,248,895 person-years of follow-up, 298 participants were diagnosed with PLC among 114,972 subjects. TC＜4.24 mmol/L for the “TC(-)” group; TC≥4.24 mmol/L for the “TC(+)” group; ALT＜22U/L for the “ALT(-)” group; ALT≥22U/L for the “ALT(+)”. Compared with the “TC(+)” group and “ALT(-)” group, respectively, the adjusted hazard ratio(HR) and 95% confidence interval(95%CI) of “TC(-)” group for PLC risk was 1.71 (1.34-2.19) and of “ALT(+)” group for PLC risk was 1.52 (1.18-1.95). In combinatorial analysis, compared with the group of “TC(+) with ALT(-)”, the significant increased risk of PLC were observed in “TC(+) with ALT(+) group”(HR=1.45; 95%CI: 1.07-1.97), “TC(-) with ALT(-)” group(HR=1.64; 95%CI: 1.21-2.22) and “TC(-) with ALT(+)” group(HR=2.70; 95%CI: 1.84-3.96), respectively. The interaction term between “TC(-)” and “ALT (+)” on the risk of PLC was not significant(Pinteraction=0.26). Conclusions: Both low TC level and normal-high ALT level were strong predictors of PLC. Individuals with low TC level and normal-high ALT level, would extremely increase the risk of PLC.Trial registration: ChiCTR-TNRC-11001489. Registered August 24, 2011 (retrospectively registered)

scholarly journals Liver Cancer: Therapeutic Challenges and the Importance of Experimental Models

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Marina Galicia-Moreno ◽  
Jorge A Silva-Gomez ◽  
Silvia Lucano-Landeros ◽  
Arturo Santos ◽  
Hugo C Monroy-Ramirez ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Hepatitis Virus ◽  
Primary Liver Cancer ◽  
Therapeutic Option ◽  
Experimental Models ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nonalcoholic Fatty Liver

Liver cancer is one of the main causes of death related to cancer worldwide; its etiology is related with infections by C or B hepatitis virus, alcohol consumption, smoking, obesity, nonalcoholic fatty liver disease, diabetes, and iron overload, among other causes. Several kinds of primary liver cancer occur, but we will focus on hepatocellular carcinoma (HCC). Numerous cellular signaling pathways are implicated in hepatocarcinogenesis, including YAP-HIPPO, Wnt-β-catenin, and nuclear factor-κB (NF-κB); these in turn are considered novel therapeutic targets. In this review, the role of lipid metabolism regulated by peroxisome proliferator-activated receptor gamma (PPARγ) in the development of HCC will also be discussed. Moreover, recent evidence has been obtained regarding the participation of epigenetic changes such as acetylation and methylation of histones and DNA methylation in the development of HCC. In this review, we provide detailed and current information about these topics. Experimental models represent useful tools for studying the different stages of liver cancer and help to develop new pharmacologic treatments. Each model in vivo and in vitro has several characteristics and advantages to offer for the study of this disease. Finally, the main therapies approved for the treatment of HCC patients, first- and second-line therapies, are described in this review. We also describe a novel option, pirfenidone, which due to its pharmacological properties could be considered in the future as a therapeutic option for HCC treatment.

scholarly journals Genetic Variant of PP2A Subunit Gene Confers an Increased Risk of Primary Liver Cancer in Chinese

2021 ◽  
Vol Volume 14 ◽  
pp. 1565-1574
Author(s):  
Youxin Wang ◽  
Qiuyue Huang ◽  
Xinglei Huang ◽  
Huiliu Zhao ◽  
Bin Guan ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Genetic Variant ◽  
Primary Liver Cancer ◽  
Subunit Gene ◽  
Increased Risk
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