title: Influence of liver cancer on lipid and lipoprotein metabolism.
abstract: Liver plays a key role in the metabolism of plasma apolipoproteins, endogenous lipids and lipoproteins. Hepatocellular carcinoma (HCC) is one of the most common fatal malignant tumors in China and in other Southeast Asian countries. This has been attributed to the high incidence of hepatitis B infection. Hepatitis B proteins, such as the hepatitis B X protein (HBx) that is large hepatitis B surface protein could regulate transcription of many candidate genes for liver carcinogenesis. It has known that patients who suffered from acute hepatitis B could have lipid disorders such as decreased plasma level of high-density lipoproteins (HDL). Furthermore, aberrations of lipid metabolism are often seen in the chronic hepatitis B infection. Plasma lipid profiles could be changed under HCC. In majority of the reports in HCC, plasma levels of triglycerides (TG), cholesterol, free fatty acids (FFA), HDL, low-density lipoproteins (LDL), lipoprotein (a) (Lp(a)), apolipoprotein AI (apoAI) and apoB were slight to significantly decreased, however, in some cases plasma levels of TG and Lp(a) might be increased. It has been suggested that analysis of plasma levels of lipids, lipoproteins and apolipoproteins in the patients suffered from HCC reflects on the hepatic cellular impairment status. Studies revealed that alterations seen in the plasma levels of lipids, lipoproteins and apolipoproteins reflecting patients' pathologic conditions. Decreased serum levels of cholesterol and apoAI may indicate a poor prognosis. Human leukaemic cells and certain tumor tissues have a higher receptor-mediated uptake of HDL and LDL than the corresponding normal cells or tissues. LDL and HDL have therefore been proposed as a carrier for the water-insoluble anti-cancer agents.
authors.affiliation: Section of Clinical Chemistry & Pharmacology, Institute of Laboratory Medicine, Lund University, S-221 85 Lund, Sweden. jingtingjiang@yahoo.com.cn
authors.forename: Jingting
authors.initials: J
authors.lastname: Jiang
authors.forename: Peter
authors.initials: P
authors.lastname: Nilsson-Ehle
authors.forename: Ning
authors.initials: N
authors.lastname: Xu
mesh_terms: D000970:Antineoplastic Agents / Q000008:administration & dosage; D001053:Apolipoproteins / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000378:metabolism*; D002784:Cholesterol / Q000378:metabolism; D004337:Drug Carriers / Q000627:therapeutic use; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000378:metabolism*; D008075:Lipoproteins, HDL / Q000627:therapeutic use; D008077:Lipoproteins, LDL / Q000627:therapeutic use; D008113:Liver Neoplasms / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D001053:Apolipoproteins; D004337:Drug Carriers; D005230:Fatty Acids, Nonesterified; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol