The identification of albumin mRNA may be a useful marker of hepatocellular carcinoma, and the demonstration of albumin mRNA by in situ hybridisation overcomes the potential background problem associated with albumin immunohistochemistry.
The hepatoma hybrid also continued to produce albumin, demonstrating the coexpression of liver and pancreas-specific genes in the hybrid-cell population.
To assess the potential role of membrane interleukin 1 (mIL-1) in modulating expression of acute phase proteins, we studied the effect of fixed mouse peritoneal macrophages and isolated cell membranes on the synthesis of C3 and albumin in human hepatoma Hep 3B cells.
However, either the regulation of such cell-specific factors breaks down in other cultured cells, or strictly cell-specific factors are not at play in controlling cell-specific transcription, because HeLa cells could transcribe the albumin promoter from the same start site about 10% as well as hepatomas could and 293 cells could transcribe both albumin and globin promoters.
This DNA showed a restriction map that was indistinguishable from that of the clone obtained from the hepatoma described above, demonstrating that no gross rearrangements of the intergenic DNA sequence are involved in control of expression of the AFP and albumin genes.
All-trans-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid (designated "acyclic retinoid") induced upregulation of the albumin gene expression at its transcriptional level, whereas all-trans-retinoic acid (RA) induced downregulation of the expression in both PLC/PRF/5 and HuH7 human hepatoma cell lines.
Also, high grade pleomorphic HCCs expressed albumin gene, and this finding is of value in the differential diagnosis with liver metastases of anaplastic tumors from lung, adrenal, pancreas, etc.
These results suggest that patients with hepatocellular carcinoma and no detectable albumin mRNA in the blood may be a subgroup with a low risk of relapse following liver transplantation.
In general, the level of aflatoxin-albumin adducts in sera and the prevalence of p53 mutation at codon 249 in HCC were lower than in other areas at high risk of HCC, including southern China and parts of Africa.
The multivariate-adjusted odds ratios of developing HCC for those who had low and high serum levels of AFB1-albumin adducts compared with those who had a undetectable adduct level as the referent (odds ratio = 1.0) were 4.1 and 12.4, respectively, for HBsAg carriers with null GST M1 genotype (P < .01, on the basis of the significance test for trend); 0.7 and 1.4 for those with non-null GST Ml genotype (P = .98); 1.8 and 10.2 for those with null GST T1 genotype (P < .05); and 1.3 and 0.8 for those with non-null GST T1 genotype (P = .93).
This suggests that the phenotypic expression of PLC cells are often not fixed, and in particular: (1) peripheral CCs have a different phenotype from hilar and large duct ones; (2) the CK profile and albumin mRNA expression in peripheral CCs show many similarities with those of some HCCs.
The present results revealed the presence of an albumin-producing human hepatic neoplastic cell, such as KMCH-2, that can differentiate to show not only the features of hepatocellular carcinoma but also those of cholangiocarcinoma under certain growth conditions.
When human hepatocellular carcinoma cell lines displaying different levels of AFP and albumin and nonhepatocyte tumor cell lines were infected with the recombinant AAV virus, ganciclovir treatment caused only AFP and albumin-positive hepatocellular carcinoma cells death, but not nonhepatocyte tumor cells or AFP and albumin-negative hepatic tumor cells.
When human Bel-7402 hepatocarcinoma cell line grew in a medium containing 10(-4) M dimethyl-4,4'-dimethoxy-5,6,5', 6'-dimethylenedioxybiphynyl-2,2'-dicarboxylate (DDB), the secretion of alpha-fetoprotein (AFP) was significantly lower than the control cells, whereas the albumin (ALB) secretion was markedly higher.
We constructed retroviral vectors carrying these cytokine genes under the control of the murine albumin enhancer and promoter and retrovirally transduced these genes into hepatoma and non-hepatoma cell lines.
The diagnosis of HCC by needle biopsy should include cytologic findings and the appropriate immunohistochemical profile, along with detection of albumin mRNA by in situ hybridization.
Albumin mRNA was detected in 22 of 23 hepatocellular carcinomas (96%); all hepatoblastomas, hepatocellular adenomas, and focal nodular hyperplasias; and within the hepatoid areas of an extrahepatic malignant mixed germ cell tumor.
These results show that the majority of patients with acute and chronic liver disease without evidence for hepatocellular carcinoma has albumin-mRNA-positive cells in their PMNC fraction indicating the nonspecificity of that parameter for the presence of circulating malignant hepatocytes.