Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatocellular carcinoma mainly affects patients with cirrhosis or with various degrees of fibrosis. From 1979 to 1990, among 87 patients who underwent hepatic resection for non fibrolamellar hepatocellular carcinoma, 12 (14%) had a non fibrolamellar hepatocellular carcinoma developed in a normal liver. There were 8 men and 4 women, aged 29 to 74 years. In 7 patients (58%) hepatocellular carcinoma was associated with clinical manifestations. Serum hepatitis B surface antigen were absent in all patients. Serum alphafetoprotein level was less than 100 mg/ml in 10 (83%), size of the tumor was greater than or less than 5 cm in 10 (83%) and capsule was present in 10 (83%). Resections included removal of 2 segments or more in 11 (91%). One patient died postoperatively. Actuarial survival rate at 3 and 5 years were respectively 57% and 38%. Intra or extrahepatic recurrence was recognized in 8 (67%), 2 patients were alive respectively 28 and 16 months after treatment of their intrahepatic recurrence (resection in one and intra-arterial embolisation in one). In conclusion, our results suggest that aggressive surgical efforts are justified in non fibrolamellar hepatocellular carcinoma arising in normal liver.
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PMID:[Hepatocellular carcinoma in undamaged liver]. 166 90

Using an automatic blood cell counter (Sysmex F500), the white blood cells of peripheral blood from patients can be accurately counted. The lymphocytes and their subsets can also be accurately counted and measured by the use of various fluorescent conjugated monoclonal antibodies and the flow cytometry (FACScan) method. This study disclosed a significant decrease in the lymphocyte, B cell, T cell and T-cell subsets of 45 hepatocellular carcinoma (HCC) patients as compared with those of 64 normal healthy individuals and those of 66 asymptomatic hepatitis B virus surface antigen carriers. The natural killer (NK) cells of HCC patients did not show any change as compared with that of the two normal control groups. A significant increase in the number of white blood cells of HCC patients was seen on the first and the seventh postoperative days as compared with the preoperative levels. However, the number of lymphocyte, T cell and NK cells of HCC patients decreased on the first postoperative day as compared with the preoperative levels. A temporary increase in B cells was observed on the seventh postoperative day. We conclude that the immunity of HCC patients is definitely reduced and is further aggravated after surgery.
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PMID:Lymphocytes and their subsets in the peripheral blood of hepatocellular carcinoma patients. 168 Oct 11

To determine serum thyroxine-binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)-positive. Among them, 38 patients had hepatocellular carcinoma (HCC), 18 had chronic persistent hepatitis, 70 had chronic lobular or active hepatitis (grouped as CAH), 31 had active cirrhosis (AC), 25 had inactive cirrhosis, 20 had decompensated cirrhosis, and 29 were "healthy" HBsAg carriers. Twenty-seven patients with acute hepatitis, 12 with cancer metastasis to the liver, and 81 normal adults served as disease or normal controls. The results showed that serum TBG level increased significantly in patients with CAH, AC, or HCC. Serum TBG did not correlate with albumin or bilirubin level, but correlated with alanine aminotransferase (ALT) positively in patients with CAH (p less than 0.001) and negatively in patients with HCC (p less than 0.01) (slope difference p less than 0.05). Serial determination of serum TBG and ALT also showed parallel changes in 15 patients with CAH, but not in nine patients with HCC. In contrast, the fall and rise of serum TBG levels in patients with HCC coincided with tumor resection and recurrence. The data suggest that serum TBG elevation in patients with hepatitis activity is the result of hepatocellular damage, whereas that in patients with HCC is due to increased synthesis. Whether serum TBG elevation without concomitant rise of ALT could be used as a marker of HCC awaits further study.
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PMID:Thyroxine-binding globulin in patients with chronic hepatitis B virus infection: different implications in hepatitis and hepatocellular carcinoma. 168 51

We studied the effects of transfection of the normal c-Ha-ras gene, rasGly-12, and its oncogenic mutant, rasVal-12, on expression of the alpha-fetoprotein (AFP) and albumin genes in a human hepatoma cell line, HuH-7. The mutant and, to a lesser extent, the normal ras gene caused reduction of the AFP mRNA but not the albumin mRNA level in transfected HuH-7 cells. Cotransfection experiments with a rasVal-12 expression plasmid and a chloramphenicol acetyltransferase reporter gene fused to AFP regulatory sequences showed that rasVal-12 suppressed the activity of enhancer and promoter regions containing A + T-rich sequences (AT motif). In contrast, rasVal-12 did not affect the promoter activity of the albumin and human hepatitis B virus pre-S1 genes even though these promoters contain homologous A + T-rich elements. ras transfection appeared to induce phosphorylation of nuclear proteins that interact with the AFP AT motif, since gel mobility analysis revealed the formation of slow-moving complexes which was reversed by phosphatase treatment. However, similar changes in complex formation were observed with the albumin and hepatitis B surface antigen pre-S1 promoters. Therefore, this effect alone cannot explain the specific down regulation of the AFP promoter and enhancer activity. ras-mediated suppression of the AFP gene may reflect the process of developmental gene regulation in which AFP gene transcription is controlled by a G-protein-linked signal transduction cascade triggered by external growth stimuli.
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PMID:c-Ha-ras down regulates the alpha-fetoprotein gene but not the albumin gene in human hepatoma cells. 169 Aug 41

Fifty-nine transgenic mice from a lineage that overproduces the hepatitis B virus large envelope polypeptide and accumulates high intrahepatic concentrations of hepatitis B surface antigen were followed for evidence of liver disease throughout their 24-month life span. By 4 months of age all mice displayed biochemical and histological evidence of moderately severe chronic hepatitis which was followed sequentially by the development of regenerative nodules and oval cell hyperplasia (by 6 months), liver cell adenomas (by 8 months), and hepatocellular carcinomas (by 12 months of age). One hundred % of mice in this lineage developed hepatocellular carcinoma by 20 months of age, whereas no histopathological changes were observed in age- and sex-matched nontransgenic littermate controls over the same period of observation. These results indicate that overproduction of the hepatitis B virus large envelope polypeptide initiates a process characterized by liver cell injury, inflammation, and regenerative hyperplasia, which places large numbers of hepatocytes at risk for the development of transforming mutations, and inexorably progresses to hepatocellular carcinoma. We suggest that this is a general mechanism of hepatocarcinogenesis that may be operative in human hepatitis B virus infection and other necroinflammatory liver diseases as well.
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PMID:Hepatocarcinogenesis due to chronic liver cell injury in hepatitis B virus transgenic mice. 169 59

Circulating immune complexes (CIC), complement and alpha-fetoprotein (AFP) were detected in 93 hepatitis B surface antigen (HBsAg)-positive patients with hepatocellular carcinoma (HCC), 16 patients with liver cirrhosis (LC) and 54 healthy controls. The CIC and complements were significantly higher in HCC patients than in LC patients. The complement and polyethylene glycol(PEG)-CIC in HCC patients with LC were higher than those in LC only (P less than 0.0001). The complement levels in LC patients were significantly lower than in controls. There was no difference in C3 and C4 between HCC patients and controls, while the C3 proactivator was higher in HCC patients (P less than 0.02). The C1q-CIC was higher in HCC and LC patients when compared to controls (P less than 0.0001). In patients with HCC, there was no difference in the CIC and complement levels between patients with cirrhosis and those without. There were inverse correlations between C1q-CIC and C3 (P less than 0.05), C1q-CIC and C4 (P less than 0.04). The mean level of 3% PEG-CIC and C1q-CIC increased significantly as AFP elevated, but decreased as AFP was higher than 1599 ng/ml (P less than 0.05). These results imply that CIC increase with tumor growth but further tumor burden may result in a fall in CIC, there was a shifting of CIC from complement-fixing to non-complement-fixing as AFP increased gradually.
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PMID:Relationship of serum alpha-fetoprotein to circulating immune complexes and complements in patients with hepatitis B surface antigen-positive hepatocellular carcinoma. 169 50

The authors successfully established 5 hepatocellular carcinoma cell lines, JHH-1, 2, 4, 5 and 6, derived from hepatitis B surface antigen seronegative patients and one line. JHH-7, from a patient considered to be a hepatitis B virus carrier. In the culture media of any of the JHH cell lines, including JHH-7, hepatitis B surface antigen was not detected by radioimmunoassay. However, in JHH-7, integration of hepatitis B virus DNA was confirmed at two sites on the chromosomes of this line by Southern blot hybridization. In contrast, in other JHH cell lines derived from hepatitis B surface antigen seronegative patients, integration of hepatitis B virus DNA into the chromosomes of cells was not detected. These cell lines will be useful in the investigation of hepatocellular carcinoma development, especially for research into non-A/non-B hepatitis viruses.
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PMID:Integration of hepatitis B virus DNA into cells of six established human hepatocellular carcinoma cell lines. 170 9

Serum alpha-fetoprotein levels were determined in patients (268) with liver disease. Markedly elevated concentrations (greater than 100 micrograms/l) were found in twelve patients with malignant tumours and two with cirrhosis. Molecular variants of alpha-fetoprotein were distinguished by lectin affinity chromatography of these sera. Reversible binding to concanavalin A (86 +/- 5%) and to lentil agglutinin (61 +/- 19%) conformed to expected values for primary hepatocellular carcinoma except in one patient with a metastatic carcinoma whose alpha-fetoprotein binding to concanavalin A was similar to non-liver alpha-fetoprotein (44 +/- 13%), and the two patients with cirrhosis in whom binding to lentil agglutinin was typical for benign liver disorders (less than 20%). Since low levels of serum alpha-fetoprotein and non-characteristic alpha-fetoprotein binding patterns assisted in the regrouping of eleven out of 24 patients initially thought to have primary hepatocellular carcinoma, it was concluded that alpha-fetoprotein determination and lectin affinity chromatography are helpful in distinguishing primary hepatocellular carcinoma from metastatic and benign liver diseases. Slight increases in the alpha-fetoprotein level in the presence of serum hepatitis B surface antigen indicated seven patients at risk for primary hepatocellular carcinoma who should be monitored frequently.
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PMID:Serum alpha-fetoprotein levels and microheterogeneity in patients with different liver diseases. 170 55

In a consecutive 440 autopsy cases of hepatocellular carcinoma (HCC), 13 patients (2.95%) were found to have a second primary malignant tumor. All of the patients were male. The age ranged from 40 to 69 years old. (mean: 56.5) Peak incidence occurred in the seventh decade. The associated neoplasms included 4 cases of colorectal adenocarcinoma, 2 cases of thyroid cancer, 2 cases of retroperitoneal sarcomas, 1 case of pancreatic adenocarcinoma, 1 case of esophageal squamous cell carcinoma, 1 case of common bile duct adenocarcinoma, 1 case of renal cell carcinoma, and 1 case of prostatic adenocarcinoma. The organ most commonly involved was large bowel (4 cases). Epithelial origin neoplasms comprised the vast majority (84.6%). Of the 13 cases, 2 associated malignancies existed metachronously, 4 and 5 years before HCC. The others were found at the same time as HCC. The clinical and pathological observations included age, sex, serum alpha-fetoprotein (AFP), serum hepatitis B surface antigen (HBsAg), cirrhosis, gross and histologic appearance. The above presentations were similar in cases with and without second malignancy. We failed to find any factor that was possibly related to the etiology of the second neoplasm. Much more such cases are needed for further evaluation.
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PMID:Hepatocellular carcinoma coexisted with second malignancy--a study of 13 cases from a consecutive 440 autopsy cases of HCC. 170 92

Flow cytometric DNA analysis was performed in 50 paraffin-embedded specimens of clinical hepatocellular carcinoma (HCC) after hepatic resections. The DNA distribution pattern was classified in two types, diploid and aneuploid, according to the degree of dispersion on the DNA histogram. The major DNA pattern of HCC in this report proved to be aneuploid (78%), although 22% of tumors revealed a diploid pattern. The serum alpha-fetoprotein level exceeded 40 ng/ml in 86.1% of the aneuploid tumors and in 13.9% of the diploid tumors (p less than 0.05). We found no correlation between DNA distribution and hepatitis B surface antigen positivity, the presence of liver cirrhosis or tumor size. Additionally we noted no significant correlation between the DNA pattern and survival rates in patients with HCC who underwent hepatic resection.
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PMID:Flow cytometric DNA analysis of hepatocellular carcinoma: preliminary report. 170 92


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