UMLS:C0019204 - FACTA Search

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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Therapeutic choices for benign liver tumours have changed over the last 20 years. From 1975 to December 1993, we observed 145 hemangiomas (HMG) (57.2% females-mean age 47.3 years, 42.8% males-mean age 50.4 years): we resected 42 symptomatic hemangiomas: mortality rate was 2.3%. 93 HMG without symptoms were only followed-up: 5 of these increased in size and were resected. 27 symptomatic cases over 50 focal nodular hyperplasia (FNH) were resected, 7 cases were resected and 3 biopsied during laparotomy performed for other pathology. Postoperative mortality was nil. 13 cases were only followed-up after diagnosis by imaging techniques and fine needle biopsy: over a mean period of 23 months. No variations have been recorded. Increases in GGT and ALP were present respectively in 34% and 22% of FNH-cases. Scintigraphic techniques were the most diagnostically accurate (96.2%). All 16 hepatocellular adenomas (HCA) were removed (11 females, 5 males), postoperative mortality was nil: oestrogen administration was present in 36.4% of female cases, histological diagnosis v/s well differentiated hepatocellular carcinoma was difficult in 2 cases, whilst 3 cases had spontaneous rupture. We resected also 8 cases of biliary adenomas in order to determine a precise diagnosis v/s liver metastases, and 4 biliary cystadenomas for their malignant potential. Asymptomatic HMG and FNH for their low tendency to increase, can be only observed, whilst HCA must be fully resected for risk of bleeding and misdiagnosis v/s well differentiated hepatocellular carcinoma.
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PMID:[The therapeutic strategy in benign liver tumors: a 20-year experience]. 802 71

This paper is a study to identify the clinical significance of high-molecular-mass alkaline phosphatase (ALP:E:C..3.1.3.1.), ALP-lipoprotein-X complex (LP-X) and intestinal variant ALP. We used cellulose acetate and agarose gels and techniques including wheat germ lectin, cetavlon-diethyl ether, thermostatability, neuraminidase and L-phenylalanine to improve the electrophoretic separation of the alkaline phosphatase isoenzymes. Patients' serum samples were electrophoresed from a diverse group of individuals ill with cholestasis, neoplastic disease metastatic to the liver, hepatocellular carcinoma, cirrhosis, diabetes mellitus, and chronic renal disease. Agarose gels provided better separation of ALP isoenzymes than cellulose acetate gels. The results also indicated that high-molecular mass ALP is present in patient's serum in conditions associated with cholestasis especially caused by hepatic malignancy. High-molecular mass ALP was frequently found to co-exist with the liver isoenzyme and LP-XALP complex. The intestinal variant was identified in patients with malignancy, cirrhosis, chronic renal disease and diabetes mellitus. Intestinal ALP coexisted concomitantly with a variant intestinal ALP. Intestinal variant ALP is most likely composed of intestinal ALP attached to a cellular membrane-binding domain, or may be an artifact produced by neuraminidase incubation.
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PMID:Clinical significance of serum high-molecular-mass alkaline phosphatase, alkaline phosphatase-lipoprotein-X complex, and intestinal variant alkaline phosphatase. 804 46

Several biochemical events accompany and mediate the development of chronic liver disease and its evolution into cancer. Low plasma zinc and high copper levels have been observed in various liver diseases, such as liver cirrhosis and viral hepatitis, while increased oestradiol levels have been documented in chronic liver damage and hepatocellular carcinoma. We administered CCL4 intragastrically to 10 female Sprague Dawley rats for 30 weeks. All animals developed cirrhosis and four also developed hepatocellular carcinoma. Plasma levels of zinc, copper and oestradiol were significantly higher in the latter group than in animals with simple cirrhosis. Progesterone, AST and bilirubin showed a trend toward significant differences whereas testosterone and ALP levels were unchanged. These findings add to the evidence that sex hormones and trace elements are involved in the process of the development of chronic liver damage and carcinogenesis.
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PMID:Sex hormones and trace elements in rat CCL4-induced cirrhosis and hepatocellular carcinoma. 835 89

We examined the prevalence of TT virus (TTV) infection in non-B, non-C, non-G chronic liver disease, in particular, in hepatocellular carcinoma (HCC), and the clinical significance of TTV infection. Among 829 cases with chronic liver disease, 30 cases (4%) had non-B, non-C, non-G chronic liver disease. The percentage of TTV-DNA positive cases among these 30 cases with non-B, non-C, non-G chronic liver disease was 57% (17/30), significantly higher than the percentage TTV-DNA positivity (14%; 5/107) among blood donors (P < 0.01). All the TTV-DNA positive cases were still positive for TTV-DNA throughout the follow-up period (4 +/- 2 years; 1-7 years), thus demonstrating that TTV infection is persistent. These findings suggest that TTV may be one of the causes of non-B, non-C, non-G chronic liver disease. When the 30 cases of non-B, non-C, non-G chronic liver disease were divided into a TTV-DNA positive group and TTV-DNA negative group and the clinical data between the two groups compared, it was found that the serum ALP and serum gamma-GTP levels in some cases in the TTV-DNA positive group were higher than those in the TTV-DNA negative group. Twelve cases of non-B, non-C, non-G HCC were divided into two groups (TTV-DNA positive and TTV-DNA negative), and the clinical data between the two groups compared. All the four cases of HCC which were not associated with liver cirrhosis were TTV-DNA positive. However, with respect to the age at the time of onset of the HCC, no significant differences were noted between the cases of HCC associated with liver cirrhosis and those not associated with liver cirrhosis. In spite of older patients, many cases of HCC associated with TTV infection are not associated with liver cirrhosis.
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PMID:[The prevalence of TTV infection in non-A to G chronic liver disease, especially non-A to G hepatocellular carcinoma, and the clinical significance of TTV infection]. 1039 Sep 98

The effect of dietary administration of cholic acid on tumorigenesis in the liver was investigated in male Fischer-344 rats after carcinogenic initiation by diethylnitrosamine (DEN); progression of liver tumors was examined in the rats fed 0.4% cholic acid-containing diet (CA group) and the rats fed standard diet (C group) at 15, 20 and 25 weeks after administration of DEN. The total bile acids and cholic acid in serum of CA group were 150 nmol/ml and 117 nmol/ml, being 31-fold and 51-fold higher than those in C group (p<0.0001, each). Serum AST and ALT were significantly higher in CA group than in C group at 15 weeks (p<0.01). Serum ALP was significantly higher in CA group than C group at each time point (p<0.01, each). Liver tumors, whose histology was hepatocellular carcinoma, developed at 15 weeks in both CA and C groups. However, tumor volume and tumor weight were significantly increased in CA group, compared to those in C group at each time point (p<0.001, p<0. 001, p<0.01, p<0.001, p<0.01 and p<0.05). The percentage of apoptotic cells in CA group at each time point was significantly lower than C group (p<0.05, p<0.01 and p<0.05). The percentage of bcl-2 positive tumor cells in C group at 20 weeks was 1.88+/-2.59%. However, it dramatically increased to 34.00+/-13.67% in CA group (p<0.0001). It was also higher in CA group than in C group at 15 and 25 weeks (p<0.05 and p<0.01). In addition, the bax-positive cells were higher in CA group than in C group at 20 weeks (p<0.05). These data suggest that oral administration of cholic acid promotes liver tumorigenesis initiated by DEN through reducing apoptosis mediated by overexpression of bcl-2.
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PMID:Oral administration of cholic acid promotes growth of liver tumors initiated by diethylnitrosamine in rats. 1040 35

We measured serum PIVKA-II concentrations in 18 patients with alcoholic liver cirrhosis. Alcoholic liver disease was diagnosed by the history of ethanol intake of more than 900 ml/day for over 10 years. Liver cirrhosis was diagnosed histologically. Infections with hepatitis B and C viruses were ruled out by assaying serum virus markers. No tumor was detected in liver by ultrasonography and computed tomography during observation period. None of the patients studied were positive for alpafetoprotein (AFP). Eight out of 18 (44.4%) patients with alcoholic liver cirrhosis showed elevated serum PIVKA-II levels. In contrast, only eight out of 93 (8.6%) patients with nonalcholic liver cirrhosis had elevated serum PIVKA-II levels. PIVKA-II is well known as a tumor marker of hepatocellular carcinoma (HCC). The rates of positive PIVKA-II found in alcoholic liver cirrhosis approached its rates in HCC. However, the time course for the elevation of serum PIVKA-II levels was different each other in alcoholic liver cirrhosis and HCC. In HCC, serum PIVKA-II "levels" continued to elevate until therapy. In contrast, its elevation was transient and its levels returned to baseline in alcoholic liver cirrhosis. The values of ALT (GPT), gamma-GTP, and ALP correlated poorly with serum PIVKA-II levels in patients with alcoholic liver cirrhosis. To investigate the mechanism by which elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis occurred, we studied the effect of vitamin K on production of PIVKA-II and AFP by hepatocytes. Hepatocytes(Alexander PLC/PRF/F cell line) were cultured in the presence of various concentrations of vitamin K (Kaytwo, Eisai, Tokyo). Vitamin K had no effect on AFP production. In contrast, PIVKA-II production was inhibited by addition of vitamin K in a dose dependent manner. Moreover, elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis was suppressed by administration of vitamin K (Kaytwo) to these patients. Taken together, these results suggest that vitamin K may have a role in the mechanism of PIVKA-II elevation in sera of these patients. Then, we measured serum concentrations of vitamin K(PK, MK-4, MK-7) in these patients. There was no correlation observed between vitamin K and PIVKA-II in these patients. This result suggests that elevation of serum PIVKA-II in these patients may not be due to vitamin K deficiency. One question not answered here is how serum PIVKA-II levels in these patients are suppressed by treatment with vitamin K (Kaytwo). More detailed analysis of the mechanism of elevation of serum PIVKA-II levels in patients with alcoholic liver cirrhosis is needed.
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PMID:[Studies on the mechanism of elevation of serum PIVKA-II levels in alcoholic liver cirrhosis]. 1198 59

Nineteen monoclonal antibodies (MAbs) against tissue-nonspecific (liver/bone/kidney) alkaline phosphatase (TNALP) were investigated in the ISOBM TD-9 Workshop. These MAbs were generated with antigens obtained from human bone tissue (n = 9), human osteosarcoma cell lines (SaOS-2 and TPX; n = 7) and human liver tissue (n = 3). The evaluation included the following antigen forms: (a) commercially available preparations of human bone ALP (BALP) and liver ALP (LALP); (b) human BALP isoforms, B/I, B1 and B2; and (c) soluble secreted epitope-tagged recombinant human TNALP (setTNALP) expressed in COS-1, osteosarcoma (SaOS-2) and hepatoma (Huh2) cell lines. In addition, 16 TNALP mutant cDNAs corresponding to a wide spectrum of reported hypophosphatasia mutations were used in an attempt to map specific immunoreactive epitopes on the surface of the TNALP molecule. The TD-9 MAbs were evaluated by immunoradiometric (IRMA) assays, cross-inhibition and different enzyme immunoassay designs. No indications of explicit tissue discriminatory immunoreactivities of the investigated MAbs against TNALP were found. However, certain IRMA combinations of MAbs increased the specificity of BALP measurements. All MAbs bound to the three BALP isoforms B/I, B1 and B2, but none of the investigated MAbs were specific for any of the isoforms. Significant differences were, however, found in immunoreactivity between these isoforms, with cross-reactivities ranging from 21 to 109% between the two major BALP isoforms B1 and B2. Desialylation with neuraminidase significantly increased the MAb affinity for the BALP isoforms B/I, B1 and B2, and also decreased the observed differences in cross-reactivity between these isoforms. We suggest, therefore, that the MAb affinity is dependent on the amount/number of terminal sialic acid residues located at the five putative N-glycosylation sites. Based on the overall results, we present a putative three-dimensional model of the TNALP molecule with positioning of the four major antigenic domains (designated A-D) of the investigated MAbs. The TNALP molecule is depicted as a homodimer, hence most, but not necessarily all, epitopes are displayed twice. The antigenic domains were positioned with the following assumptions: domain A was positioned close to the active site since most of these MAbs interfered with the catalytic activity. Interestingly, both MAbs included in the commercial BALP kits were grouped with domain A. Moreover, 4 of the 5 putative N-glycosylation sites (with terminal sialic acid residues) are located within, or with close proximity to, domain A. Domain B was localized at the top flexible loop (crown domain) of the TNALP molecule. Domain C was clearly defined by the IRMA assay combinations and by site-directed mutants of TNALP to be close to residue E281, which is located near the fourth metal binding site, likely to be occupied by a calcium ion. Domain D was positioned close to residues A115, A162 and E174, but this domain was also close to the GPI anchor site. In conclusion, none of the 19 investigated TD-9 MAbs were entirely specific for BALP or LALP, thus indicating that all MAbs bind mainly to epitopes on the common protein core of BALP and LALP and/or common glycosylated epitopes. However, some MAbs (either single or in combination with other MAbs) work sufficiently well to measure BALP when the assayed samples do not contain elevated levels of LALP.
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PMID:Monoclonal antibodies against tissue-nonspecific alkaline phosphatase. Report of the ISOBM TD9 workshop. 1249 79

Ninety individuals (76 males and 14 females) were classified into four groups. G1 (Control) included 20 healthy individuals. G2 (Chronic hepatitis) included 20 patients, G3 (Liver cirrhosis group) included 30 patients, and G4 (HCC) included 20 patients with HCC. All groups were subjected to clinical examination, abdominal ultrasonography, complete blood picture, HCV antibodies, HBs Ag, and function tests (total and direct bilirubin, total plasma proteins and albumin, prothrombin time and concentration, and liver enzymes AST, ALT and ALP). Patients of G3 & 4 were classified according to Child-Pugh classification into A. B and C. Upper endoscopic examination was done for 36/50 patients with chronic hepatitis or HCC. Circulating VEGF levels were determined by ELISA. There was a statistically high significant levels of circulating VEGF in G1, 2 & 3 than in the controls. A statistically significant higher level of circulating VEGF in G4 than in G3 & G4, and a statistically negative significant between VEGF levels and platelet count in G2. No significant correlation between VEGF and the grade of esophageal varices in G3 & G4. and no significant correlation between VEGF and upper GIT bleeding or spider naevi (vascular skin changes) in G2. A statistically significant was in correlation between VEGF and degree of hepatic dysfunction.
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PMID:Vascular endothelial growth factor level in chronic liver diseases. 1251 23

There are many molecular tumor markers for diagnosing and monitoring cancer patients. Especially, quantitative assay for serum levels of tumor markers; such as AFP, CEA, PSA, hCG, CA 19-9 and CA 125, are frequently used in daily practice because of their relative specificities and usefulness to the common cancers. Though not suitable for early diagnosis, but they are used in monitoring patients with advanced caner, especially after treatments. Two of them, AFP and PSA, are also used in the screening and monitoring of high-risk groups, namely patients with chronic viral hepatitis and old male, who are the high risk for hepatoma and proste cancer respectively. Problems in using serum markers are; relatively low specificity and low sensitivity to cancer, confusing naming for similar markers that recognize almost the same molecule of cancer. Users must understand that CA 19-9, CA 50, KM-O 1 and SPAN-1 are in the same sialylated Lewis A group, and CA 125, CA 130 and CA 602; in the mucin antigen group, and STN, CA 54/61 and CA 72-4; in the sialyl Tn antigen group. Combination of two or more markers may inform us the biological characteristics of the cancer. For example, a germ-cell tumors may produce hCG and placental marker. That is of the choriocarcinoma type. Those with hCG and fetal antigens are the ordinal type of germ cell tumors, and those with AFP, CEA and cytokeratin are teratoma, and those with LDH and ALP only but negative for hCG and AFP must be seminoma. For the bronchial and alveolar carcinomas, CEA, SCC, NSE and cytokeratin 19 fragments are useful. Combination may be difficult for beginners but once understood, it will be an art in clinical oncology.
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PMID:[Clinical usefulness of circulating tumor markers]. 1527

The presence of high-molecular intestinal alkaline phosphatase (HIALP) different from bone ALP detected in the alpha(2)beta region was recently clarified. In this study we used a novel method in which HIALP was detected after conversion to ALP(5) by protease to investigate the clinical significance of the appearance of HIALP in patients with chronic liver disease. The subjects were 241 patients with chronic liver disease. When a decrease in ALP(3) in the alpha(2)beta region and an increase in ALP(5) in the beta region were noted, the patient was judged HIALP-positive. In the patients with chronic liver disease, the total ALP activity (T-ALP) increased with progression of the pathology in the order of chronic hepatitis (CH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). HIALP appeared in 22.4% and 49.3% of patients with CH and LC, respectively, but the positivity rate decreased to 30.4% in HCC. As autoimmune liver diseases, primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH) were investigated. T-ALP was lower in PBC+AIH than in LC and HCC, but the HIALP-positive rate was high (44.4%). The HIALP-positive rate was dependent on ABO blood groups, and was high in blood groups B and O. In conclusion, the HIALP-positive rate was particularly high in patients with chronic liver disease, and was related to the pathological progression, which suggests that the method is clinically useful.
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PMID:High-molecular intestinal alkaline phosphatase in chronic liver diseases. 1750 85

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