Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sialyltransferase activity was measured in plasma samples using desialated fetuin as the acceptor and cytidine 5'-phosphate-sialic acid as donor. The data show an increased enzyme level in 56 of 65 cancer patients studied, as compared with normal control values. The enzyme was not significantly elevated during lacation or in liver cirrhosis, but it was elevated in rheumtoid arthritis. Of the patients with cancer, 35 showed plasma enzyme levels above any value encountered in rheumatoid arthritis plasmas. The determinants of enzyme level in cancer appear to be complex: monitoring of plasma sialytransferase may be of value in measuring tumor progression, metatastatic involvement, or success of therapeutic programs.
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PMID:Elevated plasma sialyltransferase in the cancer patient. 116 8

DNA stemlines of hepatocellular carcinoma (HCC) model of adult Wistar rats established by diethylnitrosamine were quantitatively measured by flow cytometry. The cancer-inducing course was divided into four stages, eg, precirrhosis stage, cirrhosis stage, early cancer stage and cancer progression stage. The advantageous DNA stemline of hepatocytes of normal adult Wistar rats was tetraploid (4C). It was from the cirrhosis stage that atavistic proliferation of hepatocytes with diploid (2C) DNA stemline started and replaced 4C hepatocytes, resulting in a new advantageous population. The features of early cancer stage were formation of HCC with 2C DNA stemline, whereas during the cancer progression stage, HCC cells with aneuploid (AN) DNA stemline presented the advantageous growth. The study clearly shows the change pattern of DNA stemline during the course of hepatocarcinogenesis from 4C-2C-AN, which is believed to be the biokinetic mechanism of the development and progression of HCC.
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PMID:Characteristic changes of DNA stemlines during hepatocarcinogenesis in rats. 145 56

Twenty-three patients with unresectable hepatocellular carcinoma were given doxorubicin 60 mg/m2 I.V. day 1 and streptozotocin 0.5 g/m2 I.V. days 1-5 every 3 weeks. This regimen was chosen because of the activity of doxorubicin and nitrosoureas in hepatocellular carcinoma and the ability to administer both drugs in full doses. Twelve patients were fully ambulatory, 14 had normal serum bilirubin, 11 had pathologic proof of cirrhosis, and 11 had no known extrahepatic tumor dissemination. Partial responses lasting 10 and 14 months occurred in two patients (9%), one had stable disease for 15 months, 12 had documented tumor progression within 4 months, and eight died within 6 weeks of the start of chemotherapy. Median survival of all patients was only 3 months (range 0.3-27), but eight (35%) lived more than 1 year. Of these eight, two responded to doxorubicin and streptozotocin, another two to subsequent chemotherapy, and four had no tumor response whatever. More than 90% of the intended doses of doxorubicin and streptozotocin was administered, with severe leukopenia in three patients, moderate thrombocytopenia in one, and moderate proteinuria in nine. There were no drug-related deaths. Various physical, radiologic, and biochemical parameters were employed in detecting tumor response and progression. Initially abnormal physical examination of the liver, hepatic radionuclide and computed tomographic (CT) scans, and serum alpha-fetoprotein levels improved in both responding patients. Tumor progression was detected by physical examination (7/12), radionuclide (10/12) and CT liver scan (3/7), rising alpha-fetoprotein (5/12), and rising carcinoembryonic antigen (3/8). Physical examination and radionuclide liver scan together documented all tumor response and progression. The combination of doxorubicin and streptozotocin has only modest activity in hepatocellular carcinoma and appears no more active than doxorubicin alone.
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PMID:Combination chemotherapy of hepatocellular carcinoma with doxorubicin and streptozotocin. 631 Sep 86

Proteoglycans are macromolecules containing a core protein to which glycosaminoglycan chains are covalently attached. The family contains several members with different structures and various functions. Some of them are elements of the extracellular matrix, while others are located to the cell surface playing important role in cell-cell and cell-extracellular matrix interactions. Present paper discusses the possible consequences of the alterations of proteoglycans observed in liver cirrhosis and liver tumors. It has to be emphasized however, that they are also involved in the pathomechanism of arteriosclerosis, Alzheimer-disease, immune diseases, arthritis, tumor progression and metastasis formation.
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PMID:[Proteoglycans (their structure, function and role in liver diseases)]. 841 46

Growing evidence indicates that lysosomal Cathepsins D (CD), B (CB) and L (CL) may promote carcinogenesis and tumor progression. Therefore, we evaluated their potential value as biochemical parameters of malignant progression in patients with benign diseases which may undergo malignant transformation, such as liver cirrhosis (LC) and chronic pancreatitis (CHP) as well as in hepatocellular carcinoma (HCC) and pancreatic cancer (DPC). CD, CB and CL serum levels were determined by immunoenzymatic assays in LC, CHP, HCC or DPC patients and correlated with a number of biochemical and clinical parameters of these diseases. CD serum levels were increased in LC, CHP and HCC, but not in the DPC group as compared to normal subjects (NS) (P < 0.01). Interestingly, higher levels of this enzyme were observed in LC patients compared to HCC patients ( P < 0.01). CB serum concentrations were increased in all patient groups (P < 0.01). However no difference was evidenced between benign and malignant diseases. CL serum levels were significantly increased only in DPC as compared to NS (P < 0.01) or CHP patients (P < 0.02) and in HCC as compared to NS (P < 0.01). The evaluation of CD, CB and CL serum pattern in LC, CHP, HCC and DPC patients may be useful as additional biochemical parameters in the differential diagnosis and therapeutic monitoring of these diseases. Prospective clinical investigations to assess the potential value of these enzymes as biochemical markers of malignant progression of LC or CHP are warranted by the present data.
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PMID:Cathepsin D, B and L circulating levels as prognostic markers of malignant progression. 869 62

Two different processes appear to be involved in the initiation of hepatocarcinogenesis by chronic hepatitis B virus (HBV) infection and by chronic hepatitis C virus (HCV) infection. Initiation of hepatocellular carcinoma (HCC) by chronic HBV infection usually occurs early in life; most patients have had onset of HBV infection before the end of childhood, although rare cases of HCC have been reported following HBV infections acquired in adulthood. In contrast, HCV-associated HCC in many cases probably develops after a chronic HCV infection that was acquired during adulthood. HBV-DNA usually is integrated in the tumor DNA of HBV-associated HCC; it produces two proteins that can transactivate known oncogenes in vitro and that theoretically could affect genes at distant sites in vivo. HCV is a nonintegrating virus and no transactivating HCV proteins have been identified so far. In the later stages of hepatocarcinogenesis, "tumor promotion" and "tumor progression," HBV-associated HCC may share certain features with those of HCV-associated HCC. Chronic inflammation and cirrhosis, accompanied by regenerative processes, may function as a tumor promoter, providing a common pathway from chronic HBV or HCV infection to HCC. Tumor progression may be brought about in HCC by mutations of the p53 tumor suppressor gene. Mutations of this gene are common in HCCs, and they are found more often in advanced human HCCs than in small, well-differentiated HCCs. The prevalences of p53 mutations are similar in HBV-associated and HCV-associated HCCs (30-50%). Even in the absence of a p53 mutation, the functions of normal p53 can be inactivated as a result of binding by viral or by cellular proteins. It is not known yet whether this type of binding contributes to the development of HCC, but p53 binding by the HBV X protein in vitro has been reported. Abnormalities of the RB tumor suppressor gene also have been found frequently in HCC patients, particularly in HCCs that contain p53 mutations.
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PMID:Hepatocarcinogenesis: hepatitis viruses and altered tumor suppressor gene function. 887 20

Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections lead to cirrhosis and increase the risk for the development of hepatocellular carcinoma (HCC). Angiogenesis is an essential step in oncogenesis and contributes to tumor progression in adult organs; however, to what extent angiogenesis occurs in the liver during chronic viral hepatitis has not been studied. Ninety-nine matched patients affected by chronic hepatitis due to either HBV or HCV were studied together with 13 controls (5 patients were affected by familial hyperbilirubinemia with normal liver histology; 6 patients with stage II primary biliary cirrhosis; and 2 patients with pseudo inflammatory tumor). Microvessel density was assessed in liver biopsies by immunostaining using two different antibodies against endothelial cell antigens, QB-END/10 and Factor VIII. In addition, the liver homogenates and sera of HCV- or HBV-positive patients and controls were tested for their capacity to stimulate the migration and proliferation of freshly isolated human endothelial cells in vitro. Evidence of angiogenesis was significantly more frequent in HCV-positive patients compared with HBV-infected subjects or controls (74% vs. 39% vs. 8%) (chi2 = 20.78; P < .0001) (HCV+ vs. HBV+ vs. controls). The degree of microvessel density was also higher in HCV- than in HBV-positive patients or controls (chi2 = 12.28; P < .005). In addition, HCV-positive sera and liver homogenates stimulated a higher migration and proliferation of human endothelial cells in vitro compared with HBV-positive or control sera and liver homogenates. These observations indicate that angiogenesis is particularly linked to HCV infection, suggesting a possible contribution to HCV-related liver oncogenesis.
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PMID:Chronic viral hepatitis induced by hepatitis C but not hepatitis B virus infection correlates with increased liver angiogenesis. 898 96

We report an autopsy case of hepatocellular carcinoma (HCC) with sarcomatous change arising in the context of primary biliary cirrhosis (PBC) in a 79-year-old man. Primary biliary cirrhosis was diagnosed (stage I according to Scheuer's classification) by findings on blood biochemical analysis, laparoscopy, and liver biopsy at age 69 years. Five years later, (at age 74 years), a mass lesion was detected in the S6 region of the liver by abdominal ultrasonography, and target biopsy revealed well differentiated HCC. Blood biochemistry, ultrasonography, and computed tomography findings showed that the PBC had progressed to stage IV (cirrhotic stage). Percutaneous ethanol injection therapy (PEIT) was administered to the HCC several times over a 5-year period; however, the patient died of liver failure in February, 1994 (at age 79 years). Viral markers for hepatitis B and C were negative during the course, and hepatitis C virus RNA was not detected by polymerase chain reaction. Autopsy findings showed liver cirrhosis and diffuse involvement of spindle-shaped sarcomatoid cells in the liver, particularly in the S6 region, associated with several nodules of trabecular HCC cells. A zone of transition between the sarcomatoid cells and the trabecular hepatocellular carcinoma cells was observed. The sarcomatoid cells were diffusely disseminated in the peritoneal cavity and had metastasized to multiple organs. Immunohistochemically, the cells were positive for fibrinogen, as were the coexisting trabecular hepatocellular carcinoma cells. The HCC had been treated several times with PEIT. Of interest, PEIT may be an important factor in this type of tumor progression.
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PMID:Hepatocellular carcinoma with sarcomatous change arising in primary biliary cirrhosis. 905 2

In our experience, the primary obstacle precluding the widespread use of orthotopic liver transplantation (OLT) for definitive therapy of hepatocellular carcinoma (HCC), even for early-stage disease, is preventing tumor recurrence. Chemoembolization is an attractive strategy to minimize tumor progression before OLT because of its shown antitumor effect, ability to be repeated, and minimal systemic toxicity. Thus, this pilot study was undertaken to determine the tolerability and treatment outcomes of pretransplantation chemoembolization of HCC followed by OLT. Between 1992 and 1997, 27 patients with HCC who had cirrhosis, no extrahepatic metastasis, less than three tumor nodules of less than 5 cm each, and no evidence of vascular invasion on preoperative imaging studies were enrolled onto the protocol. Chemoembolization was performed using Ivalon particles with mitomycin, doxorubicin, and cisplatin. Twenty-four patients completed the protocol with chemoembolization and a liver transplant. The mean United Network of Organ Sharing waiting time was 167 days. Chemoembolization was well tolerated. On examination of the explanted liver, the majority of patients had a single lesion, mean tumor size was 3.66 cm (range, 1.5 to 6 cm), and the majority of patients had stage II disease. None of the transplant recipients has developed recurrent HCC (mean follow-up, 29.2 months; range, 9 to 55 months). The 1- and 2-year disease-free survival rates are 91% and 84%, respectively. In conclusion, chemoembolization followed by OLT is well tolerated and associated with excellent outcomes in selected patients with HCC.
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PMID:Preoperative hepatic artery chemoembolization followed by orthotopic liver transplantation for hepatocellular carcinoma. 1022 9

Hepatitis C virus (HCV) is pathogenetically involved in many cases of hepatocellular carcinoma (HCC) worldwide. HCV-related HCC is on the rise in many developed countries as a consequence of past infections with HCV. The time lag between HCV infection and cancer development is several decades. HCV-related tumors arise in older patients, are almost invariably associated with cirrhosis, and often have a less aggressive course than HCC related to other etiologic factors. In most patients, HCC grows as a single hepatic node for years before generating satellite or distant tumor nodes. However, there are tumors that originate as multifocal disease. Tumor progression and hepatic failure are the leading causes of death in most patients. HCV has been almost invariably detected in tumor tissue of anti-HCV patients with HCV, but it is not clear whether the virus promotes cancer through chronic hepatocellular inflammation, which is per se an important risk factor for HCC, or has a direct role in liver carcinogenesis. No reverse transcriptase activity has been found in infected livers, but there are data suggesting that HCV has oncogenic properties, because its interacts with cellular genes regulating cell growth and differentiation.
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PMID:Hepatitis C virus and hepatocellular carcinoma. 1051 6


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