Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present paper reviews several studies performed between 1977 and 1986 in Singapore on the 10-year survival outcome of treatment for stage I and II hepatocellular carcinoma (HCC). Of 801 HCC patients evaluated, only 2 survivors (0.3%) remained in complete remission for 13 and 14 years, respectively. One had received four weekly cycles of prednisolone, Adriamycin, vincristine and 5-fluorouracil for an inoperable HCC with a 10-cm diameter, and the other had received localised synchronised hepatic irradiation and Adriamycin. As follow-up, the use of localised hepatic irradiation consisting of 131I-labeled (30 mCi) iodised oil in lipiodol infused via the hepatic artery appeared to benefit patients with small residual tumours but did not affect larger tumours measuring 2 cm in diameter. Prophylactic, intermittent long-term administration of lymphoblastoid interferon-alpha (Wellferon) was carried out in pre-cancerous, high-risk hepatitis B surface antigen (HBsAg)-positive patients with cirrhosis, in immediate male relatives of liver cancer patients, and in persons who had undergone hepatic resection. In the untreated group, 10/162 (6%) cirrhotics, 3/18 (17%) male family members, and 6/10 (60%) post-resection cases developed single or multiple HCCs within 1 year of screening done at 3-month intervals on the basis of alpha-fetoprotein (AFP) levels and real-time hepatic ultrasonography. In contrast, none of the Wellferon-treated group consisting of 518 cirrhotic patients, 82 male relatives of HCC patients and 20 post-resection cases developed HCC. Two HBsAg-positive individuals who had not been treated with interferon (IFN) developed hepatic nodules which that showed dysplasia, AFP elevation and chromosomal changes. These studies demonstrate the poor results of late diagnosis and show that early intervention and prophylaxis with Wellferon can reduce the incidence of HCC in high-risk persons. In addition, transhepatic chemoembolisation and liver resection are suitable methods for treating small HCCs (single or multiple) that are detected by screening. However, some of these early-detected HCCs remain highly malignant. Prophylactic treatment of pre-cancerous conditions appears to be a better option as a long-term programme for HCC.
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PMID:Long-term survival following treatment of hepatocellular carcinoma in Singapore: evaluation of Wellferon in the prophylaxis of high-risk pre-cancerous conditions. 133

To our knowledge, there has been only one report pertaining to the efficacy of HCFU for treatment of metastatic lung lesion of HCC, so we reported a case of HCC with lung metastasis which responded to chemotherapy with a single use of HCFU. A 64-year-old male was diagnosed as having HCC with lung metastasis by biochemical examination, abdominal CT, hepatic arteriogram and chest X-P. He had been treated previously with gamma-interferon and mitoxantrone, which were assessed as NC and PD, respectively. Two months after last chemotherapy, HCFU was administrated at a dose of 400 mg/body everyday for 8 months. After 4 weeks metastatic lung lesions showed remarkable regression (47% decrease) and disappeared completely 9 weeks later. The size of primary liver tumor gradually decreased during therapy and revealed marked improvement (85.7% decrease) after about 2 months of this therapy. During these periods serum levels of alpha-fetoprotein dropped from 430 ng/ml to less than 10 ng/ml. He is presently still alive and the duration of the PR attained to 35 weeks. As side effects, hypoproteinemia, anorexia and hot sensation were observed.
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PMID:[A case of hepatocellular carcinoma (HCC) with lung metastasis which responded to chemotherapy with a single use of 1-hexylcarbamoyl-5-fluorouracil (HCFU)]. 253 6

We investigated the expression of intercellular adhesion molecule 1 (ICAM-1) in ex vivo human hepatocellular carcinoma (HCC) cells and in vitro in eight liver cancer cell lines, including six HCC cell lines and two combined hepatocholangiocarcinoma (CHC) cell lines. Immunohistochemistry showed the expression of ICAM-1 on the HCC cell surface with honeycomblike appearance in most cases (96.2%). On the other hand, hepatocytes in noncancerous areas did not express ICAM-1, except those hepatocytes in the periportal and intra-acinar areas with inflammation. Immunohistochemical study on cultured cells revealed that four cultured HCC cell lines and one CHC cell line constitutively expressed ICAM-1 on the cell surface and in the cytoplasm. Flow cytometric analysis revealed that immunostain-positive cells expressed surface ICAM-1 with more than a 90% positive cell rate, and their expressions were upregulated by incubation of cells with inflammatory cytokines, such as interferon alfa, interferon gamma, tumor necrosis factor-alpha, and interleukin 1 beta. Soluble ICAM-1 was detected in supernatants of cell lines expressing cell surface ICAM-1 expression, and was increased in amounts 2- to 20-fold by inflammatory cytokines. These findings suggest that liver cancer cells in ex vivo may express not only surface but also a soluble form of ICAM-1, differently from normal hepatocytes, and that both expressions are upregulated by inflammatory cytokines.
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PMID:Expression of intercellular adhesion molecule 1 in human hepatocellular carcinoma. 748 78

The cytotoxicity of 5-fluorouracil (5-FU) has been related to its incorporation into RNA and blocking of DNA synthesis. Interferon may enhance the therapeutic efficacy of 5-FU in colorectal cancer. In a model of secondary liver cancer in the rat, the incorporation of 5-FU into the acid-soluble fraction (ASF), RNA and DNA of several normal tissues and the tumor was determined. The liver nucleotide profile and NADPH-cytochrome c reductase activity was examined. A therapeutic dose of 5-FU was given for 2 h via the hepatic artery and the rats were killed 1 h later. Half of them were pretreated with the interferon inducer polyinosinic-polycytidylic acid (poly(I)-poly(C) and interferon. Pretreatment increased the nucleotide (NT)/DNA and RNA/DNA ratios, decreased the cellularity and left the specific RNA labelling unchanged in the bone marrow. In the liver the pretreatment decreased the NT/DNA and RNA/DNA ratios, (F)UTP, and the NADPH-cytochrome c reductase activity. The 5-FU incorporation into liver DNA decreased. No changes were found in the tumor. The pretreated rats decreased in body weight. A decreased RNA synthesis in the liver might indicate a decreased 5-FU metabolism, explaining the increased 5-FU AUC in the clinic at interferon treatment.
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PMID:Interferon and the incorporation of 5-fluorouracil into RNA of normal tissues and a secondary liver carcinoma in rat. 751 19

The neuroendocrine-differentiated colonic carcinoma cell line (LCC-18) was transplanted to 29 nude mice (Balb/c). The purpose of the present study was to establish an animal model that would allow monitoring with magnetic resonance imaging (MRI) of changes induced by interferon (IFN) therapy and to evaluate whether the therapeutic response, as expressed by changes in MR signal characteristics and tumour proliferation activity, could be modulated by different IFN dosages. IFN did not seem to have any obvious antiproliferative effect on the LCC-18 tumour cell line transplanted to nude mice and no convincing treatment-related changes in rho values or T1 and T2 relaxation values were observed. The animal model was probably unsuitable for demonstration of IFN effects.
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PMID:Interferon treatment of neuroendocrine tumour xenografts as monitored by MRI. 752 88

Chronic viral hepatitis is prevalent worldwide in the pediatric population and can be associated with significant morbidity and mortality. Acquisition of disease in early childhood may predispose children to long-term complications, including cirrhosis and HCC. Efforts should be made to recognize, control, and prevent further spread of these infections, especially in areas where hepatitis is endemic. Alpha interferon therapy hastens disease remission in a proportion of patients with chronic hepatitis B. Further studies are needed to define the role of interferon in chronic HDV and HCV infection in children.
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PMID:Management of chronic viral hepatitis in children. 763 78

Clinically, acute hepatitis C is an asymptomatic disease in up to 90% of cases. Transaminases fluctuate characteristically. Anti-HCV (RIBA-II) and HCV-RNA (PCR) are diagnostic early in the course of the disease. The risk of chronification is high, exceeding 50% of cases, irrespective of disease transmission (parenterally or sporadic). Alpha-interferon is applicated in pilot-studies to reduce the risk of chronification, with varying results. Chronic hepatitis C is an insidious disease. Again, most cases are asymptomatic. Bilirubin is normal. GPT-activity tends to fluctuate during the course. Anti-HCV and HCV-RNA can be detected in serum. About 20% of cases progress to cirrhosis (and HCC) after a long-lasting disease (20 to 30 years after infection). Alpha-Interferon therapy is successful in about 25% of patients.
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PMID:[Hepatitis C: clinical aspects, course and therapy]. 793 55

Viral causes of acute or chronic hepatitis are the hepatitis A virus [HAV], the hepatitis B virus [HBV], the hepatitis C virus [HCV], the hepatitis delta virus [HDV], and the hepatitis E virus [HEV]. These viruses haven been characterized in great detail and can be detected by specific and sensitive serological or molecular assays. While HAV and HEV cause only acute hepatitis, infection with HBV, HCV or HDV frequently takes a chronic course. With time chronic viral hepatitis can progress to liver cirrhosis and its clinical sequelae as well as to hepatocellular carcinoma [HCC]. Apart from prophylactic measures aimed at the prevention of these viral infections, for those chronically infected natural or recombinant alpha-interferon may be a therapeutic option with the potential to prevent the development of liver cirrhosis and HCC.
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PMID:[Viral hepatitis A to E--diagnosis, clinical aspects and therapy]. 794 Apr 9

A review of the histopathology and demonstration of alpha-interferon with a monoclonal anti-alpha-interferon antibody reagent were carried out in 71 consecutive cases of acute and chronic hepatitis, and also in some cases of cirrhosis and HCC. The main cells expressing alpha-interferon were lymphocytes, plasma cells, fibroblasts and polymorphonuclears. There was no evidence for local alpha-interferon production near the site of virus replication in hepatitis B infection. Eleven cases of hepatitis were positive for alpha-interferon. The carrier state showed the highest positive rate in the different types of hepatitis. The positive rate in acute and chronic persistent hepatitis was lower than that in carrier state but higher than that in cirrhosis and HCC. The alpha-interferon positive cells were mainly located in the portal area and in the fibrotissue band around the necrotic and/or carcinomatous cells. These suggest that the function of the interferon system was related mainly to the pathological changes of liver tissue. Early use of interferon might be of therapeutic value to protect liver tissue from injury and to improve the interferon response of the host.
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PMID:[Detection of alpha-interferon positive cells in liver tissue from patients with hepatitis]. 839 41

Hepatitis C affects at least 200 million people worldwide. It can be followed by chronic hepatitis, cirrhosis, and primary liver cancer. Outcome assessments in controlled trials of antiviral therapy are based on serum transaminase values, serum HCV-RNA determinations, and liver biopsy scores. Patients most likely to respond to antiviral treatment are relatively young, have low serum HCV-RNA and transaminase levels, and do not have cirrhosis. Patients whose disease is caused by genotype 1b HCV isolates are unlikely to respond. Interferon alfa (3 million units [MU] three times a week for 6 months) is associated with a 50% response rate and a 50% relapse rate--an overall response rate of 25%. Increasing the duration of therapy may increase the sustained response rate. Ribavirin, given orally, may be used for patients who fail to respond to or relapse after interferon therapy. Its side effects are few. Treatment results in a fall in transaminase levels and some decrease in hepatic inflammation, but serum HCV RNA (viral titer) is unaltered. Combinations of interferon with ribavirin are giving promising results with increased sustained, complete responses.
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PMID:Antiviral therapy for chronic hepatitis C viral infection. 872 Feb 86


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