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

Hepatocyte growth factor (HGF) gene therapy may have potential for treating chronic hepatitis (CH) and liver cirrhosis (LC). However, the lack of an HGF gene therapy study on hepatomas that are often associated with CH or LC, together with the stimulatory effects of HGF on many types of cancer, may hamper its application. This study explored the effects of adenoviral HGF gene transduction and their mechanisms on two types of hepatoma cells (hepatoblastoma and hepatocellular carcinoma) in in vitro experiments. Both types of hepatomas were revealed to have higher adenoviral gene transduction efficiencies and more efficient expressions of the HGF transgene, which successfully activated the HGF receptor/c-Met in an autocrine fashion, than those of other types of cancer. Notably, not only HGF, but also adenoviral infection, inhibited DNA synthesis, whereas only HGF but not adenoviral infection exerted a potent apoptotic effect. Moreover, adenoviral HGF gene transduction additively exerted inhibitory effects on cisplatin-treated hepatomas. In conclusion, inhibitory and apoptotic effects of adenoviral HGF gene transduction in hepatomas in contrast to potent mitogenic and antiapoptotic effects of HGF for hepatocytes are not only of biological interest, but also pose clinical benefits for adenoviral HGF gene therapy for CH and LC.
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PMID:Adenoviral gene transduction of hepatocyte growth factor elicits inhibitory effects for hepatoma. 1594 46

End-stage liver cirrhosis because of metabolic or infectious diseases predisposes to hepatic malignancies like hepatocellular carcinoma. We report the first case of hepatoblastoma incidentally detected in the explanted liver of a 2-yr-old child undergoing liver transplantation for cirrhosis because of progressive familial intrahepatic cholestasis (PFIC). The diagnosis was difficult to obtain. The hepatoblastoma was not seen on ultrasound examination of the cirrhotic liver. As we could confirm retrospectively, alpha fetoprotein (AFP) was found elevated prior to transplantation. Two years after successful transplantation, there are no signs of malignancy detectable by clinical and radiological methods. We conclude from this case that PFIC may induce hepatoblastoma and that children with liver cirrhosis should undergo routine screening of serum AFP concentration.
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PMID:Hepatoblastoma in a child with progressive familial intrahepatic cholestasis. 1685 6

Hepatoblastoma (HB) rarely occurs in adults. We report herein the unusual case of a 19-year-old, otherwise healthy woman with no history of liver disease who presented with upper abdominal pain and hepatomegaly. Tests for hepatitis B virus (HBV), hepatitis C virus (HCV) were negative, and AFP was normal. There was no evidence of liver cirrhosis. A welldemarcated solid mass of 14 cm in diameter, which was lobulated and partly necrotic, was detected in the liver by computed tomography (CT). At surgical exploration a large liver mass was detected occupying the entire right lobe. A right trisegmentectomy was performed with tumor grossly resected with microscopic residual disease (i.e positive margins). On microscopic examination the tumor was composed mainly of two components which were intermingled: epithelial and mesenchymal elements. The epithelial component was formed of small embryonal cells, grouped into nodules, scattered in cellular mesenchymal tissue. The diagnosis was mixed hepatoblastoma. The patient received 4 cycles of systemic chemotherapy with cisplatinum and adriamycin. Post-chemotherapy evaluation revealed recurrence of the hepatoblastoma in the remaining liver. She died 6 months later.
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PMID:Hepatoblastoma in adult age. A case report and literature review. 1706 Aug 78

This prospective study analyzes the clinical features and histopathological findings in liver biopsies of pediatric patients presenting to the hospital with liver disease during a 10 year period. Only those patients in whom liver biopsy was performed for a tissue diagnosis were included. Fifty patients were investigated, all below the age of 12 years, of whom 36 were male and 14 female. Thirty-two were of neonatal-infantile group, 11 had a diagnosis of neonatal giant cell he hepatitis of infections origin and an intact biliary tree. Two had septic shock and one had leishmaniasis. The remaining 18 patients of the neonatal-infantile group constituted five case of glycogen storage disease, six of infantile obstructive cholangiopathy (biliary atreasia), four of fatty change and one each of congenital hepatic fibrosis, neuroblastoma and nonspecific reactive hepatitis. The eighteen older children had the following diagnoses: thalassemia in five, sickle cell disease in four, two each of Reye syndrome and hepatoblastoma. The remaining were one each of glycogen storage disease, Rotor syndrome, cirrhosis, fatty change and non-Hodgkin lymphoma (NHL). These findings are presented and discussed.
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PMID:Pediatric liver disease in the eastern province of Saudi Arabia: A clinicopathological study. 1758 93

Chylous ascites are the accumulation of chylomicron-rich lymphatic fluid within the peritoneal cavity, resulting from obstruction or disruption of abdominal lymphatic channels. This rare condition may be associated with neoplastic or infectious infiltration of lymphatics, with pancreatitis, and with abdominal surgery. It may occur spontaneously in 0.5% of patients with cirrhosis; but only among a few liver transplantation cases. The management of chylous ascites is controversial; the variety of described treatments include repeated paracentesis, dietary control, peritoneovenous shunting, and surgical ligation of the disrupted lymphatic channels. In this article, we report 2 cases of rapid resolution of chylous ascites after liver transplantation following 5 days of treatment using a somatostatin analog and total parenteral nutrition (TPN). A 3.5-year-old girl and a 5-year-old girl underwent living related liver transplantation for biliary atresia and hepatoblastoma, respectively. Chylous ascites, diagnosed by ascitic fluid examination, developed within the 2 weeks after transplantation in the 2 cases. Treatment by fasting, TPN, and somatostatin analog resulted in rapid resolution of the ascites within 1 week. The prevalence of chylous ascites was noted in 1.6% of children (2/119) after liver transplantation. These cases highlight the use of somatostatin analog and parenteral nutrition in chylous ascites after liver transplantation.
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PMID:Chylous ascites after living related liver transplantation treated with somatostatin analog and parenteral nutrition. 1826 17

Hepatocellular carcinoma (HCC) is a major indication of liver transplantation (LT). For HCC accessible to conventional therapies, resection or radiofrequency ablation, 5-year survival is similar after LT or conventional therapy, although recurrence-free survival is better after LT. For the other cases, the Milan criteria (single nodule < 5 cm or no more than 3 nodules, less than 3 cm), limiting the risk of recurrence to 15%, are universally used. The "liver score", established by the french Agency of biomedicine, gives a national rank on the LT waiting list. It is a sum of components, including one based on the MELD score, evaluating the severity of cirrhosis (maximum 1000 points) and an HCC component (maximum 200 points). The liver score will be regularly revisited. A treatment is often necessary during the waiting period, if the waiting time may be longer than 6 months. Hepatoblastoma, cholangiocarcinoma and neuroendocrine metastases are marginal indications of LT. LT is possible in patients with a pasthistory of extrahepatic cancer. The risk of recurrence (or transformation of hemopathies) is lower than 5% at 10 years, probably because of the extensive selection made among these patients.
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PMID:[Liver transplantation for cancer]. 1914 43

Hepatoblastoma is a rare malignancy in adults. It is often diagnosed after the appearance of symptoms, therefore, the tumor size tends to be larger. In patients with no indication for a hepatic resection, the prognosis of adult hepatoblastoma is quite poor. A 54-year-old man with hepatitis C virus-associated liver cirrhosis was initially treated with a hepatic resection for a hepatic tumor, 3 cm in diameter. The tumor consisted of osteoid-like and cartilaginous foci, myxomatous stroma, and poorly differentiated hepatocellular carcinomatous cells and was diagnosed as a mixed epithelial and mesenchymal hepatoblastoma. Two years after the first operation, multicentric hepatocellular carcinomas developed in the remnant liver and were successfully treated with a secondary hepatic resection combined with radio-frequency ablation. The patient is now alive with no recurrence at 5 years after the initial hepatectomy. To the best of our knowledge, the primary hepatoblastoma was the smallest such tumor reported and this is the first report of a metachronous hepatoblastoma and hepatocellular carcinoma in an adult hepatitis patient.
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PMID:Occurrence of hepatocellular carcinoma after hepatoblastoma resection in an adult with hepatitis C virus. 1920 87

Fibrolamellar carcinoma is a rare primary malignant liver neoplasm that usually affects adolescents and young adults with no underlying liver disease. Morphologically, the tumor cells resemble oncocytic hepatocytes arranged in cords with a stroma of lamellated collagen fibers. Immunohistochemical studies have found that fibrolamellar carcinomas express markers associated with both biliary (CK7 and epithelial membrane antigen) and hepatocytic (heppar-1and glypican-3) differentiation, as well as markers associated with hepatic progenitor cells (CK19 and EpCAM) and stem cells (CD133 and CD44). Genetic studies show fewer alterations compared with classic hepatocellular carcinoma. Pooled data from comparative genomic hybridization studies show that fibrolamellar carcinomas have fewer and less frequent genomic alterations when compared with classic hepatocellular carcinoma, cholangiocarcinoma, and hepatoblastoma. Of the alterations seen in fibrolamellar carcinoma, the most frequent are gains in 1q and 8q (also frequently seen in other hepatic tumors) and loss of 18q. Fibrolamellar carcinoma also has less frequent methylation of tumor suppressor promoters compared with hepatocellular carcinoma and minimal alterations in mitochondrial DNA. Fibrolamellar carcinoma is associated with better survival than hepatocellular carcinoma and cholangiocarcinoma, presumably due to the young age of the patients and the lack of cirrhosis. These features make more aggressive surgical therapy possible. There is currently very little information on the effectiveness of chemotherapy for fibrolamellar carcinoma.
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PMID:Fibrolamellar carcinoma: a review with focus on genetics and comparison to other malignant primary liver tumors. 2134 51

The Golgi phosphoprotein GP73 is elevated in the circulation of individuals with a diagnosis of hepatocellular carcinoma. Its usefulness as a biomarker of HCC is questioned, since it has also been reported to be elevated in the circulation of people with liver cirrhosis. Regulation of GP73 by inflammatory cytokines is therefore of interest. The interleukin-6 (IL-6) family cytokines were tested for effects on GP73 mRNA and/or protein levels in human hepatoblastoma HepG2 cells. Levels of GP73 mRNA and protein were up-regulated in HepG2 cells following treatment with either proinflammatory cytokine IL-6 or the related cytokine oncostatin M (OSM). Induction required the shared receptor subunit gp130, and correlated with increased tyrosine phosphorylation of STAT3. Maximal cytokine-mediated induction was not observed in the presence of protein synthesis inhibitor cycloheximide, suggesting additional regulatory factors play an important role. ELISA measurement of GP73 and IL-6 levels in the sera of patients with pre-malignant liver disease revealed a significant correlation between circulating levels of the two proteins. Similarly, a sensitive ELISA assay was developed to measure circulating OSM. OSM levels were elevated 6-7 fold in sera from patients with either cirrhosis or HCC relative to controls without liver disease. Although there was an association between levels of GP73 and OSM in serum from people with liver cirrhosis, there was not a statistically significant correlation in HCC, suggesting that the role of the cytokines in determining circulating levels may be complex. To our knowledge, this is the first report of OSM elevation being associated with liver disease.
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PMID:Interleukin-6 and oncostatin M are elevated in liver disease in conjunction with candidate hepatocellular carcinoma biomarker GP73. 2314 54

A young man presented with a large liver mass and positive hepatitis B virus markers. This 18-year-old male has developed ascites, jaundice, high serum alpha fetoprotein (AFP) level, liver mass and portal hypertension, without fever or calcification in the mass. All favored the diagnosis of rapidly, progressive hepatocellular carcinoma, however proven hepatoblastoma in liver biopsy. Hepatoblastoma usually manifests prior to the third year of life, but can rarely be seen in older children or adults. Although HCC rarely can be presented in young patients with HBV infection, but in patients without cirrhosis hepatoblastoma should be considered as the first possible diagnosis.
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PMID:An 18-year-old man with hepatitis B virus infection and hepatoblastoma. 2482 53


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