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)

The levels of serum somatomedin peptides were determined with a somatomedin A radioreceptor assay utilizing human placental membranes. Low levels were found in 25 patients with liver cirrhosis and 28 patients with chronic hepatitis with the mean of 0.47 +/- 0.05 and 0.60 +/- 0.04 U/ml, respectively. There was a positive correlation between somatomedin A on one hand and serum albumin, cholinesterase, total cholesterol and thrombotest on the other. There was a negative correlation between somatomedin A and the indocyanine green retention test. These findings confirm earlier results obtained with bioassay.
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PMID:Serum somatomedin peptides measured by somatomedin A radioreceptor assay in chronic liver disease. 91 86

In this study we investigated the regulation of insulin-like growth factor II gene expression to explain a role for this growth factor in concert with hepatitis B virus involvement in the development of hepatocellular carcinoma from cirrhosis. Sections of normal liver and tumor and non-tumor-bearing liver disease tissue were hybridized in situ with [35S]-labeled insulin-like growth factor II oligonucleotide probe. Parallel sections were tested for presence of insulin-like growth factor II polypeptide using immunohistochemistry. To investigate a possible role for hepatitis B virus in insulin-like growth factor II gene expression in hepatocellular carcinoma, results were analyzed against patient seropositivity for hepatitis B virus. Levels of insulin-like growth factor II transcripts in normal liver (n = 4) sections and in those from non-tumor-bearing individuals (n = 10) were so low that specific signal was not detectable above homogeneous tissue background. In contrast, 4 of 8 (50%) of the sections of hepatocellular carcinoma arising from cirrhosis or noncirrhotic chronic liver disease with hepatitis B virus involvement showed increased expression of insulin-like growth factor II messenger RNA transcripts. Up-regulation was observed in cell foci in the hepatocellular regions of the surrounding cirrhotic lobular cells and the fibrous septa. Numerous cell foci were observed in patch distribution in the tumor areas. The level of insulin-like growth factor II messenger RNA transcripts in sections of hepatocellular carcinoma arising from cirrhotic and noncirrhotic tissues obtained from patients seronegative for hepatitis B virus was similar to that of normal liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of insulin-like growth factor II gene expression by hepatitis B virus in hepatocellular carcinoma. 184 51

We investigated insulin-like growth factor II (IGF-II) mRNA in three groups of human liver samples including primary liver cancers, benign liver tumors and cirrhosis; indeed these pathological conditions would allow us to distinguish between different steps in liver carcinogenesis. A 40- to 100-fold increase in IGF-II mRNA was shown in 9/40 of the liver cancer samples as compared to normal adult liver. RNA blot analysis using both IGF-II cDNA and oligonucleotide probes showed the reexpression of two fetal (6 and 5 kilobases) IGF-II transcripts in primary liver cancers and in some cirrhotic adjacent tissues; these included all the samples with enhanced IGF-II expression. By contrast the adult (5.3 kilobases) IGF-II transcript was identified in most of the benign liver tumors and liver cirrhosis; in addition, in some of these samples, the 5-kilobase fetal transcript was also detected. The increase of IGF-II mRNA in some liver cancers is consistent with an autocrine mechanism conferring a selective growth advantage to tumorous liver cells. Furthermore, these results indicate a differential expression of IGF-II transcripts in nonmalignant hepatocyte proliferation (benign liver tumors and cirrhosis) as compared to liver cancer. Finally this study suggests that, in liver cirrhosis and in some benign liver tumors, premalignant proliferative states might be identified by the presence of IGF-II fetal transcripts.
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PMID:Differential expression of insulin-like growth factor II mRNA in human primary liver cancers, benign liver tumors, and liver cirrhosis. 318 92

In the present study we investigated the expression of transforming growth factor alpha and insulin-like growth factor II to explain the role of these growth factors in the development of hepatocellular carcinoma from chronic active hepatitis B and cirrhosis. The expression of transforming growth factor alpha and insulin-like growth factor II was tested in 38 tissue samples from patients with chronic active hepatitis B, 32 cirrhosis and 31 hepatocellular carcinoma, by immunohistochemical staining using monoclonal anti-transforming growth factor alpha and anti-insulin-like growth factor II. All patients were seropositive for HBsAg. Transforming growth factor alpha was expressed in 26 (68.4%) of 38 chronic active hepatitis B, 18 (56.3%) of 32 cirrhosis and 16 (51.6%) of 31 hepatocellular carcinoma tissue samples. Transforming growth factor alpha was found in the periportal hepatocytes of chronic active hepatitis B and in regenerating hepatocytes of cirrhotic nodules. In hepatocellular carcinoma tissues, transforming growth factor alpha-containing tumor cells were evenly distributed within the tumor tissues but focal distribution limited to a part of tumor tissues was also observed. The expression of insulin-like growth factor II was observed in 30 (93.8%) of 32 cirrhosis and all the 31 hepatocellular carcinoma tissue samples tested, but not in chronic active hepatitis B samples. Insulin-like growth factor II was expressed in most hepatocytes of regenerating nodules and in tumorous as well as non-tumorous hepatocytes of hepatocellular carcinoma tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential expression of transforming growth factor alpha and insulin-like growth factor II in chronic active hepatitis B, cirrhosis and hepatocellular carcinoma. 760 79

In this study we investigated the expression of insulin-like growth factor II (IGf-II) to explain a role for this growth factor in concert with hepatitis B virus (HBV) involvement in the development of hepatocellular carcinoma (HCC) from chronic hepatitis type B (CAH-B) and liver cirrhosis (LC). The expressions of IGF-II and HBsAg were tested in tissue samples from 38 patients with CAH-B, 32 with LC, and 31 with HCC, by immunohistochemical staining using monoclonal anti IGF-II and anti HBs. All patients were seropositive for the presence of HBsAg. The expression of IGF-II was observed in 30 out of 32 (93.8%) LC and all 31 (100%) HCC tissue samples tested. IGF-II was expressed in most hepatocytes of regenerating nodules and in tumorous as well as nontumorous cells of HCC tissues. Neither normal liver tissues nor CAH-B tissue samples expressed IGF-II. HBsAg was expressed in 34 out of 38 (89.5%) CAH-B, 24 out of 32 (75%) LC and 13 out of 31 (41.9%) HCC tissue samples. The expression sites of HBsAg were not correlated with those of IGF-II in any tissue samples tested. The present study indicates that IGF-II plays a role in cell proliferation of regenerating nodules as well as in the development of hepatocellular carcinomas. In addition, there was no direct evidence of HBV involvement in the overexpression of this growth factor.
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PMID:Expression of insulin-like growth factor II in chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma. 766

Expression of insulin-like growth factor II in two human hepatocellular carcinoma cell lines and in hepatitis B, cirrhosis and hepatocellular carcinoma in 419 cases were investigated, and its relationship with the expression of hepatitis B virus X gene was studied by means of immunohistochemical and electron microscopic techniques. The results demonstrated that hepatocellular carcinoma cells (SMMC 7721 and QGY 7703) in culture could express insulin-like growth factor II. Expression seemed to be regulated by cell density, which was suggested as the molecular basis of the contact inhibition of cell proliferation. In tissue sections, cells with high expression of insulin-like growth factor II were observed not only in hepatocellular carcinoma (93%) but also in 95% of the pericancerous liver tissues, 72% of cirrhotic livers, 64% of chronic active hepatitis and 37% of chronic persistent hepatitis. In most cases of hepatocellular carcinoma, insulin-like growth factor II was localized in the cytoplasm of the cancer cells. In the benign liver disorders, four types of cells that highly expressed insulin-like growth factor II were observed: (a) a kind of small liver cell we named the small polygonal liver cell; (b) multinuclear giant hepatocytes; (c) hepatocytes in most of hyperplastic and neoplastic nodules, small hepatocyte nodules and some of regenerative nodules; and (d) some proliferating ductular cells. Even more interestingly, insulin-like growth factor II expression was shown to be closely related to the expression of hepatitis B virus X gene product. We suggest that the activation of insulin-like growth factor II gene and its overexpression may be a crucial step in the processes of hepatitis B virus-associated hepatocarcinogenesis and that the X gene product may activate the insulin-like growth factor II gene through a transactivation mechanism. In addition, we studied the characteristics of small polygonal liver cells, and the roles they may play in the regeneration and carcinogenesis of hepatitis B virus-infected liver are discussed.
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PMID:Expression of insulin-like growth factor II in hepatitis B, cirrhosis and hepatocellular carcinoma: its relationship with hepatitis B virus antigen expression. 792 18

It has recently been reported that insulin-like growth factor II (IGF-II) may play a role in the pathogenesis of hepatocellular carcinoma (HCC). We studied the relationship between the expression of IGF-II and fatty change in human small HCC using immunohistochemical staining techniques. Liver biopsy specimens were obtained from 35 patients with HCC (consisting of 15 patients with fatty change and 20 patients without fatty change). All patients had serum markers for the hepatitis C virus (HCV) and histological findings obtained from non-tumourous lesions showed liver cirrhosis or chronic active hepatitis. Immunohistochemical staining was performed using a monoclonal antibody against rat IGF-II. A positive immunoreaction was found in 69% (24/35) of HCC. Insulin-like growth factor II was immunodetected in 80% (12/15) of HCC with fatty change but only in 60% (12/20) of those without fatty change. In most cases, IGF-II was not found in hepatocytes from non-tumourous lesions. We believe this to be the first time that IGF-II has been detected immunohistochemically in small HCC derived from HCV infection. This growth factor was more frequently immunodetected in HCC with fatty change than without. As insulin is an essential factor for the metabolism of fatty acids, IGF-II may play an important role in both fatty degeneration and in the proliferation of HCC cells. Furthermore, immunohistochemical IGF-II staining may contribute to the diagnosis of HCC, particularly in early stages accompanied by fatty change.
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PMID:Immunohistochemical evidence of insulin-like growth factor II in human small hepatocellular carcinoma with hepatitis C virus infection: relationship to fatty change in carcinoma cells. 914 39

Necrolytic migratory erythema is characterized by waves of irregular erythema in which a central bulla develops, and subsequently erodes and becomes crusted. It usually occurs in patients with an alpha-islet cell tumor of the pancreas. However, necrolytic migratory erythema has also been observed in patients without an associated glucagonoma. We describe a woman with iatrogenic necrolytic migratory erythema. She received intravenous glucagon for hypoglycemia associated with an insulin-like growth factor II-secreting hemangiopericytoma. After chemotherapy, she developed necrolytic migratory erythema. The characteristics of the previously reported patients with nonglucagonoma-associated necrolytic migratory erythema are reviewed. In patients with nonglucagonoma-associated necrolytic migratory erythema, the dermatosis-related conditions most commonly observed were celiac disease or malabsorption, cirrhosis, malignancy, and pancreatitis; less common conditions included hepatitis, inflammatory bowel disease, heroin abuse, and odontogenic abscess. Although the pathogenesis of necrolytic migratory erythema remains unknown, hyperglucagonemia appears to have had a causative role in the development of this dermatosis in our patient. Patients who develop necrolytic migratory erythema should be evaluated for the presence of a glucagonoma; if a glucagonoma is ruled out, evaluation for other conditions known to occur with necrolytic migratory erythema, such as liver disease, malabsorptive disorders, and nonislet-cell tumors is warranted.
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PMID:Iatrogenic necrolytic migratory erythema: a case report and review of nonglucagonoma-associated necrolytic migratory erythema. 959 6

The P3 promoter of the human insulin-like growth factor II (IGF-II) is the major IGF-II promoter in fetal liver (FL) and hepatocellular carcinoma (HCC). However, little information is available on the transcriptional factors (TFs) controlling IGF-II gene expression in human liver cirrhosis (LC) and HCC tissues. To evaluate the protein-binding patterns in the P3 promoter region, we performed electromobility shift assay (EMSA) and DNase I footprinting assay using nuclear extracts from human FL, LC and HCC tissues. EMSA showed considerable differences in binding patterns of proteins to P3 promoter region according to different nuclear extracts used in this study. By footprinting assay, eight footprints were observed in extracts. In addition, LC extract showed two specific binding at L1 [-80:+30] and L2 [-126:-80] regions, and HCC showed two specific binding at H1 [-176:-120] and H2 [-210:-177] as well as two liver specific binding (L1 and L2). Footprinting after immunoprecipitation indicates that Egr1, Egr2 and Sp1 could bind to P3 promoter directly, while c-jun and c-fos could not bind to these region directly. Further study is required to determine the function of these proteins.
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PMID:Different protein-binding patterns in the P3 promoter region of the human insulin-like growth factor II gene in the human liver cirrhosis and hepatocellular carcinoma tissues. 961 Jun 18

A feature of hepatocellular carcinoma (HCC) is that antecedent liver cirrhosis and chronic hepatitis are common precursor conditions and during transition to malignancy some patients develop autoantibodies which were not present during the preceding chronic liver disease phase. Serum samples from such patients can be used to immunoscreen cDNA expression libraries to identify genes encoding the new autoantigens. We demonstrate here the de novo appearance of antibodies to p62, a cytoplasmic protein which has been shown to bind to a developmentally regulated fetal species of insulin-like growth factor II (IGF-II) mRNA. Another antibody appearing during the transition period was against CENP-F, a cell cycle-related nuclear protein with maximum expression in the G2 and M phases of the cell cycle and previously shown to have a high association with malignancy. In three additional patients in whom serial serum samples were examined, new appearance of anti-p62 was detected in two patients and anti-CENP-F in one patient. This study demonstrates that transition to malignancy can be associated with autoantibody responses to certain cellular proteins which might have some role in tumorigenesis.
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PMID:De-novo humoral immune responses to cancer-associated autoantigens during transition from chronic liver disease to hepatocellular carcinoma. 1147 19


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