Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the role of insulin-like growth factor II (IGF-II) in the development of hepatocarcinoma (HCC), the expression of IGF-II, IGF-II receptor (IGF-IIR) and HBxAg in HCC was studied with immunohistochemistry (PAP method). Meanwhile DNA ploidy and S-phase fraction of hepatocytes were analyzed with flow cytometry. The results were as follows: (1) IGF-II, IGF-IIR and HBxAg showed positive staining simultaneously in the tumor tissues of 93% (n = 15) of the HCC cases with chronic liver disease and with positive evidence of HBV; (2) The mean S-phase incidence in tissues of IGF-II positive HCC was 28.6 +/- 6.4%; this was higher than 12.8 +/- 2.4% in the IGF-II negative tumors (P < 0.05); (3) The incidence of DNA-aneuploidy in IGF-II positive liver tissues was 100% (10/10); this was higher than 60% (6/10) in IGF-II negative liver tissues (P < 0.05). It is suggested that IGF-II might play an important role in the development of HCC when there is evidence of HBV and chronic liver disease involvement. IGF-II positive staining HCC have increased proliferative activity as compared with IGF-II negative staining tumors.
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PMID:[A study of the relationship between expression of IGF-II, IGF-IIR, HBxAg and the DNA ploidy, cell cycle of hepatocytes in hepatocarcinoma]. 760 Aug 62

Surgical specimens from 27 patients with hepatocellular carcinoma (HCC) were studied by in situ hybridization with 3H-labelled HBV DNA probe for detecting HBV DNA and by immunohistochemical staining (PAP) for HBsAg and HBcAg on formalin-fixed, paraffin-embedded sections respectively. The positive rate of HBV DNA was 74.07% (20/27) in the peritumor liver tissues and 48.15% (13/27) in the tumorous tissues. HBV DNA was found mainly in the cytoplasm of the hepatocytes and cancer cells, and very few in the nucleus. HBV DNA granules were more in the cytoplasm than in the nucleus, and HBV DNA positive cells were much more in the peri-tumor tissues than in the tumor tissues. These results show that most of the HCC cases selected were closely associated with the infection of HBV. HBV DNA in the peri-tumor tissues might be of the replicative form, while in the cancerous tissues, it might be of the integrated form. The relationship between HBV DNA and HBsAg, HBcAg in the liver tissues is discussed.
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PMID:[Detection of hepatitis B virus DNA in hepatocellular carcinoma by in situ hybridization]. 839 39

A case of a 62 year old Japanese woman with an endometrial adenocarcinoma producing alpha-fetoprotein (AFP) is described. Microscopically, the tumour was composed of a major medullary portion and a minor tubular adenocarcinoma which had invaded the myometrium, the myometrial lymphatics and blood vessels. Neoplastic cells in the medullary portion were polygonal with glycogen-rich cytoplasm. Vascular permeation by neoplastic cells was prominent. Extensive hepatoma-like features were observed. The tumour cells lacked features suggestive of a diagnosis of embryonal carcinoma or endodermal sinus tumour. The production of AFP by the tumour cells was demonstrated immunohistochemically using the PAP technique. Only two cases of AFP producing endometrial adenocarcinomas have been reported previously.
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PMID:Alpha-fetoprotein production by a hepatoid adenocarcinoma of the uterus. 870 61

Pancreatitis-associated protein I (PAP I) is a secretory protein first described as an acute phase reactant during acute pancreatitis. Recently, induction of the PAP I gene was also described in liver during hepatocarcinogenesis. To investigate the molecular mechanisms of this induction, we used constructs carrying progressive deletions of the PAP I promoter fused to the CAT gene. We showed that the silencer conferring tissue specificity on the PAP I gene was inactive in hepatoma cells. Then, in an vitro transcription system, we compared the transcription capacity of nuclear extracts from normal liver and HepG2 cells on constructs containing the silencer. The results confirmed that a trans-acting factor interacting with the PAP I silencer was present in liver cells and absent from hepatoma cells. On the other hand, immunohistochemistry showed that PAP I was expressed in a limited number of transformed hepatocytes. It was concluded that expression of PAP I in hepatocarcinoma occurred through inactivation of its silencer element and was not concomitant in all malignant cells. On that basis, we assayed PAP I in serum from patients with chronic hepatitis, liver cirrhosis or hepatocarcinoma. PAP I levels were normal in chronic active or persistent hepatitis, significantly higher in cirrhosis and strongly elevated in hepatocarcinoma. Because those clinical entities often develop in that sequence, serum PAP I appeared as a potential marker of hepatocarcinoma development.
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PMID:Mechanism of PAP I gene induction during hepatocarcinogenesis: clinical implications. 895 91

We have established the phenotype of a colorectal tumor by partial sequencing of 2166 transcripts that were eventually arrayed on high-density filters. These filters were used for differential screening with mRNAs of colorectal cancer and normal adjacent mucosa to characterize genes whose expression is altered in colorectal carcinoma. Three genes encoding related proteins, PAP, reg Ialpha and reg Ibeta, were over-expressed in cancer. Northern-blot analysis confirmed that their expression was very low in normal colonic epithelial cells, but elevated in 75% of tumors. Western blotting with specific antibodies to pap and reg Ialpha revealed in tumors a single band of the expected size ( 15-16 kDa), demonstrating synthesis of the proteins. Pap was localized by immunohistochemistry to the cytoplasm of epithelial cells. In cancerous tissue, many cells showed a strong staining signal, but the proportion of stained cells was variable among patients. In normal mucosa, staining was light and restricted to a few cells scattered in the epithelium. Similar results were obtained with antibodies against reg Ialpha. No significant relationship was found between concentrations of pap, reg Ialpha or reg Ibeta and clinical outcome. We looked at potential effectors of pap/reg gene over-expression by testing, in 2 adenocarcinoma cell lines, the efficacy of the pap promoter at driving a reporter gene; strong induction was observed upon exposure to IFNgamma and IL-6. By analogy with observations in hepatocellular carcinoma, our results suggest that prevention of PAP/reg expression in normal colon cells by silencing their gene promoters is relieved during colon carcinogenesis, allowing their up-regulation by mediators such as cytokines.
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PMID:pap, reg Ialpha and reg Ibeta mRNAs are concomitantly up-regulated during human colorectal carcinogenesis. 1032 17

We originally isolated the HIP/PAP gene in a differential screen of a human hepatocellular carcinoma cDNA library. This gene is expressed at high levels in 25% of primary liver cancers but not in nontumorous liver. HIP/PAP belongs to the family of C-type lectins and acts as an adhesion molecule for hepatocytes. In normal adult human tissues, HIP/PAP expression is found in pancreas (exocrine and endocrine cells) and small intestine (Paneth and neuroendocrine cells). In order to gain insight into the possible role of HIP/PAP in vivo, we have investigated the pattern of HIP/PAP expression in the developing postimplantation mouse embryo by in situ hybridization. Detailed analysis of developing mouse embryos revealed that HIP/PAP gene exhibits a restricted expression pattern during development. Thus, HIP/PAP transcripts are first observed within the nervous system from day 14.5 onwards in trigeminal ganglia, dorsal root ganglia, and spinal cord where it appears to be an early specific marker of a subpopulation of motor neurons. At laster stages, HIP/PAP transcripts were detected in intestine and pancreas at day 16.5 but not in embryonic liver. This highly restricted expression pattern suggests that HIP/PAP might participate in neuronal as well as intestinal and pancreatic cell development.
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PMID:HIP/PAP gene, encoding a C-type lectin overexpressed in primary liver cancer, is expressed in nervous system as well as in intestine and pancreas of the postimplantation mouse embryo. 1032 12

Human HIP/PAP is an adhesion protein expressed in normal pancreatic and Paneth cells and overexpressed in hepatocellular carcinoma. HIP/PAP was crystallized using the Hampton Research Crystal Screen and SAmBA software to define the optimal crystallization protocol. The crystals belong to the orthorhombic space group P2(1)2(1)2(1), with unit-cell parameters a = 30.73, b = 49.35, c = 92.15 A and one molecule in the asymmetric unit. Flash-frozen crystals diffract to 1. 78 A resolution using synchrotron radiation. A molecular-replacement solution was obtained using the human Reg/lithostathine structure and the AMoRe software.
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PMID:Crystallization and preliminary crystallographic study of HIP/PAP, a human C-lectin overexpressed in primary liver cancers. 1041 4

Hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) gene was identified because of its increased expression in 25% of human hepatocellular carcinoma. HIP/PAP protein, a C-type lectin, binds laminin, acts as an adhesion molecule for hepatocytes, and has also been described as an acute phase secretory protein during acute pancreatitis in humans and rats. We investigated HIP/PAP protein expression in patients with various liver diseases associated with ductular reaction. At the same time, we analyzed patients with hepatocellular carcinoma and cholangiocarcinoma, and tested HIP/PAP protein levels in sera to establish the pattern of secretion. Our data show that HIP/PAP expression was not restricted to hepatocellular carcinoma, but was also detected in cholangiocarcinoma cells as well as in reactive non-malignant bile ductules. In contrast, HIP/PAP protein expression was undetectable in normal mature hepatocytes, but some ductular cells localized at the interface of portal tracts with parenchyma were HIP/PAP immunoreactive in normal liver. Finally, we present evidence that HIP/PAP serum levels were increased in 21/28 (75%) patients with hepatocellular carcinoma, and in 25/51 (49%) patients with nonmalignant cirrhosis. Altogether, these results suggest that HIP/PAP protein may be implicated in hepatocytic and cholangiolar differentiation and proliferation.
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PMID:Hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) is expressed and secreted by proliferating ductules as well as by hepatocarcinoma and cholangiocarcinoma cells. 1055 Mar 9

In a review of 79 cases of gall bladder malignancy, nineteen cases were labelled as unusual tumors while sixty were diagnosed as adenocarcinoma. Alcian blue, PAS, Grimelius' and Masson trichrome stains were done. Expression of EMA, CEA and desmin was assessed (PAP). Histological subtype was revised, in eleven cases out of 19. Five tumors initially diagnosed as squamous cell carcinoma were found to be positive for mucin and CEA and hence were reclassified as adenosquamous carcinoma. Three undifferentiated carcinomas and two malignant carcinoids were labelled as adenocarcinoma and composite tumor respectively. Positive reactivity with CEA and alcian blue PAS and absence of AFP helped in differentiating one giant cell carcinoma from hepatocellular carcinoma. No definite marker could be identified in one case of malignant mesenchymal tumor. Histochemistry and immunohistochemistry also helped in confirming the diagnosis of three cases of carcinoma in situ, one of malignant carcinoid and three of clear cell carcinoma.
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PMID:Diagnostic distinction between unusual malignant tumors of gall bladder by histochemistry and antigenic phenotype. 1063 74

The present study attempts to shed more light on the role of hepatocarcinoma-intestine-pancreas/pancreatic associated protein (HIP/PAP) in hepatoma cells. We initially examined, by reverse transcription-polymerase chain reaction (RT-PCR), the HIP/PAP transcripts present in human hepatoma cell lines of different origins and with different grades of differentiation and genetic profiles. We also used DNA sequencing analysis to investigate the structure of the HIP/PAP gene. Further investigation is necessary to define the role of HIP/PAP during the development of human hepatocellular carcinoma and to ascertain whether the use of different transcripts is helpful in regulating HIP/PAP expression in transformed liver cells.
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PMID:Expression of HIP/PAP mRNA in human hepatoma cell lines. 1209 28


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