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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

135 specimens of primary hepatic carcinoma (PHC) were formalin fixed and paraffin embedded and stained for Pre-S1, Pre-S2 and HBxAg by ABC method, for HBsAg and HBcAg by PAP method. The detection rates of Pre-S1 and Pre-S2 positive cases in cancerous tissues were 22.2% and 20.0%. The detection rates of Pre-S1 and Pre-S2 in non-cancerous liver tissues were 60.0% and 59.6%. The positive ratio of Pre-S1 and Pre-S2 in the same hepatoma was 16.3% and that in the same non-cancerous liver tissue was 55.6%. Among 135 cases of PHC, HBsAg, HBxAg and HBcAg positives in tumor tissues were 16.3%, 55.6% and 8.9%, respectively. Those in non-cancerous tissues were 59.6%, 78.8% and 24.2%. This study suggested that the detection rates of Pre-S1 and Pre-S2 positivity in hepatoma tissues were higher than those of HBsAg and HBcAg but lower than that of HBxAg. The frequency of positive Pre-S1 and Pre-S2 in non-cancerous liver tissues was similar to HBsAg, and slightly lower than that of HBxAg. S1 and S2 are considered new markers for HBV infection. Their antigens could play an important role in the pathogenesis of PHC.
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PMID:[Expression and significance of Pre-S1 and Pre-S2 in human primary hepatic carcinoma (PHC)]. 131 93

Specimens of 110 cases of primary hepatic carcinoma were obtained from the pathological Laboratory of the First Teaching Hospital of the 4th Military Medical University, Xi'an. P. R. China. Sections from formalin-fixed and paraffin-embedded material were stained for HBxAg by ABC method and for HBsAg and HBcAg by PAP method. Among the 110 cases of primary hepatic carcinoma, 64 (58.2%) showed HBxAg-positive reaction in tumor tissue, and 63 (78.8%) of 80 cases of noncancerous surrounding hepatic tissue displayed HBxAg positivity. Among 64 HBxAg-positive cases in tumor tissue, 15 (23.4%) were associated with HBsAg and/or HBcAg and among 63 HBxAg-positive cases in non-tumor tissue, 45 (71.4%) were associated with HBsAg and/or HBcAg. These findings suggested a close relationship between primary hepatic carcinoma and HBV infection. The high detection rate of HBxAg indicates very active expression of the integrated HBV-DNA genome in the host cells. However, how does HBxAg act in pathogenesis of hepatocellular carcinoma remains to be further investigated.
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PMID:[Immunohistochemical study on X antigen of HBV (HBxAg) in primary hepatic carcinoma]. 133 87

Studies were carried out to test the hypothesis that exposure to aflatoxin B1 (AFB1) is common among individuals with hepatocellular carcinoma (HCC) who are also chronically infected with hepatitis B virus (HBV). Experiments were also carried out to determine whether there is a close association between the presence of AFB1-DNA adducts and the expression of one or more HBV antigens in the tumor or non-tumor regions of the liver. Twenty-seven paired tumor and non-tumor liver tissues of HCC patients from Taiwan were analyzed. Monoclonal antibody 6A10, generated against the imidazole ring-opened persistent form of the major N-7 guanine adduct of AFB1, was used for adduct detection by both indirect immunofluorescence and competitive enzyme-linked immunosorbent assay. An avidin-biotin complex staining method was used for the detection of HBsAg and HBxAg in liver sections. A total of 8 (30%) HCC samples and 7 (26%) adjacent non-tumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent non-tumorous liver samples were positive while 9 (33%) HCC samples and 11 (41%) adjacent non-tumor liver samples were HBxAg-positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These results suggest that both AFB1 exposure and carrier status of HBsAg/HBxAg may be involved in the induction of HCC in Taiwan.
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PMID:Aflatoxin B1-DNA adducts and hepatitis B virus antigens in hepatocellular carcinoma and non-tumorous liver tissue. 172 Oct 8

Detection of HBxAg was done by the immunogold-silver staining technique in 22 liver cancer specimens from patients with hepatocellular carcinoma and positive markers of hepatitis B were found to express HBxAg of hepatitis B virus, which was distributed in the perinuclear cytoplasm. The result suggests that HBxAg can be detected practically in all the liver specimens of the patients with hepatocellular carcinoma, who had been infected by hepatitis B virus. The relationship between X gene and its translation product and hepatocellular carcinoma is discussed.
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PMID:[Detection of HBxAg in liver specimens of patients with hepatocellular carcinoma]. 196 3

Human hepatoma cells (HepG2 and HUH7) transfected with a plasmid (pHBV1004) containing the transcription units for the major surface antigen (S) mRNA and the X mRNA of hepatitis B virus (HBV) secreted surface antigen (HBsAg) into the culture medium. A frameshift mutation in the X gene carried by pHBV1004 greatly reduced HBsAg production by cells transfected with an equivalent amount of the mutant (pHBV1004-B). The mutation could be complemented by cotransfection with a plasmid (pSV2HBX) containing the X structural gene under control of the SV40 early promoter. HBsAg production by cells cotransfected with pHBV1004-B and pSV2HBX was equivalent to that in cells transfected with the parent plasmid (pHBV1004) alone. Levels of HBsAg production were directly related to the amount of S mRNA produced, showing that the X-gene product (HBxAg) can modulate expression of the S gene.
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PMID:Modulation of expression of the hepatitis B virus surface antigen gene by the viral X-gene product. 197 36

To clarify the significance of the X gene of hepatitis B virus, we have tested for anti-HBx in the serum and HBxAg in the liver at different stages of the natural history of hepatitis B virus infection. Sera were screened by enzyme-linked immunosorbent assay and positive results confirmed by immunoblot. Purified recombinant MS2 Pol-HBx fusion protein was used as target for both assays. Among serial sera of patients with nonfulminant acute hepatitis, 24 of 64 patients (37.5%) were positive for anti-HBx. In fulminant cases, 15 of 36 patients (42%) had anti-HBx. In chronic hepatitis patients with high rates of hepatitis B virus replication, we found a significantly (p less than 0.01) higher prevalence of anti-HBx, 14 of 25 patients (56%), than in those with low replication, 14 of 66 patients (21%), or among asymptomatic HBsAg carrier blood donors (20 of 126 = 16%) without detectable hepatitis B virus replication (p less than 0.0001). The highest prevalence of anti-HBx was found in HBsAg carriers with cirrhosis (41 of 54 patients = 76%) and/or with hepatocellular carcinoma (18 of 33 patients = 54%). The findings suggest that anti-HBx appears as a common and early marker of hepatitis B virus infection, transient in self-limited hepatitis but persisting with progression to chronicity. In chronic hepatitis, the prevalence of anti-HBx correlated with the intensity and duration of hepatitis B virus replication but neither with the severity of the liver disease nor with malignant transformation per se.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early and frequent detection of HBxAg and/or anti-HBx in hepatitis B virus infection. 225 44

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

The expressions of c-erbB-2 oncogene and epidermal growth factor receptor (EGFR) were investigated immunohistochemically in specimens from 184 cases of hepatitis B, cirrhosis and hepatocellular carcinoma (HCC) and 29 normal liver specimens. EGFR was expressed in 36% (48/134) of the hepatocellular carcinoma and chronic liver disorder specimens and it was immunolocalized mainly in the sinusoidal endothelial cells. No significant difference was found between EGFR expression in HCC and in benign chronic liver disorders. These results indicate that EGFR may have some role in the proliferation of the sinusoidal epithelial cells in chronic liver disease. Low level c-erbB-2 expression was observed in 5/29 (17%) of normal liver specimens. In chronic hepatitis B and liver cirrhosis, its expression was found in all specimens. c-erbB-2 protein was immunolocalized mainly in small polygonal liver cells (SPLCs) and hepatocytes in small-cell dysplasia (SCD) and in ductular metaplasia (DM); c-erbB-2 expression in HCC cells was found to be weaker than in SPLCs, the hepatocytes in SCD and in DM. These results indicate that activated c-erbB-2 oncogene may have a role in human HCC genesis through promoting the development of SCD from SPLC proliferation and the progression of SCD. The close relation between the expression of c-erbB-2 and HBxAg imply that the activation of c-erbB-2 in human liver tissues may be related to HBV X gene.
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PMID:[Expression of c-erbB-2 protein and EGF receptor in hepatitis B, cirrhosis and hepatocellular carcinoma]. 778 35

A mouse monoclonal antibody directed against hepatitis B virus (HBV) X protein (HBxAg) was prepared. The antibody was used to screen by immunohistochemistry 50 liver tissue sections from patients with hepatocellular carcinoma (HCC), and 15 patients with chronic active hepatitis (CAH). 28 of 50(56%) samples were HBxAg positive in tumor tissues. The positive rates of HBxAg only in tumor tissues or in adjacent nontumor tissues were 24% and 16%. HBsAg was detected in 16% of cases in tumor tissues and 74% in surrounding nontumor tissues. In CAH samples, the positive rates of HBxAg and HBsAg were 6.6% and 73.3%. HBcAg was only detected in nontumor surrounding liver tissues, the positive rates being 18%. In CAH samples, no HBcAg was detected. The results showed that HBxAg is a common marker in liver tissue from patients with HBV-related HCC. The findings of HBxAg in the absence of detectable HBsAg and HBcAg in the liver tissues suggested that HBxAg could be independent of HBV replication and implied that the synthesis of HBxAg may be directed from integrated HBV DNA templates. It is possible to use antiHBx monoclonal antibody as a carrier for the targeting therapy of HCC.
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PMID:[Preparation of monoclonal antibody directed against hepatitis B virus X protein and detection of reactive antigen in hepatocellular carcinoma]. 784 49

60 Cases of hepatocellular carcinoma (HCC) and 47 cases of liver cirrhosis (LC) were examined with immunocytochemistry methods using antibodies against IGF-2 and HBxAg on paraffin embedded sections. 32 HCC and 37 LC were found to be positive to HBxAg, in which the positive rates of IGF-2 were 100% (32/32) and 94.6% (35/37) respectively. 28 HCC and 10 LC were found to be HBxAg negative, IGF-2 was positive in 23 HCC (82.1%) and 6 LC (60%). The positive expression rates of IGF-2 in the HBxAg positive tissues were significantly higher than those in the HBxAg negative tissues (P < 0.05). There were three types of IGF-2 distribution in HCC and LC: (1) perinucleus; (2) diffuse in cytoplasm; (3) in nucleus. Small polygonal liver cells (SPLC) were found in the liver tissue surrounding the tumor or cirrhosis, the SPLC were positive to both IGF-2 and HBxAg. The positive rates of IGF-2 in SPLC were 86.4% (38/44) in HBxAg positive group and 40.5% (15/37) in the HBxAg negative group. The above findings suggest that IGF-2 plays an important role in abnormal proliferation of HCC and SPLC. The relation of IGF-2 and HBxAg and the nature of SPLC were also discussed.
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PMID:[Comparative study of the expression of IGF-2 and HBxAg in human hepatocellular carcinoma and liver cirrhosis]. 787 60


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