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)

To characterize adenomatous hyperplasia (AH) and hepatocellular carcinoma (HCC), and to establish their histopathological differences, morphometrical and immunohistochemical analyses, namely, cellularity, thickness of cell cord, and Ki-67 labeling index (Ki-67 LI) were done on surgically obtained hepatic lesions from patients with positive serum antibody against HCV. The hepatic lesions analyzed include chronic active hepatitis (CAH) (11 specimens), regenerative nodules of liver cirrhosis (LC) (29), AH (11), small HCC Edmondson's Grade I (GI) (19), GII (26), GIII (14). The results showed that AH has relatively high cellularity, and significantly greater thickness of cell cord than LC; whereas, HCC GI has significantly higher cellularity and Ki-67 LI than AH. From the data of these markers, and from the absence of conspicuous structural atypism, AH is considered to be in a different category from HCC GI. The premalignant potential of AH is supported only by its high incidence of coexistence adjacent to HCC GI or GII(6/11). Most lesions of HCC seem to develop from the liver tissue having a background of CAH or LC without passing through AH. Focal fatty changes are frequently observed within lesions of both AH and HCC GI (5/11, 8/19). When non-fatty regions of AH and HCC GI are compared, with respect to their markers, particularly Ki-67 LI, as well as the structural atypism, such as microacinus formation and pseudoglandular structure, and invasive growth into the surrounding liver parenchyma, HCC GI can be diagnosed as an early or well-differentiated malignant lesion.
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PMID:Histopathological and immunohistochemical analysis of adenomatous hyperplasia and hepatocellular carcinoma: cellularity, thickness of cell cord, and Ki-67 proliferative activity. 754 Sep 60

To evaluate the prognostic significance and clinicopathologic correlation of proliferative activity in patients with hepatocellular carcinoma, Ki-67 antigen expression was examined using immunohistochemical staining with monoclonal antibody MIB1. Seventy-two patients (65 men, 7 women; age range 24-77 years, mean, 52 years) having hepatocellular carcinoma surgically resected were studied. Tumor and nontumorous tissues were stained with monoclonal antibody MIB1 with microwave oven pretreatment. Tumor and nontumor MIB1 (T-MIB1 and NT-MIB1) scores were assessed by counting the positive staining nuclei per 1,000 cells. The T-MIB1 score ranged from 5-630 per 1,000 cells (mean +/- standard deviation [SD] = 145 +/- 162). It was found to be significantly higher in less well-differentiated tumors (Edmondson's grades III and IV) than in well-differentiated ones (Edmondson's grades I and II) (P = .017). The T-MIB1 score was also higher in nonencapsulated tumors than in encapsulated ones, although it did not reach statistical significance (P = .069). It had no influence on tumor size, tumor invasiveness, the background disease in the nontumorous livers, patients' HBsAg status, or serum alpha-fetoprotein levels. Diseases in the nontumorous livers or patients' HBsAg status had no influence on the NT-MIB1 scores. When the tumors were stratified into two groups with T-MIB1 score < or = 20 and T-MIB1 score > 20, those patients with score < or = 20 had significantly longer disease-free survival (DFS) than those with scores > 20 (median DFS: 34 months and 4.7 months, respectively; P = .011). In addition, MIB1 and PCNA were closely correlated (P < .01). The authors conclude that proliferative activity in hepatocellular carcinoma, as defined by MIB1 immunohistochemical analysis, is significantly related to tumor cellular differentiation. It is also a potentially valuable prognostic factor in patients with this tumor.
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PMID:Ki-67 antigen expression in hepatocellular carcinoma using monoclonal antibody MIB1. A comparison with proliferating cell nuclear antigen. 754 66

We treated a patient who had previously undergone a hepatic resection for ruptured hepatocellular carcinoma (HCC) but developed a solitary peritoneal recurrence at the site of the incision 8 years and 9 months later. Since no other recurrence was evident, we resected the tumour. The primary tumour was 2.5 cm in size and histological examination revealed HCC without any histological risk factors for intrahepatic recurrence. The peritoneal tumour consisted of less differentiated cancer cells than those found in the primary tumour. The positive rates of Ki-67 were 10% in the primary tumour and 23.3% in the peritoneal recurrence. The DNA indexes in both tumours were considered to be identical. The comparison between the primary and peritoneal tumours suggested that the histological differentiation and proliferation activity can change after recurrence, in spite of consistent DNA ploidy contents. Clinically, a patient who undergoes a hepatic resection for ruptured HCC can survive for a long time, such as 10 years, if they have good liver function and small HCC without any histological risk factors for intrahepatic recurrence. However, since late recurrence is possible, a follow up for as long as 10 years is recommended.
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PMID:A long-term survivor of ruptured hepatocellular carcinoma after hepatic resection. 754 17

A total of 128 surgically resected small hepatocellular carcinomas, measuring less than or equal to 3 cm in diameter, were studied by both macroscopic and histologic examinations. In 95 single nodular-type tumors of the 128 lesions, eight tumors were associated with the cancerous areas of well differentiated hepatocellular carcinoma around the nodule. These surrounding cancerous areas went undetected by both the preoperative radiological examinations and the gross findings of resected specimens. Based on the immunohistochemical findings, the labeling index, both of the proliferating cell nuclear antigen (PCNA) and of the Ki-67 in the surrounding cancerous areas, were lower than that of the main nodules but higher than in the nontumorous liver parenchyma in seven of eight cases. These results suggest that the main nodule was generated from the surrounding cancerous area, supporting the hypothesis of a stepwise progression of HCC. Even if the tumor seems to be a small and single nodular type, it is recommended that its surrounding areas should be closely examined and the surgical cutting margin should be made more than 1.0 cm away from the main nodule at hepatic resection.
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PMID:Small hepatocellular carcinoma of single nodular type: a specific reference to its surrounding cancerous area undetected radiologically and macroscopically. 756 84

This study examined whether the monoclonal antibody Ki-67 is an indicator of hepatocellular carcinoma proliferation and whether it represents a new parameter for determining the diagnosis and prognosis. The subjects were 22 patients who were not treated preoperatively among the patients undergoing hepatectomy at our department. Fresh specimens of the cancer tissue and the noncancerous regions were stained with PI after processing them with FITC-labeled Ki-67. Then 20,000 cells were analyzed by two-color flow cytometry. A significant difference was observed between the well differentiated group and the moderately and poorly differentiated groups. However, no significant difference was observed with respect to any other factor. The average Ki-67 labeling of the cancers in the patients with and without cirrhosis was 17.0 +/- 10.5% and 5.3 +/- 3.5%, respectively (p < 0.05). The cancers showed high Ki-67 labeling rates compared with the noncancerous areas and a positive correlation was observed between the two. These findings suggested that coexistent hepatic lesions have some influence on the proliferative activity of cancer. A significant correlation was confirmed by flow cytometry after immunostaining using the antibody MIB-1. Analysis by this method was considered to be useful for assessing the proliferating activity of hepatocellular carcinoma.
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PMID:[Assessment of the proliferative activity of hepatocellular carcinoma with the monoclonal antibody Ki-67 using flow cytometry]. 767 23

The c-met protooncogene is a growth factor receptor with tyrosine kinase activity. Recently the hepatocyte growth factor was identified as the ligand for this receptor. Because the hepatocyte growth factor is a most potent mitogen in hepatocytes, possible involvement of c-met expression in hepatocarcinogenesis is suspected. In this study, we examined c-met expression in 23 hepatocellular carcinoma cases by means of Northern-blot analysis and an immunohistochemical study. Northern-blot analysis revealed c-met mRNA expression in the tumors of 6 of 19 patients (31.6%); in the immunohistochemical study, c-met protein was detected in 16 of 23 patients (69.6%). With both methods, c-met was found to be overexpressed in hepatocellular carcinoma compared with the surrounding normal liver. Comprehensive analysis showed that c-met protein expression was correlated with poor-to-moderate differentiation of cancer cells (p < 0.05). Tumor proliferative activity of hepatocellular carcinoma was evaluated by means of Ki-67 labeling index. All cases with increased tumor proliferative activity showed c-met protein expression, although the elevation of proliferative activity in the c-met-positive group was not statistically significant. These data suggest that the overexpression of c-met plays an important role in the development of hepatocellular carcinoma.
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PMID:Expression of the c-met protooncogene in human hepatocellular carcinoma. 792 56

Increased proliferative activity determined in surgical specimens of hepatocellular carcinoma (HCC) has been associated with tumor grade and patient survival. The measurement of cell proliferation in echo-guided biopsies of small focal liver lesions might provide useful information for the early recognition of malignancy and for predicting the aggressiveness of small HCCs. We assessed the diagnostic and prognostic value of cell proliferation in 91 echo-guided needle biopsies of focal liver lesions using the monoclonal antibody Ki-67, which detects a human nuclear antigen that is present in proliferating cells. Measurements were performed by image cytometry as the percentage of Ki-67 positive hepatocytes nuclei over total hepatocyte nuclei in the biopsy. At the histological examination, 27 lesions were diagnosed as chronic hepatitis, 10 as cirrhosis, 11 as macroregenerative nodule, and 43 as HCC in cirrhotic liver. Although the highest Ki-67 values (> 20%) were found in less-differentiated HCCs, most well-differentiated HCCs and nine borderline nodules were completely devoid of Ki-67-positive hepatocytes. A sustained Ki-67 labeling (up to 16%) was found in hepatitis and cirrhosis, similar to that found in several malignant tumors. In the HCC subset, Ki-67 labeling was strongly correlated to the Edmondson-Steiner histological grade. However, survival analysis did not indicate a better outcome for those patients with low-proliferating tumors.
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PMID:Cytometric measurement of cell proliferation in echo-guided biopsies from focal lesions of the liver. 865 17

In order to clarify factors which relate to AgNOR in hepatocellular carcinoma (HCC), AgNOR numbers and the expression of Ki-67 using MIB-1 antibody have been studied in paraffin-embedded specimens of 20 HCCs by means of a double staining method. We found that in individual cases the AgNOR number of MIB-1-positive cells was significantly higher than that of MIB-1-negative cells (p < 0.001). In addition, a significant correlation was seen between MIB-1 labelling index and the total mean AgNOR number (t-AgNOR) (r = 0.882, p < 0.001). The value of t-AgNORs was significantly higher in histologically less differentiated HCC (p < 0.005). The mean AgNOR number of MIB-1-negative cells (n-AgNOR) was also significantly higher in histologically less differentiated HCC (p < 0.04). By contrast, the mean AgNOR number of MIB-1-positive cells (p-AgNOR) did not significantly correlate with histologic grades (p = 0.265). However, the number of t-AgNORs was not significantly different between diploid and aneuploid tumours. In HCCs, it appears that AgNOR numbers were variably influenced by proliferative activities of tumour cells, phases of cell cycle and cell differentiation.
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PMID:Nucleolar organizer regions in hepatocellular carcinoma related to the cell cycle, cell proliferation and histologic grade. 883 63

Hepatocellular carcinoma (HCC) is a heterogeneous disease. HCC derived from different stages of cellular differentiation may have different clinical and pathobiological behavior. To test the hypothesis that HCC can be classified into two types based on its phenotypic markers (hepatocellular and biliary differentiation), liver tissues from 290 Chinese patients with HCC were studied. Expression of hepatocytic differentiation marker (HEP-PAR-reactive antigen), biliary differentiation markers (AE1-AE3, cytokeratin-19), proliferation markers (Ki-67, proliferating cell nuclear antigen), alpha-fetoprotein, p53, and transforming growth factor-alpha in the tumor tissue were assessed by immunohistochemistry. Hepatocytic differentiation marker was detected in 99.7% and biliary differentiation markers were detected in 29.3% of these tumors. Clinically, no patient with HCC with biliary markers survived for more than 27 weeks compared with a 22.6% survival rate in patients with HCC negative for biliary markers. HCCs positive for the biliary differentiation markers showed features of more aggressive disease in terms of poorer cellular differentiation (P < 0.001) and high-level expression of proliferation markers (Ki-67, P < 0.001; proliferating cell nuclear antigen, P = 0.0114) compared with HCCs without biliary markers. HCCs with biliary markers also had a higher level of expression of alpha-fetoprotein (P < 0.001) and p53 (P = 0.0077). Classification of HCCs based on its phenotypic (differentiation) markers has both clinical and pathobiological implications.
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PMID:Classification of hepatocellular carcinoma according to hepatocellular and biliary differentiation markers. Clinical and biological implications. 886 66

The ability to document nuclear proliferation in the liver is essential to our understanding of hepatic regeneration and hepatocellular carcinoma. While numerous tests are available to provide such information in experimental animals, few can be applied to patients with liver disease. Ki-67 is a proliferating nuclear antigen present in replicating cells. Recent data indicates that staining for Ki-67 reflects nuclear proliferation in these tissues. To date, the technique has had only limited application to human liver tissues in formalin-fixed paraffin embedded tissue. In the present study, we documented Ki-67 staining in archival liver tissue from patients with mild chronic hepatitis, severe chronic hepatitis, inactive cirrhosis, hepatocellular carcinoma, and in normal livers. We found that Ki-67 staining was increased in patients with mild chronic hepatitis (labelling index 29 +/- 25), severe chronic hepatitis (labelling index 41 +/- 40), and hepatocellular carcinoma (labelling index 71 +/- 61), when compared to patients with inactive cirrhosis, (labelling index 1.4 +/- 3.1), and normal livers (labelling index 2.5 +/- 3.2). In conclusion, Ki-67 maybe useful tool to assess hepatocyte proliferation in formalin-fixed paraffin-embedded human liver tissue.
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PMID:Hepatic regeneration in humans with various liver disease as assessed by Ki-67 staining of formalin-fixed paraffin-embedded liver tissue. 906 74


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