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 search for differentially expressed gene products in selected cancers of endodermal origin, cDNA libraries derived from mRNA in human hepatocellular carcinoma and adjacent grossly normal tissue were generated. From these parent libraries, subtracted cDNA libraries of tumor minus normal and normal minus tumor tissues were constructed. After screening these subtracted libraries by +/- hybridization, a cDNA clone that is overexpressed in hepatocellular carcinoma and encodes the human acidic ribosomal phosphoprotein P0 (P0) was identified. We then evaluated the expression of this phosphoprotein P0 in human colon carcinoma samples. Surgical specimens of primary tumors and liver metastases were examined by Northern hybridization of total RNA with one of 2 32P-labeled P0 probes. The mRNA level of the P0 was greater in primary colon carcinoma than in paired adjacent normal colonic epithelium in 36 of 38 cases; the mean tumor/normal ratio was 2.7 (range, up to 13). The tumor/normal ratio, when plotted against the Dukes' stage of disease, gave evidence for increasing P0 expression with increasing stage of colon carcinoma (P = 0.02). In all 8 cases of paired colon carcinoma metastatic to liver and 2 cases of paired primary hepatocellular carcinoma, the P0 mRNA level was greater in tumor than in adjacent normal liver tissue. The mean tumor/normal ratio was 4.0 (range, up to 11) for the colon cancers metastatic to liver and 4.2 for the primary hepatocellular carcinoma samples. These findings support a common increased expression of selected gene products in different tumors of endodermal origin and suggest that increased P0 expression, in line with certain other ribosomal proteins, may be associated with human colorectal cancer progression and biological aggressiveness.
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PMID:Increased expression of human ribosomal phosphoprotein P0 messenger RNA in hepatocellular carcinoma and colon carcinoma. 135 May 8

In populations with non-HIV immunodeficiency, non-Hodgkin lymphoma and soft tissue sarcoma, especially Kaposi's sarcoma, are the most prominent tumours, but Hodgkin's disease, gastric carcinoma, squamous cell skin cancer, malignant melanoma, hepatoma, myeloid leukaemia and/or colorectal carcinoma have been linked in various studies. Population based cancer registries and cohort studies of HIV infected persons have generally failed to detect HIV related increases in total cancer incidence or in specific tumours other than non-Hodgkin lymphoma and Kaposi's sarcoma; however, associations with anal carcinoma, hepatoma and Hodgkin's disease have been suggested by some studies. Although not indicating increased risk, HIV induced immunosuppression has been linked to an acceleration of cervical and anal neoplasia and to increased aggressiveness of Hodgkin's disease with a relative excess of the mixed cellularity type. Advances in treatment for HIV infection will delay progression to AIDS and may allow an altered natural history to emerge, including the occurrence of excesses of additional cancer types.
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PMID:HIV infection and cancers other than non-Hodgkin lymphoma and Kaposi's sarcoma. 182 20

Invasion and metastasis requires a series of interactions between malignant cells and the extracellular matrix (ECM). Antigen markers that relate to these interactions were evaluated for prognostic correlation in human hepatocellular carcinoma. Basement membrane type IV collagen (cIV), type IV collagenase (cIVase), laminin, and laminin receptors (LRs)--all ECM antigens previously proposed to be modulated in association with tumor aggressiveness--were immunohistochemically investigated in 30 cases of hepatocellular carcinomas (HCCs). The pattern of antigen expression was correlated with 1) 36 months' clinical follow-up and 2) the pathologic grade. As a means of estimating the proliferation fraction, an additional antigen, Ki67, was also studied in this series. There were major differences in the distribution of cIV and laminin, and in the quantity of cIVase-, LR-, and Ki67-positive cells associated with grade and prognosis. A smaller quantity of cIV and laminin and a higher number of cIVase-, LR-, and Ki67-positive cells were detected in the poorly differentiated compared with the well-differentiated HCCs. The tumors with lower immunoreactivity for cIV and laminin components accompanied by a higher number of cIVase-, LR-, and Ki67-positive cells fall into a group with the poorest overall survival (P less than 0.006). The panel of antigens is proposed as a useful prognostic tool for evaluating HCC tumor aggressiveness.
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PMID:Evaluation of hepatocellular carcinoma aggressiveness by a panel of extracellular matrix antigens. 184 41

Loss of heterozygosity on chromosome 16 is a common genetic alteration in human hepatocellular carcinoma (HCC). To clarify the pathogenetic significance of allele loss on chromosome 16, we performed restriction fragment length polymorphism analysis of 70 surgically resected tumors by using 15 polymorphic DNA markers for chromosome 16. Loss of heterozygosity on chromosome 16 was detected in 36 (52%) of 69 informative cases, and the common region of allele loss in these 36 tumors was located between the HP locus (16q22.1) and the CTRB locus (16q22.3-q23.2). These losses occurred more frequently in HCCs of poor differentiation, of larger size, and with metastasis, whereas they were not detected in HCC at the earliest stage. In addition, these losses were not associated with presence or absence of hepatitis B virus DNA integration or hepatitis C virus infection. These results show that loss of heterozygosity on chromosome 16 is a late event occurring after hepatocarcinogenesis and strongly suggest that this phenomenon is involved in enhancement of tumor aggressiveness during progression of HCC.
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PMID:Allele loss on chromosome 16 associated with progression of human hepatocellular carcinoma. 216 60

Presence of liver antigens in transplantable Morris hepatomas of varying aggressiveness was investigated by immunodiffusion and absorption methods. The most malignant and undifferentiated of these, hepatoma 7777, was found defective in two liver antigens, whereas the less malignant hepatomas, 5123tc and 9618A, did have them. Both antigens had distinct occurrence in tissues and hepatic subcellular fractions and behaved like proteins of electrophoretic mobilities of serum gamma globulins with molecular weights of 51,000 and 240,000, respectively. Since hepatoma 7777 is the least differentiated, fastest growing, and more metastatic of the tumors studied, these properties would appear to be associated with the absence of the antigens.
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PMID:Absence of liver antigens in transplantable hepatomas. A possible relationship to the tumor aggressiveness. 308 Sep 42

Nineteen children with chronic hepatitis related to the hepatitis B virus were followed for an average of 6 years. The determination of the hepatitis B virus DNA in the serum allowed us to know the state of viral replication. Thus three groups of patients could be defined: the first in which replication remained active during the total period of follow-up; the second in which the extinction of replication was observed; the third in which replication was inactive from the beginning of the serological follow-up. Symptoms, high levels of aminotransferases and histologically aggressive lesions, sometimes with cirrhosis, were more frequent in the presence of viral DNA. During the decrease of the replication, a clear-cut and time-limited increase of serum-aminotransferase levels was often noted. After the disappearance of hepatitis B virus DNA in the serum, clinical signs could be found only in children with cirrhosis or hepatocellular carcinoma. Four cases of hepatitis with initial aggressive lesions led to persistent chronic hepatitis without viral DNA in the serum. In all but one of the patients who started with an aggressive form, viral DNA disappeared in the serum. This loss occurred later and only in 2 patients of 5 who presented initially with chronic persistent hepatitis. Thus a long period of follow-up in childhood chronic hepatitis related to B virus shows frequent inactivation of viral replication. This evolution seemed to occur earlier when the initial histological lesions were aggressive as if this aggressiveness favored the elimination of the virus and the presence of specific antibodies in the serum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Course of chronic hepatitis related to B virus in children. Study of serum viral DNA]. 401 86

A considerable interest has recently been shown for the measurement of isoenzyme BB of creatine kinase as a diagnostic and prognostic indicator of tumor growth. This isoenzyme belongs to the group of oncofetal antigens and in human cancer elevated levels occur frequently in patients with metastatic disease. In this study we have attempted to quantify CK-BB serum levels during the growth of an experimental tumor (Yoshida Hepatoma AH 130) in male albino rats to determine if a significant correlation exists between isoenzyme serum levels and the rate of tumor growth. Creatine kinase-BB was measured spectrophotometrically by immunoinhibition of creatine kinase-M subunits. CK-BB normal values were 4.19 +/- 0.4 U/L and between days 5 and 9, where there is an increase in the rate of proliferation of neoplastic cells, CK-BB serum levels reaches its maximum 69.01 +/- 2.2 U/L. These data are in agreement with the hypothesis that the highest isoenzyme levels are a measure of the aggressiveness of the neoplastic clone. Moreover, this hypothesis is consistent with the proposed mathematical model, and we plan to expand this line of study to evaluate the predictive potential of this tumor marker in man.
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PMID:Evaluation of creatine kinase isoenzyme BB as a marker of neoplastic growth in Yoshida ascites hepatoma of the rat. 406 55

It has been suggested that the number of argyrophilic nucleolar organizer regions (AgNORs) correlates with cellular activity and the aggressiveness of malignancy. The mean number of AgNORs per nucleus may, therefore, be a prognostic factor for hepatocellular carcinoma (HCC). The purpose of this study was to evaluate the prognostic significance of the number of AgNORs in HCC. The silver-staining technique was applied to surgically resected specimens to indicate AgNORs. Eighty-nine of the specimens were of HCC, 23 were of normal liver adjacent to HCC, and 32 were of cirrhotic liver adjacent to HCC. The number of AgNORs of HCC (mean +/- SD, 3.26 +/- 1.23) was significantly higher than those of normal liver (1.37 +/- 0.13) and cirrhotic liver (1.49 +/- 0.14). The number of AgNORs was significantly correlated with serum alpha-fetoprotein level, tumor size, portal vein invasion, and Edmondson-Steiner histological grade. In patients undergoing curative resection, the survival rate of those with a high number (> 3.04) of AgNORs was significantly worse than that of those with a low number (< or = 3.04) of AgNORs. Multivariate analysis showed that the number of AgNORs was a significant prognostic indicator in patients without portal vein invasion, and portal vein invasion was the only significant variable when all patients undergoing curative resection were assessed together. The results of this study suggest that the number of AgNORs is useful as an indicator of the grade of malignancy and as a predictor of the prognosis of patients with HCC who do not have portal vein involvement.
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PMID:Prognostic significance of nucleolar organizer regions in hepatocellular carcinoma. 784 11

The assessment of biological markers as potential indicators of disease aggressiveness is still an open problem in hepatocellular carcinoma. Cell proliferation and extracellular matrix (ECM)-associated antigens and tumor-cell products can be associated with clinical aggressiveness in this tumor type, as has already been demonstrated for others. Cell proliferation, expressed as the in vitro [3H]thymidine labeling index, and ECM-associated antigens, such as type IV collagenase and laminin receptors, were assessed on the same paraffin-embedded samples. A strong association (P = 0.0001) was observed between the expression of collagenase and laminin receptors, with a correlation coefficient (rs) of 0.68. No relationship was found between cell proliferation and ECM-associated antigens. Moreover, the biological markers were generally independent of clinicopathologic features, except for a higher number of collagenase- and laminin receptor-positive cells in large (> or = 5 cm) compared with small (< 5 cm) tumors. In the present series of hepatocellular carcinoma patients, the 3-year clinical outcome was significantly affected by cell proliferation and ECM-associated antigens.
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PMID:Biological markers in hepatocellular carcinoma: potential clinical implications. 838 67

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


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