Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite remarkable progress of diagnostic imaging and operative procedures radiological interventions play a major role in diagnostic and therapeutic liver tumor interventions. Percutaneous biopsies should be taken by 16-20 g needles. CT control is indicated in cases when sonographically guidance is impossible or of risk. MR guidance is still seldom. Accuracy rates of percutaneous biopsies are high (>90%), and safe with complications (e.g. bleeding) of less than 1%. Palliative percutaneous therapeutic interventions of primary or secondary liver malignancies are thermoablative procedures of laser (LITT), cryoablation or radio-frequency, percutaneous ethanol injection (PEI) and intraarterial chemotherapy via port system or repetitive catheterisation with perfusion or embolization (TACE). For metastatic disease with less than five tumors of less than 4 cm LITT and PEI are recommended, more advanced cases should be treated by intra-arterial port system chemotherapy. For HCC best results are shown for PEI, in cases of UICC stage IIIB and IV only TACE is adequate.
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PMID:[Image-guided interventions in liver tumors]. 1052 32

The last ten years have seen dramatic changes in the therapeutic approach to both primary (i.e., hepatocellular carcinoma: HCC) and secondary (i.e., metastatic lesions) focal liver malignancies. This has been due to the increasing proliferation of new modalities, including percutaneous ablative therapies (ethanol injection: PEI; radiofrequency: RF; laser; microwaves), angiographic therapies (segmental chemoembolization; hypoxic perfusion) and liver transplantation (OLT), in addition to a greater acceptance of pre-existing modalities (resection; systemic chemotherapy). Thus, a main aim of current medical management is to select for each patient the therapeutic modality which will provide the highest success rate, fewest risks and lowest costs for each given situation. However, in order to decide on the appropriate therapeutic choice, the accurate diagnosis of neoplastic lesions by means of one or more imaging modalities (ultrasound: US; computed tomography: CT; magnetic resonance: MR) is mandatory. This imaging work-up can be viewed as having three purposes: lesion detection, lesion characterization, intrahepatic and extrahepatic cancer staging. The present paper is concerned primarily with the imaging approach to liver lesion detection.
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PMID:Liver cancer imaging: the need for accurate detection of intrahepatic disease spread. 1060 95

Recent data suggest that Bin1, a novel C-MYC interacting protein, is a suppressor gene whose loss of expression is a frequent aberration associated with several malignancies. The mechanism responsible for loss of BIN1 expression is not understood. The purpose of this study is to investigate DNA profile of the BIN1 gene in human hepatoma Hep G2 cells, previously documented with lack of BIN1 expression. Chromosome and molecular analyses of Hep G2 cells were initiated to exclude the possibility of genetic alterations as a factor affecting BIN1 gene expression in these cells. We used Hep G2 cell line and its hepatitis B virus (HBV) transfected variants--Hep G2T14.1 and Hep G2215 cell lines. The cytogenetic localization of BIN1 was identified in the 2q14 region. Fluorescence in situ hybridization (FISH) with the chromosome 2 whole chromosome painting probe (WCP) demonstrated three or four intact copies of chromosome 2 in all three hepatoma cell lines studied. FISH analyses with the BIN1-specific probe of the Hep G2, Hep G2T14.1, and Hep G2215 metaphase chromosomes document no rearrangement of the BIN1 gene on any of the multiple copies of chromosome 2. FISH with the specific HBV probe did not identify the HBV integration site in Hep G2T14.1 and Hep G2215 cells within the BIN1 locus. Southern blot analyses revealed no genetic rearrangements in the BIN1 gene in any of the cell lines studied. Our RNA analyses (northern blot and RT-PCR) document lack of BIN1 message in Hep G2 cells in contrast to the presence of BIN1 in Hep G2T14.1 and Hep G2215 cells. No difference was identified in other transcripts analyzed, including c-myc. Analyses of BIN1 expression of Hep G2 cells at different passages were initiated and document low levels of BIN1 transcript in Hep G2 cells of passage < 85. Furthermore, BIN1 transcript was identified in additional seven HCC cell lines analyzed. Our data indicate that lack of Bin1 expression in HepG2 cells previously documented is a characteristic of cells of passage > 85 and is not due to genetic loss, or rearrangement within the BIN1 DNA sequence. Loss of the BIN1 transcript is not a characteristic of HCCs analyzed.
Cancer Genet Cytogenet 2000 Jan 01
PMID:Investigation of the expression of Bin1, a putative suppressor, in human hepatoma cells. 1061 29

There are an increasing number of models for the study of liver cancer development with such agents as chemicals, hormones, and viruses. This process is almost always a multistep and during the long period of cancer development, discrete cells or cell populations acquire step-by-step the various properties that go to make up a cancer. The hepatocarcinogenesis models are useful in identification and analysis of the preneoplastic and neoplastic alterations, as well HCC. This article presents a review of theoretical foundation and mechanisms of various models of experimental hepatocarcinogenesis as well contain a short presentation of animals practical in those experiments, principally rats. The remarkable similarities between many models with different carcinogens in animals and humans suggest the importance of such studies in understanding of molecular basis of liver cancer development.
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PMID:[Experimental hepatocarcinogenesis--evaluation of the significance of experimental modeling. Classical models]. 1073 42

A study was performed to evaluate in vitro the sensitivity, specificity and variability of a new immunomagnetic microbead isolation technique which provides subsequent immunological staining of captured carcinoma cells. In a mixture of peripheral blood mononuclear cells (PBMCs) and human carcinoma cells the epithelial cancer cells were isolated with the Dynal((R)) RAM IgG1 CELLection Kit using Dynabeads M-280 coated with a rat monoclonal antibody (Mab) against mouse IgG1. The rat Mab was biotinylated and attached to Dynabeads via streptavidin and a DNA linker. The anti-epithelial monoclonal mouse antibody Ber-EP4 was used as the primary capture antibody. In order to permit phenotyping of the isolated carcinoma cells the magnetic beads were removed from the carcinoma cells by DN'ase digestion of the DNA linker between the magnetic bead and the secondary antibody. In an ex vivo model system an average recovery of approximately 60% of a human colon carcinoma cell line HCC-2998 seeded in 5.10(6) PBMCs was obtained, and the recovered cells could subsequently be immunologically stained for the surface antigen CD87 (urokinase plasminogen activator receptor). No positive stained cells were found in control experiments with PBMCs without carcinoma cells. Despite a relatively low recovery, the described method will be valuable for the detection of carcinoma cells in cytospin preparations with subsequent phenotyping of the cells for expression of surface antigens. Depending on the chosen antibodies, the method may be useful for the isolation and characterisation of other cell types in various cell suspensions.
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PMID:The use of the CELLection kit in the isolation of carcinoma cells from mononuclear cell suspensions. 1075 43

The aim of the present paper was to assess the utility of Levovist in defining the pathology of liver masses. Levovist is a new ultrasound contrast agent consisting of galactose microparticles, air bubbles and palmitic acid. Prospective studies were performed in patients referred for further evaluation of known liver masses. Levovist was peripherally injected and colour Doppler ultrasound studies were performed. Findings were correlated with clinicopathology and three other imaging modalities: biphasic spiral CT, CT arterial portography and contrast MRI. Twenty-five patients were studied (15 male and 10 female) in the age range 25-74 years. Liver masses ranged from 0.5 to 7 cm in maximum diameter. Thirteen lesions were benign and 12 were malignant (four hepatomas (HCC) and eight metastases). Levovist enhancement occurred in 18 lesions. Of these, six were benign (four focal nodular hyperplasias (FNH) and two haemangiomas). All 12 malignant lesions demonstrated enhancement. The HCC showed a mosaic pattern of central and peripheral enhancement, and the FNH demonstrated a spoke-wheel pattern. It was not possible to distinguish between haemangiomas and malignant lesions. Non-enhancing lesions may well be benign, with all malignancies showing some enhancement. Characteristic enhancement patterns were found for HCC (mosaic) and FNH (spoke-wheel). It was not possible to distinguish between metastases and benign lesions (haemangiomas) when the pattern of enhancement was peripheral.
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PMID:Early experience in the use of Levovist ultrasound contrast in the evaluation of liver masses. 1076 Dec 56

A ribozyme (RZ) gene targeting c-myc mRNA was synthesized and cloned. Cleavage reaction showed that cleavage of the RZ was efficient and specific. The RZ gene-containing retrovirus vector pDOR-RZ was transfected into HCC-9204 hepatoma cells, which constitutively express high levels of c-myc using Lipofectamine. Positively transfected cells were selected using G418. In situ hybridization showed that both pDOR-RZ and pDOR vectors had been integrated into the chromosome of HCC-9204 cells. Dot blot hybridization indicated that expression of the RZ was only evident in pDOR-RZ-transfected HCC-9204 cells. Avidin-biotin complex enzyme-linked immunosorbent assay showed that c-myc expression was down-regulated. Chromatin aggregation into compact masses, cytoplasmic vacuole degeneration, and blurring of cytoplasm structure were observed by transmission electron microscopy in HCC-9204-RZ cells. These results suggest that the use of a c-myc mRNA cleaving enzyme could be most effective in tumor cells that are highly proliferative and constitutively express high levels of c-myc.
Cancer Gene Ther 2000 Mar
PMID:Inhibition of cell proliferation in HCC-9204 hepatoma cells by a c-myc specific ribozyme. 1076 46

BCL10 was found to have truncated mutations at a high frequency in MALT (mucosa-associated lymphoid tissue) B cell lymphomas. We examined the mutations of BCL10 gene in human primary liver cancer using non-isotopic PCR-SSCP. Three exons were examined in both cancer and non-HCC adjacent liver tissues. For each exon, six PCR products with abnormal bands were sequenced to verify those mutations. 56.5% samples were revealed a C to G mutation at position 5744 (g5744C>G) of the first exon of BCL10 gene; 54.3% samples were revealed a T deletion mutation at position 11311 (g11311delT) of the second exon of BCL10 gene; 45.7% samples were revealed a C to T mutation at position 14116 (g14116C>T) of the third exon of BCL10 gene. Similar mutation types were found in tumor-adjacent tissues at a lower frequency. The single base changes result in a truncated BCL10 protein expression. Serum alpha-fetoprotein (AFP) level, the tumor size had no significant relationship with BCL10 mutation.
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PMID:Detection of point mutations of BCL10 gene in hepatocellular carcinoma tissues: report of 46 cases. 1079 Feb 17

There are an increasing number of models for the study of liver cancer development with such agents as chemicals, hormones, and viruses. This process is almost always a multistep and during the long period of cancer development, discrete cells or cell populations acquire step-by step the various properties that go to make up a cancer. The hepatocarcinogenesis models are useful in identification and analysis of the preneoplastic and neoplastic alterations, as well HCC. This article presents a review of theoretical foundation and mechanisms of various models of experimental hepatocarcinogenesis as well contain a short presentation of animals practical in those experiments, principally rats. The remarkable similarities between many models with different carcinogens in animals and humans suggest the importance of such studies in understanding of molecular basis of liver cancer development.
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PMID:[Experimental hepatocarcinogenesis--evaluation of the significance of theoretical models. Contemporary models]. 1080 25

Based on the fact that somatostatin (SST) analogs have given promising results for treatment of hepatocellular cancer, we performed both in vitro and in vivo investigations to define the role of a depot formulation of the long acting SST-analog lanreotide (LAN). A decrease of cells in the S-phase as compared to controls (p<0.03) followed by a significant, dose-dependent induction of apoptosis could be demonstrated in Hep G2 cells along with a dose-dependent influence of the peptide on cellular proliferation. Northern blotting demonstrated the presence of mRNA for SSTR subtypes 2, 3 and 4 in Hep G2 cells, but only slight SSTR expression in normal liver tissue. In addition, 21 untreated patients with advanced HCC not amenable to surgery were administered 30 mg of LAN by deep intramuscular injection every 14 days until documented disease progression. Fifteen of these patients also underwent scanning with commercially available 111In-DTPA-D-Phe1-Octreotide (111In-OCT) to define the in vivo expression of SSTR. No positive 111In-OCT scans were obtained, indicating the absence of relevant amounts of functional SSTR2 in HCC. One patient (5%) showed a partial response to treatment, 8 patients had stable disease (38%), while the remaining patients progressed during treatment. The median survival was 4.2 months (range 1.2-13+), and the median time to progression was 2.5 months (range, 1.5-7+). However, 4 patients (19%) had an increase in WHO performance status lasting between 2.5 and 6 months, 5 patients (24%) had an increase in body weight, while pain markedly improved in 1 additional patient (5%). In total, 5 patients (24%) had a decrease in serum-AFP levels by at least 30%. Our results clearly indicate the ability of LAN to decrease the S-phase fraction along with induction of apoptosis in Hep G2 cells in a dose-dependent manner. Our data suggest clinical potential of SST-analogs in HCC and indicate that suboptimal doses of the peptide might have been administered in our series.
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PMID:Treatment of hepatocellular cancer with the long acting somatostatin analog lanreotide in vitro and in vivo. 1081 95


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