tetracycline and Carcinoma--Hepatocellular

tetracycline has been researched along with Carcinoma--Hepatocellular* in 27 studies

Reviews

1 review(s) available for tetracycline and Carcinoma--Hepatocellular

ArticleYear
    Proceedings. Mathematical, physical, and engineering sciences, 2019, Volume: 475, Issue:2227

    Patients with POAG have lower corneal endothelial cell density than healthy controls of the same age. This may be attributed to mechanical damage from elevated IOP and toxicity of glaucoma medications.. Mycophenolic acid was detected in all cats. The dose 10 mg/kg given q12h for 1 week was tolerated (n = 3). The efficacy of MMF as an immunosuppressant and long-term safety in cats of this dosage regimen is unknown.. T

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2019

Other Studies

26 other study(ies) available for tetracycline and Carcinoma--Hepatocellular

ArticleYear
[6. Inspection of Hepatocellular Carcinoma 4: Nuclear Medicine Scan].
    Nihon Hoshasen Gijutsu Gakkai zasshi, 2016, Volume: 72, Issue:6

    Topics: Biliary Tract; Carcinoma, Hepatocellular; Humans; Liver; Liver Neoplasms; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Spleen; Technetium Tc 99m Aggregated Albumin; Technetium Tc 99m Pentetate; Tetracycline

2016
Increased expression of S100A6 promotes cell proliferation and migration in human hepatocellular carcinoma.
    Journal of molecular medicine (Berlin, Germany), 2014, Volume: 92, Issue:3

    High levels of S100A6 have been associated with poor outcome in some types of human cancers, but the role of S100A6 in the molecular pathogenesis of these cancers is largely unknown. This study was performed to explore the expression and functional roles of S100A6 in hepatocellular carcinoma (HCC). The expression level of S100A6 in HCC tumor and corresponding peritumoral tissues were determined by immunohistochemistry analysis. The potential functions of S100A6 in tumorigenesis and metastasis were analyzed by cell proliferation, migration, and invasion assays in human liver cancer cells. Moreover, through expression and purification of S100A6 recombinant protein tagged with cell-penetrating peptide, we analyzed its complex extracellular/intracellular effects in a S100A6-silenced cellular model. As a result, the expression of S100A6 was up-regulated in human HCC compared with adjacent peritumoral tissues. S100A6 silencing inhibited the growth and motility of HCC cells, while intracellular re-expression of S100A6 could rescue the proliferation and migration defects. Intracellular over-expression of S100A6 resulted in down-regulation of E-cadherin expression and promoted nuclear accumulation of β-catenin. Moreover, we found that the enhanced cell proliferation and motility after S100A6 stimulation were dependent on the activation of PI3K/AKT pathway. These results suggest that S100A6 may be involved in promotion and progression of human liver cancer.. S100A6 is overexpressed in human hepatocellular carcinoma clinical specimens. S100A6 promotes proliferation and migration of human hepatoma cells. Overexpression of S100A6 results in alteration of E-cadherin and β-catenin. The multi-effects of S100A6 may be mediated in part by PI3K/AKT pathway activation.

    Topics: Animals; beta Catenin; Cadherins; Carcinogenesis; Carcinoma, Hepatocellular; Cell Cycle Proteins; Cell Movement; Cell Nucleus; Cell Proliferation; Cell Shape; Cholangiocarcinoma; Down-Regulation; G1 Phase Cell Cycle Checkpoints; Gene Silencing; Hep G2 Cells; Humans; Immunohistochemistry; Liver Neoplasms; Mice; Phosphatidylinositol 3-Kinases; Protein Transport; Proto-Oncogene Proteins c-akt; Pseudopodia; S100 Calcium Binding Protein A6; S100 Proteins; Signal Transduction; Tetracycline

2014
A transgenic zebrafish liver tumor model with inducible Myc expression reveals conserved Myc signatures with mammalian liver tumors.
    Disease models & mechanisms, 2013, Volume: 6, Issue:2

    Myc is a pleiotropic transcription factor that is involved in many cellular activities relevant to carcinogenesis, including hepatocarcinogenesis. The zebrafish has been increasingly used to model human diseases and it is particularly valuable in helping to identify common and conserved molecular mechanisms in vertebrates. Here we generated a liver tumor model in transgenic zebrafish by liver-specific expression of mouse Myc using a Tet-On system. Dosage-dependent induction of Myc expression specifically in the liver was observed in our Myc transgenic zebrafish, TO(Myc), and the elevated Myc expression caused liver hyperplasia, which progressed to hepatocellular adenoma and carcinoma with prolonged induction. Next generation sequencing-based transcriptomic analyses indicated that ribosome proteins were overwhelmingly upregulated in the Myc-induced liver tumors. Cross-species analyses showed that the zebrafish Myc model correlated well with Myc transgenic mouse models for liver cancers. The Myc-induced zebrafish liver tumors also possessed molecular signatures highly similar to human those of hepatocellular carcinoma. Finally, we found that a small Myc target gene set of 16 genes could be used to identify liver tumors due to Myc upregulation. Thus, our zebrafish model demonstrated the conserved role of Myc in promoting hepatocarcinogenesis in all vertebrate species.

    Topics: Animals; Animals, Genetically Modified; Carcinoma, Hepatocellular; Disease Models, Animal; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Humans; Liver; Liver Neoplasms; Liver Neoplasms, Experimental; Mammals; Mice; Mice, Transgenic; Neoplasm Staging; Proto-Oncogene Proteins c-myc; Reproducibility of Results; Sequence Analysis, RNA; Tetracycline; Zebrafish

2013
SPECT/CT imaging in 99mTc-PMT hepatobiliary scintigraphy to detect bone metastases from hepatocellular carcinoma.
    Clinical nuclear medicine, 2012, Volume: 37, Issue:10

    We report a 62-year-old man who presented with pain on the right side of his hip. CT revealed destructive masses in the right femur and left ilium. Histological examination indicated metastases from hepatocellular carcinoma, and further investigations revealed the primary tumor in the liver. Hepatobiliary scintigraphy using 99mTc N-pyrydoxyl-5-methyltryptophan and fused SPECT/CT clearly showed abnormal accumulation in these bone metastases from hepatocellular carcinoma.

    Topics: Biliary Tract; Bone Neoplasms; Carcinoma, Hepatocellular; Humans; Liver; Liver Neoplasms; Male; Middle Aged; Multimodal Imaging; Organotechnetium Compounds; Positron-Emission Tomography; Pyrrolidines; Tetracycline; Tomography, X-Ray Computed

2012
Cytoplasmic accumulation of connexin32 expands cancer stem cell population in human HuH7 hepatoma cells by enhancing its self-renewal.
    International journal of cancer, 2011, Jan-01, Volume: 128, Issue:1

    Although the connexin32 (Cx32)-mediated gap junction is abolished in hepatocellular carcinoma (HCC), the expression of cytoplasmic Cx32 tends to increase in correspondence with the grade of malignancy. Establishing a Tet-off expression system in human nonmetastatic HuH7 HCC cells where cytoplasmic Cx32 was overexpressed by doxycycline (Dox) withdrawal, we previously demonstrated that overexpression of cytoplasmic Cx32 made HuH7 cells metastatic in mice. In our study, hypothesizing that the cytoplasmic Cx32-induced metastasis may involve expansion of the cancer stem cell (CSC) population, we examined whether cytoplasmic Cx32 controlled the size of the side population (SP) in HuH7 Tet-off Cx32 cells. Fluorescence-activated cell sorting revealed that SP was expanded in a Dox-free medium compared with a Dox-supplemented one. Although cytoplasmic Cx32 did not block maturation from SP to non-SP, purified SP reconstituted a larger SP fraction in the Dox-free medium than in the Dox-supplemented one. Furthermore, although SP from HuH7 Tet-off mock cells formed a similar number of CSC spheres of a similar size whether with or without Dox, SP from HuH7 Tet-off Cx32 cells developed a greater number of larger CSC spheres in the Dox-free medium than in the Dox-supplemented one. Taken together, these results suggest that accumulation of cytoplasmic Cx32 should enhance self-renewal of CSC to expand the CSC population in HCC.

    Topics: Animals; Anti-Bacterial Agents; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Proliferation; Connexins; Cytoplasm; Doxycycline; Flow Cytometry; Fluorescent Antibody Technique, Indirect; Gap Junction beta-1 Protein; Gene Expression; Humans; Immunoblotting; Liver Neoplasms, Experimental; Male; Mice; Mice, SCID; Neoplasm Metastasis; Neoplastic Stem Cells; Tetracycline; Transplantation, Heterologous

2011
Induction of vesicular steatosis by amiodarone and tetracycline is associated with up-regulation of lipogenic genes in HepaRG cells.
    Hepatology (Baltimore, Md.), 2011, Volume: 53, Issue:6

    Drug-induced liver injury occurs in general after several weeks and is often unpredictable. It is characterized by a large spectrum of lesions that includes steatosis and phospholipidosis. Many drugs such as amiodarone and tetracycline have been reported to cause phospholipidosis and/or steatosis. In this study, acute and chronic hepatic effects of these two drugs were investigated using well-differentiated human hepatoma HepaRG cells. Accumulation of typical lipid droplets, labeled with Oil Red O, was observed in hepatocyte-like HepaRG cells after repeat exposure to either drug. Amiodarone caused the formation of additional intracytoplasmic vesicles that did not stain in all HepaRG cells. At the electron microscopic level, these vesicles appeared as typical lamellar bodies and were associated with an increase of phosphatidylethanolamine and phosphatidylcholine. A dose-dependent induction of triglycerides (TG) was observed after repeat exposure to either amiodarone or tetracycline. Several genes known to be related to lipogenesis were induced after treatment by these two drugs. By contrast, opposite deregulation of some of these genes (FASN, SCD1, and THSRP) was observed in fat HepaRG cells induced by oleic acid overload, supporting the conclusion that different mechanisms were involved in the induction of steatosis by drugs and oleic acid. Moreover, several genes related to lipid droplet formation (ADFP, PLIN4) were up-regulated after exposure to both drugs and oleic acid.. Our results show that amiodarone causes phospholipidosis after short-term treatment and, like tetracycline, induces vesicular steatosis after repeat exposure in HepaRG cells. These data represent the first demonstration that drugs can induce vesicular steatosis in vitro and show a direct relationship between TG accumulation and enhanced expression of lipogenic genes.

    Topics: Amiodarone; Carcinoma, Hepatocellular; Carrier Proteins; Cell Line, Tumor; Down-Regulation; Fatty Acid Synthase, Type I; Fatty Liver; Humans; Lipid Metabolism; Lipogenesis; Liver Neoplasms; Membrane Proteins; Oleic Acid; Perilipin-2; Perilipin-4; Phosphoproteins; Stearoyl-CoA Desaturase; Tetracycline; Triglycerides; Up-Regulation

2011
Inhibition of hepatitis C virus (HCV) core protein- induced cell growth by non-structural protein 4A (NS4A) is mediated by mitochondrial dysregulation.
    Bosnian journal of basic medical sciences, 2008, Volume: 8, Issue:1

    Hepatitis C virus (HCV) is a significant health problem facing the world. More than 170 million people are infected with HCV worldwide. HCV encodes a large polyprotein precursor that is processed into at least 10 distinct products including structural (core, E1 and E2) and non-structural (NS2, NS3, NS4A, NS4B, NS5A and NS5B). Besides its importance in virus replication, NS4A functions as a cofactor for NS3 and contributes to viral pathogenesis by influencing cellular functions. Here, we investigated the effect of NS4A protein on the growth rate induced by core protein in liver cells. Using our established tetracycline inducible system, we demonstrated the ability of NS4A protein to inhibit core protein-induced cell growth in Hepatoma cell line, HepG2. Induction of both core and NS4A proteins in HepG2-core/NS4A transfectants inhibited core-induced growth advantage in HepG2-core transfectants and blocked NS4A protein-induced cell growth inhibition in HepG2-NS4A transfectants. Using both immune fluorescence staining and Western blot analysis, we confirmed the localization of NS4A protein to the mitochondria in HepG2-NS4A transfectants expressing NS4A protein. Data obtained from flow cytometry analysis, using JC-1 demonstrated the loss of mitochondrial membrane potential (DeltaPsim) by the expression of NS4A protein in HepG2-NS4A transfectants, but not by the expression of core protein in HepG2-core transfectants. Whereas, the induction of the expression of both core and NS4A proteins in HepG2-core/NS4A transfectants blocked NS4A-induced loss of DeltaPsim in HepG2 cells. Taken together, our data suggest an important role for mitochondria in the modulation HCV NS4A-induced inhibition of HCV core-mediated cell growth.

    Topics: Carcinoma, Hepatocellular; Carrier Proteins; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Viral; Hepacivirus; Humans; Intracellular Signaling Peptides and Proteins; Liver Neoplasms; Membrane Potential, Mitochondrial; Mitochondria, Liver; Protein Synthesis Inhibitors; Tetracycline; Viral Core Proteins; Viral Nonstructural Proteins; Viral Proteins

2008
Different levels of p53 induced either apoptosis or cell cycle arrest in a doxycycline-regulated hepatocellular carcinoma cell line in vitro.
    Apoptosis : an international journal on programmed cell death, 2007, Volume: 12, Issue:2

    Induction of p53 gene expression in cancer cells can lead to both cell cycle arrest and apoptosis. To clarify whether the level of p53 expression determines the apoptotic response of hepatocellular carcinoma (HCC) cells, we assessed the effect of various levels of expression of p53 gene on a p53-deficient HCC cell line, Hep3B, utilizing a doxycycline (Dox)-regulated inducible p53 expression system. Our results showed that apoptosis was induced in HCC cells with high levels of p53 expression. However, lower level of p53 expression induced only cell cycle arrest but not apoptosis. Bax expression was up-regulated following high levels of p53 expression, while bcl-2 expression was not altered by the level of p53 expression. Moreover, p21 expression was observed in both high and low expression of p53. These results suggest the level of p53 expression could determine if the HCC cells would go into cell cycle arrest or apoptosis. Bax may participate, at least in part, in inducing p53-dependent apoptosis and the induction of p21 alone was able to cause cell cycle arrest but not apoptosis.

    Topics: Anti-Bacterial Agents; Apoptosis; bcl-2-Associated X Protein; Carcinoma, Hepatocellular; Cell Cycle; Cell Line, Tumor; Clone Cells; Cyclin-Dependent Kinase Inhibitor p21; Doxycycline; Gene Expression Regulation, Neoplastic; Humans; Liver Neoplasms; Tetracycline; Tumor Suppressor Protein p53; Up-Regulation

2007
Development of a transactivator in hepatoma cells that allows expression of phase I, phase II, and chemical defense genes.
    American journal of physiology. Cell physiology, 2006, Volume: 290, Issue:1

    Precise control of the level of protein expression in cells can yield quantitative and temporal information on the role of a given gene in normal cellular physiology and on exposure to chemicals and drugs. This is particularly relevant to liver cells, in which the expression of many proteins, such as phase I and phase II drug-metabolizing enzymes, vary widely between species, among individual humans, and on exposure to xenobiotics. The most widely used gene regulatory system has been the tet-on/off approach. Although a second-generation tet-on transactivator was recently described, it has not been widely investigated for its potential as a tool for regulating genes in cells and particularly in cells previously recalcitrant to the first-generation tet-on approach, such as hepatocyte-derived cells. Here we demonstrate the development of two human (HepG2 and HuH7) and one mouse (Hepa1c1c7) hepatoma-derived cell lines incorporating a second-generation doxycycline-inducible gene expression system and the application of the human lines to control the expression of different transgenes. The two human cell lines were tested for transient or stable inducibility of five transgenes relevant to liver biology, namely phase I (cytochrome P-450 2E1; CYP2E1) and phase II (glutathione S-transferase P1; GSTP1) drug metabolism, and three transcription factors that respond to chemical stress [nuclear factor erythroid 2 p45-related factors (NRF)1 and 2 and NFKB1 subunit of NF-kappaB]. High levels of functional expression were obtained in a time- and dose-dependent manner. Importantly, doxycycline did not cause obvious changes in the cellular proteome. In conclusion, we have generated hepatocyte-derived cell lines in which expression of genes is fully controllable.

    Topics: Amino Acid Sequence; Animals; Anti-Bacterial Agents; Carcinoma, Hepatocellular; Cell Line, Tumor; Cytochrome P-450 CYP2E1; Doxycycline; Gene Expression Regulation, Neoplastic; Glutathione Transferase; Hepatocytes; Humans; Liver; Liver Neoplasms; Mice; Molecular Sequence Data; NF-E2-Related Factor 1; NF-E2-Related Factor 2; NF-kappa B p50 Subunit; Protein Synthesis Inhibitors; Tetracycline; Transgenes; Xenobiotics

2006
The mitogenic function of hepatitis B virus X protein resides within amino acids 51 to 140 and is modulated by N- and C-terminal regulatory regions.
    Journal of virology, 2006, Volume: 80, Issue:21

    The hepatitis B virus (HBV) X protein (pX) is implicated in hepatocarcinogenesis by an unknown mechanism. pX variants encoded by HBV genomes found integrated in genomic DNA from liver tumors of patients with hepatocellular carcinoma (HCC) generally lack amino acids 134 to 154. Since deregulation of mitogenic pathways is linked to oncogenic transformation, herein we define the pX region required for mitogenic pathway activation. A series of pX deletions was used to construct tetracycline-regulated pX-expressing cell lines. The activation of the mitogenic pathways by these pX deletions expressed in the constructed cell lines was measured by transient transreporter assays, effects on endogenous cyclin A expression, and apoptosis. Conditional expression of pX51-140 in AML12 clone 4 cell line activates the mitogenic pathways, induces endogenous cyclin A expression, and sensitizes cells to apoptosis, similar to wild-type (WT) pX. By contrast, pX1-115 is inactive, supporting the idea that amino acids 116 to 140 are required for mitogenic pathway activation. Moreover, this pX deletion analysis demonstrates that WT pX function is modulated by two regions spanning amino acids 1 to 78 and 141 to 154. The N-terminal X1-78, expressed via a retroviral vector in WT pX-expressing 4pX-1 cells, coimmunoprecipitates with WT pX, indicating this pX region participates in protein-protein interactions leading to pX oligomerization. Interestingly, pX1-78 interferes with WT pX in mediating mitogenic pathway activation, endogenous gene expression, and apoptosis. The C-terminal pX region spanning amino acids 141 to 154 decreases pX stability, determined by pulse-chase studies of WT pX and pX1-140, suggesting that increased stability of naturally occurring pX variants lacking amino acids 134 to 154 may play a role in HCC development.

    Topics: Animals; Apoptosis; Carcinoma, Hepatocellular; Cell Line; Cyclin A; Gene Expression; Genes, Viral; Hepatitis B virus; Humans; Liver Neoplasms; Mice; Mitogens; Recombinant Proteins; Sequence Deletion; Signal Transduction; Tetracycline; Trans-Activators; Transfection; Viral Regulatory and Accessory Proteins

2006
Accumulation of 99mTc-PMT in renal metastasis of hepatocellular carcinoma.
    Annals of nuclear medicine, 2003, Volume: 17, Issue:4

    We describe here a case in which 99mTc-Sn-N-pyridoxy-5-methyltryptophan (99mTc-PMT) scintigraphy was useful in diagnosing renal metastasis of hepatocellular carcinoma (HCC). A 62-year-old man who had undergone hepatectomy for HCC presented 6 years after initial diagnosis with left flank pain and was found on CT and MRI to have a tumor in the left kidney. Hepatobiliary scintigraphy using 99Tc-PMT was performed, and 99mTc-PMT accumulation was found in the tumor. Nephrectomy was performed and metastasis of HCC was confirmed.

    Topics: Carcinoma, Hepatocellular; Humans; Kidney Neoplasms; Liver Neoplasms; Male; Middle Aged; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Radiopharmaceuticals; Tetracycline

2003
Inducible system in human hepatoma cell lines for hepatitis C virus production.
    Virology, 2002, Nov-10, Volume: 303, Issue:1

    We cloned the complete complementary DNA of an isolate of the hepatitis C virus, HCV-S1, into a tetracycline-inducible expression vector and stably transfected it into two human hepatoma cell lines, Huh7 and HepG2. Twenty-six Huh7 and two HepG2-positive clones were obtained after preliminary screening. Two Huh7 (SH-7 and -9) and one HepG2 (G-19) clones were chosen for further characterisation. Expression of HCV proteins in these cells accumulated from 6 h to 4 days posttreatment. Full-length viral plus-strand RNA was detected by Northern analyses. Using RT-PCR and ribonuclease protection assay, we also detected the synthesis of minus-strand HCV RNA. Plus- and minus-strand viral RNA was still detected after treatment with actinomycin D. Indirect immunofluorescence staining with anti-E2, NS4B, and NS5A revealed that these proteins were mostly localised to the endoplasmic reticulum (ER). Culture media from tet-induced SH-9 cells was separated on sucrose density gradients and analysed for the presence of HCV RNA. Viral RNA levels peaked at two separate ranges, one with a buoyant density of 1.08 g/ml and another from 1.17 to 1.39 g/ml. Electron microscopy demonstrated the presence of subviral-like particles (approximately 20-25 nm in diameter) in the cytoplasm of SH-9 and G-19 cells, which were positively labelled by anti-HCV core antibodies. Anti-E2 antibodies strongly labelled cytoplasmic vesicular structures and some viral-like particles. Complete viral particles of about 50 nm which reacted with anti-E2 antibodies were observed in the culture media of tet-induced SH-9 cells following negative staining. Supernatant from tet-treated SH-9 cells was found to infect nai;ve Huh7 and stable Huh7-human CD81 cells.

    Topics: Carcinoma, Hepatocellular; Centrifugation, Density Gradient; Culture Media; Endoplasmic Reticulum; Genetic Vectors; Hepacivirus; Hepatitis C Antigens; Humans; Liver Neoplasms; RNA, Viral; Tetracycline; Transfection; Tumor Cells, Cultured; Viral Core Proteins; Viral Envelope Proteins; Viral Nonstructural Proteins; Viral Proteins; Virion; Virus Replication

2002
Synergistic effect of basic fibroblast growth factor and vascular endothelial growth factor in murine hepatocellular carcinoma.
    Hepatology (Baltimore, Md.), 2002, Volume: 35, Issue:4

    The growth of any solid tumor depends on angiogenesis. Among the known angiogenic factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), are potent and representative factors involved in tumor development. It has been reported that bFGF and VEGF showed a synergistic effect in both in vitro and in vivo angiogenesis. However, the interaction of these factors on tumor development and angiogenesis, including hepatocellular carcinoma (HCC), has not yet been elucidated. In this study, we examined the combined effect of bFGF and VEGF overexpression by means of a combination of a retroviral tetracycline (tet)-regulated (Retro-Tet) gene expression system, which can manipulate the gene expression in vivo by providing tet in the drinking water, and a conventional plasmid gene expression system. In an allograft study, bFGF and VEGF overexpression synergistically increased tumor growth and angiogenesis in the murine HCC cells. This synergistic effect also was found in established tumors. VEGF messenger RNA (mRNA) expression in the tumor was increased 3.1-fold by bFGF-overexpression, and the bFGF-induced tumor development was significantly attenuated by treatment with KDR/Flk-1 neutralizing monoclonal antibody. In conclusion, these results suggest that bFGF synergistically augments VEGF-mediated HCC development and angiogenesis at least partly by induction of VEGF through KDR/Flk-1.

    Topics: Animals; Carcinoma, Hepatocellular; Drug Synergism; Endothelial Growth Factors; Fibroblast Growth Factor 2; Gene Transfer Techniques; Genetic Vectors; Injections, Subcutaneous; Liver Neoplasms; Lymphokines; Mice; Mice, Inbred BALB C; Neoplasm Transplantation; Neovascularization, Pathologic; Protein Synthesis Inhibitors; Receptor Protein-Tyrosine Kinases; Receptors, Growth Factor; Receptors, Vascular Endothelial Growth Factor; Retroviridae; Tetracycline; Tumor Cells, Cultured; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

2002
Multiple bone metastases of hepatocellular carcinoma.
    Annals of nuclear medicine, 2001, Volume: 15, Issue:6

    Topics: Bone Neoplasms; Carcinoma, Hepatocellular; Clavicle; Humans; Ilium; Liver Neoplasms; Male; Middle Aged; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Radiopharmaceuticals; Ribs; Scapula; Skull; Technetium Tc 99m Medronate; Tetracycline

2001
Discordant uptake of Tc-99m PMT and Tc-99m GSA by two hepatocellular carcinoma lesions.
    Annals of nuclear medicine, 2000, Volume: 14, Issue:6

    Tc-99m PMT and Tc-99m GSA can be taken up by hepatocellular carcinoma (HCC), but there has been no report concerning HCC showing accumulation of both of Tc-99m PMT and Tc-99m GSA. In this paper we describe a case of two simultaneously developed HCCs, one of which took up both tracers but the other took up neither of them.

    Topics: Aged; Carcinoma, Hepatocellular; Female; Humans; Liver Neoplasms; Magnetic Resonance Imaging; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Radiopharmaceuticals; Reproducibility of Results; Technetium Tc 99m Aggregated Albumin; Technetium Tc 99m Pentetate; Tetracycline; Tissue Distribution; Tomography, X-Ray Computed

2000
Vascular endothelial growth factor tightly regulates in vivo development of murine hepatocellular carcinoma cells.
    Hepatology (Baltimore, Md.), 1998, Volume: 28, Issue:6

    Angiogenesis is essential for the development of a solid tumor, including hepatocellular carcinoma (HCC). HCC is a well-known hypervascular tumor. Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic factors. Its role has not been clarified in vivo in HCC development. We used a self-contained, tetracycline-regulated retroviral vector system to elucidate the effect of VEGF on murine HCC development in a xenograft experimental model. By delivering the VEGF gene within the retroviral vector and under the control of a tetracycline-regulated promoter, we were able to manipulate VEGF expression in vivo tumor by providing tetracycline in the drinking water. Overexpression of VEGF showed a marked increase in tumor development accompanied by augmentation of neovascularization. The degree of tumor enlargement corresponded to the level of VEGF gene expression. Suppression of VEGF led to a decrease in tumor growth at the established tumor size, whether relatively small or large. The level of VEGF expression did not alter the proliferation of HCC cells in vitro. In a double-chamber chemoinvasion assay, the in vitro invasion activity of VEGF-transduced cells was not changed. In the presence of endothelial cells (EC), however, VEGF-transduced cells showed a marked increase in their in vitro invasion activity. These results suggested that VEGF plays a critical role in the development of HCC in cooperation with EC

    Topics: Animals; Carcinoma, Hepatocellular; Cell Division; Cell Movement; Endothelial Growth Factors; Endothelium, Vascular; Gene Expression Regulation; Genetic Vectors; Humans; Liver Neoplasms; Lymphokines; Mice; Neoplasm Invasiveness; Platelet Endothelial Cell Adhesion Molecule-1; Protein Synthesis Inhibitors; Retroviridae; Tetracycline; Tumor Cells, Cultured; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors

1998
Reversible intercellular coupling by regulated expression of a gap junction channel gene.
    Cell adhesion and communication, 1995, Volume: 3, Issue:4

    Direct intercellular coupling through gap junction channels has been implicated in diverse processes including cellular differentiation, growth control, metabolic cooperativity and electronic coupling and natural and induced mutations in connexin genes have been described in human and experimental disease states. Genetic systems in which the extent of coupling could be reversibly regulated would provide an important approach for examining these potential functional roles, both in vitro and in vivo. Here we describe the generation and characterization of cell lines in which the extent of coupling is reversibly controlled at the transcriptional level. Plasmids encoding a tetracycline-controlled transactivator and a tetracycline-responsive connexin32 target gene were introduced in the communication-deficient SKHep1 cell line. Quantitative immunoblotting and confocal immunofluorescence microscopy with connexin32-specific antibodies demonstrated that expression of connexin32 in stable transfectants was tightly regulated by tetracycline treatment. Moreover, transfectants exhibited a highly coupled phenotype which was rapidly and reversibly converted to the communication deficient parental state after tetracycline treatment. Time constants for decay of the messenger RNA, protein and functional coupling were similar (approximately 4 hrs), implying that transcription was rate-limiting and that separate long-lived pools of connexin32 protein were absent. In contrast to other approaches in which the extent of coupling is pharmacologically regulated by altering channel gating characteristics or by generalized blockade of transcription or translation, in this system intercellular communication is regulated by directly controlling connexin gene expression.

    Topics: Carcinoma, Hepatocellular; Connexins; Gap Junction beta-1 Protein; Gap Junctions; Gene Expression Regulation; Genes, Reporter; Genetic Vectors; Humans; Luciferases; Protein Synthesis Inhibitors; Repressor Proteins; RNA, Messenger; Tetracycline; Transcription, Genetic; Transcriptional Activation; Tumor Cells, Cultured

1995
[Clinical usefulness of 99mTc-PMT whole body scans in the diagnosis of bone metastases from hepatocellular carcinoma].
    Nihon Igaku Hoshasen Gakkai zasshi. Nippon acta radiologica, 1992, Feb-25, Volume: 52, Issue:2

    The diagnostic value of whole body scanning using 99mTc-N-pyridoxylmethyltryptophan (PMT) was evaluated in 16 patients with bone metastases from hepatocellular carcinoma, in comparison with 99mTc-MDP. Of the 72 known lesions of bone metastases, 63 (87.5%) were detected by 99mTc-PMT scintigraphy, which demonstrated increased uptake of radionuclide. However, 99mTc-MDP bone scintigraphy detected only 45 lesions (62.5%), which were shown as increased, decreased, or mixed patterns of uptake. Thus 99mTc-PMT scintigraphy was more sensitive than 99mTc-MDP bone scintigraphy. In addition, the latter showed poor specificity because of its high false positive rate due to degenerative change. All lesions undetected by 99mTc-PMT scintigraphy were located in areas that overlapped the liver or bowel activity. In conclusion, it is recommended that whole body 99mTc-PMT scintigraphy be combined with 99mTc-MDP bone scintigraphy for the detection of bone metastases from hepatocellular carcinoma.

    Topics: Aged; Aged, 80 and over; Bone Neoplasms; Carcinoma, Hepatocellular; Female; Humans; Japan; Liver Neoplasms; Male; Middle Aged; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Retrospective Studies; Tetracycline; Tetracyclines

1992
Discordant hepatic uptake of Tc-99m NGA and Tc-99m PMT in a patient with hepatoma.
    Clinical nuclear medicine, 1992, Volume: 17, Issue:10

    The authors report discordant hepatic uptake of Tc-99m NGA and Tc-99m PMT in a patient with hepatoma. Tc-99m PMT uptake was delayed and Tc-99m NGA concentrated in another area, thereby demonstrating that the uptake mechanisms for Tc-99m NGA and Tc-99m PMT are different. Tc-99m NGA imaging may be useful in characterizing the focal hepatic lesion of Tc-99m IDA or Tc-99m PMT concentration.

    Topics: Albumins; Carcinoma, Hepatocellular; Humans; Liver Neoplasms; Male; Middle Aged; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Tetracycline; Tetracyclines

1992
Accumulation of Tc-99m PMT in adrenal metastasis of hepatoma.
    Clinical nuclear medicine, 1991, Volume: 16, Issue:12

    Topics: Adrenal Gland Neoplasms; Aged; Aged, 80 and over; Carcinoma, Hepatocellular; Humans; Liver Neoplasms; Male; Organotechnetium Compounds; Pyrrolidines; Radionuclide Imaging; Tetracycline; Tetracyclines

1991
[Detection of neoplastic cells in the bloodstream].
    Biulleten' eksperimental'noi biologii i meditsiny, 1975, Volume: 80, Issue:7

    A study was made of the efficacy of trypan blue, acridine orange, tetracycline and oxytetracycline for detection of tumour cells injected into the blood stream of rats. The cells were identified in the mesenteric microvessels by intravital microscopy. Fluorescence of fluorochromized cells was observed in the blue-violet (lambda max = 400 nm) and ultra-violet (lambda max = 365 nm) irradiation of the fluorescent lamp and in the laser irradiation (lambda = 337 nm). The cells stained with acridine orange had a higher fluorescence intensity and a more distinct structure than those labelled with tetracyclines. Identification of cells with trypan blue was more difficult. The fluorescent method of determination is rather simple and permits to indentify tumour cells directly in the blood stream.

    Topics: Acridines; Animals; Carcinoma, Hepatocellular; Liver Neoplasms; Microscopy, Fluorescence; Neoplasms, Experimental; Neoplastic Cells, Circulating; Oxytetracycline; Rats; Staining and Labeling; Tetracycline; Trypan Blue

1975
Tumor detection and localization with 99mTc-tetracycline.
    Radiology, 1974, Volume: 112, Issue:1

    Topics: Adenocarcinoma; Animals; Carcinoma, Bronchogenic; Carcinoma, Hepatocellular; Gallium; Glioblastoma; Hodgkin Disease; Humans; L-Lactate Dehydrogenase; Liver Neoplasms; Lung Neoplasms; Mediastinal Neoplasms; Methane; Mice; Muscular Diseases; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms, Experimental; Nitrosourea Compounds; Osteosarcoma; Rabbits; Radioisotopes; Radionuclide Imaging; Rats; Sarcoma; Sarcoma, Experimental; Technetium; Tetracycline; Transplantation, Homologous

1974
Stability studies and tumor uptake of a technetium-tetracycline complex.
    Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 1974, Volume: 15, Issue:11

    Topics: Animals; Carcinoma, Hepatocellular; Drug Stability; Gastric Mucosa; Kidney; Liver; Liver Neoplasms; Neoplasm Transplantation; Neoplasms, Experimental; Radionuclide Imaging; Rats; Rats, Inbred BUF; Technetium; Tetracycline

1974
[On biliary excretion of minocycline (minomycin 'Lederle') injected by intravenous drip (author's transl)].
    The Japanese journal of antibiotics, 1974, Volume: 27, Issue:3

    Topics: Aged; Bile; Carcinoma, Hepatocellular; Cholelithiasis; Humans; Infusions, Parenteral; Liver Neoplasms; Male; Middle Aged; Minocycline; Postoperative Complications; Tetracycline; Time Factors

1974
[Effects of x-rays on the cells of ascites tumors, studied with fluorescence microscopy].
    Bollettino della Societa italiana di biologia sperimentale, 1971, May-15, Volume: 47, Issue:9

    Topics: Acridines; Animals; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Liver Neoplasms; Mice; Microscopy, Fluorescence; Neoplasms, Experimental; Radiation Effects; Rats; Tetracycline

1971
BACTERIOSTATIC CHEMOTHERAPEUTIC AGENTS AND THE GROWTH OF MALIGNANT TUMOR.
    The Journal of the International College of Surgeons, 1964, Volume: 41

    Topics: Adenoma; Aminosalicylic Acid; Aminosalicylic Acids; Animals; Anti-Bacterial Agents; Antineoplastic Agents; Antitubercular Agents; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Chloramphenicol; Isonicotinic Acids; Leukemia; Leukemia, Experimental; Liver Neoplasms; Neoplasms; Neoplasms, Experimental; Oleandomycin; Pharmacology; Pyrazinamide; Research; Rolitetracycline; Sarcoma; Sarcoma, Experimental; Sarcoma, Yoshida; Streptomycin; Tetracycline

1964