[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 29 of about 29
1. Jagan S, Ramakrishnan G, Anandakumar P, Kamaraj S, Devaki T: Antiproliferative potential of gallic acid against diethylnitrosamine-induced rat hepatocellular carcinoma. Mol Cell Biochem; 2008 Dec;319(1-2):51-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiproliferative potential of gallic acid against diethylnitrosamine-induced rat hepatocellular carcinoma.
  • One of the focuses in current cancer chemoprevention studies is the search for nontoxic chemopreventive agents that inhibit the initiation of malignant transformation.
  • In the present study, we investigated the antiproliferative effect of gallic acid during diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) in male wistar albino rats.
  • These finding suggests that gallic acid is a potent antiproliferative agent against DEN-induced HCC.
  • [MeSH-major] Antioxidants / pharmacology. Biomarkers, Tumor / metabolism. Carcinogens / metabolism. Carcinoma, Hepatocellular / metabolism. Cell Proliferation / drug effects. Diethylnitrosamine / toxicity. Gallic Acid / pharmacology
  • [MeSH-minor] Alkylating Agents / toxicity. Animals. Male. Neoplasms, Experimental / chemically induced. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / metabolism. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. GALLIC ACID .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Free Radic Biol Med. 2004 Aug 1;37(3):287-303 [15223063.001]
  • [Cites] Histochem J. 1986 Jan;18(1):5-14 [2423479.001]
  • [Cites] Int J Cancer. 1996 Nov 15;68(4):493-500 [8945621.001]
  • [Cites] Cancer Causes Control. 1991 Sep;2(5):325-57 [1834240.001]
  • [Cites] Cancer Lett. 2005 Aug 8;226(1):17-25 [16004929.001]
  • [Cites] J Natl Cancer Inst. 1980 Sep;65(3):529-34 [6251302.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2004 Nov;3(4):564-70 [15567746.001]
  • [Cites] Carcinogenesis. 1984 Nov;5(11):1381-93 [6386215.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):156-62 [16488533.001]
  • [Cites] Mol Cell Biochem. 1998 Aug;185(1-2):85-94 [9746215.001]
  • [Cites] Life Sci. 2005 May 27;77(2):230-40 [15862607.001]
  • [Cites] Biochim Biophys Acta. 1972 Sep 1;282(1):447-52 [4341793.001]
  • [Cites] Br J Cancer. 2002 May 20;86(10):1645-51 [12085217.001]
  • [Cites] Urology. 1981 Jul;18(1):50-3 [7257039.001]
  • [Cites] Biol Pharm Bull. 2007 Dec;30(12):2268-73 [18057710.001]
  • [Cites] Chem Biol Interact. 2006 Jun 10;161(2):104-14 [16643877.001]
  • [Cites] Oncogene. 1997 Feb 13;14(6):629-40 [9038370.001]
  • [Cites] World J Gastroenterol. 2000 Apr;6(2):234-238 [11819564.001]
  • [Cites] Nat Rev Cancer. 2006 Sep;6(9):674-87 [16929323.001]
  • [Cites] J Agric Food Chem. 1999 Oct;47(10):3954-62 [10552749.001]
  • [Cites] Exp Oncol. 2007 Mar;29(1):39-44 [17431387.001]
  • [Cites] World J Gastroenterol. 1999 Aug;5(4):356-358 [11819467.001]
  • [Cites] J Histochem Cytochem. 1995 Sep;43(9):887-93 [7642962.001]
  • [Cites] World J Gastroenterol. 2000 Apr;6(2):216-219 [11819559.001]
  • [Cites] Pharmacol Ther. 2000 Aug-Sep;87(2-3):161-73 [11007998.001]
  • [Cites] Ann N Y Acad Sci. 1975 Aug 22;259:234-8 [54025.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S27-34 [15508094.001]
  • [Cites] Chem Biol Interact. 2005 Oct 20;156(2-3):101-11 [16144695.001]
  • [Cites] Melanoma Res. 2006 Jun;16(3):213-22 [16718268.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] J Ethnopharmacol. 2007 Jan 19;109(2):214-8 [17049775.001]
  • [Cites] Indian J Exp Biol. 1998 Mar;36(3):264-72 [9754059.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Oct 28;204(2):898-904 [7980558.001]
  • [Cites] Anticancer Drugs. 2001 Nov;12(10):847-52 [11707653.001]
  • [Cites] Clin Chim Acta. 1972 Jun;39(1):41-7 [5038763.001]
  • [Cites] J Ethnopharmacol. 2006 Apr 6;104(3):407-9 [16257158.001]
  • [Cites] Biochem J. 1992 Jul 15;285 ( Pt 2):345-65 [1637327.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Mol Cell Biochem. 2008 Jun;313(1-2):53-61 [18373278.001]
  • (PMID = 18629614.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antioxidants; 0 / Biomarkers, Tumor; 0 / Carcinogens; 3IQ78TTX1A / Diethylnitrosamine; 632XD903SP / Gallic Acid
  •  go-up   go-down


2. Holmes EW, Bingham CM, Cunningham ML: Hepatic expression of polymerase beta, Ref-1, PCNA, and Bax in WY 14,643-exposed rats and hamsters. Exp Mol Pathol; 2002 Dec;73(3):209-19
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The hepatic levels of three protein markers of oxidative stress, polymerase beta, Ref-1, and PCNA, and of the pro-apoptotic protein, Bax, were quantitated after exposure to WY 14,643 (500 ppm in the feed) for 6 or 34 days in a rodent that is susceptible peroxisome proliferator (PP)-induced liver tumors (the Sprague Dawley rat) and in a rodent that is relatively resistant PP-induced liver tumors (the Syrian hamster).
  • Dose-response studies in the rat showed that the hepatic expression of the polymerase beta and Ref-1 were significantly increased after 6 days of exposure to WY 14,643 at levels of 5 and 50 ppm, respectively.
  • The analysis of subcellular fractions of rat liver showed that the pathological increases in the levels of polymerase beta, Ref-1, and PCNA were especially prominent in mitochondria-enriched particulate liver subfractions.
  • Our data are consistent with the hypothesis that the chronic overexpression of mutagenic or oncogenic effectors like polymerase beta and Ref-1 in a setting of increased hepatocyte proliferation and decreased apoptosis may facilitate peroxisome proliferator-induced hepatocellular carcinoma in the rat.
  • [MeSH-major] Carbon-Oxygen Lyases / metabolism. DNA Polymerase beta / metabolism. DNA-(Apurinic or Apyrimidinic Site) Lyase. Liver / drug effects. Peroxisome Proliferators / pharmacology. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Cell Fractionation. Cricetinae. Dose-Response Relationship, Drug. Endodeoxyribonucleases / metabolism. Immunoblotting. Male. Rats. Rats, Sprague-Dawley. Time Factors. bcl-2-Associated X Protein

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Pirinixic acid .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12565796.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 1 R03 ES09783-01
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bax protein, rat; 0 / Peroxisome Proliferators; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrimidines; 0 / bcl-2-Associated X Protein; 86C4MRT55A / pirinixic acid; EC 2.7.7.- / DNA Polymerase beta; EC 3.1.- / Endodeoxyribonucleases; EC 4.2.- / Carbon-Oxygen Lyases; EC 4.2.99.18 / Apex1 protein, rat; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  •  go-up   go-down


3. Wang SS, Zhang T, Wang XL, Hong L, Qi QH: Effect of arsenic trioxide on rat hepatocellular carcinoma and its renal cytotoxity. World J Gastroenterol; 2003 May;9(5):930-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of arsenic trioxide on rat hepatocellular carcinoma and its renal cytotoxity.
  • AIM: To study the effect of arsenic trioxide (As(2)O(3)) on rat experimental hepatocellular carcinoma and its renal cytotoxicity.
  • METHODS: The hepatocellular carcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks.
  • Before the treatment, the rat models were randomly divided into 5 groups.
  • In the treatment groups, three doses of As(2)O(3) were injected into rat abdominal cavity; the total time of drug administration was 4 weeks.
  • On the 7th, 14th and 28th day after the treatment, the hepatocellular carcinoma nodules were obtained and the morphologic changes of hepatocellular carcinoma cells were observed under light and electron microscopes; Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocellular carcinoma tissues; flow cytometry (TUNEL assay) was used to detect the apoptosis of liver cancer cells and the change of cytokinetics.
  • RESULTS: As(2)O(3) could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes.
  • The incidence of apoptosis of hapatocellular carcinoma cells was elevated (P=0.001).
  • Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013).
  • CONCLUSION: As(2)O(3) can induce apoptosis of rat hepatocellular carcinoma cells.
  • As(2)O(3) can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner; Compared with cisplatin, As(2)O(3) didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects.
  • [MeSH-major] Arsenicals / therapeutic use. Kidney / drug effects. Liver Neoplasms, Experimental / drug therapy. Oxides / therapeutic use. Oxides / toxicity
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Antineoplastic Agents / toxicity. Apoptosis / drug effects. Cell Division / drug effects. Cisplatin / therapeutic use. Cisplatin / toxicity. Female. Immunohistochemistry. Male. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. Rats, Wistar

  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12717832.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; Q20Q21Q62J / Cisplatin; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4611399
  •  go-up   go-down


Advertisement
4. Tan B, Huang JF, Wei Q, Zhang H, Ni RZ: Anti-hepatoma effect of arsenic trioxide on experimental liver cancer induced by 2-acetamidofluorene in rats. World J Gastroenterol; 2005 Oct 14;11(38):5938-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: To study the anti-hepatoma efficiency of arsenic trioxide (As(2)O(3)) in the treatment of experimental rat hepatocellular carcinoma (HCC) induced by 2-acetamidofluorene (2-FAA) and to elucidate the possible mechanisms.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Liver Neoplasms, Experimental / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] 2-Acetylaminofluorene / toxicity. Animals. Apoptosis / drug effects. Carcinogens / toxicity. Cell Cycle / drug effects. Rats. Rats, Sprague-Dawley. Vascular Endothelial Growth Factor A / metabolism

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • Hazardous Substances Data Bank. 2-ACETYLAMINOFLUORENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16273603.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Carcinogens; 0 / Oxides; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, rat; 9M98QLJ2DL / 2-Acetylaminofluorene; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4436714
  •  go-up   go-down


5. Zhang T, Wang SS, Hong L, Wang XL, Qi QH: Arsenic trioxide induces apoptosis of rat hepatocellular carcinoma cells in vivo. J Exp Clin Cancer Res; 2003 Mar;22(1):61-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide induces apoptosis of rat hepatocellular carcinoma cells in vivo.
  • The aim of this work was to study the effect of arsenic trioxide (As2O3) on rat hepatocellular carcinoma (HCC), and investgate on the mechanisms of its antitumor effect.
  • The histological and ultrastructural changes in liver tissue were observed under microscope and electronic microscope on the 7th, 14th and 28th day after drug administration.
  • The expression of bcl-2, bax, and proliferation cell nuclear antigen (PCNA) of rat liver cancer cells on the 7th day after drug administration was determined by using immunohistochemical technique.
  • In conclusion, these data demonstrate that As2O3 induces apoptosis of rat HCC cells, and it is closely associated with G2/M restriction when apoptosis reaches the top.
  • It is suggested that arsenic trioxide may be an atypical cell cycle specific agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Arsenicals / therapeutic use. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Oxides / therapeutic use
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Female. Male. Microscopy, Electron. Rats. Rats, Wistar. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12725324.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


6. Pourgholami MH, Lu Y, Wang L, Stephens RW, Morris DL: Regression of Novikoff rat hepatocellular carcinoma following locoregional administration of a novel formulation of clofazimine in lipiodol. Cancer Lett; 2004 Apr 15;207(1):37-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of Novikoff rat hepatocellular carcinoma following locoregional administration of a novel formulation of clofazimine in lipiodol.
  • We report here that, clofazimine (CFZ) treatment (0.1-10 microM) led to inhibition of in vitro proliferation of hepatocellular carcinoma (HCC) cell lines Hep3-beta, HuH-7, HepG2, SKHEP-1, PLC/PRF-5 and Novikoff.
  • In vivo, direct intratumoural and intrahepatic arterial injection (IHA) of CFZ-L led to profound inhibition of orthotopic growth of rat Novikoff liver tumours (P < 0.0001 and P < 0.005, respectively).
  • Histological examination of rat tumours, revealed the presence of lipiodol in tumour cells, 7 days after treatment with a single IHA dose.
  • Histopathology did not show any abnormality in liver, lung or bowel sections taken from animals 1 week after IHA administration of CFZ-L.
  • Similarly, liver function tests were all normal compared to saline treated animals.
  • Thus, intraarterial administration of the highly lipophilic antiproliferative agent CFZ in lipiodol solution may represent an effective and yet safe strategy for the regional treatment of HCCs.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Clofazimine / therapeutic use. Iodized Oil / therapeutic use. Liver Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis. Azo Compounds / pharmacology. Cell Division. Cell Line, Tumor. Cell Survival. Coloring Agents / pharmacology. Contrast Media / pharmacology. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Inhibitory Concentration 50. Lipid Metabolism. Rats. Time Factors

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15050732.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Azo Compounds; 0 / Coloring Agents; 0 / Contrast Media; 1320-06-5 / oil red O; 8001-40-9 / Iodized Oil; D959AE5USF / Clofazimine
  •  go-up   go-down


7. Nagata H, Hatano E, Tada M, Murata M, Kitamura K, Asechi H, Narita M, Yanagida A, Tamaki N, Yagi S, Ikai I, Matsuzaki K, Uemoto S: Inhibition of c-Jun NH2-terminal kinase switches Smad3 signaling from oncogenesis to tumor- suppression in rat hepatocellular carcinoma. Hepatology; 2009 Jun;49(6):1944-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of c-Jun NH2-terminal kinase switches Smad3 signaling from oncogenesis to tumor- suppression in rat hepatocellular carcinoma.
  • TGF-beta activates the TGF-beta type I receptor (TbetaRI) and c-Jun N-terminal kinase (JNK), which differentially phosphorylate the mediator Smad3 to become COOH-terminally phosphorylated Smad3 (pSmad3C) and linker-phosphorylated Smad3 (pSmad3L).
  • The aim of this study is to elucidate how SP600125, a JNK inhibitor, affected rat hepatocellular carcinoma (HCC) development, while focusing on the domain-specific phosphorylation of Smad3.
  • JNK/pSmad3L/c-Myc was enhanced in the rat hepatocytes exposed to DEN.
  • [MeSH-major] Anthracenes / pharmacology. Carcinoma, Hepatocellular / enzymology. Genes, Tumor Suppressor / drug effects. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. Liver Neoplasms / enzymology. Smad3 Protein / drug effects. Smad3 Protein / physiology
  • [MeSH-minor] Animals. Male. Rats. Rats, Wistar. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19418558.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracenes; 0 / Madh3 protein, rat; 0 / Smad3 Protein; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  •  go-up   go-down


8. Ogawa T, Tashiro H, Miyata Y, Ushitora Y, Fudaba Y, Kobayashi T, Arihiro K, Okajima M, Asahara T: Rho-associated kinase inhibitor reduces tumor recurrence after liver transplantation in a rat hepatoma model. Am J Transplant; 2007 Feb;7(2):347-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rho-associated kinase inhibitor reduces tumor recurrence after liver transplantation in a rat hepatoma model.
  • Tumor recurrence after liver transplantation still remains a significant problem in patients with hepatocellular carcinoma.
  • We investigated whether tacrolimus activated the Rho/ROCK signal pathway to promote the invasiveness of rat hepatocellular carcinoma cells.
  • We also investigated whether the ROCK inhibitor Y-27632 suppressed tumor recurrence after experimental liver transplantation in a rat hepatocellular carcinoma model.
  • Orthotopic liver transplantation was performed in hepatocellular carcinoma cell line McA-RH7777-bearing rats.
  • Tacrolimus stimulates the Rho/ROCK signal pathway to enhance the invasiveness of hepatocellular carcinoma, and the ROCK inhibitor Y-27632 can be used as a new antimetastatic agent for the prevention of tumor recurrence after liver transplantation.
  • [MeSH-major] Carcinoma, Hepatocellular / physiopathology. Immunosuppressive Agents / pharmacology. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Liver Neoplasms, Experimental / physiopathology. Liver Transplantation. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Tacrolimus / pharmacology
  • [MeSH-minor] Amides / pharmacology. Animals. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Cell Proliferation / drug effects. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Male. Neoplasm Invasiveness / physiopathology. Neoplasm Recurrence, Local / physiopathology. Neoplasm Recurrence, Local / prevention & control. Pyridines / pharmacology. Rats. Rats, Inbred BUF. Signal Transduction / drug effects. Signal Transduction / physiology. rho-Associated Kinases

  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17229077.001).
  • [ISSN] 1600-6135
  • [Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
  • [ISO-abbreviation] Am. J. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Amides; 0 / Enzyme Inhibitors; 0 / Immunosuppressive Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / Pyridines; 138381-45-0 / Y 27632; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / rho-Associated Kinases; WM0HAQ4WNM / Tacrolimus
  •  go-up   go-down


9. Ramakrishnan G, Elinos-Báez CM, Jagan S, Augustine TA, Kamaraj S, Anandakumar P, Devaki T: Silymarin downregulates COX-2 expression and attenuates hyperlipidemia during NDEA-induced rat hepatocellular carcinoma. Mol Cell Biochem; 2008 Jun;313(1-2):53-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Silymarin downregulates COX-2 expression and attenuates hyperlipidemia during NDEA-induced rat hepatocellular carcinoma.
  • In the present study, we investigated whether dietary supplementation of silymarin has any role in lipid components, lipid-metabolizing enzymes, free fatty acid profile, and expression of cyclooxygenase-2 (COX-2) in N-nitrosodiethylamine (NDEA)-induced hepatocellular carcinoma in rats.
  • Thus we conclude that compounds like silymarin with potent hypolipidemic effect are strong candidates as chemopreventive agents for the treatment of liver cancer.
  • [MeSH-major] Carcinoma, Hepatocellular / complications. Cyclooxygenase 2 / metabolism. Down-Regulation / drug effects. Hyperlipidemias / complications. Hyperlipidemias / enzymology. Liver Neoplasms / complications. Silymarin / pharmacology
  • [MeSH-minor] Animals. Arachidonic Acid / metabolism. Cholesterol, HDL / blood. Diethylnitrosamine. Hydroxymethylglutaryl CoA Reductases / metabolism. Immunoblotting. Lipid Metabolism / drug effects. Liver / drug effects. Liver / enzymology. Liver / pathology. Male. Phytotherapy. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochimie. 2004 Sep-Oct;86(9-10):633-42 [15556273.001]
  • [Cites] Hepatology. 2006 Sep;44(3):602-11 [16941710.001]
  • [Cites] Clin Sci (Lond). 1994 Sep;87(3):349-55 [7955912.001]
  • [Cites] Clin Chem. 1975 Sep;21(10):1523-5 [1157326.001]
  • [Cites] Cancer Lett. 2004 May 10;208(1):43-9 [15105044.001]
  • [Cites] J Lipid Res. 1964 Oct;5:600-8 [14221106.001]
  • [Cites] Biosci Biotechnol Biochem. 2004 Jan;68(1):72-8 [14745166.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Life Sci. 1996;58(18):1591-600 [8649189.001]
  • [Cites] Int J Epidemiol. 2006 Apr;35(2):361-9 [16373377.001]
  • [Cites] J Biol Chem. 1959 Mar;234(3):466-8 [13641241.001]
  • [Cites] Hepatology. 2003 Sep;38(3):756-68 [12939602.001]
  • [Cites] J Leukoc Biol. 2006 Aug;80(2):215-6 [16735695.001]
  • [Cites] Pharmacol Rep. 2006 May-Jun;58(3):413-9 [16845216.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 1997 Apr;56(4):285-93 [9150374.001]
  • [Cites] J Lipid Res. 1981 Feb;22(2):377-81 [7240964.001]
  • [Cites] Carcinogenesis. 2002 May;23(5):787-94 [12016151.001]
  • [Cites] HPB (Oxford). 2005;7(1):5-15 [18333156.001]
  • [Cites] Chem Biol Interact. 2006 Jun 10;161(2):104-14 [16643877.001]
  • [Cites] Biochem J. 1981 Nov 15;200(2):453-6 [7340847.001]
  • [Cites] Exp Oncol. 2007 Mar;29(1):39-44 [17431387.001]
  • [Cites] Clin Chem. 1973 Mar;19(3):338-40 [4347544.001]
  • [Cites] Nat Rev Cancer. 2003 Aug;3(8):582-91 [12894246.001]
  • [Cites] World J Gastroenterol. 2005 Apr 7;11(13):1896-902 [15800977.001]
  • [Cites] Nat Rev Cancer. 2005 Dec;5(12):930-42 [16341084.001]
  • [Cites] Exp Eye Res. 2000 Apr;70(4):503-17 [10865999.001]
  • [Cites] Br J Surg. 1996 Sep;83(9):1219-22 [8983610.001]
  • [Cites] Anticancer Drugs. 2004 Jul;15(6):625-32 [15205608.001]
  • [Cites] Mol Cell Biochem. 2003 Nov;253(1-2):141-9 [14619964.001]
  • [Cites] Clin Chim Acta. 1983 Sep 15;133(1):85-96 [6627678.001]
  • [Cites] Environ Health Perspect. 2001 Sep;109(9):943-7 [11673124.001]
  • [Cites] Clin Biochem. 2003 Feb;36(1):61-5 [12554062.001]
  • [Cites] Chem Biol Interact. 2007 Feb 20;165(3):239-50 [17275799.001]
  • [Cites] Lipids Health Dis. 2006 Mar 03;5:4 [16515689.001]
  • [Cites] Cancer. 2003 Aug 15;98(4):661-7 [12910508.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] Methods Enzymol. 1981;72:325-38 [7031422.001]
  • [Cites] Biochem Pharmacol. 1990 Oct 1;40(7):1663-5 [2171536.001]
  • [Cites] Br J Surg. 2004 Feb;91(2):191-8 [14760667.001]
  • [Cites] Eur J Pharmacol. 2007 Apr 10;560(2-3):110-6 [17300777.001]
  • (PMID = 18373278.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cholesterol, HDL; 0 / Silymarin; 27YG812J1I / Arachidonic Acid; 3IQ78TTX1A / Diethylnitrosamine; EC 1.1.1.- / Hydroxymethylglutaryl CoA Reductases; EC 1.14.99.1 / Cyclooxygenase 2
  •  go-up   go-down


10. Ledda-Columbano GM, Perra A, Concas D, Cossu C, Molotzu F, Sartori C, Shinozuka H, Columbano A: Different effects of the liver mitogens triiodo-thyronine and ciprofibrate on the development of rat hepatocellular carcinoma. Toxicol Pathol; 2003 Jan-Feb;31(1):113-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different effects of the liver mitogens triiodo-thyronine and ciprofibrate on the development of rat hepatocellular carcinoma.
  • Previous work has shown that treatment with thyroid hormone (T3) decreased the incidence of rat hepatocellular carcinoma (HCC).
  • Hepatic nodules were induced in Fischer rats by a single dose of DENA, followed by a 2-week exposure of the animals to 2-AAF and partial hepatectomy.
  • [MeSH-major] Clofibric Acid / analogs & derivatives. Clofibric Acid / therapeutic use. Cocarcinogenesis. Liver Neoplasms, Experimental / drug therapy. Mitogens / therapeutic use. Triiodothyronine / therapeutic use
  • [MeSH-minor] 2-Acetylaminofluorene / toxicity. Animals. Diethylnitrosamine / toxicity. Fibric Acids. Hepatectomy. Liver / drug effects. Liver / pathology. Male. Rats. Rats, Inbred F344. Time Factors

  • Hazardous Substances Data Bank. 2-ACETYLAMINOFLUORENE .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • Hazardous Substances Data Bank. LIOTHYRONINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12597455.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibric Acids; 0 / Mitogens; 06LU7C9H1V / Triiodothyronine; 3IQ78TTX1A / Diethylnitrosamine; 53PF01Q249 / Clofibric Acid; 9M98QLJ2DL / 2-Acetylaminofluorene; F8252JGO9S / ciprofibrate
  •  go-up   go-down


11. Di Stefano G, Fiume L, Baglioni M, Busi C, Chieco P, Kratz F, Mattioli A: Coupling of lactose molecules to the carrier protein hinders the spleen and bone marrow uptake of doxorubicin conjugated with human albumin. Eur J Pharm Sci; 2007 Feb;30(2):136-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Several attempts have been made to enhance doxorubicin (DOXO) concentrations in tumour cells by drug conjugation with human albumin (HSA).
  • This result can be explained by higher amounts of the former conjugate entering in these cells and suggests macrophages as the cell type responsible for the spleen and bone marrow internalization of HSA-DOXO hindered by lactose coupling.
  • Importantly, lactosamination of HSA did not reduce the marked uptake of HSA-DOXO by chemically induced rat hepatocellular carcinoma.
  • L-HSA-DOXO, by avoiding DOXO accumulation in bone marrow is an attractive candidate for clinical trials against tumors which were found to actively internalize this conjugate in laboratory animals, such as hepatocellular carcinoma.
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / chemistry. Antibiotics, Antineoplastic / pharmacokinetics. Antibiotics, Antineoplastic / pharmacology. Carbon Radioisotopes. Carcinoma, Hepatocellular / chemically induced. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / prevention & control. Cell Proliferation / drug effects. Diethylnitrosamine / toxicity. Dose-Response Relationship, Drug. Drug Carriers. Female. Humans. Liver Neoplasms, Experimental / chemically induced. Liver Neoplasms, Experimental / metabolism. Liver Neoplasms, Experimental / prevention & control. Lymphocytes / cytology. Lymphocytes / drug effects. Lymphocytes / metabolism. Macrophages / cytology. Macrophages / drug effects. Macrophages / metabolism. Male. Mice. Rats. Rats, Wistar. Time Factors. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • Hazardous Substances Data Bank. Lactose .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17218086.001).
  • [ISSN] 0928-0987
  • [Journal-full-title] European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
  • [ISO-abbreviation] Eur J Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Carbon Radioisotopes; 0 / Drug Carriers; 0 / Serum Albumin; 0 / lactosaminated serum albumin; 3IQ78TTX1A / Diethylnitrosamine; 80168379AG / Doxorubicin; J2B2A4N98G / Lactose
  •  go-up   go-down


12. Lum CT, Yang ZF, Li HY, Wai-Yin Sun R, Fan ST, Poon RT, Lin MC, Che CM, Kung HF: Gold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinoma. Int J Cancer; 2006 Mar 15;118(6):1527-38
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinoma.
  • In the present study, the antitumor effects of one of these compounds, gold(III) meso-tetraarylporphyrin 1a (gold-1a) was investigated in an orthotopic rat hepatocellular carcinoma (HCC) model as well as using a HCC cell line.
  • The rat HCC model was induced by injection of rat hepatoma cells, McA-RH7777, into the left lobe of the liver.
  • Results from our study demonstrated that gold-1a might be a novel promising chemocytotoxic agent for treating HCC.
  • [MeSH-major] Gold Compounds / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms, Experimental / drug therapy. Metalloporphyrins / therapeutic use
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Antigens, Differentiation / genetics. Antigens, Differentiation / metabolism. Apoptosis / drug effects. Aspartate Aminotransferases / blood. Blotting, Western. Body Weight / drug effects. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Administration Schedule. Gene Expression Regulation, Neoplastic / drug effects. Injections, Intraperitoneal. Male. Necrosis / chemically induced. Oligonucleotide Array Sequence Analysis. Rats. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Time Factors. Transcription Factor CHOP / genetics. Transcription Factor CHOP / metabolism

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Hazardous Substances Data Bank. GOLD COMPOUNDS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16206274.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Cell Cycle Proteins; 0 / Ddit3 protein, rat; 0 / Gold Compounds; 0 / Metalloporphyrins; 0 / gold (III) porphyrin 1a; 147336-12-7 / Transcription Factor CHOP; EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase
  •  go-up   go-down


13. Sakagami H, Satoh K, Hakeda Y, Kumegawa M: Apoptosis-inducing activity of vitamin C and vitamin K. Cell Mol Biol (Noisy-le-grand); 2000 Feb;46(1):129-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Higher concentrations of vitamin C induce apoptotic cell death in various tumor cell lines including oral squamous cell carcinoma and salivary gland tumor cell lines, possibly via its prooxidant action.
  • On the other hand, at lower concentrations, ascorbic acid displays an antioxidant property, preventing the spontaneous and stress or antitumor agent-induced apoptosis.
  • Sodium 5,6-benzylidene-L-ascorbate, intravenous administration of which induces degeneration of human inoperable tumors and rat hepatocellular carcinoma in vivo, induces apoptotic or non-apoptotic cell death, depending on the types of target cells.
  • Synergistic apoptosis-inducing actions have been found between vitamins C and K, and between these vitamins and antiproliferative agents.
  • [MeSH-major] Apoptosis / drug effects. Ascorbic Acid / pharmacology. Vitamin K / pharmacology
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Bone Density / drug effects. Humans. Molecular Structure. Rats. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Vitamin C.
  • MedlinePlus Health Information. consumer health - Vitamin K.
  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10726979.001).
  • [ISSN] 0145-5680
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] FRANCE
  • [Chemical-registry-number] 0 / Antioxidants; 12001-79-5 / Vitamin K; PQ6CK8PD0R / Ascorbic Acid
  • [Number-of-references] 112
  •  go-up   go-down


14. Sivaramakrishnan V, Niranjali Devaraj S: Morin regulates the expression of NF-kappaB-p65, COX-2 and matrix metalloproteinases in diethylnitrosamine induced rat hepatocellular carcinoma. Chem Biol Interact; 2009 Aug 14;180(3):353-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morin regulates the expression of NF-kappaB-p65, COX-2 and matrix metalloproteinases in diethylnitrosamine induced rat hepatocellular carcinoma.
  • Morin--a bioflavonoid is a naturally available dietary agent believed to impede cancer promotion and progression.
  • Reverse transcriptase polymerase chain reaction (RT-PCR) analysis revealed that administration of DEN (200 mg/kg bodyweight in drinking water) to experimental animals caused inflammation of the liver due to up-regulation of NF-kappaB-p65 and COX-2.
  • RT-PCR and immunoblot analysis also revealed that the oral supplementation of morin (500 ppm in diet) to DEN-induced hepatocellular carcinoma rats down-regulated the expression of COX-2 and NF-kappaB-p65, thereby preventing inflammation and angiogenesis mediated hepatocellular carcinogenesis.
  • Gelatin zymography was performed for matrix metalloproteinase MMP-2 and MMP-9 expression to confirm their role in angiogenesis in DEN induced hepatocellular carcinoma and its modulation by morin.
  • Both MMP-2 and MMP-9 levels were found to be increased in DEN-induced animals when compared to control.
  • MMP-2 and MMP-9 levels were down-regulated in morin post-treated animals when compared to DEN-induced animals favouring prevention of angiogenesis.
  • In conclusion, our findings indicate that morin possessed anti-inflammatory and anti-cancer properties favouring suppression of DEN-induced hepatocellular carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / metabolism. Cyclooxygenase 2 / metabolism. Flavonoids / pharmacology. Liver Neoplasms, Experimental / metabolism. Matrix Metalloproteinases / metabolism. Transcription Factor RelA / metabolism
  • [MeSH-minor] Administration, Oral. Animals. Anti-Inflammatory Agents, Non-Steroidal / chemistry. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Diethylnitrosamine. Down-Regulation. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Rats. Rats, Wistar. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19539802.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Transcription Factor RelA; 3IQ78TTX1A / Diethylnitrosamine; 8NFQ3F76WR / morin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


15. Ebert O, Shinozaki K, Huang TG, Savontaus MJ, García-Sastre A, Woo SL: Oncolytic vesicular stomatitis virus for treatment of orthotopic hepatocellular carcinoma in immune-competent rats. Cancer Res; 2003 Jul 1;63(13):3605-11
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncolytic vesicular stomatitis virus for treatment of orthotopic hepatocellular carcinoma in immune-competent rats.
  • Tumor-targeted replicating viruses are being developed as a novel class of oncolytic agents.
  • Using this GFP-expressing virus, we have demonstrated the oncolytic potential of VSV against human and rat hepatocellular carcinoma (HCC).
  • We found that rVSV-GFP replicated efficiently in cultured human and rat HCC cells, whereas normal human and rat hepatocytes were refractory.
  • Our results show that VSV is an effective oncolytic agent against HCC in immune-competent hosts and warrants further development for future therapy in patients with HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. Vesicular stomatitis Indiana virus / physiology
  • [MeSH-minor] Animals. Cell Division. Hepatocytes / virology. Humans. Liver Neoplasms, Experimental / pathology. Liver Neoplasms, Experimental / therapy. Liver Neoplasms, Experimental / virology. RNA, Viral / genetics. Rats. Rats, Inbred BUF. Recombination, Genetic. Tumor Cells, Cultured. Virus Replication

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12839948.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-100830
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral
  •  go-up   go-down


16. Qiao L, Yu J, Dent P, Farrell G: NF-kappaB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis. Cancer Biol Ther; 2005 Nov;4(11):1195-202
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-kappaB protects rat ARL-6 hepatocellular carcinoma cells against hydrogen peroxide-induced apoptosis.
  • We compared NF-kappaB activation profiles between normal rat hepatocytes and ARL-6 rat hepatocellular carcinoma (HCC) cells exposed to hydrogen peroxide (H2O2), and examined whether NF-kappaB activation could explain the observed resistance to apoptosis of ARL-6 cells.
  • METHODS: Cultured primary rat hepatocytes and ARL-6 cells were treated with graded doses of H2O2.
  • [MeSH-major] Apoptosis / drug effects. Carcinoma, Hepatocellular / pathology. Cytoprotection. Hepatocytes / drug effects. Hydrogen Peroxide / pharmacology. Liver Neoplasms / pathology. NF-kappa B / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Male. Oxidants / pharmacology. Rats. Rats, Wistar. Time Factors

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. HYDROGEN PEROXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16177566.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Oxidants; BBX060AN9V / Hydrogen Peroxide
  •  go-up   go-down


17. Zhang Y, Mi L, Xiong R, Wang PN, Chen JY, Yang W, Wang C, Peng Q: Subcellular Localization of Thiol-Capped CdTe Quantum Dots in Living Cells. Nanoscale Res Lett; 2009;4(7):606-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These unfunctionalized QDs were well internalized into human hepatocellular carcinoma and rat basophilic leukemia cells in vitro.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20596411.001).
  • [ISSN] 1931-7573
  • [Journal-full-title] Nanoscale research letters
  • [ISO-abbreviation] Nanoscale Res Lett
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Ganslmayer M, Ocker M, Kraemer G, Zopf S, Hahn EG, Schuppan D, Herold C: The combination of tamoxifen and 9cis retinoic acid exerts overadditive anti-tumoral efficacy in rat hepatocellular carcinoma. J Hepatol; 2004 Jun;40(6):952-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The combination of tamoxifen and 9cis retinoic acid exerts overadditive anti-tumoral efficacy in rat hepatocellular carcinoma.
  • BACKGROUND/AIMS: Medical treatment for hepatocellular carcinoma (HCC) remains elusive.
  • Combination therapy of both agents has not been investigated in vitro and in vivo.
  • [MeSH-major] Liver Neoplasms / drug therapy. Liver Neoplasms, Experimental / drug therapy. Tamoxifen / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Tumor. DNA Replication / drug effects. In Situ Nick-End Labeling. Rats. Rats, Inbred BUF


19. Futakuchi M, Ogawa K, Tamano S, Takahashi S, Shirai T: Suppression of metastasis by nuclear factor kappaB inhibitors in an in vivo lung metastasis model of chemically induced hepatocellular carcinoma. Cancer Sci; 2004 Jan;95(1):18-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of metastasis by nuclear factor kappaB inhibitors in an in vivo lung metastasis model of chemically induced hepatocellular carcinoma.
  • To evaluate the suppressive effects of nuclear factor kappa B (NF-kappaB) inhibitors on metastasis, three agents, pentoxifylline (PTX, 0.5% in diet), N-acetyl-L-cysteine (NAC, 0.5% in diet), and aspirin (ASP, 0.5% in diet) were applied in an in vivo highly metastatic rat hepatocellular carcinoma (HCC) model in F344 male rats.
  • Although no lung metastasis was observed in the rats killed at the end of the period of carcinogen exposure, lung metastasis was found in 100% of animals in all the groups at the end of the experiment.
  • In conclusion, the present study demonstrated that NF-kappaB inhibitors have the potential to inhibit lung metastasis from rat HCCs in vivo, and PTX is especially promising.
  • [MeSH-major] Liver Neoplasms, Experimental / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. NF-kappa B / drug effects. Neoplasm Metastasis / drug therapy
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Aspirin / pharmacology. Blotting, Western. Carcinogens / toxicity. Diethylnitrosamine / toxicity. E-Selectin / biosynthesis. E-Selectin / drug effects. Enzyme Inhibitors / pharmacology. Free Radical Scavengers / pharmacology. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / drug effects. Male. Nitrosamines / toxicity. Pentoxifylline / pharmacology. RNA, Messenger / analysis. Rats. Reverse Transcriptase Polymerase Chain Reaction. Vascular Cell Adhesion Molecule-1 / biosynthesis. Vascular Cell Adhesion Molecule-1 / drug effects

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • Hazardous Substances Data Bank. N-NITROSOMORPHOLINE .
  • Hazardous Substances Data Bank. N-ACETYLCYSTEINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14720322.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Carcinogens; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Free Radical Scavengers; 0 / NF-kappa B; 0 / Nitrosamines; 0 / RNA, Messenger; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 3IQ78TTX1A / Diethylnitrosamine; 3L25FO7FN7 / N-nitrosomorpholine; R16CO5Y76E / Aspirin; SD6QCT3TSU / Pentoxifylline; WYQ7N0BPYC / Acetylcysteine
  •  go-up   go-down


20. Futakuchi M, Ogawa K, Sano M, Tamano S, Takeshita F, Shirai T: Suppression of lung metastasis by aspirin but not indomethacin in an in vivo model of chemically induced hepatocellular carcinoma. Jpn J Cancer Res; 2002 Oct;93(10):1175-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of lung metastasis by aspirin but not indomethacin in an in vivo model of chemically induced hepatocellular carcinoma.
  • To examine the effect of non-steroidal anti-inflammatory drugs on metastasis formation, aspirin (ASP, 0.5% in diet) and indomethacin (IM, 0.005% in drinking water) were applied to an in vivo highly metastatic rat hepatocellular carcinoma (HCC) model in F344 male rats.
  • Both agents suppressed cell proliferation in HCCs, without any alteration of pan-cadherin expression.
  • Thus, the present study demonstrated that ASP, but not IM, has the potential to inhibit lung metastasis of rat HCC in vivo, possibly via reduced attachment of tumor cells to the vascular endothelium.
  • Moreover, these data indicate this in vivo model for induction of rat highly metastatic HCC to be a useful tool for the assessment of the efficacy of therapeutic treatments to block metastasis formation.
  • [MeSH-major] Aspirin / therapeutic use. Indomethacin / therapeutic use. Liver Neoplasms, Experimental / drug therapy. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary
  • [MeSH-minor] Animals. Intercellular Adhesion Molecule-1 / analysis. Male. Rats. Rats, Inbred F344. Vascular Cell Adhesion Molecule-1 / analysis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • Hazardous Substances Data Bank. INDOMETHACIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12417048.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; R16CO5Y76E / Aspirin; XXE1CET956 / Indomethacin
  •  go-up   go-down


21. Fiume L, Baglioni M, Busi C, Manerba M, Di Stefano G: The enhancement of interstitial transport of a doxorubicin-lactosaminated albumin conjugate by imatinib: in rat hepatocellular carcinoma it is not preferentially higher than that in liver and bone marrow. Eur J Pharm Biopharm; 2009 Aug;72(3):630-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The enhancement of interstitial transport of a doxorubicin-lactosaminated albumin conjugate by imatinib: in rat hepatocellular carcinoma it is not preferentially higher than that in liver and bone marrow.
  • The finding that imatinib enhances the drug transport from bloodstream to neoplastic cells suggested a possible role of this drug as an adjuvant to the chemotherapeutics given in the treatment of solid malignancies.The present experiments aimed to verify whether imatinib can selectively increase the penetration of a doxorubicin-lactosaminated human albumin conjugate (L-HSA-DOXO) in chemically induced rat hepatocellular carcinomas (HCCs).
  • To our knowledge, this is the first demonstration that the enhancing effect of imatinib on interstitial drug transport is not restricted to the tumors, but can be also displayed in normal tissues.
  • This observation casts some doubts about the possibility that the value of anticancer agents with toxic side effects on liver and bone marrow can be improved by imatinib.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Doxorubicin / pharmacokinetics. Extracellular Fluid / metabolism. Liver Neoplasms, Experimental / metabolism. Piperazines / pharmacokinetics. Pyrimidines / pharmacokinetics. Serum Albumin / pharmacokinetics
  • [MeSH-minor] Animals. Benzamides. Biological Transport / drug effects. Biological Transport / physiology. Bone Marrow / drug effects. Bone Marrow / metabolism. Drug Synergism. Humans. Imatinib Mesylate. Liver / drug effects. Liver / metabolism. Male. Rats. Rats, Wistar

  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19572414.001).
  • [ISSN] 1873-3441
  • [Journal-full-title] European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft für Pharmazeutische Verfahrenstechnik e.V
  • [ISO-abbreviation] Eur J Pharm Biopharm
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Serum Albumin; 0 / lactosaminated serum albumin; 80168379AG / Doxorubicin; 8A1O1M485B / Imatinib Mesylate
  •  go-up   go-down


22. Ajith TA, Janardhanan KK: Chemopreventive activity of a macrofungus Phellinus rimosus against N-nitrosodiethylamine induced hepatocellular carcinoma in rat. J Exp Ther Oncol; 2006;5(4):309-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemopreventive activity of a macrofungus Phellinus rimosus against N-nitrosodiethylamine induced hepatocellular carcinoma in rat.
  • Chemical substances with multiple inhibitory properties would be a welcome addition to the class of chemopreventive drugs.
  • The concentration required to inhibit 50% of Fe2+ induced lipid peroxidation in rat liver homogenate was 318 +/- 2.4 microg/ml.
  • Anticarcinogenic activity was evaluated using N-nitrosodiethylamine (NDEA) induced hepatocellular carcinoma (HCC) in rats.
  • Serum gamma glutamyl transpeptidase (GGT), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) activities and lipid peroxidation level (MDA) were elevated significantly (P<0.05) in the NDEA alone treated group of animals.
  • The NDEA alone treated animals showed altered serum albumin/globulin ratio (A:G ratio), hyperfibrinogenaemia, increased hepatic glutathione S-transferase (GST) activity, glutathione-peroxidsae (GPx) activity and reduced glutathione (GSH) level compared to the extract plus NDEA treated group.
  • The extract also inhibited in vitro aniline hydroxylase (AH) activity of rat liver induced by phenobarbitone in a dose dependent manner.
  • The results, thus suggest the significant chemopreventive properties of the aqueous extract of the Phellinus rimosus against NDEA induced hepatocellular carcinoma by its antioxidant, anti-inflammatory and antimutagenic activities.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / prevention & control. Diethylnitrosamine / pharmacology. Fungi / metabolism. Liver Neoplasms / drug therapy. Liver Neoplasms / prevention & control
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Hydroxyl Radical. Inhibitory Concentration 50. Lipid Peroxidation. Liver / metabolism. Male. Mutagens. Nitric Oxide / metabolism. Rats

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Molds.
  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17024971.001).
  • [ISSN] 1359-4117
  • [Journal-full-title] Journal of experimental therapeutics & oncology
  • [ISO-abbreviation] J. Exp. Ther. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Mutagens; 31C4KY9ESH / Nitric Oxide; 3352-57-6 / Hydroxyl Radical; 3IQ78TTX1A / Diethylnitrosamine
  •  go-up   go-down


23. Shinozaki K, Ebert O, Kournioti C, Tai YS, Woo SL: Oncolysis of multifocal hepatocellular carcinoma in the rat liver by hepatic artery infusion of vesicular stomatitis virus. Mol Ther; 2004 Mar;9(3):368-76
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oncolysis of multifocal hepatocellular carcinoma in the rat liver by hepatic artery infusion of vesicular stomatitis virus.
  • Hepatocellular carcinoma (HCC) is a lethal malignancy with poor prognosis and few effective treatments, as well as ever-increasing frequencies in the Western world.
  • Viruses that replicate selectively in cancer cells hold considerable promise as novel therapeutic agents for the treatment of malignancy.
  • The aim of this study was to evaluate the potential of VSV, administered via the hepatic artery, as an effective and safe therapeutic agent for treating "multifocal" HCC in the rat liver.
  • Finally, survival of vector-treated rats was substantially prolonged over that of animals in the control treatment group (p < 0.028).
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Genetic Therapy / methods. Hepatic Artery / metabolism. Infusions, Intra-Arterial. Liver / metabolism. Liver Neoplasms / therapy. Vesicular stomatitis Indiana virus / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytokines / biosynthesis. Galactosides / metabolism. Genetic Vectors. Humans. Immunohistochemistry. Indoles / metabolism. Inflammation. Kinetics. Male. Rats. Time Factors. beta-Galactosidase / genetics

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15006603.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100830
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Galactosides; 0 / Indoles; EC 3.2.1.23 / beta-Galactosidase; V595OG374W / 5-bromo-4-chloro-3-indolyl beta-galactoside
  •  go-up   go-down


24. Fang M, Dewaele S, Zhao YP, Stärkel P, Vanhooren V, Chen YM, Ji X, Luo M, Sun BM, Horsmans Y, Dell A, Haslam SM, Grassi P, Libert C, Gao CF, Chen CC: Serum N-glycome biomarker for monitoring development of DENA-induced hepatocellular carcinoma in rat. Mol Cancer; 2010 Aug 12;9:215
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum N-glycome biomarker for monitoring development of DENA-induced hepatocellular carcinoma in rat.
  • We previously found that serum N-linked sugar chains are altered in hepatocellular carcinoma (HCC).
  • Here, we studied glycomic alterations during development of HCC in a rat model.
  • RESULTS: Rat HCC was induced by the hepatocarcinogen, diethylnitrosamine (DENA).
  • We thus propose a GlycoTest model using the above-mentioned serum glycan markers to monitor the progression of cirrhosis and HCC in the DENA-treated rat model.
  • When DENA-treated rats were subsequently treated with farnesylthiosalicyclic acid, an anticancer drug, progression to HCC was prevented and GlycoTest markers (P5, R5a and R5b) reverted towards non-DENA levels, and the HCC-specific markers, log(R5a/P1) and log(R5b/P1), normalized completely.
  • Our GlycoTest model can be used to monitor progression of HCC and to follow up treatment of liver tumors in the DENA rat.
  • This GlycoTest model is particularly important because a rapid non-invasive diagnostic procedure for tumour progression in this rat model would greatly facilitate the search for anticancer drugs.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Hepatol. 1991 Nov;13(3):372-4 [1808228.001]
  • [Cites] J Biol Chem. 1989 Feb 15;264(5):2415-23 [2536709.001]
  • [Cites] Cancer Res. 1993 Nov 15;53(22):5419-23 [7693340.001]
  • [Cites] Methods Enzymol. 1994;230:108-32 [8139492.001]
  • [Cites] J Hepatol. 1995 Jan;22(1):112-4 [7751577.001]
  • [Cites] Adv Exp Med Biol. 1995;376:231-8 [8597253.001]
  • [Cites] J Biol Chem. 1997 Jan 31;272(5):2866-72 [9006930.001]
  • [Cites] Hepatology. 2005 Feb;41(2):307-14 [15660382.001]
  • [Cites] Cancer Res. 1999 May 1;59(9):2237-43 [10232614.001]
  • [Cites] Dev Biol Stand. 1998;96:43-7 [9890515.001]
  • [Cites] Methods. 2005 Apr;35(4):328-37 [15804604.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15791-6 [16236725.001]
  • [Cites] Immunol Cell Biol. 2005 Dec;83(6):674-86 [16266320.001]
  • [Cites] J Biol Chem. 2006 Feb 3;281(5):2572-7 [16316986.001]
  • [Cites] Am J Gastroenterol. 2006 Mar;101(3):513-23 [16542288.001]
  • [Cites] Int J Cancer. 2006 Jun 1;118(11):2803-8 [16385567.001]
  • [Cites] Methods Enzymol. 2006;415:59-86 [17116468.001]
  • [Cites] J Proteome Res. 2007 May;6(5):1822-32 [17432893.001]
  • [Cites] J Biol Chem. 2007 May 25;282(21):15700-8 [17383961.001]
  • [Cites] Mol Cancer Ther. 2007 Jun;6(6):1765-73 [17541036.001]
  • [Cites] Hepatology. 2007 Nov;46(5):1426-35 [17683101.001]
  • [Cites] J Hepatol. 2008 May;48(5):858-79 [18314222.001]
  • [Cites] J Proteome Res. 2008 Apr;7(4):1650-9 [18311910.001]
  • [Cites] J Biochem. 2008 Jun;143(6):725-9 [18218651.001]
  • [Cites] Biogerontology. 2008 Oct;9(5):351-6 [18431686.001]
  • [Cites] Arch Toxicol. 2008 Sep;82(9):623-31 [18204979.001]
  • [Cites] Mech Ageing Dev. 2009 Jan-Feb;130(1-2):92-7 [19070631.001]
  • [Cites] Mol Cell Proteomics. 2009 May;8(5):986-94 [19181623.001]
  • [Cites] Int J Cancer. 2010 Jul 1;127(1):148-59 [19904744.001]
  • [Cites] Liver Int. 2010 Feb;30(2):259-67 [19951379.001]
  • [Cites] Eur J Cancer. 2009 Jul;45(11):2050-60 [19427195.001]
  • [Cites] Scand J Immunol. 2000 Mar;51(3):300-6 [10736100.001]
  • [Cites] Clin Liver Dis. 2001 Feb;5(1):145-59 [11218912.001]
  • [Cites] Biochimie. 2001 Jul;83(7):557-63 [11522383.001]
  • [Cites] Int J Cancer. 2001 Oct 15;94(2):153-6 [11668491.001]
  • [Cites] Biomed Chromatogr. 2002 Sep;16(6):365-72 [12228891.001]
  • [Cites] J Clin Gastroenterol. 2002 Nov-Dec;35(5 Suppl 2):S72-8 [12394209.001]
  • [Cites] J Hepatol. 2003 Mar;38(3):357-60 [12586303.001]
  • [Cites] J Hepatol. 2003;38 Suppl 1:S38-53 [12591185.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6282-9 [14559815.001]
  • [Cites] Dig Liver Dis. 2004 Apr;36(4):231-42 [15115333.001]
  • [Cites] Nat Med. 2004 Apr;10(4):429-34 [15152612.001]
  • [Cites] Clin Chem. 2004 Aug;50(8):1299-300 [15277345.001]
  • [Cites] Hepatology. 1993 Jan;17(1):50-2 [7678576.001]
  • (PMID = 20704698.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBF0083091
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carcinogens; 0 / Polysaccharides; 3713-31-3 / Fucose; 3IQ78TTX1A / Diethylnitrosamine; EC 2.4.1.- / Fucosyltransferases
  • [Other-IDs] NLM/ PMC2925372
  •  go-up   go-down


25. Yang FC, Zheng SS, Jiang TA: A modified rat model for hepatocellular carcinoma. Hepatobiliary Pancreat Dis Int; 2004 Nov;3(4):585-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A modified rat model for hepatocellular carcinoma.
  • BACKGROUND: Rat hepatocellular carcinoma (HCC) model which has a high analogy to clinical liver cancer is of great value in understanding the pathogenesis and evolution of liver cancer, in searching effective anti-cancer treatments (drug, hepatectomy and liver transplantation), and designing cancer prevention strategies.
  • In this study we established a modified rat model of hepatocellular carcinoma to enhance rats' physique and surgical endurance.
  • METHODS: Wistar rats were fed with diethylnitrosamine (DENA) by three methods for evaluation of general conditions for 130 days: Doppler ultrasonographic measurement, laparotomy and histopathological examination.
  • RESULTS: No rat died in control group (group A) and modified DENA-induction-HCC group(group C), but 6 deaths in classical DENA-induction-HCC group (group B) (survival rate 80%).
  • All survived rats in groups B and C developed diffusive hepatocellular carcinoma and liver cirrhosis.
  • General appearance of rats in the group C was better than that in the group B.
  • CONCLUSION: With good general conditions for surgery, the modified rat model for hepatocellular carcinoma has a high carcinogenic rate and a high survival rate.
  • [MeSH-major] Carcinoma, Hepatocellular / chemically induced. Diethylnitrosamine. Disease Models, Animal. Liver Neoplasms, Experimental / chemically induced
  • [MeSH-minor] Animals. Body Weight. Laparotomy. Male. Rats. Rats, Wistar. Survival Analysis. Ultrasonography, Doppler

  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15567750.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 3IQ78TTX1A / Diethylnitrosamine
  •  go-up   go-down


26. Taras D, Blanc JF, Rullier A, Dugot-Senant N, Laurendeau I, Vidaud M, Rosenbaum J: Pravastatin reduces lung metastasis of rat hepatocellular carcinoma via a coordinated decrease of MMP expression and activity. J Hepatol; 2007 Jan;46(1):69-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pravastatin reduces lung metastasis of rat hepatocellular carcinoma via a coordinated decrease of MMP expression and activity.
  • BACKGROUND/AIMS: Statins have beneficial effects in early pre-clinical models of hepatocellular carcinoma (HCC).
  • Our aim was to test the efficacy of pravastatin on the progression of established HCC in rat, and to study its mechanisms.
  • Every CG rat surviving at 24 weeks (4/4) had lung metastasis, against only 5/8 in PG.
  • [MeSH-major] Liver Neoplasms, Experimental / drug therapy. Lung Neoplasms / prevention & control. Matrix Metalloproteinase Inhibitors. Matrix Metalloproteinases / genetics. Pravastatin / pharmacology
  • [MeSH-minor] Animals. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Male. Matrix Metalloproteinase 14 / genetics. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 9 / genetics. Rats. Rats, Inbred F344

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16935385.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Matrix Metalloproteinase Inhibitors; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.80 / Matrix Metalloproteinase 14; KXO2KT9N0G / Pravastatin
  •  go-up   go-down


27. Waehler R, Ittrich H, Mueller L, Krupski G, Ameis D, Schnieders F: Low-dose adenoviral immunotherapy of rat hepatocellular carcinoma using single-chain interleukin-12. Hum Gene Ther; 2005 Mar;16(3):307-17
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose adenoviral immunotherapy of rat hepatocellular carcinoma using single-chain interleukin-12.
  • In a rat model of hepatocellular carcinoma, this vector revealed antitumor effects even at a low dosage of 4.6 x 10(5) i.u. in a dose-dependent manner.
  • Long-term antitumor effects were determined at 2.3 x 10(6) and 2.3 x 10(7) i.u. per animal, resulting in 82% and 90% surviving animals, respectively.
  • Animals rechallenged with tumor cells remained tumor-free.
  • Compared to studies applying native IL-12, our data show that the fusion of IL-12 subunits provides approximately 1000-fold higher biological activity.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Genetic Therapy / methods. Genetic Vectors / therapeutic use. Immunotherapy / methods. Interleukin-12 / therapeutic use. Liver Neoplasms, Experimental / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Histological Techniques. Magnetic Resonance Imaging. Mice. Rats

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15812226.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 187348-17-0 / Interleukin-12
  •  go-up   go-down


28. Das T, Patra F, Mukherjee B: Effect of antisense oligomer in controlling c-raf.1 overexpression during diethylnitrosamine-induced hepatocarcinogenesis in rat. Cancer Chemother Pharmacol; 2010 Jan;65(2):309-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of antisense oligomer in controlling c-raf.1 overexpression during diethylnitrosamine-induced hepatocarcinogenesis in rat.
  • PURPOSE: In ras-mediated signal transduction pathway, c-raf.1 is believed to have predominant oncogenic potential and has been found to be highly expressed in certain human and animal malignancies including hepatocellular carcinoma.
  • METHODS: Initially antiproliferating effect of the antisense oligomers was studied in vitro by measuring the rate of tritiated thymidine incorporation into DNA in rat hepatocellular carcinoma cells in culture medium.
  • Based on the findings, the antisense treatment was carried out in rat hepatocarcinogenesis model-initiated with diethylnitrosamine and promoted using 2-acetylaminoflourene.
  • Different drug-metabolizing enzymes, lipid peroxidation, liver morphology and histopathological studies along with c-raf.1 gene expression by in situ hybridization were performed.
  • Treatment of antisense c-raf.1 oligomers enhanced cytochrome P-450 content (81%) and reduced glutathione S-transferase activity (33%), UDP glucuronosyltransferase activity (74%) and MDA concentration (30%) in carcinogen and antisense oligomer-treated group as compared with carcinogen control animals.
  • CONCLUSION: The study demonstrates that the antisense oligomer targeted against c-raf.1 mRNA inhibits the overexpression of c-raf.1 gene during hepatocellular carcinoma in rats.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Transformation, Neoplastic / metabolism. Diethylnitrosamine. Liver Neoplasms / metabolism. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-raf / biosynthesis
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Cytochrome P-450 Enzyme System / metabolism. Hyperplasia. Lipid Peroxidation. Male. Precancerous Conditions / chemically induced. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. RNA, Messenger / biosynthesis. Rats. Rats, Sprague-Dawley

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19499222.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 3IQ78TTX1A / Diethylnitrosamine; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf
  •  go-up   go-down


29. Premalatha B, Sachdanandam P: Stabilization of lysosomal membrane and cell membrane glycoprotein profile by Semecarpus anacardium linn. nut milk extract in experimental hepatocellular carcinoma. Phytother Res; 2000 Aug;14(5):352-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stabilization of lysosomal membrane and cell membrane glycoprotein profile by Semecarpus anacardium linn. nut milk extract in experimental hepatocellular carcinoma.
  • Semecarpus anacardium Linn. nut milk extract administered orally at a dose of 200 mg/kg/day for 14 days exerted an in vivo stabilizing effect on lysosomal membrane and glycoprotein content in rat hepatocellular carcinoma.
  • This was demonstrated in normal rats and in animals whose biomembranes were rendered fragile by induction of hepatocellular carcinoma with aflatoxin B(1) and subsequent treatment with Semecarpus anacardium nut extract.
  • The nut extract administration reversed these adverse changes to near normal in treated animals.
  • Such stabilization of biomembranes by Semecarpus anacardium nut extract may have a beneficial effect in the treatment of hepatocellular carcinoma and other cancers involving abnormal fragility of lysosomes and glycoprotein content providing the extract demonstrates safety in a full toxicity study.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Carcinoma, Hepatocellular / prevention & control. Glycoproteins / drug effects. Liver Neoplasms, Experimental / prevention & control. Lysosomes / drug effects. Rosales
  • [MeSH-minor] Administration, Oral. Animals. Cell Membrane / drug effects. Disease Models, Animal. Male. Membrane Proteins / drug effects. Plant Extracts / administration & dosage. Plant Extracts / chemistry. Plant Extracts / pharmacology. Plant Extracts / therapeutic use. Rats. Rats, Wistar

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 John Wiley & Sons, Ltd.
  • (PMID = 10925401.001).
  • [ISSN] 0951-418X
  • [Journal-full-title] Phytotherapy research : PTR
  • [ISO-abbreviation] Phytother Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Glycoproteins; 0 / Membrane Proteins; 0 / Plant Extracts
  •  go-up   go-down






Advertisement