[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 28 of about 28
1. Hoshida Y, Toffanin S, Lachenmayer A, Villanueva A, Minguez B, Llovet JM: Molecular classification and novel targets in hepatocellular carcinoma: recent advancements. Semin Liver Dis; 2010 Feb;30(1):35-51
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular classification and novel targets in hepatocellular carcinoma: recent advancements.
  • Hepatocellular carcinoma (HCC) is one of most lethal cancers worldwide.
  • Strategic decisions for the advancement of molecular therapies in this neoplasm require a clear understanding of its molecular classification.
  • Such a framework will allow systematic understanding of the frequently co-occurring molecular aberrations to design treatment strategy for each specific subclass of tumors.
  • Accompanied by a growing number of clinical trials of molecular targeted drugs, diagnostic and prognostic biomarker development will be facilitated with special attention on study design and with new assay technologies specialized for archived fixed tissues.
  • A new class of genomic information, microRNA dysregulation and epigenetic alterations, will provide insight for more precise understanding of disease mechanism and expand the opportunity of biomarker/therapeutic target discovery.

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • 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] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Hepatology. 2001 Mar;33(3):561-8 [11230735.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2129-37 [11280777.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3225-9 [11309270.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4238-43 [11358850.001]
  • [Cites] Gastroenterology. 2001 Jun;120(7):1763-73 [11375957.001]
  • [Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61 [11459866.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15089-94 [11752456.001]
  • [Cites] Cancer Lett. 2002 Feb 25;176(2):149-58 [11804742.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2593-604 [11971194.001]
  • [Cites] Hepatology. 2002 May;35(5):1134-43 [11981763.001]
  • [Cites] J Natl Cancer Inst. 2002 May 15;94(10):755-61 [12011226.001]
  • [Cites] Mol Biol Cell. 2002 Jun;13(6):1929-39 [12058060.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3939-44 [12124323.001]
  • [Cites] Nat Genet. 2002 Aug;31(4):339-46 [12149612.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] J Hepatol. 2003 Feb;38(2):200-7 [12547409.001]
  • [Cites] BMC Cancer. 2002 Nov 15;2:29 [12433278.001]
  • [Cites] Lancet. 2003 Mar 15;361(9361):923-9 [12648972.001]
  • [Cites] Nat Med. 2003 Apr;9(4):416-23 [12640447.001]
  • [Cites] Rev Gastroenterol Disord. 2003 Winter;3(1):8-24 [12684589.001]
  • [Cites] Nat Rev Cancer. 2003 May;3(5):321-9 [12724730.001]
  • [Cites] Am J Pathol. 2003 Sep;163(3):1101-7 [12937151.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1423-32 [14534335.001]
  • [Cites] Lancet. 2003 Nov 1;362(9394):1439-44 [14602436.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7646-51 [14633684.001]
  • [Cites] Lancet. 2003 Dec 6;362(9399):1907-17 [14667750.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] Hepatology. 2004 Feb;39(2):518-27 [14768006.001]
  • [Cites] Semin Liver Dis. 2004 Feb;24(1):77-88 [15085488.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3030-6 [15126338.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 22;101(25):9309-14 [15184677.001]
  • [Cites] J Hepatol. 2004 Aug;41(2):284-91 [15288478.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6058-64 [15342387.001]
  • [Cites] Hepatology. 2004 Sep;40(3):667-76 [15349906.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):461-6 [15329734.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7263-70 [15492245.001]
  • [Cites] J Hepatol. 1992 Mar;14(2-3):342-6 [1323601.001]
  • [Cites] Hepatogastroenterology. 1998 Sep-Oct;45(23):1753-9 [9840141.001]
  • [Cites] Nat Genet. 2004 Dec;36(12):1306-11 [15565109.001]
  • [Cites] BMC Cancer. 2005 Jan 10;5:3 [15642117.001]
  • [Cites] Lancet. 2005 Feb 5-11;365(9458):488-92 [15705458.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2115-24 [15781621.001]
  • [Cites] Nat Methods. 2004 Nov;1(2):155-61 [15782179.001]
  • [Cites] Semin Liver Dis. 2005;25(2):143-54 [15918143.001]
  • [Cites] Semin Liver Dis. 2005;25(2):212-25 [15918149.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] J Clin Oncol. 2005 Jul 1;23(19):4265-74 [15911866.001]
  • [Cites] J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4 [16106022.001]
  • [Cites] J Clin Oncol. 2005 Sep 20;23(27):6657-63 [16170173.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1768-71 [16251533.001]
  • [Cites] Hepatology. 2005 Nov;42(5):1208-36 [16250051.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2006 Mar;18(3):239-47 [16462536.001]
  • [Cites] Hepatology. 2006 Feb;43(2 Suppl 1):S145-50 [16447291.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Nat Rev Drug Discov. 2006 Jan;5(1):37-50 [16485345.001]
  • [Cites] Nat Med. 2006 Apr;12(4):410-6 [16532004.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1117-28 [16618406.001]
  • [Cites] Oncogene. 2006 Apr 20;25(17):2537-45 [16331254.001]
  • [Cites] Semin Liver Dis. 2006 May;26(2):153-61 [16673293.001]
  • [Cites] J Clin Invest. 2006 Jun;116(6):1582-95 [16710476.001]
  • [Cites] Hepatology. 2006 May;43(5):891-902 [16628664.001]
  • [Cites] Ann Surg Oncol. 2006 Jul;13(7):947-54 [16788756.001]
  • [Cites] Oncogene. 2006 Jun 26;25(27):3778-86 [16799619.001]
  • [Cites] Oncogene. 2006 Jun 26;25(27):3787-800 [16799620.001]
  • [Cites] Oncogene. 2006 Jun 26;25(27):3823-33 [16799624.001]
  • [Cites] J Biol Chem. 2006 Aug 11;281(32):22429-33 [16793760.001]
  • [Cites] Cancer Cell. 2006 Aug;10(2):99-111 [16904609.001]
  • [Cites] Nat Rev Cancer. 2006 Sep;6(9):674-87 [16929323.001]
  • [Cites] Oncogene. 2006 Sep 7;25(40):5581-90 [16785998.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1929-35 [17008526.001]
  • [Cites] Dev Cell. 2006 Oct;11(4):441-50 [17011485.001]
  • [Cites] Hepatology. 2006 Oct;44(4):1012-24 [17006932.001]
  • [Cites] Semin Liver Dis. 2006 Nov;26(4):373-84 [17051451.001]
  • [Cites] Nat Biotechnol. 2006 Sep;24(9):1151-61 [16964229.001]
  • [Cites] Hepatology. 2001 Mar;33(3):676-91 [11230749.001]
  • [Cites] Hepatology. 2006 Nov;44(5):1122-38 [17058214.001]
  • [Cites] Hepatology. 2006 Dec;44(6):1543-54 [17133492.001]
  • [Cites] Hepatology. 2007 Jan;45(1):42-52 [17187432.001]
  • [Cites] J Natl Cancer Inst. 2007 Jan 17;99(2):147-57 [17227998.001]
  • [Cites] Oncogene. 2007 Feb 1;26(5):774-80 [16964294.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):944-52 [17289889.001]
  • [Cites] Semin Liver Dis. 2007 Feb;27(1):55-76 [17295177.001]
  • [Cites] Nat Rev Cancer. 2007 Feb;7(2):139-47 [17218951.001]
  • [Cites] Liver Int. 2007 Mar;27(2):174-85 [17311611.001]
  • [Cites] Hepatology. 2007 Apr;45(4):938-47 [17393520.001]
  • [Cites] Cancer. 2007 May 15;109(10):2132-41 [17407132.001]
  • [Cites] Hum Mol Genet. 2007 Jun 1;16(11):1335-42 [17412760.001]
  • [Cites] J Pathol. 2007 Jun;212(2):134-42 [17471463.001]
  • [Cites] Int J Mol Med. 2007 Jul;20(1):65-73 [17549390.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Jun;22 Suppl 1:S108-11 [17567457.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2557-76 [17570226.001]
  • [Cites] Science. 2007 Jul 6;317(5834):121-4 [17615358.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6092-9 [17616664.001]
  • [Cites] BMC Biotechnol. 2007;7:36 [17603869.001]
  • [Cites] Gastroenterology. 2007 Aug;133(2):647-58 [17681183.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2713-22 [17717605.001]
  • [Cites] Gene. 2007 Oct 15;401(1-2):12-8 [17651921.001]
  • [Cites] Cancer. 2007 Sep 1;110(5):1059-67 [17623837.001]
  • [Cites] Br J Cancer. 2007 Nov 5;97(9):1260-5 [17968429.001]
  • [Cites] Clin Cancer Res. 2007 Nov 1;13(21):6275-83 [17975138.001]
  • [Cites] Liver Transpl. 2007 Nov;13(11 Suppl 2):S13-6 [17969094.001]
  • [Cites] Gastroenterology. 2007 Nov;133(5):1475-86 [17983802.001]
  • [Cites] APMIS. 2007 Oct;115(10):1039-59 [18042143.001]
  • [Cites] JAMA. 2008 Jan 2;299(1):53-60 [18167406.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):419-27 [18223217.001]
  • [Cites] Adv Genet. 2008;61:247-67 [18282509.001]
  • [Cites] Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609.001]
  • [Cites] Hepatology. 2008 Mar;47(3):908-18 [18161048.001]
  • [Cites] Hepatology. 2008 Mar;47(3):897-907 [18176954.001]
  • [Cites] Cell Signal. 2008 May;20(5):795-802 [18160255.001]
  • [Cites] J Hepatol. 2008;48 Suppl 1:S20-37 [18304676.001]
  • [Cites] Clin Cancer Res. 2008 Apr 1;14(7):2056-64 [18381945.001]
  • [Cites] Nat Biotechnol. 2008 Apr;26(4):462-9 [18362881.001]
  • [Cites] Int J Cancer. 2008 Jun 15;122(12):2800-4 [18351580.001]
  • [Cites] Int J Oncol. 2008 May;32(5):1057-63 [18425332.001]
  • [Cites] J Biol Chem. 2008 May 9;283(19):13205-15 [18319255.001]
  • [Cites] J Natl Cancer Inst. 2008 May 21;100(10):698-711 [18477802.001]
  • [Cites] Hepatology. 2008 Jun;47(6):1955-63 [18433021.001]
  • [Cites] Hepatology. 2008 Jun;47(6):2059-67 [18506891.001]
  • [Cites] Curr Opin Oncol. 2008 Jul;20(4):444-53 [18525342.001]
  • [Cites] Int J Cancer. 2008 Sep 1;123(5):998-1004 [18546260.001]
  • [Cites] Int J Cancer. 2008 Sep 1;123(5):1043-52 [18553387.001]
  • [Cites] J Gastroenterol. 2008;43(5):378-89 [18592156.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):5049-58 [18593903.001]
  • [Cites] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514.001]
  • [Cites] Int J Cancer. 2008 Oct 1;123(7):1616-22 [18649363.001]
  • [Cites] Cancer Res. 2008 Aug 15;68(16):6779-88 [18701503.001]
  • [Cites] Histol Histopathol. 2008 Oct;23(10):1171-5 [18712668.001]
  • [Cites] J Natl Cancer Inst. 2008 Aug 20;100(16):1121-3 [18695130.001]
  • [Cites] Oncogene. 2008 Sep 25;27(43):5651-61 [18521080.001]
  • [Cites] Carcinogenesis. 2008 Oct;29(10):1901-10 [18632756.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):5984-93 [18829477.001]
  • [Cites] Hepatology. 2008 Oct;48(4):1312-27 [18821591.001]
  • [Cites] Mol Cancer Ther. 2008 Oct;7(10):3129-40 [18852116.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1061-8 [18772890.001]
  • [Cites] N Engl J Med. 2008 Nov 6;359(19):1995-2004 [18923165.001]
  • [Cites] N Engl J Med. 2008 Nov 6;359(19):2045-7 [18923166.001]
  • [Cites] Cancer Cell. 2008 Dec 9;14(6):471-84 [19061838.001]
  • [Cites] Virus Res. 2009 Jan;139(1):14-21 [18948152.001]
  • [Cites] J Hepatol. 2009 Feb;50(2):323-33 [19041150.001]
  • [Cites] Cancer Lett. 2009 Mar 8;275(1):44-53 [19006648.001]
  • [Cites] Cancer Res. 2009 Feb 1;69(3):1135-42 [19155302.001]
  • [Cites] J Clin Oncol. 2009 Feb 20;27(6):843-50 [19139433.001]
  • [Cites] Cell. 2009 Mar 6;136(5):823-37 [19269363.001]
  • [Cites] Eur J Cancer. 2009 Mar;45(5):881-9 [19167881.001]
  • [Cites] Liver Int. 2009 Apr;29(4):502-10 [19141028.001]
  • [Cites] BioDrugs. 2009;23(1):15-23 [19344188.001]
  • [Cites] Hepatology. 2009 Apr;49(4):1194-202 [19133651.001]
  • [Cites] Hepatology. 2009 Apr;49(4):1098-112 [19173277.001]
  • [Cites] Expert Rev Gastroenterol Hepatol. 2009 Apr;3(2):101-3 [19351279.001]
  • [Cites] Curr Opin Gastroenterol. 2009 May;25(3):186-94 [19387255.001]
  • [Cites] Cancer Res. 2009 May 1;69(9):4059-66 [19366792.001]
  • [Cites] Hepatology. 2009 May;49(5 Suppl):S56-60 [19399807.001]
  • [Cites] PLoS Med. 2008 Sep 30;5(9):e184 [18767902.001]
  • [Cites] J Exp Med. 2009 Jun 8;206(6):1327-37 [19451266.001]
  • [Cites] Future Oncol. 2009 Jun;5(5):601-12 [19519200.001]
  • [Cites] Cell. 2009 Jun 12;137(6):1005-17 [19524505.001]
  • [Cites] J Clin Oncol. 2009 Jun 20;27(18):3027-35 [19470923.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):843-8 [19483683.001]
  • [Cites] Hepatology. 2009 Jul;50(1):113-21 [19441017.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Lancet Oncol. 2009 Aug;10(8):794-800 [19586800.001]
  • [Cites] Hepatology. 2009 Aug;50(2):490-9 [19472311.001]
  • [Cites] Hepatology. 2009 Aug;50(2):472-80 [19585654.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5073-81 [19671867.001]
  • [Cites] J Hepatol. 2009 Oct;51(4):810-20 [19545926.001]
  • [Cites] Cancer Res. 2009 Sep 15;69(18):7385-92 [19723656.001]
  • [Cites] Int J Oncol. 2009 Nov;35(5):1081-9 [19787262.001]
  • [Cites] Cancer Cell. 2009 Oct 6;16(4):281-94 [19800574.001]
  • [Cites] N Engl J Med. 2009 Oct 8;361(15):1437-47 [19812400.001]
  • [Cites] Oncogene. 2009 Oct 8;28(40):3526-36 [19617899.001]
  • [Cites] J Hepatol. 2009 Nov;51(5):890-7 [19747749.001]
  • [Cites] Liver Int. 2010 Jan;30(1):112-8 [19840254.001]
  • [Cites] J Hepatol. 2010 Mar;52(3):370-9 [19720422.001]
  • [Cites] Carcinogenesis. 2010 May;31(5):766-76 [19843643.001]
  • [Cites] Med Oncol. 2010 Sep;27(3):654-60 [19572217.001]
  • (PMID = 20175032.001).
  • [ISSN] 1098-8971
  • [Journal-full-title] Seminars in liver disease
  • [ISO-abbreviation] Semin. Liver Dis.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / P20 AA017067; United States / NIDDK NIH HHS / DK / R01 DK037340; United States / NIDDK NIH HHS / DK / R01 DK056601; United States / NIDDK NIH HHS / DK / R01 DK076986
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / RNA, Messenger
  • [Number-of-references] 185
  • [Other-IDs] NLM/ NIHMS466332; NLM/ PMC3668687
  •  go-up   go-down


2. Xiao EH, Li JQ, Huang JF: Effects of p53 on apoptosis and proliferation of hepatocellular carcinoma cells treated with transcatheter arterial chemoembolization. World J Gastroenterol; 2004 Jan 15;10(2):190-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of p53 on apoptosis and proliferation of hepatocellular carcinoma cells treated with transcatheter arterial chemoembolization.
  • AIM: To evaluate the effects of p53 on apoptosis and proliferation of hepatocellular carcinoma (HCC) cells treated with transcatheter arterial chemoembolization (TACE).
  • TACE group included 79 patients who had 1-5 courses of TACE before surgery, of them, 11 patients had 1-4 courses of chemotherapy (group A), 33 patients had 1-5 courses of chemotherapy combined with iodized oil (group B), 23 patients had 1-3 courses of chemotherapy, iodized oil and gelatin sponge (group C), 12 patients had 1-3 courses of chemotherapy combined with iodized oil, ethanol and gelatin sponge (group D).
  • RESULTS: P53 protein expressions in trabecular and clear cells in HCC specimens were significantly lower than that in pseudoglandular, solid, poorly differentiated or undifferentiated and sclerosis HCC (P<0.05).
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Hepatocellular / therapy. Chemoembolization, Therapeutic. Liver Neoplasms / therapy. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Aged. Cell Division / physiology. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Middle Aged. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-2-Associated X Protein

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14716820.001).
  • [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 / BAX protein, human; 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein
  • [Other-IDs] NLM/ PMC4717001
  •  go-up   go-down


3. Altomonte J, Marozin S, Schmid RM, Ebert O: Engineered newcastle disease virus as an improved oncolytic agent against hepatocellular carcinoma. Mol Ther; 2010 Feb;18(2):275-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Engineered newcastle disease virus as an improved oncolytic agent against hepatocellular carcinoma.
  • Several clinical trials have reported NDV to be a safe and effective agent for cancer therapy; however, there remains a clear need for improvement in therapeutic outcome.
  • The endogenous NDV fusion (F) protein directs membrane fusion, which is required for virus entry and cell-cell fusion.
  • Here, we report a novel NDV vector harboring an L289A mutation within the F gene, which resulted in enhanced fusion and cytotoxicity of hepatocellular carcinoma (HCC) cells in vitro, as compared with the rNDV/F3aa control virus.
  • In vivo administration of the recombinant vector, termed rNDV/F3aa(L289A), via hepatic arterial infusion in immune-competent Buffalo rats bearing multifocal, orthotopic liver tumors resulted in tumor-specific syncytia formation and necrosis, with no evidence of toxicity to the neighboring hepatic parenchyma.
  • Taken together, rNDV/F(L289A) represents a safe, yet more effective vector than wild-type NDV for the treatment of HCC, making it an ideal candidate for clinical application in HCC patients.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. Newcastle disease virus / physiology. Oncolytic Virotherapy / methods
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Chickens. Genetic Vectors / drug effects. Genetic Vectors / genetics. Genetic Vectors / physiology. Humans. Interferon Type I / pharmacology. Male. Rats

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Oct 1;98(7):2002-7 [11567982.001]
  • [Cites] IUBMB Life. 2000 Aug;50(2):135-8 [11185959.001]
  • [Cites] J Virol. 2001 Dec;75(23):11868-73 [11689668.001]
  • [Cites] Nat Immunol. 2002 Nov;3(11):1006-12 [12407408.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6566-78 [12438252.001]
  • [Cites] Oncology (Williston Park). 2002 Nov;16(11):1483-92; discussion 1495-7 [12469927.001]
  • [Cites] J Gen Virol. 2003 Feb;84(Pt 2):475-84 [12560582.001]
  • [Cites] J Virol. 2003 Sep;77(17):9522-32 [12915566.001]
  • [Cites] Cancer Cell. 2003 Oct;4(4):263-75 [14585354.001]
  • [Cites] Ann Intern Med. 2003 Nov 18;139(10):817-23 [14623619.001]
  • [Cites] Lancet. 2003 Dec 6;362(9399):1907-17 [14667750.001]
  • [Cites] Mol Ther. 2004 Mar;9(3):368-76 [15006603.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):83-93 [15072452.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3265-70 [15126368.001]
  • [Cites] Nat Immun Cell Growth Regul. 1986;5(4):169-99 [2430177.001]
  • [Cites] Virology. 1991 Oct;184(2):504-12 [1887586.001]
  • [Cites] J Surg Res. 1992 May;52(5):448-53 [1619912.001]
  • [Cites] Virology. 1993 Nov;197(1):1-11 [8212546.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6017-21 [7954437.001]
  • [Cites] J Virol. 1995 Jul;69(7):3967-71 [7769654.001]
  • [Cites] Lancet. 1998 Jan 17;351(9097):214-5 [9449893.001]
  • [Cites] Nat Med. 1998 May;4(5):581-7 [9585232.001]
  • [Cites] Aliment Pharmacol Ther. 1998 Feb;12(2):111-26 [9692685.001]
  • [Cites] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408.001]
  • [Cites] J Virol. 1999 Jun;73(6):5001-9 [10233962.001]
  • [Cites] Cancer. 1965 Jul;18:863-8 [14308233.001]
  • [Cites] J Virol. 2005 Jan;79(2):1180-90 [15613345.001]
  • [Cites] Hepatology. 2005 Jan;41(1):196-203 [15619242.001]
  • [Cites] Aliment Pharmacol Ther. 2005 Jul 1;22(1):17-22 [15963075.001]
  • [Cites] Mol Ther. 2006 Jan;13(1):221-8 [16257582.001]
  • [Cites] J Virol. 2006 Jun;80(11):5145-55 [16698995.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 23;103(21):8203-8 [16717196.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):977-85 [17289893.001]
  • [Cites] Otolaryngol Head Neck Surg. 2007 May;136(5):811-7 [17478221.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8285-92 [17804743.001]
  • [Cites] Gene Ther. 2007 Dec;14(23):1639-49 [17914407.001]
  • [Cites] J Clin Invest. 2008 Mar;118(3):1165-75 [18259609.001]
  • [Cites] Curr Opin Mol Ther. 2008 Aug;10(4):356-61 [18683100.001]
  • [Cites] Mol Ther. 2008 Nov;16(11):1789-97 [18781139.001]
  • [Cites] Hepatology. 2008 Dec;48(6):1864-73 [19003878.001]
  • [Cites] Gene Ther. 2009 Jun;16(6):796-804 [19242529.001]
  • [Cites] J Virol. 2009 Aug;83(16):8108-21 [19515783.001]
  • [Cites] Virology. 1999 Oct 25;263(2):364-75 [10544109.001]
  • [Cites] Cancer Gene Ther. 1999 Nov-Dec;6(6):499-504 [10608346.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1492-7 [10749110.001]
  • [Cites] J Virol. 2000 Jun;74(11):5101-7 [10799584.001]
  • [Cites] Nat Med. 2000 Jul;6(7):821-5 [10888934.001]
  • [Cites] Int J Cancer. 2001 Oct 15;94(2):153-6 [11668491.001]
  • (PMID = 19809404.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I
  • [Other-IDs] NLM/ PMC2839313
  •  go-up   go-down


Advertisement
4. Ueno S, Aoki D, Kubo F, Hiwatashi K, Matsushita K, Oyama T, Maruyama I, Aikou T: Roxithromycin inhibits constitutive activation of nuclear factor {kappa}B by diminishing oxidative stress in a rat model of hepatocellular carcinoma. Clin Cancer Res; 2005 Aug 1;11(15):5645-50
Hazardous Substances Data Bank. N-NITROSODIETHYLAMINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Roxithromycin inhibits constitutive activation of nuclear factor {kappa}B by diminishing oxidative stress in a rat model of hepatocellular carcinoma.
  • We investigated the suppressive effect of roxithromycin on accelerated hepatocellular carcinoma growth in a rat hepatocarcinogenetic model and compared results with effects from TNP-470.
  • RESULTS: Carcinomatous tissue growing outside dysplastic nodules and a marked expression of placental glutathione S-transferase were detected in rats with induced carcinogenesis.
  • The inhibitory effect of roxithromycin was dose dependent and no clear differences were noted between groups given roxithromycin 100 mg/kg and TNP-470 50 mg/kg.
  • The data provide additional evidence for the potential use of roxithromycin in treatment of hepatocellular carcinoma prevention.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. NF-kappa B / metabolism. Roxithromycin / pharmacology
  • [MeSH-minor] Animals. Anti-Bacterial Agents / pharmacology. Antineoplastic Agents / pharmacology. Carcinogens. Cell Nucleus / metabolism. Cyclohexanes. Diethylnitrosamine. Disease Models, Animal. Dose-Response Relationship, Drug. Glutathione Transferase / metabolism. Lipid Peroxidation. Liver / pathology. Male. Models, Biological. Nitric Oxide Synthase / metabolism. Oxidative Stress. Placenta / enzymology. Rats. Rats, Wistar. Sesquiterpenes / pharmacology

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16061884.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Cyclohexanes; 0 / NF-kappa B; 0 / Sesquiterpenes; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; 21KOF230FA / Roxithromycin; 3IQ78TTX1A / Diethylnitrosamine; EC 1.14.13.39 / Nitric Oxide Synthase; EC 2.5.1.18 / Glutathione Transferase
  •  go-up   go-down


5. Thin L, Macquillan G, Adams L, Garas G, Seow C, Cannell P, Augustson B, Mitchell A, Delriveire L, Jeffrey G: Acute graft-versus-host disease after liver transplant: novel use of etanercept and the role of tumor necrosis factor alpha inhibitors. Liver Transpl; 2009 Apr;15(4):421-6
Hazardous Substances Data Bank. Etanercept .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute graft-versus-host disease after liver transplant: novel use of etanercept and the role of tumor necrosis factor alpha inhibitors.
  • Acute graft-versus-host disease following orthotopic liver transplantation is a rare but feared complication arising in 1% to 2% of cases with a dismal prognosis.
  • Because of its low incidence, there is no clear treatment protocol for this complication.
  • Although anti-tumor necrosis factor alpha therapy has been widely used for the treatment of steroid-resistant acute graft-versus-host disease in the hematopoietic stem cell transplant setting, there previously have been no reported cases of its use in liver transplantation.
  • Etanercept has never previously been used in liver transplantation complicated by acute graft-versus-host disease.
  • However, preliminary results are encouraging and offer insight into its use as a potentially viable therapeutic option.
  • We report the first successful use of etanercept in liver transplantation-associated graft-versus-host disease, albeit complicated by invasive aspergillosis, and recommend concurrent antifungal prophylaxis when the drug is used in this setting.
  • [MeSH-major] Carcinoma, Hepatocellular / surgery. Graft vs Host Disease / drug therapy. Hepatitis B, Chronic / surgery. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Liver Neoplasms / surgery. Liver Transplantation / adverse effects. Receptors, Tumor Necrosis Factor / therapeutic use. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Aged. Antifungal Agents / therapeutic use. Aspergillosis / chemically induced. Aspergillosis / drug therapy. Dermatomycoses / chemically induced. Dermatomycoses / drug therapy. Etanercept. Humans. Male. Treatment Outcome

  • Genetic Alliance. consumer health - Liver Disease.
  • Genetic Alliance. consumer health - Liver Transplant.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 AASLD.
  • (PMID = 19326415.001).
  • [ISSN] 1527-6473
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  •  go-up   go-down


6. Papoulas M, Theocharis S: Primary liver tumors: origin and target therapy. Expert Opin Ther Targets; 2009 Aug;13(8):957-65
MedlinePlus Health Information. consumer health - Stem Cells.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary liver tumors: origin and target therapy.
  • BACKGROUND: The liver is the largest gland and chief metabolic organ of the human body possessing a unique ability to regenerate.
  • The general interest of primary liver tumors is noteworthy because of their increasing worldwide incidence and mortality.
  • OBJECTIVE: To provide a brief and up-to-date review on the cellular origin of primary liver tumors and to examine the use of stem cells in potential future therapeutic attempts.
  • RESULTS: It is clear that hepatic progenitor cells (HPCs) could be the basis of some hepatocellular carcinomas (HCC), cholangiocarcinomas (CHC), hepatocellular adenomas and hepatoblastomas.
  • Cancer stem cell (CSC) theory emphasizes the role of hepatic stem cells in the development and progression of liver tumors.
  • Conventional treatments for HCC do not seem to be beneficial for the majority of patients and new therapeutic approaches such as gene therapy and targeted drug therapy are of great clinical interest.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / therapy. Cell Transformation, Neoplastic / pathology. Drug Delivery Systems / methods. Hepatocytes / pathology. Liver Neoplasms / pathology. Liver Neoplasms / therapy. Stem Cells / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor / genetics. Cell Differentiation / genetics. Cell Lineage / genetics. Cholangiocarcinoma / genetics. Cholangiocarcinoma / pathology. Cholangiocarcinoma / therapy. Humans

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19606929.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 84
  •  go-up   go-down


7. Basile J, Caldwell S, Nolan N, Hammerle C: Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma. Ann Hepatol; 2010 Oct-Dec;9(4):465-7
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma.
  • Primary liver tumors in children are rare with hepatoblastoma (HB) being the most common malignancy.
  • Clear cell carcinoma, a variant of hepatocellular carcinoma (HCC), is another rare tumor of the liver that tends to affect adults.
  • We describe the diagnosis and management of the only known documented case of a primary clear cell HCC arising twenty-five years after the patient was successfully treated with chemotherapy and surgical resection for a malignant HB as an infant.
  • While some evidence has shown a genetic link between HB and various types of HCC, other research has shown distinct chromosomal alterations and molecular mechanisms unique to both.
  • Further knowledge of liver tumorigenesis will help elucidate the complicated genetic, molecular, and environmental factors involved in the development of these two rare hepatic malignancies.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Hepatoblastoma / drug therapy. Hepatoblastoma / surgery. Liver Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biopsy. Combined Modality Therapy. Genetic Predisposition to Disease / genetics. Humans. Magnetic Resonance Imaging. Male. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Hepatoblastoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21057168.001).
  • [ISSN] 1665-2681
  • [Journal-full-title] Annals of hepatology
  • [ISO-abbreviation] Ann Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Mexico
  •  go-up   go-down


8. Pang R, Poon RT: Angiogenesis and antiangiogenic therapy in hepatocellular carcinoma. Cancer Lett; 2006 Oct 28;242(2):151-67
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiogenesis and antiangiogenic therapy in hepatocellular carcinoma.
  • Hepatocellular carcinoma (HCC) is a hypervascular tumor characterized by neovascularization, which plays an important role in the growth and progression of HCC.
  • Angiogenesis provides a target for novel prognostic and therapeutic approaches to HCC.
  • Assessment of microvessel density using immunohistochemical staining for specific endothelial cell markers such as CD34 has been shown to provide prognostic information independent of conventional pathological parameters in HCC patients.
  • Recent studies have unveiled the important angiogenic factors involved in the regulation of angiogenesis in HCC, although the exact molecular pathways are far from clear.
  • VEGF is an important molecular target for antiangiogenic therapy.
  • Antiangiogenic therapy has already entered clinical trials in HCC patients and holds the promise of providing an effective novel treatment for HCC, which is of great clinical significance because there is no existing effective systemic therapy for HCC.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Gene Expression Regulation, Neoplastic. Liver Neoplasms / drug therapy. Neovascularization, Pathologic
  • [MeSH-minor] Antigens, CD34 / biosynthesis. Cell Proliferation. Disease Progression. Fibroblast Growth Factor 2 / metabolism. Humans. Models, Biological. Prognosis. Time Factors. Vascular Endothelial Growth Factor A / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16564617.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD34; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2
  • [Number-of-references] 160
  •  go-up   go-down


9. Xiao E, Hu G, Liu P, Hu D, Liu S, Hao C: The effect of different interventional treatment on P-Glycoprotein in different histopathological types and grades of primary hepatocellular carcinoma. J Tongji Med Univ; 2000;20(3):231-4
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of different interventional treatment on P-Glycoprotein in different histopathological types and grades of primary hepatocellular carcinoma.
  • To study the effect of the different interventional treatment on P-Glycoprotein (Pgp) in different histopathological types of primary hepatocellular carcinoma (PHC), 98 surgically and histologically verified PHC specimens were obtained.
  • The patients included 57 patients treated by surgical resection alone and 41 patients receiving second-stage surgical resection after four kinds of interventional treatment.
  • SABC immunohistochemical staining with a monoclonal antibody against human Pgp was used to observe the Pgp in all specimens.
  • The positive rate of Pgp was 100% in group of chemotherapy alone (P < 0.05), 62.5% in group of chemotherapy combined with iodized oil (P > 0.05), 46.6% in group of chemotherapy combined with iodized oil and spongia gelatini absorbens (Sga) (P > 0.05), 18.18% in group of chemotherapy combined with Ethanol-iodized-oil and Sga (P < 0.05) and 52.63% in group of surgical resection alone.
  • The positive rate of Pgp varied with different histopathological types, with rate of clear cell PHC being the lowest, and that of poorly differentiated or undifferentiated PHC the highest.
  • Overexpression of Pgp may be responsible for the intrinsic and acquired drug resistance of PHC.
  • Multidrug resistance (MDR) varied with different histological types.
  • Therapy of PHC should be tailored according to individual.
  • Local chemotherapy combined with ethanol-iodized-oil and Sga embolization may become a new way to overcome MDR of PHC.
  • [MeSH-major] Adenocarcinoma / therapy. Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. P-Glycoprotein / metabolism
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Radiography, Interventional

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11215058.001).
  • [ISSN] 0257-716X
  • [Journal-full-title] Journal of Tongji Medical University = Tong ji yi ke da xue xue bao
  • [ISO-abbreviation] J. Tongji Med. Univ.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / P-Glycoprotein
  •  go-up   go-down


10. Yip EC, Chan AS, Pang H, Tam YK, Wong YH: Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism. Cell Biol Toxicol; 2006 Jul;22(4):293-302
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protocatechuic acid induces cell death in HepG2 hepatocellular carcinoma cells through a c-Jun N-terminal kinase-dependent mechanism.
  • Cytotoxicity assays showed that PCA, CA and LT (at 100 micromol/L) effectively killed the HepG2 hepatocellular carcinoma cells.
  • Coincidently, PCA-induced cell death was rescued by specific inhibitors for JNK and p38, while the cytotoxicities of CA and LT were partially eliminated by the antioxidant effect of N-acetyl-L-cysteine (NAC).
  • Further investigation demonstrated that the aqueous extract of Lonicera japonica also triggered HepG2 cell death in a JNK-dependent manner, but the amount of PCA alone in this herbal extract was insufficient to contribute the subsequent cytotoxic effect.
  • Collectively, our results suggest that PCA is a naturally occurring compound capable of inducing JNK-dependent hepatocellular carcinoma cell death.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Hydroxybenzoates / pharmacology. JNK Mitogen-Activated Protein Kinases / metabolism. Liver Neoplasms / drug therapy
  • [MeSH-minor] Cell Death. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Lonicera / metabolism. MAP Kinase Signaling System. Models, Chemical. Phosphorylation. Plant Extracts / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • [ErratumIn] Cell Biol Toxicol. 2007 Mar;23(2):139
  • (PMID = 16835731.001).
  • [ISSN] 0742-2091
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxybenzoates; 0 / Plant Extracts; 36R5QJ8L4B / protocatechuic acid; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  •  go-up   go-down


11. Kumada H: Long-term treatment of chronic hepatitis C with glycyrrhizin [stronger neo-minophagen C (SNMC)] for preventing liver cirrhosis and hepatocellular carcinoma. Oncology; 2002;62 Suppl 1:94-100
Hazardous Substances Data Bank. GLYCYRRHIZIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term treatment of chronic hepatitis C with glycyrrhizin [stronger neo-minophagen C (SNMC)] for preventing liver cirrhosis and hepatocellular carcinoma.
  • In Japan, hepatitis C virus (HCV) is the single most frequent cause of hepatocellular carcinoma (HCC), resulting in yearly deaths of over 30,000.
  • Although the mechanism of how HCV induces HCC is not clear, persistent HCV infection and necro-inflammatory changes in chronic hepatitis C accelerate the development of liver cirrhosis and can eventuate in HCC.
  • Hence, means of eradicating HCV as well as suppressing inflammation in the liver, even if patients stay infected with HCV, would decrease the incidence of HCC with chronic hepatitis C.
  • For more than 40 years, a preparation of glycyrrhizin [Stronger Neo-Minophagen C (SNMC)] has been used for the treatment of 'allergic' hepatitis in Japan.
  • In 1977, intravenous injection with SNMC was started in patients with chronic hepatitis or liver cirrhosis, most of whom have turned out to be infected with hepatitis viruses.
  • Furthermore, SNMC 100 ml/day for 8 weeks improved liver histology in 40 patients with chronic hepatitis, in correlation with improved ALT levels in serum.
  • Liver cirrhosis occurred less frequently in 178 patients on long-term SNMC than in 100 controls (28 vs. 40% at year 13, p < 0.002).
  • Finally, HCC developed less frequently in the 84 patients on long-term SNMC than in the 109 controls (13 vs. 25% at year 15, p < 0.002).
  • Combined, these results indicate that a long-term treatment with SNMC prevents the development of HCC in the patients with chronic hepatitis.
  • [MeSH-major] Antiviral Agents / therapeutic use. Carcinoma, Hepatocellular / prevention & control. Glycyrrhizic Acid / therapeutic use. Hepatitis C / drug therapy. Liver Cirrhosis / prevention & control. Liver Neoplasms / prevention & control
  • [MeSH-minor] Alanine Transaminase / metabolism. Cell Transformation, Neoplastic / drug effects. Chronic Disease. Humans. Survival Analysis

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Cirrhosis.
  • MedlinePlus Health Information. consumer health - Hepatitis C.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11868794.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antiviral Agents; 6FO62043WK / Glycyrrhizic Acid; EC 2.6.1.2 / Alanine Transaminase
  •  go-up   go-down


12. Warmann SW, Frank H, Heitmann H, Ruck P, Herberts T, Seitz G, Fuchs J: Bcl-2 gene silencing in pediatric epithelial liver tumors. J Surg Res; 2008 Jan;144(1):43-8
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bcl-2 gene silencing in pediatric epithelial liver tumors.
  • BACKGROUND: Proteins of the Bcl-2 family prevent cells of various tumor types from undergoing apoptosis and thus contribute to their chemotherapy resistance.
  • The phenotype of multidrug resistance is a major factor for poor treatment results of advanced epithelial liver tumors in children.
  • The purpose of this study was to analyze the influence of Bcl-2 on the chemotherapy resistance of hepatoblastoma (HB) and pediatric hepatocellular carcinoma (HCC).
  • MATERIALS AND METHODS: Bcl-2 expression was analyzed in the HB cell lines HUH6 and HepT1 as well as in the HCC cell line HepG2 before and after treatment with cisplatin, doxorubicin, taxol, and etoposid.
  • Treatment efficiencies of cytotoxic agents were assessed against original and Bcl-2 siRNA transfected tumor cells.
  • RESULTS: The mixed HB cell line HUH6 showed a relevant amount of Bcl-2 expression, which increased after chemotherapy.
  • Treatment with all cytotoxic agents was significantly improved through Bcl-2 siRNA (P < 0.001-0.0054) in this cell line.
  • Thus, this gene might serve as target for a gene-directed adjuvant therapy.
  • Further studies seem necessary to clear the susceptibility of pediatric epithelial liver tumors toward the described approach.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Drug Resistance, Neoplasm / genetics. Gene Silencing. Liver Neoplasms / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Child. Cisplatin / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Multiple / genetics. Epithelium. Etoposide / pharmacology. Genetic Therapy / methods. Humans. Paclitaxel / pharmacology. Transfection

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17574594.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


13. Gao Y, Lin LP, Zhu CH, Chen Y, Hou YT, Ding J: Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma. Cancer Biol Ther; 2006 Aug;5(8):978-85
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth arrest induced by C75, A fatty acid synthase inhibitor, was partially modulated by p38 MAPK but not by p53 in human hepatocellular carcinoma.
  • In this study, we reveal that C75 is a cell cycle arrest inducer and explore the potential mechanisms for this effect in hepatocellular carcinoma (HCC) cell lines with abundant FAS expression: HepG2 and SMMC7721 cells with wt-p53, and Hep3B cells with null p53.
  • The results showed FAS protein expression and basal activity levels were higher in HepG2 cells than in the other two HCC cell lines.
  • Treatment with C75 inhibited FAS activity within 30 min of administration and induced G(2) phase arrest accompanied by p53 overexpression in HepG2 and SMMC7721 cells.
  • However, we observed a clear correlation between p38 MAPK activation triggered by C75 and the induction of cell cycle arrest in all three HCC cells.
  • Furthermore, treatment with the p38 MAPK inhibitor SB203580 reduced p38 MAPK activity and cell cycle arrest, and also partially restored cyclin A, cyclin B1, cyclin D1 and p21 protein levels.
  • Collectively, it was p38 MAPK but not p53 involved in C75-mediated tumor cell growth arrest in HCC cells.
  • [MeSH-major] 4-Butyrolactone / analogs & derivatives. Carcinoma, Hepatocellular / metabolism. Fatty Acid Synthases / antagonists & inhibitors. G2 Phase / drug effects. Liver Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Antigens, CD95 / metabolism. Blotting, Western. Cell Proliferation. Cyclin A / metabolism. Cyclin B / metabolism. Cyclin B1. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Flow Cytometry. Humans. Immunoprecipitation. Plasmids / genetics. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BUTYROLACTONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [CommentIn] Cancer Biol Ther. 2006 Aug;5(8):986-7 [16998303.001]
  • (PMID = 16855382.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methylene-2-octyl-5-oxofuran-3-carboxylic acid; 0 / Antigens, CD95; 0 / CCNB1 protein, human; 0 / Cyclin A; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 2.3.1.85 / Fatty Acid Synthases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; OL659KIY4X / 4-Butyrolactone
  •  go-up   go-down


14. Yan J, Gong Y, Wang G, Gong Y, Burczynski FJ: Regulation of liver fatty acid binding protein expression by clofibrate in hepatoma cells. Biochem Cell Biol; 2010 Dec;88(6):957-67
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of liver fatty acid binding protein expression by clofibrate in hepatoma cells.
  • Peroxisome proliferator-activated receptor (PPAR) agonists such as clofibrate are known to affect liver fatty acid binding protein (L-FABP) levels, which in turn influence hepatocellular oxidant status.
  • The mechanism of clofibrate's modulation of L-FABP levels is not clear.
  • RT-PCR and mRNA stability assay showed that clofibrate treatment enhanced L-FABP mRNA stability, which resulted in increased L-FABP levels.
  • Levels of superoxide dismutase, glutathione peroxidase, and catalase were not affected by clofibrate treatment.
  • [MeSH-minor] Anilides / pharmacology. Animals. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / enzymology. Catalase / analysis. Catalase / metabolism. Cell Line, Tumor. Fluoresceins / analysis. Gene Expression Regulation, Neoplastic / drug effects. Glutathione Peroxidase / analysis. Glutathione Peroxidase / metabolism. Hepatocytes / drug effects. Hepatocytes / enzymology. Humans. Hydrogen Peroxide / administration & dosage. Indoles / pharmacology. Liver Neoplasms / drug therapy. Liver Neoplasms / enzymology. Oxidative Stress. RNA Stability / drug effects. RNA, Messenger / metabolism. Rats. Superoxide Dismutase / analysis. Superoxide Dismutase / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CLOFIBRATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21102658.001).
  • [ISSN] 1208-6002
  • [Journal-full-title] Biochemistry and cell biology = Biochimie et biologie cellulaire
  • [ISO-abbreviation] Biochem. Cell Biol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Fatty Acid-Binding Proteins; 0 / Fluoresceins; 0 / Indoles; 0 / PPAR alpha; 0 / RNA, Messenger; 118414-82-7 / L 663536; 76-54-0 / 2',7'-dichlorofluorescein; BBX060AN9V / Hydrogen Peroxide; EC 1.11.1.6 / Catalase; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; HPN91K7FU3 / Clofibrate
  •  go-up   go-down


15. Wu XZ, Zhang L, Shi BZ, Hu P: Inhibitory effects of N-(4-hydrophenyl) retinamide on liver cancer and malignant melanoma cells. World J Gastroenterol; 2005 Oct 7;11(37):5763-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of N-(4-hydrophenyl) retinamide on liver cancer and malignant melanoma cells.
  • AIM: To investigate the effect of N-(4-hydrophenyl) retinamide (4-HPR), the derivative of retinoic acid, on inhibition of migration, invasion, cell growth, and induction of apoptosis in hepatocellular carcinoma cells (HCCs) and malignant melanoma cells.
  • Cell growth was assayed by MTT chromometry.
  • The invasion through reconstituted basement membrane was also significantly reduced by 4-HPR treatment to 11.2+/-3.3 in SMMC 7721-k3 HCC (control 27+/-13.1), and to 24.3+/-3.2 in melanoma cells (control 67.5+/-10.1, P<0.05, n = 3).
  • Cell growth, especially in melanoma cells, was also significantly inhibited.
  • The mechanism for 4-HPR-induced apoptosis was not clear, but we observed that 4-HPR could regulate p27(kip1), and overexpression of cerebroside sulfotransferase (CST) diminished the apoptosis induced by 4-HPR in melanoma cells.
  • CONCLUSION: 4-HPR is a potent inhibitor of HCC migration and inducer of melanoma cell apoptosis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Fenretinide / therapeutic use. Liver Neoplasms / drug therapy. Melanoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor / drug effects. Cell Movement / drug effects. Humans. Mice. Mice, Nude. Sulfotransferases / genetics. Sulfotransferases / metabolism

  • Genetic Alliance. consumer health - Liver cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16270382.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 187EJ7QEXL / Fenretinide; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.11 / galactosylceramide sulfotransferase
  • [Other-IDs] NLM/ PMC4479673
  •  go-up   go-down


16. Sharma A, Upadhyay AK, Bhat MK: Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells. Cancer Biol Ther; 2009 Nov;8(22):2106-13
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Hsp27 and Hsp40 potentiates 5-fluorouracil and carboplatin mediated cell killing in hepatoma cells.
  • Heat shock proteins (Hsps) modulate several cellular functions and are ubiquitously present in cell.
  • Moreover, effect of quercetin (Qctn), an inhibitor of Hsps, on chemotherapeutic drugs treatment in hepatoma cells Hep3B and HepG2 was investigated.
  • We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells.
  • Induction of Hsps following exposure to sub lethal dose of drugs is a cellular challenge to survival.
  • However, under lethal environmental conditions with reduced cell viability, cells fail to sustain the induction of survival proteins, Hsp27 and Hsp40.
  • The increased cell killing correlates with decreased levels of procaspase-3.
  • Furthermore, siRNA mediated knockdown of Hsp27 and Hsp40 diminishes survival of drugs exposed cells.
  • Altogether, our data provides clear evidence that Hsp27 and 40 promote cell survival and inhibition of their expression does not allow cells to adapt to drug exposure and survive.
  • Collectively, our novel findings on compelling action of 5-FU or carboplatin following knockdown of Hsp40 and that of Hsp27 highlights their strategic implications towards an effective therapy against HCC.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Agents, Alkylating / pharmacology. Apoptosis / drug effects. Carboplatin / pharmacology. Carcinoma, Hepatocellular / pathology. Fluorouracil / pharmacology. HSP27 Heat-Shock Proteins / physiology. HSP40 Heat-Shock Proteins / physiology. Liver Neoplasms / pathology. Neoplasm Proteins / physiology. Quercetin / pharmacology
  • [MeSH-minor] Cell Line, Tumor / cytology. Cell Line, Tumor / drug effects. Drug Resistance, Neoplasm. Drug Synergism. Gene Expression Regulation, Neoplastic / drug effects. Humans. RNA Interference. RNA, Small Interfering / pharmacology. Transfection

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. QUERCETIN .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19901540.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / DNAJB1 protein, human; 0 / HSP27 Heat-Shock Proteins; 0 / HSP40 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 9IKM0I5T1E / Quercetin; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


17. Plumlee CR, Lazaro CA, Fausto N, Polyak SJ: Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells. Virol J; 2005 Dec 02;2:89
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of ethanol on innate antiviral pathways and HCV replication in human liver cells.
  • Alcohol abuse reduces response rates to IFN therapy in patients with chronic hepatitis C.
  • To model the molecular mechanisms behind this phenotype, we characterized the effects of ethanol on Jak-Stat and MAPK pathways in Huh7 human hepatoma cells, in HCV replicon cell lines, and in primary human hepatocytes.
  • High physiological concentrations of acute ethanol activated the Jak-Stat and p38 MAPK pathways and inhibited HCV replication in several independent replicon cell lines.
  • With a propensity to progress to chronic infection, approximately 70% of patients with chronic viremia develop histological evidence of chronic liver diseases including chronic hepatitis, cirrhosis, and hepatocellular carcinoma.
  • The situation is even more dire for patients who abuse ethanol, where the risk of developing end stage liver disease is significantly higher as compared to HCV patients who do not drink 12.Recombinant interferon alpha (IFN-alpha) therapy produces sustained responses (ie clearance of viremia) in 8-12% of patients with chronic hepatitis C 3.
  • Significant improvements in response rates can be achieved with IFN plus ribavirin combination 456 and pegylated IFN plus ribavirin 78 therapies.
  • However, over 50% of chronically infected patients still do not clear viremia.
  • Moreover, HCV-infected patients who abuse alcohol have extremely low response rates to IFN therapy 9, but the mechanisms involved have not been clarified.MAPKs play essential roles in regulation of differentiation, cell growth, and responses to cytokines, chemokines and stress.
  • In the current report, we postulated that alcohol and HCV proteins modulate MAPK and Jak-Stat pathways in human liver cells.

  • Hazardous Substances Data Bank. ETHANOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [Cites] Science. 1999 Jul 2;285(5424):110-3 [10390360.001]
  • [Cites] FEBS Lett. 1999 Aug 20;457(1):162-8 [10486586.001]
  • [Cites] EMBO J. 1999 Sep 15;18(18):4969-80 [10487749.001]
  • [Cites] J Virol. 2005 Mar;79(5):2689-99 [15708988.001]
  • [Cites] Alcohol Clin Exp Res. 1999 Nov;23(11):1711-20 [10591586.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3690-5 [10725368.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2628-37 [10851062.001]
  • [Cites] JAMA. 2000 Jul 26;284(4):450-6 [10904508.001]
  • [Cites] Science. 2000 Dec 8;290(5498):1972-4 [11110665.001]
  • [Cites] J Virol. 2001 Feb;75(3):1437-49 [11152517.001]
  • [Cites] Drug Metab Dispos. 2001 Feb;29(2):141-4 [11159803.001]
  • [Cites] EMBO J. 2001 Jan 15;20(1-2):91-100 [11226159.001]
  • [Cites] J Virol. 2001 May;75(10):4614-24 [11312331.001]
  • [Cites] J Virol. 2002 Sep;76(18):9207-17 [12186904.001]
  • [Cites] N Engl J Med. 2002 Sep 26;347(13):975-82 [12324553.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12859-64 [12232043.001]
  • [Cites] J Virol. 2003 Mar;77(5):3181-90 [12584342.001]
  • [Cites] J Clin Gastroenterol. 2003 Mar;36(3):242-52 [12590237.001]
  • [Cites] Pharmacol Ther. 2003 May;98(2):129-42 [12725866.001]
  • [Cites] J Biol Chem. 2003 May 16;278(20):17775-84 [12621033.001]
  • [Cites] Hepatology. 2003 Jul;38(1):57-65 [12829987.001]
  • [Cites] Hepatology. 2003 Nov;38(5):1095-106 [14578848.001]
  • [Cites] Gene. 2003 Nov 27;320:3-21 [14597384.001]
  • [Cites] Nat Immunol. 2003 Dec;4(12):1169-76 [14639467.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):970-9 [14578350.001]
  • [Cites] J Gen Virol. 2004 Mar;85(Pt 3):721-9 [14993658.001]
  • [Cites] Life Sci. 2004 Mar 26;74(19):2339-64 [15027449.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12232-41 [14709551.001]
  • [Cites] Annu Rev Nutr. 2004;24:55-78 [15189113.001]
  • [Cites] J Clin Microbiol. 2004 Sep;42(9):4130-6 [15365000.001]
  • [Cites] J Interferon Res. 1981;1(4):613-20 [6180094.001]
  • [Cites] J Biol Chem. 1992 Jan 25;267(3):1741-5 [1309794.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):607-14 [7509043.001]
  • [Cites] Science. 1994 Jun 3;264(5164):1415-21 [8197455.001]
  • [Cites] Cell. 1995 Jul 28;82(2):241-50 [7543024.001]
  • [Cites] Science. 1995 Sep 22;269(5231):1721-3 [7569900.001]
  • [Cites] J Biol Chem. 1995 Dec 29;270(52):30837-40 [8537333.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1996;36:185-201 [8725387.001]
  • [Cites] J Biol Chem. 1996 Sep 27;271(39):23914-9 [8798623.001]
  • [Cites] Arch Biochem Biophys. 1996 Nov 1;335(1):123-30 [8914842.001]
  • [Cites] Hepatology. 1997 Sep;26(3 Suppl 1):39S-42S [9305662.001]
  • [Cites] Hepatology. 1997 Sep;26(3 Suppl 1):71S-77S [9305668.001]
  • [Cites] Alcohol. 1998 Feb;15(2):147-60 [9476961.001]
  • [Cites] Lancet. 1998 Oct 31;352(9138):1426-32 [9807989.001]
  • [Cites] N Engl J Med. 1998 Nov 19;339(21):1485-92 [9819446.001]
  • [Cites] N Engl J Med. 1998 Nov 19;339(21):1493-9 [9819447.001]
  • [Cites] Physiol Rev. 1999 Jan;79(1):143-80 [9922370.001]
  • [Cites] Hepatology. 1999 Apr;29(4):1262-71 [10094974.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5533-8 [10318918.001]
  • (PMID = 16324217.001).
  • [ISSN] 1743-422X
  • [Journal-full-title] Virology journal
  • [ISO-abbreviation] Virol. J.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK62187; United States / NIAAA NIH HHS / AA / AA13301; United States / NIDDK NIH HHS / DK / R01 DK062187; United States / NIAAA NIH HHS / AA / AA013301-02; United States / NIAAA NIH HHS / AA / R21 AA013301-02; United States / NIAID NIH HHS / AI / AI048214; United States / NIAID NIH HHS / AI / U19 AI048214; United States / NIAAA NIH HHS / AA / R21 AA013301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Viral; 3K9958V90M / Ethanol; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1318489
  •  go-up   go-down


18. Koizumi N, Hatano E, Nitta T, Tada M, Harada N, Taura K, Ikai I, Shimahara Y: Blocking of PI3K/Akt pathway enhances apoptosis induced by SN-38, an active form of CPT-11, in human hepatoma cells. Int J Oncol; 2005 May;26(5):1301-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatocellular carcinoma (HCC) is a common malignancy and often resistant to chemotherapy.
  • Many chemotherapy regimens have been tried to control advanced HCC, but have produced a low response rate and no clear impact.
  • CPT-11, a derivative of camptothecin, works as type-I DNA topoisomerase inhibitor and showed a major objective response rate in patients with metastatic colorectal cancer.
  • Hep3B was the most resistant to SN-38 among three hepatoma cell lines.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Phosphatidylinositol 3-Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Drug Resistance, Neoplasm. Humans. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt. Tumor Cells, Cultured

  • 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 = 15809721.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins; 7673326042 / irinotecan; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; XT3Z54Z28A / Camptothecin
  •  go-up   go-down


19. Torresi J, Bharadwaj M, Jackson DC, Gowans EJ: Neutralising antibody, CTL and dendritic cell responses to hepatitis C virus: a preventative vaccine strategy. Curr Drug Targets; 2004 Jan;5(1):41-56
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutralising antibody, CTL and dendritic cell responses to hepatitis C virus: a preventative vaccine strategy.
  • Hepatitis C virus (HCV) accounts for the majority of cases of transfusion acquired hepatitis and hepatitis transmitted by injecting drug use.
  • The patients who do not clear the infection become chronic carriers of HCV and form a reservoir of infection within human populations.
  • Furthermore, these carriers are at serious risk of developing cirrhosis of the liver and hepatocellular carcinoma.
  • The disease is of major concern in developing as well as in developed countries and yet there are no vaccines against HCV, treatment is confined to the use of chemotherapy which is expensive and not always effective.
  • The major obstacle in vaccine development is a limited understanding of the type of immune response that is necessary for viral clearance and the occurrence of various genotypes and quasispecies of HCV.

  • Genetic Alliance. consumer health - Hepatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14738217.001).
  • [ISSN] 1389-4501
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hepatitis C Antibodies; 0 / Viral Hepatitis Vaccines
  • [Number-of-references] 168
  •  go-up   go-down


20. Djeha AH, Thomson TA, Leung H, Searle PF, Young LS, Kerr DJ, Harris PA, Mountain A, Wrighton CJ: Combined adenovirus-mediated nitroreductase gene delivery and CB1954 treatment: a well-tolerated therapy for established solid tumors. Mol Ther; 2001 Feb;3(2):233-40
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined adenovirus-mediated nitroreductase gene delivery and CB1954 treatment: a well-tolerated therapy for established solid tumors.
  • Gene-directed enzyme prodrug therapy (GDEPT) is a refinement of cancer chemotherapy that generates a potent cell-killing drug specifically in tumor cells by enzymatic activation of an inert prodrug.
  • We describe in vivo studies that evaluate the efficacy and safety of intratumoral (i.t.) injection of an adenovirus vector (CTL102) expressing Escherichia coli nitroreductase (NTR) combined with systemic prodrug (CB1954) treatment.
  • A single i.t. injection of CTL102 (7.5 x 10(9) to -2 x 10(10) particles) followed by CB1954 treatment produced clear anti-tumor effects in subcutaneous (s.c.) xenograft models of four cancers that are likely candidates for GDEPT (i.e., primary liver, head and neck, colorectal and prostate).
  • Virus dose-response studies (s.c. liver model) revealed a steep increase and subsequent rapid plateauing of both NTR gene delivery and anti-tumor efficacy.
  • Evidence of minor virus spread (toxicity) was observed in a s.c. head and neck xenograft model.
  • Preexisting anti-Ad5 neutralizing antibodies may therefore be an advantage rather than an issue in the clinical use of this new therapy.
  • [MeSH-major] Adenoviridae / genetics. Antineoplastic Agents / therapeutic use. Aziridines / therapeutic use. Gene Transfer Techniques. Genetic Therapy / methods. Nitroreductases / genetics. Prodrugs / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / therapy. Colorectal Neoplasms / therapy. Dose-Response Relationship, Drug. Escherichia coli / enzymology. Head and Neck Neoplasms / therapy. Humans. Liver Neoplasms / therapy. Luciferases / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Prostatic Neoplasms / therapy. Transduction, Genetic. Transfection. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11237680.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aziridines; 0 / Prodrugs; 7865D5D01M / tretazicar; EC 1.13.12.- / Luciferases; EC 1.7.- / Nitroreductases
  •  go-up   go-down


21. Qin X, Liu C, Zhou Y, Wang G: Cisplatin induces programmed death-1-ligand 1(PD-L1) over-expression in hepatoma H22 cells via Erk /MAPK signaling pathway. Cell Mol Biol (Noisy-le-grand); 2010;56 Suppl:OL1366-72
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cisplatin has been widely used in cancer treatment.
  • However, the prognosis of the cancer patients following chemotherapy has not been substantially improved and several different mechanisms could be involved.
  • Clinically alternative strategies such as immunotherapy and their combinations with chemotherapy have being used.
  • Cancer immunoresistance and immune escape are major obstacles in chemotherapy.
  • However, the effects of cisplatin on the immune responses of cancer cells are not clear.
  • We demonstrated that cisplatin was able to induce H22 cell apoptosis and when the concentration less than IC50 cisplatin could up-regulate PD-L1 expression in hepatoma H22 cells.
  • Meanwhile, cisplatin could induce the phosphorylation of Erk1/2.The lack of effect during treatment with a specific MAPK pathway inhibitor PD98059, demonstrated that cisplatin-induced PD-L1 expression is dependent of Erk1/2 phosphorylation.
  • Our studies reveal a potential link between chemotherapy and cancer immunoresistance.
  • PD-L1 and its signaling pathway appear to be a potential therapeutic target for the cisplatin treatment of hepatoma.
  • [MeSH-minor] Animals. Antigens, CD274. Apoptosis. Carcinoma, Hepatocellular / metabolism. Cell Line, Tumor. Flavonoids / pharmacology. Liver Neoplasms / metabolism. Mice. Phosphorylation. Signal Transduction

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20937224.001).
  • [ISSN] 1165-158X
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antigens, CD274; 0 / Antigens, CD80; 0 / Antineoplastic Agents; 0 / Cd274 protein, mouse; 0 / Flavonoids; 0 / Membrane Glycoproteins; 0 / Peptides; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


22. Hoshida Y, Moriyama M, Otsuka M, Kato N, Taniguchi H, Shiratori Y, Seki N, Omata M: Gene expressions associated with chemosensitivity in human hepatoma cells. Hepatogastroenterology; 2007 Mar;54(74):489-92
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND/AIMS: Only limited patients with hepatoma benefit from chemotherapy without a clear explanation.
  • Chemosensitivities to 8 anticancer drugs (nimustine, mitomycin C, cisplatin, carboplatin, doxorubicin, epirubicin, mitoxantrone, and 5-fluorouracil) were measured by obtaining 50% growth inhibitory concentrations (GI50) using MTT assay.
  • Genes having drug-specific association with chemosensitivity were selected.
  • Drug inactivators reported in non-liver cancers such as multidrug transporters and drug metabolizers showed less diversity of chemosensitivity in hepatoma cells.
  • CONCLUSIONS: To evaluate these gene expressions may be useful to select anticancer drugs, and possibly to consider new therapeutic target to modify drug action.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / pathology. Cell Division / drug effects. Cell Survival / drug effects. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Liver Neoplasms / genetics. Liver Neoplasms / pathology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cell Line, Tumor. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic / genetics. Humans. In Vitro Techniques. Membrane Transport Proteins / genetics. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Superoxide Dismutase / genetics. Up-Regulation / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17523305.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Membrane Transport Proteins; 97599-47-8 / peptide permease; EC 1.15.1.1 / Superoxide Dismutase; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  •  go-up   go-down


23. Frese M, Schwärzle V, Barth K, Krieger N, Lohmann V, Mihm S, Haller O, Bartenschlager R: Interferon-gamma inhibits replication of subgenomic and genomic hepatitis C virus RNAs. Hepatology; 2002 Mar;35(3):694-703
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Persistent infection with hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma.
  • All treatments known so far rely on the antiviral activity of interferon alfa (IFN-alpha) that is given alone or in combination with ribavirin.
  • Unfortunately, only a fraction of the patients clear the virus during therapy and for those who do not respond there is currently no alternative treatment.
  • In conclusion, our results suggest that cytotoxic T cells and natural killer cells may contribute to HCV clearance not only by cell killing but also by producing IFN-gamma, thereby enhancing the intracellular inhibition of viral replication.
  • [MeSH-major] Hepacivirus / drug effects. Interferon-gamma / pharmacology. RNA, Viral / biosynthesis. Virus Replication / drug effects
  • [MeSH-minor] Humans. Interferon Type I / biosynthesis. Nitric Oxide / biosynthesis. Nitric Oxide Synthase / physiology. Nitric Oxide Synthase Type II. Replicon / drug effects. Tryptophan / metabolism. Tumor Cells, Cultured. Viral Nonstructural Proteins / metabolism

  • Genetic Alliance. consumer health - Hepatitis.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. (L)-Tryptophan .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11870386.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Type I; 0 / NS-5 protein, hepatitis C virus; 0 / NS3 protein, hepatitis C virus; 0 / RNA, Viral; 0 / Viral Nonstructural Proteins; 31C4KY9ESH / Nitric Oxide; 82115-62-6 / Interferon-gamma; 8DUH1N11BX / Tryptophan; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  •  go-up   go-down


24. Lin HL, Liu TY, Chau GY, Lui WY, Chi CW: Comparison of 2-methoxyestradiol-induced, docetaxel-induced, and paclitaxel-induced apoptosis in hepatoma cells and its correlation with reactive oxygen species. Cancer; 2000 Sep 1;89(5):983-94
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Previously, the authors observed that paclitaxel treatment of hepatoma cells resulted in differential cytotoxicity.
  • Whether other antimicrotubule agents (docetaxel and 2-methoxyestradiol) are more effective than paclitaxel is not clear.
  • Moreover, whether the modulation of reactive oxygen species (ROS) is involved in the drug-induced growth inhibition of hepatoma cells is not known.
  • METHODS: The authors examined the effects of 2-methoxyestradiol, paclitaxel, and docetaxel on HepG2, Hep3B, HA22T/VGH, and Hepa1-6 hepatoma cell lines.
  • The parameters examined included cell viability, cell membrane permeability, cell cycle distribution, DNA fragmentation, and ROS generation.
  • This drug-induced growth inhibition was cell cycle dependent.
  • High dose (0.1 microM) docetaxel- and paclitaxel-treated cells resulted in a G2/M arrest followed by generation of polyploidy or apoptosis; however, low dose (0.01 microM) treatment induced apoptosis without G2/M arrest.
  • Although these antimicrotubule agents increased the formation of ROS, antioxidant treatment did not block drug-induced cell cycle and growth inhibition effects.
  • The drug-induced apoptosis was independent of ROS formation.
  • The potential of using 2-methoxyestradiol and docetaxel for the treatment of patients with hepatoma is worthy of further study.
  • [MeSH-major] Apoptosis. Carcinoma, Hepatocellular / drug therapy. Estradiol / analogs & derivatives. Estradiol / pharmacology. Liver Neoplasms / drug therapy. Paclitaxel / analogs & derivatives. Paclitaxel / pharmacology. Reactive Oxygen Species / metabolism. Taxoids
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Cell Cycle / drug effects. Cell Survival / drug effects. DNA Fragmentation. Flow Cytometry. Humans. Microtubules / drug effects. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10964328.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Reactive Oxygen Species; 0 / Taxoids; 15H5577CQD / docetaxel; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


25. Mulder K, Koski S, Scarfe A, Chu Q, King K, Spratlin J: Antiangiogenic agents in advanced gastrointestinal malignancies: past, present and a novel future. Oncotarget; 2010 Nov;1(7):515-29
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Advanced gastrointestinal (GI) malignancies are varied in presentation, prognosis, and treatment options.
  • Cytotoxic chemotherapies have been the mainstay of therapy for decades but limited extension of survival or clinical benefit has been achieved in non-colorectal GI cancers.
  • Clear benefits have been identified with bevacizumab and sorafenib in colorectal cancer and hepatocellular cancer, respectively; other GI tumor sites have lacked impressive results with antiangiogenic agents.
  • In this review, we will present the benefits, or lack thereof, of clinically tested antiangiogenic compounds in GI malignancies and explore some potential new therapeutic anti-angiogenesis options for these diseases.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma / drug therapy. Gastrointestinal Neoplasms / drug therapy. Medical Oncology / trends
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Biliary Tract Neoplasms / drug therapy. Biliary Tract Neoplasms / pathology. Disease Progression. Drugs, Investigational / therapeutic use. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology. Models, Biological. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology. Protein Kinase Inhibitors / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2003 Jan 1;21(1):60-5 [12506171.001]
  • [Cites] Cancer Res. 2003 Jun 15;63(12):3121-6 [12810638.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4221-6 [14519649.001]
  • [Cites] Eur J Surg Oncol. 2003 Dec;29(10):879-83 [14624781.001]
  • [Cites] World J Gastroenterol. 2004 Mar 1;10(5):643-8 [14991930.001]
  • [Cites] J Clin Invest. 2004 Apr;113(7):1040-50 [15057311.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23):2335-42 [15175435.001]
  • [Cites] FASEB J. 1999 Jan;13(1):9-22 [9872925.001]
  • [Cites] Semin Cancer Biol. 1999 Jun;9(3):211-20 [10343072.001]
  • [Cites] Br J Cancer. 1999 Jul;80(10):1630-4 [10408410.001]
  • [Cites] Anticancer Res. 1999 May-Jun;19(3B):2257-60 [10472340.001]
  • [Cites] Expert Opin Pharmacother. 2005 Feb;6(2):211-23 [15757418.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):179-86 [15863033.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3509-16 [15908661.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3697-705 [15738537.001]
  • [Cites] Br J Cancer. 2005 Jun;92 Suppl 1:S14-20 [15928653.001]
  • [Cites] Ann Oncol. 2005 Aug;16(8):1391-7 [15905307.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):299-309 [16226705.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):8033-40 [16258101.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):483-9 [16052530.001]
  • [Cites] Oncology. 2005;69 Suppl 3:11-6 [16301831.001]
  • [Cites] Nature. 2005 Dec 15;438(7070):932-6 [16355210.001]
  • [Cites] Oncologist. 2005;10 Suppl 3:40-8 [16368870.001]
  • [Cites] Science. 1992 Feb 21;255(5047):989-91 [1312256.001]
  • [Cites] Nature. 1993 Apr 29;362(6423):841-4 [7683111.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):37-41 [8508427.001]
  • [Cites] Cancer Res. 1993 Dec 1;53(23):5822-7 [7694795.001]
  • [Cites] Int J Cancer. 1994 Nov 15;59(4):520-9 [7525492.001]
  • [Cites] Br J Cancer. 1995 Mar;71(3):587-91 [7533517.001]
  • [Cites] Cancer Res. 1995 Sep 15;55(18):3964-8 [7664263.001]
  • [Cites] Nat Med. 1995 Jan;1(1):27-31 [7584949.001]
  • [Cites] Cancer. 1996 Mar 1;77(5):858-63 [8608475.001]
  • [Cites] Hepatology. 1996 Mar;23(3):455-64 [8617424.001]
  • [Cites] Cytokine Growth Factor Rev. 1996 Oct;7(3):259-70 [8971481.001]
  • [Cites] Ann Oncol. 1997 Feb;8(2):163-8 [9093725.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2403-13 [9196156.001]
  • [Cites] Br J Cancer. 1997;76(2):238-43 [9231925.001]
  • [Cites] Int J Cancer. 1998 Sep 11;77(6):933-6 [9714067.001]
  • [Cites] Int J Cancer. 2000 Jan 1;85(1):27-34 [10585578.001]
  • [Cites] Aliment Pharmacol Ther. 2006 Jun 1;23(11):1535-47 [16696801.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2903-9 [16782930.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4293-300 [16908937.001]
  • [Cites] Clin Cancer Res. 2006 Nov 1;12(21):6573-84 [17085673.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5201-6 [17114652.001]
  • [Cites] J Med Chem. 2007 Apr 5;50(7):1584-97 [17343372.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1539-44 [17442997.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1960-6 [17452677.001]
  • [Cites] Ann Surg Oncol. 2007 Jun;14(6):1835-45 [17406950.001]
  • [Cites] J Clin Oncol. 2007 Oct 20;25(30):4779-86 [17947725.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2007;21(6):1089-108 [18070705.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2340-8 [18381441.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):2013-9 [18421054.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):2992-8 [18565886.001]
  • [Cites] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514.001]
  • [Cites] Lancet Oncol. 2009 Jan;10(1):25-34 [19095497.001]
  • [Cites] Invest New Drugs. 2009 Jun;27(3):253-61 [19002384.001]
  • [Cites] Mol Cancer Ther. 2004 Sep;3(9):1041-8 [15367698.001]
  • [Cites] Science. 1989 Dec 8;246(4935):1306-9 [2479986.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1898-903 [16622265.001]
  • [Cites] Mol Cancer Ther. 2006 Apr;5(4):995-1006 [16648571.001]
  • [Cites] J Clin Oncol. 2009 May 1;27(13):2231-7 [19307500.001]
  • [Cites] Science. 2009 Jun 12;324(5933):1457-61 [19460966.001]
  • [Cites] J Clin Oncol. 2009 Jun 20;27(18):3027-35 [19470923.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Sep;64(4):665-72 [19184020.001]
  • [Cites] Lancet Oncol. 2009 Aug;10(8):794-800 [19586800.001]
  • [Cites] J Clin Oncol. 2009 Oct 1;27(28):4718-26 [19720910.001]
  • [Cites] J Clin Oncol. 2009 Nov 20;27(33):5513-8 [19858379.001]
  • [Cites] Clin Cancer Res. 2010 Jan 1;16(1):358-66 [20028764.001]
  • [Cites] Br J Cancer. 2010 Jan 5;102(1):68-72 [19935794.001]
  • [Cites] J Clin Oncol. 2010 Jan 10;28(2):207-14 [19949018.001]
  • [Cites] Clin Cancer Res. 2010 Jan 15;16(2):390-7 [20068087.001]
  • [Cites] Lancet Oncol. 2010 Jan;11(1):48-54 [19932054.001]
  • [Cites] J Clin Oncol. 2010 Feb 10;28(5):780-7 [20048182.001]
  • [Cites] Br J Cancer. 2010 Mar 16;102(6):981-6 [20160718.001]
  • [Cites] N Engl J Med. 2010 Apr 8;362(14):1273-81 [20375404.001]
  • [Cites] J Clin Oncol. 2010 Jun 20;28(18):2947-51 [20458043.001]
  • [Cites] Future Oncol. 2010 Jul;6(7):1085-94 [20624120.001]
  • [Cites] J Clin Oncol. 2010 Aug 1;28(22):3617-22 [20606091.001]
  • [Cites] Invest New Drugs. 2011 Dec;29(6):1449-58 [20461441.001]
  • [Cites] Cancer Lett. 2000 May 29;153(1-2):7-12 [10779624.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):249-57 [11001068.001]
  • [Cites] Gastroenterology. 2000 Nov;119(5):1358-72 [11054395.001]
  • [Cites] Int J Cancer. 2001 May 1;92(3):361-9 [11291072.001]
  • [Cites] J Biol Chem. 2001 Feb 2;276(5):3222-30 [11058584.001]
  • [Cites] Am J Surg. 2001 Sep;182(3):298-304 [11587697.001]
  • [Cites] Lab Invest. 2001 Oct;81(10):1439-51 [11598156.001]
  • [Cites] Am J Clin Pathol. 2001 Dec;116(6):838-45 [11764072.001]
  • [Cites] Cancer Biother Radiopharm. 2001 Oct;16(5):359-70 [11776753.001]
  • [Cites] Int J Cancer. 2002 Jan 20;97(3):393-9 [11774295.001]
  • [Cites] Cancer Res. 2002 Apr 1;62(7):1996-2003 [11929816.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):193-202 [12086877.001]
  • [Cites] Ann Surg. 2002 Jul;236(1):37-42 [12131083.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3270-5 [12149301.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4645-55 [12183421.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11393-8 [12177445.001]
  • [Cites] Int J Cancer. 2002 Nov 10;102(2):101-8 [12385004.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7284-90 [12499271.001]
  • (PMID = 21317448.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drugs, Investigational; 0 / Protein Kinase Inhibitors
  • [Other-IDs] NLM/ PMC3248127
  •  go-up   go-down


26. Chen Y, Cheng G, Mahato RI: RNAi for treating hepatitis B viral infection. Pharm Res; 2008 Jan;25(1):72-86
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic hepatitis B virus (HBV) infection is one of the leading causes of liver cirrhosis and hepatocellular carcinoma (HCC).
  • Current treatment strategies of HBV infection including the use of interferon (IFN)-alpha and nucleotide analogues such as lamivudine and adefovir have met with only partial success.
  • Therefore, it is necessary to develop more effective antiviral therapies that can clear HBV infection with fewer side effects.
  • The successful use of chemically synthesized siRNA, endogenous expression of small hairpin RNA (shRNA) or microRNA (miRNA) to silence the target gene make this technology towards a potentially rational therapeutics for HBV infection.
  • In this review, we discuss several strategies for improving the anti-HBV therapeutic efficacy of siRNAs, while avoiding their off-target effects and immunostimulation.
  • There is an in-depth discussion on the (1) mechanisms of RNAi, (2) methods for siRNA/shRNA production, (3) barriers to RNAi-based therapies, and (4) delivery strategies of siRNA for treating HBV infection.

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • COS Scholar Universe. author profiles.
  • 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] J Control Release. 2002 Apr 23;80(1-3):283-94 [11943405.001]
  • [Cites] Genes Dev. 2002 Apr 15;16(8):948-58 [11959843.001]
  • [Cites] Science. 2002 Apr 19;296(5567):550-3 [11910072.001]
  • [Cites] FEBS Lett. 2002 Jun 19;521(1-3):195-9 [12096714.001]
  • [Cites] RNA. 2002 Jul;8(7):855-60 [12166640.001]
  • [Cites] J Virol. 2002 Sep;76(18):9225-31 [12186906.001]
  • [Cites] Biomacromolecules. 2002 Nov-Dec;3(6):1197-207 [12425656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):2014-8 [12566571.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2783-8 [12594341.001]
  • [Cites] Hepatology. 2003 Apr;37(4):764-70 [12668968.001]
  • [Cites] Cancer Biol Ther. 2003 Mar-Apr;2(2):206-10 [12750565.001]
  • [Cites] FEBS Lett. 2003 May 22;543(1-3):51-4 [12753904.001]
  • [Cites] Nucleic Acids Res. 2003 Jun 1;31(11):2705-16 [12771196.001]
  • [Cites] Nat Biotechnol. 2003 Jun;21(6):639-44 [12740585.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Jun;4(6):457-67 [12778125.001]
  • [Cites] Biochemistry. 2003 Jul 8;42(26):7967-75 [12834349.001]
  • [Cites] Gastroenterology. 2003 Jul;125(1):9-18 [12851866.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5712-5 [12944921.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Sep 19;309(2):482-4 [12951075.001]
  • [Cites] Nat Cell Biol. 2003 Sep;5(9):834-9 [12942087.001]
  • [Cites] Hepatology. 2003 Oct;38(4):842-50 [14512871.001]
  • [Cites] Gene. 2003 Oct 16;316:137-41 [14563560.001]
  • [Cites] Gene Ther. 2005 Mar;12(5):461-6 [15616603.001]
  • [Cites] J Zhejiang Univ Sci B. 2005 Apr;6(4):236-41 [15754419.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):708-16 [15765406.001]
  • [Cites] Nat Biotechnol. 2005 Apr;23(4):457-62 [15778705.001]
  • [Cites] Trends Cell Biol. 2005 May;15(5):251-8 [15866029.001]
  • [Cites] Hepatology. 2005 Jun;41(6):1349-56 [15880588.001]
  • [Cites] J Gene Med. 2005 Jul;7(7):918-25 [15756649.001]
  • [Cites] Nat Biotechnol. 2005 Aug;23(8):1002-7 [16041363.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Oct 7;335(4):1051-9 [16111658.001]
  • [Cites] J Pharm Sci. 2005 Oct;94(10):2266-75 [16136555.001]
  • [Cites] AAPS J. 2005;7(1):E61-77 [16146351.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Oct 28;336(3):820-30 [16153600.001]
  • [Cites] FEBS J. 2005 Nov;272(22):5910-22 [16279954.001]
  • [Cites] Expert Opin Drug Deliv. 2005 Jan;2(1):3-28 [16296732.001]
  • [Cites] J Gen Virol. 2005 Dec;86(Pt 12):3227-34 [16298967.001]
  • [Cites] Mol Ther. 2006 Feb;13(2):411-21 [16337206.001]
  • [Cites] Mol Ther. 2006 Mar;13(3):494-505 [16343994.001]
  • [Cites] Gene Ther. 2006 Jun;13(11):883-92 [16496015.001]
  • [Cites] Nucleic Acids Res. 2006;34(10):e73 [16740739.001]
  • [Cites] RNA. 2006 Jul;12(7):1179-87 [16682560.001]
  • [Cites] RNA. 2006 Jul;12(7):1197-205 [16682562.001]
  • [Cites] Hum Gene Ther. 2006 Jul;17(7):751-66 [16839274.001]
  • [Cites] Gene Ther. 2000 Feb;7(4):292-9 [10694809.001]
  • [Cites] Microbiol Mol Biol Rev. 2000 Mar;64(1):51-68 [10704474.001]
  • [Cites] Hepatology. 2000 Oct;32(4 Pt 1):828-34 [11003630.001]
  • [Cites] Mol Ther. 2000 Oct;2(4):302-17 [11020345.001]
  • [Cites] J Control Release. 2000 Dec 3;69(3):369-77 [11102677.001]
  • [Cites] Nature. 2001 May 24;411(6836):494-8 [11373684.001]
  • [Cites] J Mol Med (Berl). 2001 May;79(4):205-12 [11409712.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1146-50 [11498593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1443-8 [11818553.001]
  • [Cites] Nucleic Acids Res. 2002 Apr 15;30(8):1757-66 [11937629.001]
  • [Cites] Int J Mol Med. 2007 Apr;19(4):705-11 [17334648.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jun 1;357(2):511-6 [17434451.001]
  • [Cites] World J Gastroenterol. 2007 Apr 28;13(16):2324-7 [17511031.001]
  • [Cites] Hepatology. 2007 Jul;46(1):84-94 [17596868.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Sep 14;361(1):122-6 [17658482.001]
  • [Cites] Bioconjug Chem. 2007 Sep-Oct;18(5):1391-6 [17630789.001]
  • [Cites] Nat Biotechnol. 2007 Oct;25(10):1149-57 [17873866.001]
  • [Cites] RNA. 2007 Nov;13(11):1887-93 [17804643.001]
  • [Cites] BMC Biotechnol. 2002 Aug 28;2:15 [12199908.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Nov 14;311(2):398-404 [14592428.001]
  • [Cites] Mol Ther. 2003 Nov;8(5):769-76 [14599810.001]
  • [Cites] Pharmacol Rev. 2003 Dec;55(4):629-48 [14657420.001]
  • [Cites] Nucleic Acids Res. 2004;32(3):936-48 [14769950.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Mar 8;14(5):1139-43 [14980652.001]
  • [Cites] Pharm Res. 2004 Jan;21(1):1-7 [14984251.001]
  • [Cites] Virology. 2004 Mar 1;320(1):135-43 [15003869.001]
  • [Cites] Pharm Res. 2004 Mar;21(3):458-66 [15070097.001]
  • [Cites] Nucleic Acids Res. 2004;32(7):2102-12 [15087489.001]
  • [Cites] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W113-20 [15215362.001]
  • [Cites] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W124-9 [15215364.001]
  • [Cites] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W130-4 [15215365.001]
  • [Cites] World J Gastroenterol. 2004 Jul 1;10(13):1898-901 [15222032.001]
  • [Cites] World J Gastroenterol. 2004 Jul 15;10(14):2050-4 [15237432.001]
  • [Cites] Cell. 2004 Jul 9;118(1):57-68 [15242644.001]
  • [Cites] N Engl J Med. 1997 Dec 11;337(24):1733-45 [9392700.001]
  • [Cites] J Gastroenterol Hepatol. 1997 Oct;12(9-10):S354-69 [9407358.001]
  • [Cites] J Immunol. 1998 Feb 15;160(4):2013-21 [9469465.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):806-11 [9486653.001]
  • [Cites] Oncogene. 1998 Apr 23;16(16):2051-63 [9572486.001]
  • [Cites] N Engl J Med. 1998 Jul 9;339(2):61-8 [9654535.001]
  • [Cites] Genes Cells. 1998 Jul;3(7):477-84 [9753428.001]
  • [Cites] Annu Rev Biochem. 1998;67:227-64 [9759489.001]
  • [Cites] J Med Chem. 1999 Feb 25;42(4):609-18 [10052968.001]
  • [Cites] Zhonghua Gan Zang Bing Za Zhi. 1999 Jun;7(2):80-3 [10488413.001]
  • [Cites] Adv Genet. 1999;41:95-156 [10494618.001]
  • [Cites] Nature. 2004 Nov 11;432(7014):173-8 [15538359.001]
  • [Cites] World J Gastroenterol. 2005 Jan 28;11(4):498-502 [15641133.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):773-8 [15640346.001]
  • [Cites] Trends Biochem Sci. 2005 Feb;30(2):106-14 [15691656.001]
  • [Cites] J Med Chem. 2005 Feb 24;48(4):901-4 [15715458.001]
  • [Cites] Mol Cell. 2004 Jul 23;15(2):185-97 [15260970.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Oct 4;14(19):4975-7 [15341962.001]
  • [Cites] Lancet. 1970 Apr 4;1(7649):695-8 [4190997.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 May;84(9):2678-82 [3033659.001]
  • [Cites] J Virol. 1987 Oct;61(10):3322-5 [3041052.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6599-603 [2395863.001]
  • [Cites] Jpn J Cancer Res. 1990 Dec;81(12):1191-4 [2125986.001]
  • [Cites] N Engl J Med. 1991 Sep 5;325(10):729-31 [1651454.001]
  • [Cites] J Virol. 1992 Feb;66(2):1223-7 [1731101.001]
  • [Cites] J Biol Chem. 1992 Jun 25;267(18):12436-9 [1618751.001]
  • [Cites] J Virol. 1992 Sep;66(9):5682-4 [1501300.001]
  • [Cites] Oncogene. 1993 May;8(5):1109-17 [8386823.001]
  • [Cites] Lancet. 1993 Nov 27;342(8883):1335-40 [7901639.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 15;91(6):2230-4 [8134379.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10350-4 [7937954.001]
  • [Cites] Infect Agents Dis. 1994 Apr-Jun;3(2-3):85-93 [7529120.001]
  • [Cites] J Virol. 1995 Feb;69(2):1107-14 [7815490.001]
  • [Cites] Clin Investig. 1994 Oct;72(10):737-41 [7865975.001]
  • [Cites] J Cancer Res Clin Oncol. 1995;121(9-10):593-601 [7559743.001]
  • [Cites] N Engl J Med. 1997 Jan 30;336(5):347-56 [9011789.001]
  • [Cites] Methods Enzymol. 1996;275:195-208 [9026639.001]
  • [Cites] Pharm Res. 1997 Jul;14(7):853-9 [9244140.001]
  • [Cites] Hepatology. 1997 Aug;26(2):251-5 [9252130.001]
  • [Cites] Nature. 1997 Sep 18;389(6648):239-42 [9305836.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11681-5 [9326670.001]
  • [Cites] Gastroenterology. 1997 Nov;113(5):1660-7 [9352870.001]
  • [Cites] Mol Biosyst. 2005 Dec;1(5-6):382-90 [16881007.001]
  • [Cites] Nat Biotechnol. 2006 Aug;24(8):1005-15 [16823371.001]
  • [Cites] Gene Ther. 2007 Jan;14(1):11-9 [16929350.001]
  • [Cites] Antiviral Res. 2007 Jan;73(1):24-30 [16844238.001]
  • [Cites] J Control Release. 2007 Feb 12;117(2):281-90 [17196291.001]
  • [Cites] Mol Ther. 2007 Mar;15(3):534-41 [17213835.001]
  • (PMID = 18074201.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK069968; United States / NIDDK NIH HHS / DK / R01 DK 064633; United States / NIDDK NIH HHS / DK / R01 DK 069968
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Excipients; 0 / RNA, Small Interfering
  • [Number-of-references] 126
  • [Other-IDs] NLM/ PMC2217617
  •  go-up   go-down


27. Durantel D, Carrouée-Durantel S, Branza-Nichita N, Dwek RA, Zitzmann N: Effects of interferon, ribavirin, and iminosugar derivatives on cells persistently infected with noncytopathic bovine viral diarrhea virus. Antimicrob Agents Chemother; 2004 Feb;48(2):497-504
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In chronic carriers, the viral infection induces liver damage that predisposes the patient for cirrhosis and can lead to hepatocellular carcinoma.
  • In addition to its limited efficacy, this treatment is frequently poorly tolerated because of its side effects.
  • The urgently needed development of new drugs is made difficult by the lack of an in vitro or in vivo infectivity model, and no cell line has been found so far to reliably and reproducibly support HCV infection.
  • In this study we used an MDBK cell line persistently infected with noncytopathic BVDV to assess the antiviral effect of IFN-alpha and RBV, the two drugs currently in clinical use against HCV.
  • The same system was then used to evaluate the potential of two classes of iminosugar derivates to clear noncytopathic BVDV infection from MDBK cells.
  • We show that treatment with long-alkyl-chain deoxynojirimycin derivatives, which are inhibitors of the endoplasmic reticulum (ER)-resident alpha-glucosidases, can greatly reduce the amount of secreted enveloped viral RNA.
  • [MeSH-major] Antiviral Agents / pharmacology. Bovine Virus Diarrhea-Mucosal Disease / drug therapy. Bovine Virus Diarrhea-Mucosal Disease / virology. Diarrhea Viruses, Bovine Viral / drug effects. Diarrhea Viruses, Bovine Viral / pathogenicity. Interferon Type I / pharmacology. Ribavirin / pharmacology
  • [MeSH-minor] Animals. Cattle. Cell Line. Cytopathogenic Effect, Viral / drug effects. Fluorescent Antibody Technique. Imino Acids / chemistry. RNA, Viral / biosynthesis. RNA, Viral / genetics. Recombinant Proteins. Reverse Transcriptase Polymerase Chain Reaction. Viral Plaque Assay. Virus Replication / drug effects

  • Hazardous Substances Data Bank. RIBAVIRIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Forum (Genova). 2000 Jan-Mar;10(1):22-8 [10717255.001]
  • [Cites] Curr Top Microbiol Immunol. 2000;242:135-48 [10592659.001]
  • [Cites] J Gen Virol. 2000 Jul;81(Pt 7):1631-48 [10859368.001]
  • [Cites] J Viral Hepat. 2000 Jul;7(4):250-7 [10886533.001]
  • [Cites] Baillieres Best Pract Res Clin Gastroenterol. 2000 Apr;14(2):211-28 [10890317.001]
  • [Cites] Baillieres Best Pract Res Clin Gastroenterol. 2000 Apr;14(2):255-64 [10890320.001]
  • [Cites] Semin Liver Dis. 2000;20(1):17-35 [10895429.001]
  • [Cites] Vet Microbiol. 2000 Nov 15;77(1-2):117-28 [11042405.001]
  • [Cites] Gastroenterology. 2001 Mar;120(4):1000-8 [11231955.001]
  • [Cites] J Virol. 2001 Apr;75(8):3527-36 [11264342.001]
  • [Cites] Nature. 2001 Apr 19;410(6831):995-1001 [11309630.001]
  • [Cites] Hepatology. 2001 Jun;33(6):1488-95 [11391538.001]
  • [Cites] J Virol. 2001 Sep;75(18):8516-23 [11507197.001]
  • [Cites] Drug Resist Updat. 2001 Apr;4(2):118-28 [11512520.001]
  • [Cites] Antiviral Res. 2001 Oct;52(1):1-17 [11530183.001]
  • [Cites] J Virol. 2001 Oct;75(19):8987-98 [11533162.001]
  • [Cites] Prog Drug Res. 2001;Spec No:1-34 [11548206.001]
  • [Cites] Expert Opin Pharmacother. 2001 Aug;2(8):1317-24 [11585000.001]
  • [Cites] Drugs. 2002;62(3):507-56 [11827565.001]
  • [Cites] J Virol. 2002 Apr;76(8):3596-604 [11907199.001]
  • [Cites] Antivir Chem Chemother. 2001 Nov;12(6):317-25 [12018676.001]
  • [Cites] Nat Rev Drug Discov. 2002 Jan;1(1):65-75 [12119611.001]
  • [Cites] Antiviral Res. 2002 Sep;55(3):425-35 [12206880.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Jul;47(7):2293-8 [12821481.001]
  • [Cites] Arch Virol. 1987;94(1-2):43-53 [3034204.001]
  • [Cites] J Gen Virol. 1988 Jun;69 ( Pt 6):1399-403 [2838577.001]
  • [Cites] Vet Microbiol. 1989 Jan;19(1):13-21 [2538022.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 1;91(3):913-7 [8302866.001]
  • [Cites] Science. 1994 Oct 21;266(5184):456-8 [7939687.001]
  • [Cites] Cell. 1995 May 5;81(3):425-33 [7736594.001]
  • [Cites] J Vet Med Sci. 1995 Aug;57(4):677-81 [8519897.001]
  • [Cites] FEBS Lett. 1998 Jun 23;430(1-2):17-22 [9678587.001]
  • [Cites] Vet Microbiol. 1998 Oct;63(2-4):117-24 [9850992.001]
  • [Cites] J Vet Med Sci. 1998 Dec;60(12):1329-33 [9879534.001]
  • [Cites] Semin Liver Dis. 1999;19 Suppl 1:57-65 [10349693.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):11878-82 [10518544.001]
  • [Cites] Virus Res. 1995 Oct;38(2-3):231-9 [8578861.001]
  • [Cites] J Virol. 1996 Feb;70(2):778-86 [8551615.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1995;60:405-15 [8824414.001]
  • [Cites] J Virol. 1997 Jan;71(1):697-704 [8985401.001]
  • [Cites] J Virol. 1997 Apr;71(4):3255-8 [9060690.001]
  • [Cites] J Virol. 1998 May;72(5):3851-8 [9557669.001]
  • [Cites] Nat Med. 1998 May;4(5):610-4 [9585237.001]
  • [Cites] J Virol. 2000 Jan;74(1):564-72 [10590151.001]
  • [Cites] Antimicrob Agents Chemother. 2000 Apr;44(4):859-66 [10722482.001]
  • (PMID = 14742201.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Imino Acids; 0 / Interferon Type I; 0 / RNA, Viral; 0 / Recombinant Proteins; 49717AWG6K / Ribavirin
  • [Other-IDs] NLM/ PMC321564
  •  go-up   go-down


28. Selvendiran K, Koga H, Ueno T, Yoshida T, Maeyama M, Torimura T, Yano H, Kojiro M, Sata M: Luteolin promotes degradation in signal transducer and activator of transcription 3 in human hepatoma cells: an implication for the antitumor potential of flavonoids. Cancer Res; 2006 May 1;66(9):4826-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A clear apoptosis was found in the luteolin-treated HLF hepatoma cells in a time- and dosage-dependent manner.
  • The expression level of Ser(727)-phosphorylated STAT3 was gradually decreased by the luteolin treatment, followed by a fast and clear down-regulation in the active forms of CDK5, which can phosphorylate STAT3 at Ser(727).
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Luteolin / pharmacology. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Animals. Antigens, CD95 / biosynthesis. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Cell Growth Processes / drug effects. Cell Line, Tumor. Down-Regulation. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Phosphorylation / drug effects. Receptors, Tumor Necrosis Factor, Type I / biosynthesis. Ubiquitin / metabolism. Xenograft Model Antitumor Assays






Advertisement