[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 100 of about 802
36. Ishii T, Ishida T, Utsunomiya A, Inagaki A, Yano H, Komatsu H, Iida S, Imada K, Uchiyama T, Akinaga S, Shitara K, Ueda R: Defucosylated humanized anti-CCR4 monoclonal antibody KW-0761 as a novel immunotherapeutic agent for adult T-cell leukemia/lymphoma. Clin Cancer Res; 2010 Mar 1;16(5):1520-31
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defucosylated humanized anti-CCR4 monoclonal antibody KW-0761 as a novel immunotherapeutic agent for adult T-cell leukemia/lymphoma.
  • PURPOSE: Adult T-cell leukemia/lymphoma (ATLL) has a very poor prognosis.
  • The first aim of the present study was to evaluate whether the antitumor activity of KW-0761 would likely be sufficient for therapeutic clinical application against ATLL.
  • EXPERIMENTAL DESIGN: The antitumor activity of KW-0761 against ATLL cell lines was evaluated in vitro using human cells and in mice in vivo.
  • Primary ATLL cells from 23 patients were evaluated for susceptibility to autologous ADCC with KW-0761 by two independent methods.
  • RESULTS: KW-0761 showed potent antitumor activity against ATLL cell lines both in vitro and in the ATLL mouse model in vivo.
  • In addition, KW-0761 showed potent antitumor activity mediated by highly enhanced ADCC against primary ATLL cells both in vitro and ex vivo in an autologous setting.
  • The degree of KW-0761 ADCC against primary ATLL cells in an autologous setting was mainly determined by the amount of effector natural killer cells present, but not the amount of the target molecule CCR4 on the ATLL cell surface.
  • CONCLUSION: KW-0761 should be sufficiently active for therapeutic clinical application for ATLL.
  • In addition, combination treatment strategies that augment natural killer cell activity should be promising for amplifying the effect of KW-0761.
  • In the near future, the actual efficacy of KW-0761 will be established in pivotal clinical trials.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotherapy / methods. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Animals. Antibodies, Monoclonal, Humanized. Antibody-Dependent Cell Cytotoxicity / drug effects. Antibody-Dependent Cell Cytotoxicity / immunology. Biosensing Techniques. Cell Separation. Flow Cytometry. Humans. Male. Mice. Mice, SCID. Receptors, CCR4 / immunology

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20160057.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / mogamulizumab
  •  go-up   go-down


37. Kawakami H, Tomita M, Okudaira T, Ishikawa C, Matsuda T, Tanaka Y, Nakazato T, Taira N, Ohshiro K, Mori N: Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells. Int J Cancer; 2007 Apr 15;120(8):1811-20
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells.
  • The geldanamycin derivative 17-AAG is currently tested in clinical trials and known to inhibit the function of Hsp90 and promote the proteasomal degradation of its misfolded client proteins.
  • ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.
  • Since Hsp90 is overexpressed in HTLV-I-infected T-cell lines and primary ATL cells, we analyzed the effects of 17-AAG on cell survival, apoptosis and expression of signal transduction proteins.
  • HTLV-I-infected T-cell lines and primary ATL cells were significantly more sensitive to 17-AAG in cell survival assays than normal PBMCs.
  • 17-AAG induced the inhibition of cell cycle and apoptosis.
  • These effects could be mediated by inactivation of NF-kappaB, AP-1 and PI3K/Akt pathways, as well as reduction of expression of proteins involved in the G1-S cell cycle transition and apoptosis.
  • Collectively, our results indicate that 17-AAG suppresses ATL cell survival through, at least in part, destabilization of several client proteins and suggest that 17-AAG is a potentially useful chemotherapeutic agent for ATL.
  • [MeSH-major] Apoptosis / drug effects. Benzoquinones / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Human T-lymphotropic virus 1 / drug effects. Lactams, Macrocyclic / therapeutic use. Leukemia, T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. T-Lymphocytes / virology
  • [MeSH-minor] Adult. Cell Cycle / drug effects. Humans. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [RetractionIn] Int J Cancer. 2011 Dec 1;129(11):2762-3 [21960263.001]
  • (PMID = 17230513.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 4GY0AVT3L4 / tanespimycin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


38. Bench BJ, Suarez VH, Watanabe CM: An efficient one-pot synthesis of tethered cyclohexadiene enaminonitriles from methyl-ketones: an effective route to quinazolines. Bioorg Med Chem Lett; 2008 May 15;18(10):3126-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The substituted enaminonitrile intermediates also exhibited weak anti-microbial activity and cytotoxicity against human T-cell leukemia.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17967539.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM008523
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Cyclohexenes; 0 / Ketones; 0 / Nitriles; 0 / Quinazolines; 0F8Z5909QZ / 1,4-cyclohexadiene
  •  go-up   go-down


39. Rauch D, Gross S, Harding J, Niewiesk S, Lairmore M, Piwnica-Worms D, Ratner L: Imaging spontaneous tumorigenesis: inflammation precedes development of peripheral NK tumors. Blood; 2009 Feb 12;113(7):1493-500
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We developed a mouse model of spontaneous lymphoma in which malignant transformation is coupled with light emission that can be detected noninvasively using bioluminescent imaging.
  • The human T-cell leukemia virus (HTLV) type 1 transcriptional transactivator Tax is an oncogene sufficient to produce lymphoma in transgenic animal models.
  • Using the granzyme B promoter to restrict Tax expression to the mature natural killer (NK)/T-cell compartment, we have reproduced many elements of HTLV-associated adult T-cell leukemia/lymphoma.
  • Tax activates signaling cascades associated with transformation, inflammation, and tumorigenesis.
  • Based on these findings, we propose that Tax expression in activated lymphocytes initiates a cascade of events that leads to NK/T cell recruitment, activation, and transformation.

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [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] Oncogene. 2005 Sep 5;24(39):6005-15 [16155607.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] Virology. 2001 Mar 1;281(1):10-20 [11222091.001]
  • [Cites] J Biol Chem. 2005 Oct 21;280(42):35713-22 [16105841.001]
  • [Cites] J Virol. 2005 Nov;79(22):14069-78 [16254341.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4294-302 [16118323.001]
  • [Cites] Carcinogenesis. 2006 Apr;27(4):673-81 [16308315.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Mol Cancer Res. 2006 Apr;4(4):221-33 [16603636.001]
  • [Cites] EMBO J. 2006 Apr 19;25(8):1741-52 [16601696.001]
  • [Cites] Virology. 2006 May 10;348(2):354-69 [16458341.001]
  • [Cites] Immunol Res. 2006;34(1):1-12 [16720895.001]
  • [Cites] Nature. 2006 May 25;441(7092):431-6 [16724054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9220-5 [16751281.001]
  • [Cites] J Leukoc Biol. 2006 Sep;80(3):640-50 [16829632.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] J Biol Chem. 2007 Nov 23;282(47):34581-93 [17897946.001]
  • [Cites] Cell Death Differ. 2008 Feb;15(2):226-33 [17541426.001]
  • [Cites] J Virol. 2008 Sep;82(17):8442-55 [18596104.001]
  • [Cites] EMBO J. 1986 Nov;5(11):2883-8 [3024966.001]
  • [Cites] Nature. 1989 Sep 7;341(6237):72-4 [2788824.001]
  • [Cites] Am J Pathol. 1989 Dec;135(6):1025-33 [2688429.001]
  • [Cites] J Virol. 1991 Aug;65(8):4398-407 [2072456.001]
  • [Cites] Hokkaido Igaku Zasshi. 1991 Jul;66(4):534-43 [1916630.001]
  • [Cites] J Biol Chem. 1991 Dec 25;266(36):24433-8 [1761544.001]
  • [Cites] Virology. 1992 Apr;187(2):705-10 [1546464.001]
  • [Cites] Oncogene. 1992 Sep;7(9):1749-55 [1501887.001]
  • [Cites] Oncogene. 1992 Dec;7(12):2399-405 [1461648.001]
  • [Cites] Virology. 1993 Sep;196(1):309-18 [8356801.001]
  • [Cites] Virology. 1993 Nov;197(1):196-204 [8212554.001]
  • [Cites] J Virol. 1994 Jun;68(6):3544-9 [8189493.001]
  • [Cites] J Virol. 1995 Mar;69(3):1907-12 [7853532.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] J Virol. 1995 Jun;69(6):3420-32 [7745688.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S162-9 [8797719.001]
  • [Cites] J Neurovirol. 1996 Oct;2(5):336-44 [8912210.001]
  • [Cites] Blood. 1997 Jul 15;90(2):783-94 [9226179.001]
  • [Cites] Virology. 1999 Feb 15;254(2):279-87 [9986794.001]
  • [Cites] J Immunol. 1999 Mar 1;162(5):2956-63 [10072546.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Virology. 2004 Nov 24;329(2):395-411 [15518818.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3305-11 [15292059.001]
  • [Cites] Cancer Cell. 2005 Jan;7(1):5-15 [15652745.001]
  • [Cites] Oncogene. 2005 Jan 20;24(4):525-40 [15580311.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1200-8 [11493471.001]
  • [Cites] Exp Cell Res. 2001 Nov 15;271(1):169-79 [11697893.001]
  • [Cites] Nat Rev Cancer. 2002 Apr;2(4):301-10 [12001991.001]
  • [Cites] Int J Mol Med. 2003 Jan;11(1):3-11 [12469209.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] Methods. 2003 Jan;29(1):110-22 [12543076.001]
  • [Cites] Nucleic Acids Res. 2004;32(9):2829-37 [15155851.001]
  • [Cites] J Virol. 2004 Jul;78(13):6735-43 [15194748.001]
  • [Cites] Blood. 2004 Aug 1;104(3):802-9 [15090453.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):461-6 [15329734.001]
  • [Cites] J Virol. 2005 Jun;79(11):6932-9 [15890932.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] J Virol. 2000 Dec;74(24):11988-92 [11090202.001]
  • (PMID = 18971418.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA094056; United States / NCI NIH HHS / CA / CA100730-06; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / P01 CA100730-06; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / CA94056; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; EC 1.13.12.- / Luciferases; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse
  • [Other-IDs] NLM/ PMC2644076
  •  go-up   go-down


40. Nitta T, Kanai M, Sugihara E, Tanaka M, Sun B, Nagasawa T, Sonoda S, Saya H, Miwa M: Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells. Cancer Sci; 2006 Sep;97(9):836-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells.
  • Centrosomes play pivotal roles in cell polarity, regulation of the cell cycle and chromosomal segregation.
  • Centrosome amplification was recently described as a possible cause of aneuploidy in certain solid tumors and leukemias.
  • ATL is a T-cell malignancy caused by HTLV-1.
  • Although the precise mechanism of cell transformation is unclear, the HTLV-1-encoded protein, Tax, is thought to play a crucial role in leukemogenesis.
  • Here we demonstrate that lymphocytes isolated from patients with ATL show centrosome amplification and that a human T cell line shows centrosome amplification after induction of Tax, which was suppressed by CDK inhibitors.
  • Micronuclei formation was also observed after centrosome amplification in Tax-induced human T cells.
  • These findings suggest that Tax deregulates CDK activity and induces centrosome amplification, which might be associated with cellular transformation by HTLV-1 and chromosomal instability in HTLV-1-infected human T cells.
  • [MeSH-major] Cell Transformation, Viral / genetics. Centrosome / physiology. Gene Products, tax / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes / virology

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16805820.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax
  •  go-up   go-down


41. Jones KS, Petrow-Sadowski C, Bertolette DC, Huang Y, Ruscetti FW: Heparan sulfate proteoglycans mediate attachment and entry of human T-cell leukemia virus type 1 virions into CD4+ T cells. J Virol; 2005 Oct;79(20):12692-702
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heparan sulfate proteoglycans mediate attachment and entry of human T-cell leukemia virus type 1 virions into CD4+ T cells.
  • Heparan sulfate proteoglycans (HSPGs) are used by a number of viruses to facilitate entry into host cells.
  • For the retrovirus human T-cell leukemia virus type 1 (HTLV-1), it has recently been reported that HSPGs are critical for efficient binding of soluble HTLV-1 SU and the entry of HTLV pseudotyped viruses into non-T cells.
  • However, the primary in vivo targets of HTLV-1, CD4(+) T cells, have been reported to express low or undetectable levels of HSPGs.
  • For this study, we reexamined the expression of HSPGs in CD4(+) T cells and examined their role in HTLV-1 attachment and entry.
  • Enzymatic modification of HSPGs on the surfaces of either established CD4(+) T-cell lines or primary CD4(+) T cells dramatically reduced the binding of both soluble HTLV-1 SU and HTLV-1 virions.
  • HSPGs also affected the efficiency of HTLV-1 entry, since blocking the interaction with HSPGs markedly reduced both the internalization of HTLV-1 virions and the titer of HTLV-1 pseudotyped viral infection in CD4(+) T cells.
  • Thus, HSPGs play a critical role in the binding and entry of HTLV-1 into CD4(+) T cells.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1992 Oct 5;267(28):20435-43 [1400362.001]
  • [Cites] J Cell Biol. 1992 Nov;119(4):961-75 [1385449.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8392-6 [7690960.001]
  • [Cites] Antiviral Res. 1994 Feb;23(2):143-59 [7908510.001]
  • [Cites] J Virol. 1995 Oct;69(10):6297-303 [7666530.001]
  • [Cites] Virology. 1995 Sep 10;212(1):196-203 [7676629.001]
  • [Cites] Virology. 1996 Apr 1;218(1):279-84 [8615036.001]
  • [Cites] J Virol. 1996 Oct;70(10):7322-6 [8794391.001]
  • [Cites] J Virol. 1997 Jun;71(6):4571-80 [9151851.001]
  • [Cites] J Clin Invest. 1997 Oct 15;100(8):2043-53 [9329969.001]
  • [Cites] J Virol. 1998 Jan;72(1):535-41 [9420256.001]
  • [Cites] J Virol. 1998 Feb;72(2):1577-85 [9445060.001]
  • [Cites] J Virol. 1998 Mar;72(3):2208-12 [9499078.001]
  • [Cites] J Virol. 1998 Sep;72(9):7357-66 [9696832.001]
  • [Cites] Annu Rev Biochem. 1998;67:609-52 [9759499.001]
  • [Cites] Virology. 1999 Feb 15;254(2):235-44 [9986790.001]
  • [Cites] Virus Res. 1999 Apr;60(2):159-69 [10392724.001]
  • [Cites] J Virol. 2000 Feb;74(4):1948-60 [10644368.001]
  • [Cites] Biochem J. 2000 Mar 1;346 Pt 2:463-8 [10677367.001]
  • [Cites] Virology. 2000 Mar 1;268(1):41-8 [10683325.001]
  • [Cites] Annu Rev Biochem. 1999;68:729-77 [10872465.001]
  • [Cites] J Virol. 2000 Oct;74(20):9553-61 [11000226.001]
  • [Cites] Virology. 2000 Oct 10;276(1):93-103 [11021998.001]
  • [Cites] J Gen Virol. 2000 Nov;81(Pt 11):2715-22 [11038384.001]
  • [Cites] Genes Dev. 2000 Nov 1;14(21):2677-88 [11069884.001]
  • [Cites] J Virol. 2001 Feb;75(3):1565-70 [11152531.001]
  • [Cites] J Virol. 2001 May;75(10):4528-39 [11312323.001]
  • [Cites] J Virol. 2001 Jun;75(12):5627-37 [11356970.001]
  • [Cites] J Virol. 2001 Jul;75(14):6303-9 [11413296.001]
  • [Cites] Blood. 2001 Aug 1;98(3):721-6 [11468172.001]
  • [Cites] J Virol. 2001 Sep;75(17):8317-28 [11483777.001]
  • [Cites] Virus Res. 2001 Oct 30;78(1-2):17-34 [11520577.001]
  • [Cites] Biochimie. 2001 Aug;83(8):811-7 [11530214.001]
  • [Cites] J Virol. 2001 Oct;75(19):9187-200 [11533182.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1858-61 [11535522.001]
  • [Cites] J Gen Virol. 2001 Oct;82(Pt 10):2405-13 [11562534.001]
  • [Cites] J Virol. 2001 Nov;75(22):11166-77 [11602756.001]
  • [Cites] J Dent Res. 2001 Aug;80(8):1704-10 [11669479.001]
  • [Cites] J Virol. 2001 Dec;75(24):12439-45 [11711634.001]
  • [Cites] J Virol. 2002 Jun;76(12):6332-43 [12021366.001]
  • [Cites] J Biol Chem. 1999 Aug 20;274(34):24113-23 [10446183.001]
  • [Cites] Cell. 1999 Oct 1;99(1):13-22 [10520990.001]
  • [Cites] Curr Pharm Des. 2004;10(30):3701-12 [15579065.001]
  • [Cites] AIDS Res Hum Retroviruses. 2005 Jan;21(1):43-50 [15665643.001]
  • [Cites] J Virol. 2005 Apr;79(7):4150-8 [15767416.001]
  • [Cites] J Immunol. 2005 Apr 1;174(7):4262-70 [15778389.001]
  • [Cites] J Cell Sci. 2003 Sep 1;116(Pt 17):3591-600 [12876215.001]
  • [Cites] J Virol. 2003 Sep;77(18):9922-30 [12941902.001]
  • [Cites] Nat Rev Immunol. 2003 Sep;3(9):697-709 [12949494.001]
  • [Cites] J Virol. 2003 Oct;77(19):10179-85 [12970403.001]
  • [Cites] J Biol Chem. 2003 Oct 17;278(42):41003-12 [12867431.001]
  • [Cites] J Virol. 2003 Nov;77(22):12140-51 [14581551.001]
  • [Cites] Cell. 2003 Nov 14;115(4):449-59 [14622599.001]
  • [Cites] J Virol. 2003 Dec;77(24):13125-35 [14645569.001]
  • [Cites] Nat Med. 2004 Jan;10(1):20-1 [14702624.001]
  • [Cites] J Virol. 2004 Feb;78(3):1375-83 [14722292.001]
  • [Cites] J Biochem. 2004 Jan;135(1):129-37 [14999018.001]
  • [Cites] J Virol. 2002 Oct;76(20):10128-37 [12239287.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):36272-9 [12138122.001]
  • [Cites] J Virol. 2002 Dec;76(24):12723-34 [12438598.001]
  • [Cites] Immunity. 2003 Jan;18(1):27-39 [12530973.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1913-8 [12393496.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3085-92 [12506039.001]
  • [Cites] Virus Res. 2003 May;93(1):31-9 [12727340.001]
  • [Cites] Cancer Invest. 2003 Apr;21(2):253-77 [12743991.001]
  • [Cites] J Virol. 2003 Aug;77(15):8562-9 [12857926.001]
  • [Cites] Cell Microbiol. 2004 May;6(5):401-10 [15056211.001]
  • [Cites] Microbes Infect. 2004 May;6(6):617-22 [15158197.001]
  • [Cites] J Virol. 2004 Jun;78(12):6567-84 [15163749.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 Jul 12;2(8498):104-5 [2873363.001]
  • [Cites] Science. 1988 Dec 16;242(4885):1557-9 [3201246.001]
  • [Cites] Virology. 1990 May;176(1):58-69 [1691887.001]
  • [Cites] J Acquir Immune Defic Syndr. 1990;3(10):965-74 [2398460.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] Clin Immunol Immunopathol. 1991 Mar;58(3):419-30 [1705874.001]
  • [Cites] Immunology. 1991 Feb;72(2):231-8 [2016120.001]
  • [Cites] J Exp Med. 1992 Jul 1;176(1):293-6 [1351922.001]
  • (PMID = 16188972.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heparan Sulfate Proteoglycans
  • [Other-IDs] NLM/ PMC1235841
  •  go-up   go-down


42. Kuhlmann AS, Villaudy J, Gazzolo L, Castellazzi M, Mesnard JM, Duc Dodon M: HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT). Retrovirology; 2007;4:92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT).
  • Thus, in patients with adult-T cell leukaemia (ATL), an HTLV-1 (Human T cell Leukaemia virus type 1)-associated disease, leukemic cells display a high telomerase activity, mainly through transcriptional up-regulation of the human telomerase catalytic subunit (hTERT).
  • The HBZ (HTLV-1 bZIP) protein coded by the minus strand of HTLV-1 genome and expressed in ATL cells has been shown to increase the transcriptional activity of JunD, an AP-1 protein.
  • CONCLUSION: These observations establish for the first time that HBZ by intervening in the re-activation of telomerase, may contribute to the development and maintenance of the leukemic process.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / metabolism. Human T-lymphotropic virus 1 / physiology. Proto-Oncogene Proteins c-jun / metabolism. Telomerase / biosynthesis. Transcription, Genetic. Up-Regulation. Viral Proteins / metabolism

  • 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] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] J Virol. 2006 Mar;80(5):2495-505 [16474156.001]
  • [Cites] Blood. 2006 May 15;107(10):3976-82 [16424388.001]
  • [Cites] Retrovirology. 2006;3:15 [16512901.001]
  • [Cites] Nucleic Acids Res. 2006;34(9):2761-72 [16717281.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Retrovirology. 2005;2:77 [16354306.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(18):8037-43 [16135795.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Oncogene. 2002 Nov 14;21(52):7991-8000 [12439749.001]
  • [Cites] J Biol Chem. 2001 Jun 15;276(24):21797-808 [11259418.001]
  • [Cites] J Biol Chem. 2000 Nov 17;275(46):35665-8 [10986277.001]
  • [Cites] Nucleic Acids Res. 2000 Feb 1;28(3):669-77 [10637317.001]
  • [Cites] Oncogene. 2003 Jun 12;22(24):3734-41 [12802280.001]
  • [Cites] Oncogene. 2003 Jun 26;22(26):4047-61 [12821939.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] Adv Cancer Res. 2003;89:69-132 [14587871.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45848-57 [12954631.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):165-70 [15044019.001]
  • [Cites] J Virol. 2004 Oct;78(19):10348-59 [15367601.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2523-31 [15226182.001]
  • [Cites] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Mol Cell Biol. 1994 Oct;14(10):6886-95 [7935406.001]
  • [Cites] Leuk Res. 1999 Mar;23(3):311-6 [10071087.001]
  • [Cites] J Biol Chem. 1999 Oct 8;274(41):29572-81 [10506225.001]
  • [Cites] Leuk Lymphoma. 2005 Mar;46(3):393-9 [15621829.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1001-10 [15592508.001]
  • [Cites] J Cell Sci. 2005 Apr 1;118(Pt 7):1355-62 [15755797.001]
  • [Cites] Oncogene. 2005 Apr 7;24(15):2547-57 [15735704.001]
  • [Cites] Crit Rev Oncol Hematol. 2005 May;54(2):85-93 [15843091.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Retrovirology. 2005;2:15 [15743525.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • (PMID = 18078517.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Messenger; 0 / Sp1 Transcription Factor; 0 / Viral Proteins; 9007-49-2 / DNA; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2235888
  •  go-up   go-down


43. Kobayashi H, Ngato T, Sato K, Aoki N, Kimura S, Tanaka Y, Aizawa H, Tateno M, Celis E: In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes. Clin Cancer Res; 2006 Jun 15;12(12):3814-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes.
  • PURPOSE: Adult T-cell leukemia/lymphoma induced by human T-cell leukemia virus type 1 (HTLV-1) is usually a fatal lymphoproliferative malignant disease.
  • HTLV-1 Tax protein plays a critical role in HTLV-1-associated leukemogenesis and is an attractive target for vaccine development.
  • Although HTLV-1 Tax is the most dominant antigen for HTLV-1-specific CD8(+) CTLs in HTLV-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in HTLV-1 Tax protein have been described.
  • The aim of the present study was to study T-helper-cell responses to HTLV-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.
  • EXPERIMENTAL DESIGN: An MHC class II binding peptide algorithm was used to predict potential T-helper cell epitope peptides from HTLV-1 Tax.
  • We assessed the ability of the corresponding peptides to elicit helper T-cell responses by in vitro vaccination of purified CD4(+) T lymphocytes.
  • RESULTS: Peptides Tax(191-205) and Tax(305-319) were effective in inducing T-helper-cell responses.
  • Both these epitopes were found to be naturally processed by HTLV-1(+) T-cell lymphoma cells and by autologous antigen-presenting cells that were pulsed with HTLV-1 Tax(+) tumor lysates.
  • Notably, the two newly identified helper T-cell epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.
  • CONCLUSION: Our data suggest that HTLV-1 Tax protein could serve as tumor-associated antigen for CD4(+) helper T cells and that the present epitopes might be used for T-cell-based immunotherapy against tumors expressing HTLV-1.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 1995 Mar 15;85(6):1547-54 [7534136.001]
  • [Cites] J Virol. 1994 May;68(5):2860-8 [7512153.001]
  • [Cites] Clin Diagn Lab Immunol. 1994 Mar;1(2):176-81 [7496941.001]
  • [Cites] Annu Rev Immunol. 1997;15:15-37 [9143680.001]
  • [Cites] J Immunol. 1998 Apr 1;160(7):3363-73 [9531296.001]
  • [Cites] J Exp Med. 1999 Jan 18;189(2):371-80 [9892619.001]
  • [Cites] J Virol. 1999 Jul;73(7):6031-40 [10364355.001]
  • [Cites] Int J Cancer. 2005 Mar 20;114(2):257-67 [15551352.001]
  • [Cites] Clin Cancer Res. 2005 May 15;11(10):3869-78 [15897588.001]
  • [Cites] Cancer Immunol Immunother. 2006 Jul;55(7):850-60 [16220325.001]
  • [Cites] J Immunol. 1995 Jan 1;154(1):399-412 [7527817.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1386-92 [10666215.001]
  • [Cites] J Exp Med. 2000 Feb 7;191(3):567-72 [10662802.001]
  • [Cites] J Virol. 2000 Oct;74(20):9610-6 [11000233.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5228-36 [11016652.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4773-8 [11406551.001]
  • [Cites] Int J Exp Pathol. 2001 Jun;82(3):135-47 [11488989.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7577-84 [11606397.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] Blood. 2002 Jan 1;99(1):88-94 [11756157.001]
  • [Cites] Blood. 2002 May 1;99(9):3335-41 [11964301.001]
  • [Cites] J Immunol. 2002 Aug 15;169(4):2172-9 [12165547.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3219-25 [12374692.001]
  • [Cites] Vaccine. 2003 Jun 20;21(21-22):2767-81 [12798617.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5386-93 [14614024.001]
  • [Cites] Leukemia. 2004 Jan;18(1):126-32 [14574331.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] J Immunol. 2004 Feb 1;172(3):1735-43 [14734756.001]
  • [Cites] Expert Rev Anticancer Ther. 2004 Jun;4(3):369-76 [15161436.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):7053-62 [15501985.001]
  • [Cites] Leukemia. 1994 Apr;8 Suppl 1:S54-9 [8152305.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Science. 1984 Apr 20;224(4646):297-9 [6231724.001]
  • [Cites] J Immunol. 1984 Aug;133(2):1037-41 [6203964.001]
  • [Cites] Ann Neurol. 1988;23 Suppl:S143-50 [2894806.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] J Clin Invest. 1991 Mar;87(3):761-6 [1999493.001]
  • [Cites] Int J Cancer. 1991 Jun 19;48(4):623-30 [1710610.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] Virology. 1992 Jun;188(2):628-36 [1374983.001]
  • [Cites] J Virol. 1992 Oct;66(10):5879-89 [1326649.001]
  • [Cites] J Exp Med. 1993 Jun 1;177(6):1567-73 [8496677.001]
  • [Cites] Int J Cancer. 1993 Jun 19;54(4):582-8 [8514449.001]
  • [Cites] J Immunol. 1993 Jul 15;151(2):1013-24 [7687611.001]
  • [Cites] J Virol. 1995 Oct;69(10):6077-89 [7545241.001]
  • (PMID = 16778109.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA103921; United States / NCI NIH HHS / CA / R01CA80782; United States / NCI NIH HHS / CA / R01CA103921; United States / NCI NIH HHS / CA / R01 CA080782; United States / NCI NIH HHS / CA / P50CA91956; United States / NCI NIH HHS / CA / P50 CA091956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / HLA-D Antigens; 0 / Peptides
  • [Other-IDs] NLM/ NIHMS14245; NLM/ PMC1986724
  •  go-up   go-down


4
Advertisement
4. Bogenberger JM, Laybourn PJ: Human T Lymphotropic Virus Type 1 protein Tax reduces histone levels. Retrovirology; 2008;5:9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T Lymphotropic Virus Type 1 protein Tax reduces histone levels.
  • BACKGROUND: Human T-Lymphotropic Virus Type-1 (HTLV-1) is an oncogenic retrovirus that causes adult T-cell leukemia/lymphoma (ATLL).
  • The virally encoded Tax protein is thought to be necessary and sufficient for T-cell leukemogenesis.
  • Tax promotes inappropriate cellular proliferation, represses multiple DNA repair mechanisms, deregulates cell cycle checkpoints, and induces genomic instability.
  • All of these Tax effects are thought to cooperate in the development of ATLL.
  • RESULTS: In this study, we demonstrate that histone protein levels are reduced in HTLV-1 infected T-cell lines (HuT102, SLB-1 and C81) relative to uninfected T-cell lines (CEM, Jurkat and Molt4), while the relative amount of DNA per haploid complement is unaffected.
  • In addition, we show that replication-dependent core and linker histone transcript levels are reduced in HTLV-1 infected T-cell lines.
  • Further, our findings suggest that HTLV-1 infection uncouples replication-dependent histone gene expression and DNA replication, allowing the depletion of histone proteins with cell division.
  • [MeSH-major] Gene Products, tax / physiology. Histones / biosynthesis. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Cell Growth Processes / physiology. Cell Line. DNA / genetics. Flow Cytometry. Gene Expression Regulation. Humans. Jurkat Cells. RNA, Messenger / chemistry. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Microbiol. 1992 Apr;30(4):905-10 [1572977.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] Virology. 1993 Mar;193(1):456-9 [8438579.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] Intern Med. 1995 Oct;34(10):947-52 [8563094.001]
  • [Cites] Virology. 1996 Mar 1;217(1):373-9 [8599225.001]
  • [Cites] Genes Dev. 1996 Dec 1;10(23):3028-40 [8957003.001]
  • [Cites] Mol Cell Biol. 1997 Feb;17(2):545-52 [9001207.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3561-70 [10207079.001]
  • [Cites] Biochem Cell Biol. 2006 Aug;84(4):568-77 [16936829.001]
  • [Cites] Genes Dev. 2006 Dec 1;20(23):3215-31 [17158741.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Clin Infect Dis. 2007 Mar 1;44(5):689-92 [17278060.001]
  • [Cites] Curr Opin Genet Dev. 2007 Apr;17(2):126-31 [17320375.001]
  • [Cites] Mutat Res. 2007 May 1;618(1-2):65-80 [17291544.001]
  • [Cites] J Neurovirol. 1997 May;3 Suppl 1:S50-1 [9179793.001]
  • [Cites] Mol Cell. 2003 Feb;11(2):341-51 [12620223.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Mol Cell Biol. 2003 Apr;23(8):2821-33 [12665581.001]
  • [Cites] Science. 2003 Apr 18;300(5618):455 [12702868.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] J Virol. 2001 Sep;75(18):8461-8 [11507191.001]
  • [Cites] J Virol. 2002 Apr;76(8):4022-33 [11907241.001]
  • [Cites] Mol Cell. 2002 May;9(5):1091-100 [12049744.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3562-71 [12068005.001]
  • [Cites] Curr Opin Cell Biol. 2002 Jun;14(3):269-78 [12067648.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):34424-33 [12093802.001]
  • [Cites] Mol Cell Biol. 2002 Oct;22(20):7093-104 [12242288.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7230-4 [12370813.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(22):7853-67 [12391154.001]
  • [Cites] Genomics. 2002 Nov;80(5):487-98 [12408966.001]
  • [Cites] Cell. 2002 Nov 1;111(3):285-91 [12419240.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Curr Opin Cell Biol. 2002 Dec;14(6):692-9 [12473341.001]
  • [Cites] Cancer Sci. 2004 May;95(5):411-7 [15132768.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Cell Cycle. 2004 Jun;3(6):695-7 [15153807.001]
  • [Cites] Cell Mol Life Sci. 2004 Sep;61(17):2137-47 [15338043.001]
  • [Cites] Cancer Biol Ther. 2004 Jul;3(7):617-23 [15136760.001]
  • [Cites] Biochemistry. 1974 Feb 12;13(4):746-9 [4359465.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Mol Cell Biol. 1983 Apr;3(4):539-50 [6406835.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Cell. 1983 Dec;35(2 Pt 1):433-40 [6317188.001]
  • [Cites] Mol Cell Biol. 1983 Nov;3(11):1920-9 [6656760.001]
  • [Cites] Nature. 1984 Jun 14-20;309(5969):640-2 [6328324.001]
  • [Cites] Blood. 1998 Jun 15;91(12):4701-7 [9616168.001]
  • [Cites] Blood. 1998 Dec 1;92(11):4296-307 [9834236.001]
  • [Cites] Nature. 1998 Dec 17;396(6712):643-9 [9872311.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Feb;109(1):1-13 [9973953.001]
  • [Cites] Cancer Genet Cytogenet. 1999 Feb;109(1):34-9 [9973957.001]
  • [Cites] Gan. 1984 Sep;75(9):747-51 [6094295.001]
  • [Cites] Science. 1985 Jun 28;228(4707):1532-4 [2990031.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8359-63 [3001699.001]
  • [Cites] Jpn J Cancer Res. 1985 Dec;76(12):1127-31 [3005203.001]
  • [Cites] J Mol Biol. 1986 May 5;189(1):189-204 [3023620.001]
  • [Cites] FEBS Lett. 1986 Dec 15;209(2):187-90 [3025015.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] EMBO J. 1988 Feb;7(2):519-23 [2835230.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7124-8 [3174625.001]
  • [Cites] J Virol. 2003 Jun;77(11):6227-34 [12743279.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5141-9 [12910251.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3963-9 [12907436.001]
  • [Cites] Cell. 2003 Nov 26;115(5):537-49 [14651846.001]
  • [Cites] Nat Rev Cancer. 2004 Feb;4(2):143-53 [14732866.001]
  • [Cites] Int J Colorectal Dis. 2004 Mar;19(2):95-101 [14534800.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Int J Cancer. 2004 May 10;109(6):875-81 [15027121.001]
  • [Cites] J Virol. 2004 Apr;78(8):3837-45 [15047799.001]
  • [Cites] Mol Cell. 2005 Jan 21;17(2):301-11 [15664198.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(4):1526-36 [15684401.001]
  • [Cites] Curr Opin Struct Biol. 2005 Apr;15(2):188-96 [15837178.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):6178-98 [15988028.001]
  • [Cites] Biochimie. 2005 Jul;87(7):625-35 [15989979.001]
  • [Cites] Nucleic Acids Res. 2005;33(15):4928-39 [16141196.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5986-95 [16155605.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] J Virol. 2005 Dec;79(23):14473-81 [16282446.001]
  • [Cites] Retrovirology. 2005;2:64 [16242045.001]
  • [Cites] Nat Rev Genet. 2006 Jan;7(1):21-33 [16369569.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Apr;80(7):3469-76 [16537614.001]
  • [Cites] Development. 2006 Jun;133(11):2089-94 [16672331.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(12):4188-98 [10825184.001]
  • [Cites] Baillieres Best Pract Res Clin Haematol. 2000 Jun;13(2):231-43 [10942623.001]
  • [Cites] Genes Dev. 2000 Sep 15;14(18):2283-97 [10995386.001]
  • [Cites] Genes Dev. 2000 Sep 15;14(18):2298-313 [10995387.001]
  • [Cites] J Biol Chem. 2000 Oct 20;275(42):32906-10 [10969065.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(5):1854-65 [11238922.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] J Virol. 2001 Jul;75(13):6086-94 [11390610.001]
  • [Cites] J Virol. 2001 Aug;75(16):7672-82 [11462039.001]
  • [Cites] Biochemistry. 1988 Aug 23;27(17):6542-50 [3146349.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):413-7 [2403646.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1071-5 [2300570.001]
  • [Cites] Virology. 1991 Apr;181(2):433-44 [2014632.001]
  • [Cites] Annu Rev Biochem. 1991;60:827-61 [1883210.001]
  • [Cites] J Clin Invest. 1991 Sep;88(3):1038-42 [1832173.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1481-93 [1540956.001]
  • (PMID = 18237376.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Histones; 0 / RNA, Messenger; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2276518
  •  go-up   go-down


46. Pancewicz J, Taylor JM, Datta A, Baydoun HH, Waldmann TA, Hermine O, Nicot C: Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia. Proc Natl Acad Sci U S A; 2010 Sep 21;107(38):16619-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia.
  • Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemia (ATL).
  • The disease has a dismal prognosis and is invariably fatal.
  • In this study, we report a high frequency of constitutively activated Notch in ATL patients.
  • We found activating mutations in Notch in more than 30% of ATL patients.
  • These activating mutations are phenotypically different from those previously reported in T-ALL leukemias and may represent polymorphisms for activated Notch in human cancers.
  • Compared with the exclusive activating frameshift mutations in the proline, glutamic acid, serine, and threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in this domain leading to reduced CDC4/Fbw7-mediated degradation and stabilization of the intracellular cleaved form of Notch1 (ICN1).
  • Finally, we demonstrated that inhibition of Notch signaling by γ-secretase inhibitors reduced tumor cell proliferation and tumor formation in ATL-engrafted mice.
  • These data suggest that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for therapeutic intervention in ATL patients.


47. Siu YT, Chin KT, Siu KL, Yee Wai Choy E, Jeang KT, Jin DY: TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats. J Virol; 2006 Jul;80(14):7052-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats.
  • Human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription from the long terminal repeats (LTR).
  • Thus, both TORC and p300 families of coactivators are essential for optimal activation of HTLV-1 transcription by Tax.
  • [MeSH-major] Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / physiology. Phosphoproteins / metabolism. Terminal Repeat Sequences / physiology. Transcription Factors / metabolism. Virus Activation / physiology

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):34646-52 [9852138.001]
  • [Cites] Nature. 2005 Oct 20;437(7062):1109-11 [16148943.001]
  • [Cites] Curr Biol. 2004 Dec 14;14(23):2156-61 [15589160.001]
  • [Cites] Science. 2005 Dec 9;310(5754):1642-6 [16308421.001]
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8136-45 [10567539.001]
  • [Cites] EMBO J. 2000 Feb 15;19(4):729-40 [10675342.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):11852-7 [10766811.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3470-81 [10779337.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1689-94 [11080811.001]
  • [Cites] EMBO J. 2001 Mar 15;20(6):1331-40 [11250899.001]
  • [Cites] J Biol Chem. 2001 Aug 3;276(31):28933-8 [11384994.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1443-8 [11818553.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38755-63 [12161448.001]
  • [Cites] FEBS Lett. 2002 Nov 20;531(3):494-8 [12435599.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5141-9 [12910251.001]
  • [Cites] Mol Cell. 2003 Aug;12(2):413-23 [14536081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12147-52 [14506290.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(14):6117-26 [15226416.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Cell. 2004 Oct 1;119(1):61-74 [15454081.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11445-9 [1763059.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4269-78 [8223437.001]
  • [Cites] Nature. 1996 Apr 18;380(6575):642-6 [8602268.001]
  • [Cites] Nature. 1996 Jul 25;382(6589):319-24 [8684459.001]
  • [Cites] J Virol. 1996 Dec;70(12):8368-74 [8970957.001]
  • [Cites] Nucleic Acids Res. 1997 Jan 15;25(2):379-87 [9016568.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3662-7 [9108034.001]
  • [Cites] Oncogene. 1997 Jun 12;14(23):2785-92 [9190894.001]
  • [Cites] Mol Cell Biol. 1998 Feb;18(2):967-77 [9447994.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13768-75 [9593719.001]
  • [Cites] J Biol Chem. 1998 Jul 24;273(30):19251-9 [9668114.001]
  • [Cites] Mol Cell Biol. 1998 Sep;18(9):5052-61 [9710589.001]
  • [Cites] J Biol Chem. 2004 Dec 17;279(51):52978-83 [15466468.001]
  • [Cites] FEBS Lett. 2005 Feb 7;579(4):909-15 [15680973.001]
  • [Cites] Nucleic Acids Res. 2005;33(6):1859-73 [15800215.001]
  • [Cites] Mol Cell Biol. 2005 May;25(9):3575-82 [15831463.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4467-70 [15930259.001]
  • [Cites] J Virol. 2005 Jul;79(14):9346-50 [15994832.001]
  • [Cites] Retrovirology. 2004;1:18 [15285791.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • (PMID = 16809310.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATF4 protein, human; 0 / CREB1 protein, human; 0 / CRTC1 protein, human; 0 / CRTC2 protein, human; 0 / CRTC3 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / Phosphoproteins; 0 / Trans-Activators; 0 / Transcription Factors; 145891-90-3 / Activating Transcription Factor 4; EC 2.3.1.48 / p300-CBP Transcription Factors
  • [Other-IDs] NLM/ PMC1489057
  •  go-up   go-down


48. Tholouli E, Liu Yin JA: Successful treatment of HTLV-1-associated acute adult T-cell leukemia lymphoma by allogeneic bone marrow transplantation: a 12 year follow-up. Leuk Lymphoma; 2006 Aug;47(8):1691-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of HTLV-1-associated acute adult T-cell leukemia lymphoma by allogeneic bone marrow transplantation: a 12 year follow-up.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Remission Induction. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16966289.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  •  go-up   go-down


49. Schlecht-Louf G, Renard M, Mangeney M, Letzelter C, Richaud A, Ducos B, Bouallaga I, Heidmann T: Retroviral infection in vivo requires an immune escape virulence factor encrypted in the envelope protein of oncoretroviruses. Proc Natl Acad Sci U S A; 2010 Feb 23;107(8):3782-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we genetically "switched off' the envelope-mediated immunosuppression of an infectious retrovirus, the Friend murine leukemia virus, while preserving mutant envelope infectivity both ex vivo and in vivo, thus allowing us to test the functional importance of envelope-mediated immunosuppression in retrovirus physiology.
  • Remarkably, we show, in vivo, that the non-IS mutant virus displays the same propagation kinetics as its WT counterpart in irradiated immunocompromised mice but that it is rapidly and totally cleared from normal immunocompetent mice, which become fully protected against a challenge with the WT retrovirus.
  • Using cell depletion strategies, we further establish that envelope-mediated immunosuppression enables the retrovirus to escape innate (natural killer cells) and adaptive (CD8 T cells) antiviral effectors.
  • In conclusion, our work demonstrates the critical role of Env-induced immunosuppression for retrovirus propagation in vivo and identifies a unique definite target for antiretroviral therapies and vaccine strategies, also characterized in the human T-cell leukemia virus (HTLV) and xenotropic murine leukemia virus-related virus (XMRV) retroviruses, opening unprecedented prospects for the treatment of retroviral diseases.
  • [MeSH-major] Friend murine leukemia virus / immunology. Immune Tolerance. Leukemia, Experimental / immunology. Retroviridae Infections / immunology. Tumor Virus Infections / immunology. Viral Envelope Proteins / immunology. Virulence Factors / immunology

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 18;104(51):20534-9 [18077339.001]
  • [Cites] J Virol. 2007 Nov;81(22):12368-74 [17686853.001]
  • [Cites] J Virol. 2008 Apr;82(8):4135-48 [18272584.001]
  • [Cites] Cell Host Microbe. 2008 Jun 12;3(6):388-98 [18541215.001]
  • [Cites] Nat Rev Immunol. 2008 Dec;8(12):911-22 [18989317.001]
  • [Cites] Nat Rev Immunol. 2009 Jul;9(7):503-13 [19498380.001]
  • [Cites] J Immunol. 2009 Aug 1;183(3):1636-43 [19587016.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3199-207 [19671923.001]
  • [Cites] J Gen Virol. 2001 Jul;82(Pt 7):1597-600 [11413370.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 31;98(16):9226-30 [11459933.001]
  • [Cites] Annu Rev Immunol. 2002;20:621-67 [11861614.001]
  • [Cites] Science. 2002 Apr 19;296(5567):553-5 [11968185.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):13013-8 [14557543.001]
  • [Cites] J Virol. 2004 Jan;78(2):1050-4 [14694139.001]
  • [Cites] Immunity. 2004 Mar;20(3):293-303 [15030773.001]
  • [Cites] J Virol. 2004 Nov;78(21):11641-7 [15479805.001]
  • [Cites] Science. 1985 Oct 25;230(4724):453-5 [2996136.001]
  • [Cites] J Virol. 1990 May;64(5):2135-40 [2182908.001]
  • [Cites] J Virol. 1993 Aug;67(8):4533-42 [7687300.001]
  • [Cites] J Exp Med. 1995 Aug 1;182(2):477-86 [7629507.001]
  • [Cites] J Virol. 1996 Nov;70(11):7773-82 [8892898.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14920-5 [9843991.001]
  • [Cites] Mol Immunol. 2005 Feb;42(4):547-55 [15607812.001]
  • [Cites] J Virol. 2005 Aug;79(16):10619-26 [16051854.001]
  • [Cites] J Mol Biol. 2005 Oct 7;352(5):1029-34 [16140326.001]
  • [Cites] J Leukoc Biol. 2006 Jan;79(1):16-35 [16204622.001]
  • [Cites] J Immunol. 2006 Mar 15;176(6):3342-9 [16517701.001]
  • [Cites] PLoS Pathog. 2006 Mar;2(3):e25 [16609730.001]
  • [Cites] J Gen Virol. 2006 Jun;87(Pt 6):1423-38 [16690907.001]
  • [Cites] Immunol Rev. 2006 Aug;212:272-86 [16903920.001]
  • [Cites] Eur J Immunol. 2006 Oct;36(10):2658-70 [16981182.001]
  • [Cites] J Leukoc Biol. 2007 Jan;81(1):144-53 [16959895.001]
  • [Cites] Curr Opin Immunol. 2008 Feb;20(1):30-8 [18206359.001]
  • (PMID = 20142478.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Viral Envelope Proteins; 0 / Viral Vaccines; 0 / Virulence Factors
  • [Other-IDs] NLM/ PMC2840525
  •  go-up   go-down


50. Yano H, Ishida T, Imada K, Sakai T, Ishii T, Inagaki A, Iida S, Uchiyama T, Ueda R: Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF. Br J Haematol; 2008 Mar;140(5):586-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / therapy. Receptors, CCR4 / immunology
  • [MeSH-minor] Adult. Animals. Antineoplastic Agents / therapeutic use. Disease Models, Animal. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Mice. Mice, SCID

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3625-34 [14506150.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2127-33 [15026353.001]
  • [Cites] J Exp Med. 2004 Jun 21;199(12):1659-69 [15210744.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Leukemia. 2006 Dec;20(12):2162-8 [17039235.001]
  • [Cites] Clin Cancer Res. 2004 Nov 15;10(22):7529-39 [15569983.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Nat Rev Immunol. 2006 May;6(5):343-57 [16622479.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1139-46 [16952304.001]
  • [Cites] Jpn J Cancer Res. 1996 Sep;87(9):887-92 [8878449.001]
  • (PMID = 18205860.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 134088-74-7 / nartograstim; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2268953
  •  go-up   go-down


51. Yoshie O: Expression of CCR4 in adult T-cell leukemia. Leuk Lymphoma; 2005 Feb;46(2):185-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CCR4 in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a malignancy of mature T cells that is etiologically associated with human T-cell leukemia virus type 1 (HTLV-1).
  • The frequent manifestation of ATL is infiltration of leukemic cells into various organs.
  • Besides certain cell adhesion molecules and matrix metalloproteineses, chemokine receptors may play important roles in tissue infiltration of ATL.
  • Identification of a unique set of chemokine receptors expressed by ATL would thus provide valuable information about the molecular mechanism of tissue infiltration of ATL.
  • This may also reveal that ATL frequently develops from a certain subset of T cells that express a particular set of chemokine receptors.
  • Since HTLV-1 encodes a potent viral transcriptional activator Tax, which is known to induce various cellular genes, expression of some chemokine receptors may be affected by Tax.
  • This, however, may relate more to HTLV-1-infected T cells, since ATL cells usually do not express Tax.
  • Finally, identification of a unique set of chemokine receptors expressed by ATL may also provide a new therapeutic target.
  • These considerations prompted us to examine the chemokine receptor expression in ATL.
  • We found that in the majority of ATL cases, leukemic cells consistently express CCR4.
  • Since CCR4 is known to be involved in T cell migration into skin, this may in part explain the frequent skin infiltration in ATL.
  • Thus, the majority of ATL may predominantly originate from either Th2 or regulatory T cells.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Chemokine / analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15621800.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
  • [Number-of-references] 44
  •  go-up   go-down


52. Tanosaki R, Tobinai K: Adult T-cell leukemia-lymphoma: current treatment strategies and novel immunological approaches. Expert Rev Hematol; 2010 Dec;3(6):743-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia-lymphoma: current treatment strategies and novel immunological approaches.
  • Adult T-cell leukemia-lymphoma (ATL) is a peripheral T-cell malignancy, closely associated with human T-cell lymphotropic virus type I infection.
  • Clinically, ATL is classified into four subtypes: acute, lymphoma, chronic and smoldering type.
  • Although the prognosis of chronic and smoldering-type ATL is relatively good, that of patients with acute- or lymphoma-type ATL still remains extremely poor.
  • Allogeneic stem cell transplantation is promising and approximately 40% of aggressive ATL patients are expected to survive long-term, although transplantation-related mortality is as high as 40-50%.
  • Stem cell transplantation using reduced-intensity conditioning is also effective and safer, with graft-versus-ATL and graft-versus-human T-cell lymphotropic virus type I effects observed after transplantation.
  • Novel approaches including new agents such as purine nucleoside phosphorylase inhibitors and histone deacetylase inhibitors, or targeted immunotherapy using antichemokine receptor-4 antibody or dendritic cell/peptide vaccine are also warranted.
  • [MeSH-major] Immunotherapy. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Humans. Interferon-alpha / therapeutic use. Kaplan-Meier Estimate. Stem Cell Transplantation. Transplantation, Homologous

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21091150.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Interferon-alpha
  •  go-up   go-down


53. Lee SH, Wiernik PH: Adult T-cell leukemia/lymphoma presenting with bilateral hearing loss: a case report. Med Oncol; 2007;24(1):109-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma presenting with bilateral hearing loss: a case report.
  • A 44-yr-old Jamaican male who presented only with bilateral hearing loss was found to have hypercalcemia, which, upon further investigation, was found to be due to adult T-cell leukemia/lymphoma (ATLL) syndrome.
  • This is the first case of ATLL presenting with bilateral auditory conduction hearing loss, which responded to combination chemotherapy along with alleviation of other manifestations of ATLL.
  • [MeSH-major] Hearing Loss, Bilateral / etiology. Leukemia-Lymphoma, Adult T-Cell / complications
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Hypercalcemia / etiology. Hypercalcemia / therapy. Male

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1985 Aug 29;313(9):529-33 [2862584.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S20-5 [8797699.001]
  • [Cites] Int J Cancer. 1999 Oct 29;83(3):291-8 [10495418.001]
  • [Cites] No Shinkei Geka. 1999 Jan;27(1):55-9 [10024985.001]
  • [Cites] Am J Hematol. 1985 Oct;20(2):129-37 [2994470.001]
  • [Cites] Blood. 1993 May 15;81(10):2810-5 [8490187.001]
  • [Cites] J Clin Oncol. 1985 Jun;3(6):782-8 [3874266.001]
  • [Cites] Leukemia. 1993 Aug;7 Suppl 2:S75-7 [8361238.001]
  • [Cites] Int J Cancer. 2004 May 10;109(6):875-81 [15027121.001]
  • [Cites] Int J Cancer. 1982 Jun 15;29(6):631-5 [6980846.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Blood. 1991 Jun 1;77(11):2419-30 [2039822.001]
  • [Cites] N Engl J Med. 1983 Aug 4;309(5):257-64 [6602943.001]
  • [Cites] Ann Intern Med. 1989 Oct 1;111(7):555-60 [2789009.001]
  • [Cites] J Am Acad Dermatol. 1997 May;36(5 Pt 2):869-71 [9146571.001]
  • [Cites] Cancer Res. 1985 Sep;45(9 Suppl):4644s-4645s [2861896.001]
  • [Cites] Curr Top Microbiol Immunol. 1985;115:53-66 [2983946.001]
  • [Cites] Cancer Res. 1985 Sep;45(9 Suppl):4633s-4636s [2990698.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Int J Hematol. 1995 Feb;61(2):97-102 [7734717.001]
  • [Cites] Int J Hematol. 2000 Jan;71(1):66-9 [10729996.001]
  • (PMID = 17673820.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


54. Jeang KT: Human T cell leukemia virus type 1 (HTLV-1) and oncogene or oncomiR addiction? Oncotarget; 2010 Oct;1(6):453-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T cell leukemia virus type 1 (HTLV-1) and oncogene or oncomiR addiction?
  • The mechanism of HTLV-1 transformation of cells to Adult T cell leukemia (ATL) remains not fully understood.
  • Emerging evidence suggests that Tax is not needed to maintain the transformed ATL phenotype.
  • Recent studies have shown that HTLV-1 transformed cells show deregulated expression of cellular microRNAs (miRNAs).
  • Here we discuss the possibility that early ATL cells are Tax-oncogene-addicted while late ATL cells are oncogenic microRNA (oncomiR) - addicted.
  • [MeSH-major] Gene Expression Regulation. Gene Products, tax. Human T-lymphotropic virus 1 / genetics. MicroRNAs / genetics. Oncogenes / genetics
  • [MeSH-minor] Adult. HTLV-I Infections / genetics. HTLV-I Infections / virology. Humans

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Aug;3(8):448-57 [16894390.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Nat Med. 2007 May;13(5):527-8 [17479090.001]
  • [Cites] J Cell Biochem. 2007 Oct 15;102(3):531-8 [17661351.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16170-5 [17911264.001]
  • [Cites] Retrovirology. 2007;4:82 [18036240.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8976-85 [18974142.001]
  • [Cites] Retrovirology. 2008;5:100 [19014482.001]
  • [Cites] Blood. 2009 May 14;113(20):4914-7 [19246560.001]
  • [Cites] Virus Res. 2009 Aug;143(2):195-208 [19540281.001]
  • [Cites] Nat Rev Genet. 2009 Oct;10(10):704-14 [19763153.001]
  • [Cites] Genes Dev. 2009 Dec 1;23(23):2700-4 [19903759.001]
  • [Cites] Retrovirology. 2009;6:117 [20017952.001]
  • [Cites] Retrovirology. 2010;7:17 [20222966.001]
  • [Cites] J Biol Chem. 2010 Aug 6;285(32):24707-16 [20529860.001]
  • [Cites] Mol Aspects Med. 2010 Oct;31(5):367-82 [20600265.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] J Biol Chem. 1998 Mar 20;273(12):6698-703 [9506967.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5931-7 [16155600.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • (PMID = 21311101.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AI001023-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS242806; NLM/ PMC3058865
  •  go-up   go-down


55. Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K: Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines. Cancer Lett; 2007 Nov 18;257(2):206-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.
  • The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing HTLV-I-infected cells.
  • In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient ATL cell lines caused rapid death, whereas DHMEQ-treated mice survived.
  • Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted ATL cells.
  • These results demonstrate that DHMEQ has therapeutic efficacy on ATL cells, regardless of Tax expression.
  • [MeSH-major] Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency. Leukemia, T-Cell / prevention & control. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cell Line, Tumor. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17764832.001).
  • [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
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin
  •  go-up   go-down


56. Hsi ED: T-cell lymphoma in the head and neck? Think about adult T-cell leukemia/lymphoma. Leuk Lymphoma; 2009 Feb;50(2):150-1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell lymphoma in the head and neck? Think about adult T-cell leukemia/lymphoma.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Adult. HTLV-I Infections / complications. HTLV-I Infections / pathology. Human T-lymphotropic virus 1 / physiology. Humans

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Leuk Lymphoma. 2009 Feb;50(2):187-95 [19197730.001]
  • (PMID = 19235010.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  •  go-up   go-down


57. Saito M: Immunogenetics and the Pathological Mechanisms of Human T-Cell Leukemia VirusType 1- (HTLV-1-)Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). Interdiscip Perspect Infect Dis; 2010;2010:478461
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunogenetics and the Pathological Mechanisms of Human T-Cell Leukemia VirusType 1- (HTLV-1-)Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP).
  • Human T-cell leukemia virus type 1 (HTLV-1) is a replication-competent human retrovirus associated with two distinct types of disease only in a minority of infected individuals: the malignancy known as adult T-cell leukemia (ATL) and a chronic inflammatory central nervous system disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
  • Although the factors that cause these different manifestations of HTLV-1 infection are not fully understood, accumulating evidence suggests that complex virus-host interactions play an important role in determining the risk of HAM/TSP.
  • This review focuses on the role of the immune response in controlling or limiting viral persistence in HAM/TSP patients, and the reason why some HTLV-1-infected people develop HAM/TSP whereas the majority remains asymptomatic carriers of the virus.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] J Neuroimmunol. 1991 Aug;33(2):121-8 [2066395.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] J Neurol Sci. 1990 Apr;96(1):103-23 [2351985.001]
  • [Cites] Ann Neurol. 1990 Jul;28(1):50-6 [2375633.001]
  • [Cites] J Neuroimmunol. 1989 Jul;23(2):175-8 [2723044.001]
  • [Cites] Jpn J Cancer Res. 1987 Jul;78(7):674-80 [2887539.001]
  • [Cites] Neurology. 1988 Aug;38(8):1302-7 [2899862.001]
  • [Cites] Jpn J Cancer Res. 1985 Jun;76(6):474-80 [2991060.001]
  • [Cites] EMBO J. 1986 Nov;5(11):2883-8 [3024966.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Am J Epidemiol. 1995 Dec 1;142(11):1212-20 [7485068.001]
  • [Cites] Blood. 1993 Nov 1;82(9):2823-8 [7693049.001]
  • [Cites] J Infect Dis. 1994 Mar;169(3):496-503 [8158021.001]
  • [Cites] J Acquir Immune Defic Syndr. 1994 Feb;7(2):199-203 [8301532.001]
  • [Cites] AIDS Res Hum Retroviruses. 1993 May;9(5):381-6 [8318266.001]
  • [Cites] Virology. 1993 Sep;196(1):25-33 [8356797.001]
  • [Cites] Clin Exp Immunol. 1993 Oct;94(1):32-7 [8403513.001]
  • [Cites] J Neurovirol. 1996 Oct;2(5):345-55 [8912211.001]
  • [Cites] Blood. 1997 Jan 1;89(1):346-8 [8978312.001]
  • [Cites] J Neurovirol. 1995 Mar;1(1):50-61 [9222342.001]
  • [Cites] Clin Exp Immunol. 1998 Feb;111(2):278-85 [9486393.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7568-73 [9636190.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):586-93 [10065900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3848-53 [10097126.001]
  • [Cites] Clin Diagn Lab Immunol. 1999 May;6(3):316-22 [10225829.001]
  • [Cites] J Neurol. 1999 May;246(5):358-64 [10399866.001]
  • [Cites] J Infect Dis. 1999 Nov;180(5):1487-93 [10515807.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1386-92 [10666215.001]
  • [Cites] Curr Opin Immunol. 2000 Aug;12(4):397-402 [10899027.001]
  • [Cites] J Infect Dis. 2000 Nov;182(5):1343-9 [11010842.001]
  • [Cites] Neuropathology. 2000 Sep;20 Suppl:S65-8 [11037191.001]
  • [Cites] J Infect Dis. 2001 Jan 15;183(2):197-205 [11120926.001]
  • [Cites] J Virol. 2001 Jan;75(2):1065-71 [11134322.001]
  • [Cites] Ann Neurol. 2001 Dec;50(6):807-12 [11761481.001]
  • [Cites] J Cell Physiol. 2002 Feb;190(2):133-59 [11807819.001]
  • [Cites] Blood. 2002 May 1;99(9):3335-41 [11964301.001]
  • [Cites] J Infect Dis. 2002 Oct 1;186(7):932-9 [12232833.001]
  • [Cites] J Infect Dis. 2002 Nov 1;186(9):1231-41 [12402192.001]
  • [Cites] J Infect Dis. 2002 Dec 1;186 Suppl 2:S187-92 [12424696.001]
  • [Cites] Blood. 2003 Jul 15;102(2):577-84 [12560226.001]
  • [Cites] J Neurovirol. 2003 Feb;9(1):29-35 [12587066.001]
  • [Cites] J Virol. 2003 Sep;77(17):9716-22 [12915584.001]
  • [Cites] J Exp Med. 2004 May 17;199(10):1367-77 [15136590.001]
  • [Cites] J Infect Dis. 2004 Jun 15;189(12):2294-8 [15181578.001]
  • [Cites] J Infect Dis. 2004 Oct 1;190(7):1279-85 [15346339.001]
  • [Cites] J Neuroimmunol. 2004 Nov;156(1-2):188-94 [15465610.001]
  • [Cites] J Infect Dis. 2004 Nov 1;190(9):1605-9 [15478065.001]
  • [Cites] J Gen Virol. 2005 Mar;86(Pt 3):773-81 [15722539.001]
  • [Cites] J Infect Dis. 2005 May 1;191(9):1490-7 [15809908.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1361-8 [15864353.001]
  • [Cites] J Neurol Sci. 2005 Oct 15;237(1-2):75-81 [15961107.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] J Infect Dis. 2006 Jun 1;193(11):1557-66 [16652285.001]
  • [Cites] Immunol Rev. 2006 Aug;212:8-27 [16903903.001]
  • [Cites] J Neurovirol. 2006 Dec;12(6):456-65 [17162661.001]
  • [Cites] Lancet Infect Dis. 2007 Apr;7(4):266-81 [17376384.001]
  • [Cites] Blood. 2008 May 15;111(10):5047-53 [18094326.001]
  • [Cites] J Infect Dis. 2007 Dec 15;196(12):1761-72 [18190256.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2411-20 [18502825.001]
  • [Cites] J Neuroimmunol. 2008 Aug 30;200(1-2):115-24 [18639344.001]
  • [Cites] J Neurovirol. 2008 Oct;14(5):459-63 [18989817.001]
  • [Cites] J Leukoc Biol. 2009 Nov;86(5):1205-16 [19656902.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3208-15 [19666871.001]
  • [Cites] Immunology. 2009 Sep;128(1 Suppl):e777-86 [19740339.001]
  • [Cites] Clin Exp Immunol. 2009 Dec;158(3):294-9 [19778295.001]
  • [Cites] AIDS Res Hum Retroviruses. 1992 Sep;8(9):1699-706 [1457215.001]
  • [Cites] J Neurol Sci. 1992 Jan;107(1):98-104 [1578240.001]
  • [Cites] J Neurol Sci. 1991 Jun;103(2):203-8 [1880539.001]
  • (PMID = 20169122.001).
  • [ISSN] 1687-7098
  • [Journal-full-title] Interdisciplinary perspectives on infectious diseases
  • [ISO-abbreviation] Interdiscip Perspect Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2821641
  •  go-up   go-down


58. Javier RT: Cell polarity proteins: common targets for tumorigenic human viruses. Oncogene; 2008 Nov 24;27(55):7031-46
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell polarity proteins: common targets for tumorigenic human viruses.
  • Loss of polarity and disruption of cell junctions are common features of epithelial-derived cancer cells, and mounting evidence indicates that such defects have a direct function in the pathology of cancer.
  • Supporting this idea, results with several different human tumor viruses indicate that their oncogenic potential depends in part on a common ability to inactivate key cell polarity proteins.
  • For example, adenovirus (Ad) type 9 is unique among human Ads by causing exclusively estrogen-dependent mammary tumors in experimental animals and in having E4 region-encoded open reading frame 1 (E4-ORF1) as its primary oncogenic determinant.
  • Most notably, the E4-ORF1 PBM mediates interactions with a selected group of cellular PDZ proteins, three of which include the cell polarity proteins Dlg1, PATJ and ZO-2.
  • Data further indicate that these interactions promote disruption of cell junctions and a loss of cell polarity.
  • In addition, one or more of the E4-ORF1-interacting cell polarity proteins, as well as the cell polarity protein Scribble, are common targets for the high-risk human papillomavirus (HPV) E6 or human T-cell leukemia virus type 1 (HTLV-1) Tax oncoproteins.
  • Underscoring the significance of these observations, in humans, high-risk HPV and HTLV-1 are causative agents for cervical cancer and adult T-cell leukemia, respectively.
  • Consequently, human tumor viruses should serve as powerful tools for deciphering mechanisms whereby disruption of cell junctions and loss of cell polarity contribute to the development of many human cancers.
  • This review article discusses evidence supporting this hypothesis, with an emphasis on the human Ad E4-ORF1 oncoprotein.
  • [MeSH-major] Cell Polarity. Membrane Proteins / physiology. Neoplasms / etiology. Virus Attachment. Virus Diseases / complications
  • [MeSH-minor] Adenovirus Infections, Human / virology. Adenoviruses, Human / physiology. Animals. Cell Transformation, Viral / physiology. Gene Products, tax / physiology. Human T-lymphotropic virus 1 / metabolism. Human T-lymphotropic virus 1 / physiology. Human papillomavirus 6 / metabolism. Human papillomavirus 6 / physiology. Humans. Models, Biological. Oncogene Proteins, Viral / metabolism. Oncogene Proteins, Viral / physiology. Protein Binding

  • MedlinePlus Health Information. consumer health - Viral Infections.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12974-82 [11150294.001]
  • [Cites] Nature. 2001 May 17;411(6835):355-65 [11357143.001]
  • [Cites] Cell. 2001 Aug 24;106(4):489-98 [11525734.001]
  • [Cites] J Cell Sci. 2001 Jul;114(Pt 13):2375-82 [11559746.001]
  • [Cites] Oncogene. 2001 Sep 6;20(39):5431-9 [11571640.001]
  • [Cites] J Cell Sci. 2001 Sep;114(Pt 18):3219-31 [11591811.001]
  • [Cites] EMBO J. 2001 Oct 15;20(20):5578-86 [11598001.001]
  • [Cites] Curr Biol. 2001 Dec 11;11(24):1958-62 [11747822.001]
  • [Cites] Oncogene. 2001 Nov 26;20(54):7874-87 [11753670.001]
  • [Cites] J Biol Chem. 2002 Jan 4;277(1):455-61 [11689568.001]
  • [Cites] J Cell Sci. 2002 Jan 1;115(Pt 1):39-50 [11801722.001]
  • [Cites] Biochem J. 2002 Feb 1;361(Pt 3):525-36 [11802782.001]
  • [Cites] J Gen Virol. 2002 Feb;83(Pt 2):283-9 [11807220.001]
  • [Cites] J Virol. 2002 Mar;76(6):2648-53 [11861831.001]
  • [Cites] Genes Dev. 2002 Mar 15;16(6):693-706 [11914275.001]
  • [Cites] Steroids. 2002 May;67(6):471-5 [11960623.001]
  • [Cites] Exp Cell Res. 2002 May 1;275(2):155-70 [11969287.001]
  • [Cites] J Steroid Biochem Mol Biol. 2002 Apr;80(4-5):369-81 [11983484.001]
  • [Cites] Science. 2002 May 31;296(5573):1642-4 [12040178.001]
  • [Cites] J Biol Chem. 2002 Aug 16;277(33):30183-90 [12042308.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):30928-34 [12050163.001]
  • [Cites] J Cell Biol. 2002 Sep 2;158(5):967-78 [12196510.001]
  • [Cites] Oncogene. 2002 Nov 21;21(53):8140-8 [12444549.001]
  • [Cites] Nature. 2002 Dec 12;420(6916):629-35 [12478284.001]
  • [Cites] Curr Opin Cell Biol. 2003 Feb;15(1):67-72 [12517706.001]
  • [Cites] J Cell Biol. 2003 Feb 3;160(3):423-32 [12566432.001]
  • [Cites] Oncogene. 2003 Feb 6;22(5):710-21 [12569363.001]
  • [Cites] J Virol. 2003 Mar;77(5):2807-18 [12584304.001]
  • [Cites] Nature. 2003 Feb 13;421(6924):753-6 [12610628.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Mar;4(3):225-36 [12612641.001]
  • [Cites] Breast Cancer Res. 2003;5(2):117-9 [12631393.001]
  • [Cites] Development. 2003 May;130(9):1927-35 [12642496.001]
  • [Cites] Nature. 2003 Mar 20;422(6929):322-6 [12646923.001]
  • [Cites] Genes Dev. 2003 May 1;17(9):1090-100 [12695331.001]
  • [Cites] Curr Top Microbiol Immunol. 2003;272:287-330 [12747554.001]
  • [Cites] Bioessays. 2003 Jun;25(6):542-53 [12766944.001]
  • [Cites] J Virol. 1987 Feb;61(2):543-52 [2949089.001]
  • [Cites] Nature. 1987 Apr 16-22;326(6114):714-7 [3031513.001]
  • [Cites] J Virol. 1989 Feb;63(2):631-8 [2911117.001]
  • [Cites] J Natl Cancer Inst. 1989 Feb 15;81(4):294-8 [2913327.001]
  • [Cites] J Virol. 1989 Jun;63(6):2605-15 [2724411.001]
  • [Cites] Dev Biol. 1989 Jul;134(1):222-35 [2471660.001]
  • [Cites] Genes Dev. 1989 Nov;3(11):1699-710 [2532611.001]
  • [Cites] Virology. 1990 Feb;174(2):345-53 [2137659.001]
  • [Cites] Nucleic Acids Res. 1990 May 25;18(10):3065-6 [2349112.001]
  • [Cites] Virology. 1990 Aug;177(2):419-26 [2142553.001]
  • [Cites] Pathol Res Pract. 1990 Aug;186(4):427-38 [2174150.001]
  • [Cites] J Virol. 1991 Jun;65(6):3192-202 [2033670.001]
  • [Cites] Cell. 1991 Aug 9;66(3):451-64 [1651169.001]
  • [Cites] Adv Cancer Res. 1991;57:47-85 [1835254.001]
  • [Cites] J Virol. 1992 Jul;66(7):4606-11 [1534854.001]
  • [Cites] Science. 1992 Aug 28;257(5074):1267-71 [1519063.001]
  • [Cites] J Cell Biol. 1994 Mar;124(6):949-61 [8132716.001]
  • [Cites] J Virol. 1994 Jun;68(6):3917-24 [8189528.001]
  • [Cites] J Neurosci. 1995 Mar;15(3 Pt 2):2354-66 [7891172.001]
  • [Cites] Science. 1995 Apr 21;268(5209):411-5 [7536343.001]
  • [Cites] Science. 1995 Sep 22;269(5231):1737-40 [7569905.001]
  • [Cites] Nature. 1995 Nov 2;378(6552):85-8 [7477295.001]
  • [Cites] Curr Opin Cell Biol. 1995 Oct;7(5):641-9 [8573338.001]
  • [Cites] J Virol. 1996 Feb;70(2):862-72 [8551625.001]
  • [Cites] Science. 1996 May 17;272(5264):1020-3 [8638125.001]
  • [Cites] Science. 1996 Jun 7;272(5267):1470-3 [8633237.001]
  • [Cites] Breast Cancer Res Treat. 1996;39(1):57-67 [8738606.001]
  • [Cites] Structure. 1996 Sep 15;4(9):1077-92 [8805593.001]
  • [Cites] J Biol Chem. 1996 Oct 18;271(42):25723-6 [8824195.001]
  • [Cites] J Cell Biol. 1996 Sep;134(6):1469-82 [8830775.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11295-301 [8876129.001]
  • [Cites] Neuron. 1996 Oct;17(4):575-8 [8893015.001]
  • [Cites] Curr Opin Neurobiol. 1996 Oct;6(5):602-8 [8937823.001]
  • [Cites] Science. 1997 Jan 3;275(5296):73-7 [8974395.001]
  • [Cites] Trends Biochem Sci. 1996 Dec;21(12):455-8 [9009824.001]
  • [Cites] J Virol. 1997 Mar;71(3):1857-70 [9032316.001]
  • [Cites] Curr Biol. 2003 Sep 2;13(17):R661-2 [12956964.001]
  • [Cites] Nat Cell Biol. 2003 Nov;5(11):987-93 [14562058.001]
  • [Cites] Science. 2003 Nov 14;302(5648):1227-31 [14551319.001]
  • [Cites] J Cell Sci. 2003 Dec 15;116(Pt 24):4925-34 [14625386.001]
  • [Cites] J Virol. 1997 Oct;71(10):7873-80 [9311876.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11612-6 [9326658.001]
  • [Cites] Genes Dev. 1997 Oct 1;11(19):2532-44 [9334318.001]
  • [Cites] Oncogene. 1998 Feb 5;16(5):643-54 [9482110.001]
  • [Cites] J Virol. 1999 Dec;73(12):10095-103 [10559324.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5967-72 [10557085.001]
  • [Cites] Oncogene. 2000 Jan 20;19(3):365-72 [10656683.001]
  • [Cites] J Virol. 2000 Mar;74(5):2084-93 [10666238.001]
  • [Cites] Oncogene. 2000 Feb 10;19(6):719-25 [10698489.001]
  • [Cites] Nature. 2000 Apr 13;404(6779):782-7 [10783894.001]
  • [Cites] J Virol. 2000 Jun;74(11):5168-81 [10799592.001]
  • [Cites] Nat Cell Biol. 2000 Aug;2(8):531-9 [10934474.001]
  • [Cites] J Cell Biochem. 2000 Aug 2;79(2):213-24 [10967549.001]
  • [Cites] Semin Cell Dev Biol. 2000 Aug;11(4):315-24 [10966866.001]
  • [Cites] J Virol. 2000 Oct;74(20):9680-93 [11000240.001]
  • [Cites] Biochim Biophys Acta. 2000 Oct 2;1493(3):319-24 [11018256.001]
  • [Cites] Mol Cell Biol. 2000 Nov;20(21):8244-53 [11027293.001]
  • [Cites] Oncogene. 2000 Nov 2;19(46):5270-80 [11077444.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1661-8 [11080807.001]
  • [Cites] J Virol. 2001 Jan;75(2):557-68 [11134268.001]
  • [Cites] Oncogene. 2000 Nov 30;19(51):5884-91 [11127819.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):136-41 [11134523.001]
  • [Cites] J Virol. 2001 Apr;75(7):3089-94 [11238835.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(5):1475-83 [11238884.001]
  • [Cites] Front Biosci. 2005;10:1106-17 [15769610.001]
  • [Cites] EMBO J. 2005 Mar 23;24(6):1211-21 [15775987.001]
  • [Cites] Development. 2005 May;132(10):2273-85 [15829519.001]
  • [Cites] Cell. 2005 May 6;121(3):451-63 [15882626.001]
  • [Cites] Immunity. 2005 Jun;22(6):737-48 [15963788.001]
  • [Cites] Oncogene. 2005 Jun 23;24(27):4330-9 [15806148.001]
  • [Cites] Blood. 2005 Aug 1;106(3):988-95 [15831709.001]
  • [Cites] J Biol Chem. 2005 Aug 12;280(32):28936-43 [15951562.001]
  • [Cites] Kidney Int. 2005 Sep;68(3):955-65 [16105026.001]
  • [Cites] Cell Cycle. 2005 Jul;4(7):883-8 [15970698.001]
  • [Cites] J Cell Sci. 2005 Sep 1;118(Pt 17):4049-57 [16129888.001]
  • [Cites] Retrovirology. 2005;2:46 [16042787.001]
  • [Cites] J Cell Sci. 2005 Sep 15;118(Pt 18):4283-93 [16141229.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25408-15 [11964389.001]
  • [Cites] Nature. 2002 Jul 18;418(6895):348-52 [12124628.001]
  • [Cites] J Neurosci. 2002 Aug 1;22(15):6415-25 [12151521.001]
  • [Cites] J Cell Biol. 2005 Sep 12;170(6):895-901 [16157700.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8266-73 [16166303.001]
  • [Cites] Breast Cancer Res. 2005;7(5):190-7 [16168137.001]
  • [Cites] Oncogene. 2005 Nov 21;24(52):7686-96 [16299529.001]
  • [Cites] J Cell Biol. 2005 Dec 19;171(6):1061-71 [16344308.001]
  • [Cites] Mol Biol Cell. 2006 Feb;17(2):966-76 [16339077.001]
  • [Cites] J Biol Chem. 2006 Feb 17;281(7):4267-73 [16332687.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1980-8 [16263794.001]
  • [Cites] J Cell Sci. 2006 Mar 15;119(Pt 6):979-87 [16525119.001]
  • [Cites] EMBO J. 2006 Mar 22;25(6):1406-17 [16511562.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1121-3 [16564003.001]
  • [Cites] J Med Virol. 2006 Apr;78(4):501-7 [16482544.001]
  • [Cites] J Androl. 2006 May-Jun;27(3):390-404 [16452527.001]
  • [Cites] Mol Biol Cell. 2006 May;17(5):2303-11 [16525015.001]
  • [Cites] J Virol. 2006 Jun;80(11):5301-7 [16699010.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Jul;10(3):197-8 [16807799.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Jul;10(3):231-47 [16807803.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Jul;10(3):261-72 [16807805.001]
  • [Cites] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462.001]
  • [Cites] Oncogene. 2006 Jul 20;25(31):4276-85 [16532034.001]
  • [Cites] J Virol. 2003 Jun;77(12):6957-64 [12768014.001]
  • [Cites] Mol Cell Biol. 2003 Jun;23(12):4267-82 [12773569.001]
  • [Cites] Cell Mol Biol (Noisy-le-grand). 2003 Feb;49(1):13-21 [12839333.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3735-42 [12839967.001]
  • [Cites] Retrovirology. 2006;3:71 [17042961.001]
  • [Cites] Nat Cell Biol. 2006 Nov;8(11):1235-45 [17060907.001]
  • [Cites] Trends Cell Biol. 2006 Dec;16(12):622-30 [17067797.001]
  • [Cites] Retrovirology. 2006;3:88 [17140451.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(24):8970-81 [14645510.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;273:163-214 [14674602.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):194-9 [14710229.001]
  • [Cites] Exp Cell Res. 2004 Jan 1;292(1):51-66 [14720506.001]
  • [Cites] Virology. 2004 Jan 5;318(1):327-36 [14972558.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):10157-66 [14699157.001]
  • [Cites] Virology. 2004 Mar 1;320(1):52-62 [15003862.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):19051-63 [14960569.001]
  • [Cites] Rev Clin Exp Hematol. 2003 Dec;7(4):336-61 [15129647.001]
  • [Cites] J Cell Biol. 2004 Jul 19;166(2):173-8 [15263016.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1909-25 [15314019.001]
  • [Cites] Oncogene. 2004 Oct 21;23(49):8033-9 [15378012.001]
  • [Cites] J Virol. 2004 Nov;78(22):12366-77 [15507623.001]
  • [Cites] Int J Cancer. 1974 Mar 15;13(3):286-90 [4822103.001]
  • [Cites] Virology. 1979 Mar;93(2):481-92 [452413.001]
  • [Cites] Virology. 1980 Sep;105(2):537-50 [7423858.001]
  • [Cites] Nucleic Acids Res. 1981 Aug 25;9(16):4023-42 [6985482.001]
  • [Cites] Virology. 1983 Jul 30;128(2):377-90 [6310863.001]
  • [Cites] J Virol. 1985 Oct;56(1):250-7 [4032537.001]
  • [Cites] Cancer Surv. 1986;5(2):389-404 [2946407.001]
  • [Cites] J Virol. 2007 Nov;81(21):11900-7 [17715223.001]
  • [Cites] J Biol Chem. 2007 Nov 9;282(45):33132-41 [17855372.001]
  • [Cites] Science. 2008 Feb 22;319(5866):1096-100 [18202256.001]
  • [Cites] Oncogene. 2008 Feb 28;27(10):1412-20 [17828302.001]
  • [Cites] Int J Cancer. 2006 Sep 15;119(6):1285-90 [16619250.001]
  • [Cites] Cell. 2006 Aug 25;126(4):741-54 [16923393.001]
  • [Cites] Annu Rev Cell Dev Biol. 2006;22:207-35 [16771626.001]
  • [Cites] Nat Immunol. 2006 Nov;7(11):1143-9 [17053799.001]
  • [Cites] Curr Biol. 2006 Dec 19;16(24):2395-405 [17081755.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19872-7 [17172448.001]
  • [Cites] J Biol Chem. 2007 Jan 5;282(1):65-71 [17085449.001]
  • [Cites] Neoplasia. 2006 Dec;8(12):1019-27 [17217619.001]
  • [Cites] Nat Immunol. 2007 Feb;8(2):154-61 [17187070.001]
  • [Cites] Nat Immunol. 2007 Feb;8(2):126-7 [17242684.001]
  • [Cites] EMBO Rep. 2007 Feb;8(2):158-64 [17235357.001]
  • [Cites] J Neurochem. 2007 Feb;100(4):1032-46 [17156128.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):4162-71 [17145756.001]
  • [Cites] J Biol Chem. 2007 Feb 16;282(7):5085-99 [17170109.001]
  • [Cites] Genes Cells. 2007 Feb;12(2):219-33 [17295841.001]
  • [Cites] J Neurosci. 2007 Feb 14;27(7):1682-91 [17301176.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1626-35 [17308103.001]
  • [Cites] Genes Dev. 2007 Mar 1;21(5):483-96 [17344411.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] J Cell Biol. 2007 Mar 26;176(7):1035-47 [17371830.001]
  • [Cites] J Virol. 2007 Apr;81(8):4080-90 [17287269.001]
  • [Cites] Genes Cells. 2007 Apr;12(4):473-86 [17397395.001]
  • [Cites] Genes Cells. 2007 Apr;12(4):535-46 [17397400.001]
  • [Cites] Oncogene. 2007 Apr 5;26(16):2272-82 [17043654.001]
  • [Cites] Dev Cell. 2007 Apr;12(4):487-502 [17419990.001]
  • [Cites] J Virol. 2007 May;81(9):4787-97 [17314165.001]
  • [Cites] Development. 2007 May;134(9):1799-807 [17435047.001]
  • [Cites] Exp Cell Res. 2007 May 1;313(8):1533-47 [17374535.001]
  • [Cites] Mol Biol Cell. 2007 May;18(5):1744-55 [17332497.001]
  • [Cites] Trends Immunol. 2007 May;28(5):196-200 [17395537.001]
  • [Cites] J Cell Biol. 2007 Jun 4;177(5):893-903 [17548515.001]
  • [Cites] Nat Cell Biol. 2007 Sep;9(9):1016-24 [17762893.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1206-11 [9037031.001]
  • [Cites] Mech Dev. 1997 Mar;62(2):161-74 [9152008.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6670-5 [9192623.001]
  • [Cites] FEBS Lett. 1997 Aug 18;413(2):243-8 [9280290.001]
  • [Cites] Oncogene. 2008 Nov 24;27(55):7018-30 [19029942.001]
  • [Cites] J Virol. 1992 Oct;66(10):5867-78 [1326648.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7834-8 [8395056.001]
  • [Cites] Cancer Res. 1993 Dec 1;53(23):5624-8 [8242616.001]
  • [Cites] J Cell Sci. 1998 Apr;111 ( Pt 8):1071-80 [9512503.001]
  • [Cites] J Cell Biol. 1998 Apr 6;141(1):199-208 [9531559.001]
  • [Cites] J Cell Sci. 1998 Aug;111 ( Pt 16):2365-76 [9683631.001]
  • [Cites] J Virol. 1999 Feb;73(2):1591-600 [9882365.001]
  • [Cites] Ultrastruct Pathol. 1998 Nov-Dec;22(6):413-20 [9891919.001]
  • [Cites] Dev Biol. 1999 Feb 1;206(1):88-99 [9918697.001]
  • [Cites] Oncogene. 1999 Jan 7;18(1):9-17 [9926915.001]
  • [Cites] J Cell Physiol. 1999 Feb;178(2):235-46 [10048588.001]
  • [Cites] J Virol. 1999 Apr;73(4):3071-9 [10074157.001]
  • [Cites] Int J Cancer. 1999 Jul 2;82(1):137-44 [10360833.001]
  • [Cites] Carcinogenesis. 1999 Aug;20(8):1425-31 [10426787.001]
  • [Cites] Int J Cancer. 1999 Oct 29;83(3):349-58 [10495427.001]
  • [Cites] Oncogene. 1999 Sep 30;18(40):5487-96 [10523825.001]
  • [Cites] Science. 1962 Sep 14;137(3533):835-41 [13922417.001]
  • [Cites] Eur J Cancer. 2004 Dec;40(18):2717-25 [15571953.001]
  • [Cites] FASEB J. 2005 Jan;19(1):115-7 [15629897.001]
  • [Cites] Cell Tissue Res. 2005 Feb;319(2):341-7 [15558322.001]
  • [Cites] Bioessays. 2005 Feb;27(2):153-63 [15666353.001]
  • [Cites] J Exp Med. 2005 Feb 7;201(3):419-30 [15699074.001]
  • [Cites] J Cell Biol. 2005 Feb 28;168(5):705-11 [15738264.001]
  • (PMID = 19029943.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058541
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E4 protein, Adenovirus 9; 0 / Gene Products, tax; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Number-of-references] 233
  • [Other-IDs] NLM/ NIHMS411909; NLM/ PMC3501650
  •  go-up   go-down


59. Zhang X, Hakata Y, Tanaka Y, Shida H: CRM1, an RNA transporter, is a major species-specific restriction factor of human T cell leukemia virus type 1 (HTLV-1) in rat cells. Microbes Infect; 2006 Mar;8(3):851-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CRM1, an RNA transporter, is a major species-specific restriction factor of human T cell leukemia virus type 1 (HTLV-1) in rat cells.
  • Rat ortholog of human CRM1 has been found to be responsible for the poor activity of viral Rex protein, which is essential for RNA export of human T cell leukemia virus type 1 (HTLV-1).
  • Here, we examined the species-specific barrier of HTLV-1 by establishing rat cell lines, including both adherent and CD4(+) T cells, which express human CRM1 at physiological levels.
  • We demonstrated that expression of human CRM1 in rat cells is not harmful to cell growth and is sufficient to restore the synthesis of the viral structural proteins, Gag and Env, at levels similar to those in human cells.
  • An HTLV-1 pseudovirus infection system suggested that the released virus particles are fully infectious.
  • Our newly developed reporter cell system revealed that Env proteins produced in rat cells are fully fusogenic, which is the basis for cell-cell HTLV-1 infection.
  • These results, in conjunction with reports describing efficient entry of HTLV-1 into rat cells, may indicate that HTLV-1 is unique in that its major species-specific barrier is determined by CRM1 at a viral RNA export step.
  • These observations will enable us to construct a transgenic rat model expressing human CRM1 that is sensitive to HTLV-1 infection.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16504563.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Karyopherins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Viral Proteins; 0 / exportin 1 protein
  •  go-up   go-down


60. Ueda M, Imada K, Imura A, Koga H, Hishizawa M, Uchiyama T: Expression of functional interleukin-21 receptor on adult T-cell leukaemia cells. Br J Haematol; 2005 Jan;128(2):169-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of functional interleukin-21 receptor on adult T-cell leukaemia cells.
  • Adult T-cell leukaemia (ATL) is caused by human T-cell leukaemia virus type I (HTLV-I).
  • It has been suggested that cytokines play a role in the development and in the neoplastic cell growth of ATL.
  • In this study, we examined the expression of IL-21R and the effect of IL-21 on ATL cells.
  • Real-time reverse transcription polymerase chain reaction showed that HTLV-I-infected cell lines and primary ATL cells expressed IL-21R mRNA.
  • Cell surface expression of IL-21R on these cells was confirmed by flow cytometric analysis using a newly developed monoclonal antibody against human IL-21R.
  • Notably, IL-21 induced the proliferation of ATL-43T and ED-40515(+) cells, both of which were derived from leukaemic cell clones of ATL.
  • Taken together, these findings provide the first evidence that ATL cells express functional IL-21R, suggesting that it may contribute to the pathophysiology of ATL.
  • In addition, the IL-21/IL-21R system may represent a new target for the treatment of ATL.
  • [MeSH-major] Leukemia, T-Cell / immunology. RNA, Messenger / analysis. Receptors, Interleukin / genetics. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Blotting, Western / methods. Cell Line, Transformed. Cell Line, Tumor. Cell Proliferation. DNA-Binding Proteins / metabolism. Flow Cytometry. Human T-lymphotropic virus 1. Humans. Interleukin-21 Receptor alpha Subunit. Milk Proteins / metabolism. Phosphorylation. Receptors, Interleukin-21. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor. STAT5 Transcription Factor. Signal Transduction. Trans-Activators / metabolism


61. Shembade N, Harhaj NS, Yamamoto M, Akira S, Harhaj EW: The human T-cell leukemia virus type 1 Tax oncoprotein requires the ubiquitin-conjugating enzyme Ubc13 for NF-kappaB activation. J Virol; 2007 Dec;81(24):13735-42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The human T-cell leukemia virus type 1 Tax oncoprotein requires the ubiquitin-conjugating enzyme Ubc13 for NF-kappaB activation.
  • Ubiquitination of the human T-cell leukemia virus 1 Tax oncoprotein provides an important regulatory mechanism that promotes the Tax-mediated activation of NF-kappaB.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • 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] Nat Cell Biol. 2005 Aug;7(8):758-65 [16056267.001]
  • [Cites] Biochem Biophys Res Commun. 2007 May 25;357(1):225-30 [17418100.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5986-95 [16155605.001]
  • [Cites] EMBO J. 2005 Oct 5;24(19):3353-9 [16148945.001]
  • [Cites] Mol Cell. 2005 Oct 28;20(2):301-12 [16246731.001]
  • [Cites] Front Biosci. 2000 Jan 1;5:D138-68 [10702386.001]
  • [Cites] Oncogene. 2000 Mar 9;19(11):1448-56 [10723136.001]
  • [Cites] Gene Ther. 2000 Jun;7(12):1063-6 [10871756.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34060-7 [10906125.001]
  • [Cites] Cell. 2000 Oct 13;103(2):351-61 [11057907.001]
  • [Cites] Mol Cell. 2001 Feb;7(2):401-9 [11239468.001]
  • [Cites] Science. 2001 Aug 24;293(5534):1495-9 [11520989.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23):6805-15 [11726516.001]
  • [Cites] J Cell Physiol. 2002 Feb;190(2):133-59 [11807819.001]
  • [Cites] Sci STKE. 1999 Oct 26;1999(5):RE1 [11865184.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] Nat Immunol. 2002 Oct;3(10):958-65 [12352969.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):1487-93 [12419799.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(15):5331-45 [12861019.001]
  • [Cites] Oncogene. 2003 Oct 16;22(46):7101-7 [14562038.001]
  • [Cites] EMBO J. 2004 Jan 28;23(2):322-32 [14713952.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Biochem J. 2004 Sep 1;382(Pt 2):393-409 [15214841.001]
  • [Cites] Virology. 2007 May 25;362(1):99-108 [17258259.001]
  • [Cites] EMBO Rep. 2007 May;8(5):510-5 [17363973.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3214-26 [17496917.001]
  • [Cites] J Biol Chem. 2007 Aug 31;282(35):25177-81 [17626013.001]
  • [Cites] EMBO J. 2007 Sep 5;26(17):3910-22 [17703191.001]
  • [Cites] Oncogene. 2008 Mar 13;27(12):1665-76 [17891179.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6371-6 [17404240.001]
  • [Cites] Genes Dev. 2004 Sep 15;18(18):2195-224 [15371334.001]
  • [Cites] J Virol. 2004 Nov;78(21):11686-95 [15479810.001]
  • [Cites] J Virol. 2004 Nov;78(21):11823-32 [15479824.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Science. 1989 Mar 24;243(4898):1576-83 [2538923.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8797-801 [8090726.001]
  • [Cites] Cell. 1998 Jun 26;93(7):1231-40 [9657155.001]
  • [Cites] Annu Rev Biochem. 1998;67:425-79 [9759494.001]
  • [Cites] Genes Dev. 1999 Apr 15;13(8):1015-24 [10215628.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):22911-4 [10438454.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jan;6(1):9-20 [15688063.001]
  • [Cites] Virology. 2005 Mar 1;333(1):145-58 [15708600.001]
  • [Cites] IUBMB Life. 2005 Feb;57(2):83-91 [16036567.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10391-406 [16287853.001]
  • [Cites] EMBO J. 2005 Nov 16;24(22):3859-68 [16252010.001]
  • [Cites] J Cell Biochem. 2006 Feb 15;97(3):572-82 [16215985.001]
  • [Cites] EMBO J. 2006 Apr 19;25(8):1635-45 [16601694.001]
  • [Cites] Blood. 2006 May 15;107(10):4021-9 [16424386.001]
  • [Cites] Nat Immunol. 2006 Sep;7(9):962-70 [16862162.001]
  • [Cites] Sci STKE. 2006 Oct 17;2006(357):re13 [17047224.001]
  • [Cites] Mol Cell Biol. 2006 Dec;26(23):8901-13 [17000756.001]
  • [Cites] J Immunol. 2006 Dec 1;177(11):7520-4 [17114420.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):4102-12 [17135271.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):4185-92 [17145747.001]
  • [Cites] Mol Cell Biol. 2007 Apr;27(8):2910-8 [17296724.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • (PMID = 17942533.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099926; United States / NCI NIH HHS / CA / R01 CA99926
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / IKBKG protein, human; 0 / NF-kappa B; 0 / Ubiquitin; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.10 / I-kappa B Kinase; EC 6.3.2.19 / Ubc13 protein, mouse; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
  • [Other-IDs] NLM/ PMC2168884
  •  go-up   go-down


62. Sargent JT, Smith OP: Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders. Br J Haematol; 2010 May;149(4):465-77
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypercalcaemia is a common metabolic complication of malignant disease often requiring emergency intervention.
  • Although it is more frequently associated with solid tumours, malignancy-associated hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.
  • Its association with myeloma and adult T-cell leukaemia/lymphoma is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.
  • Haematologists need to be familiar with the clinical manifestations of, the differential diagnosis to be considered and the most effective management strategies that are currently available for MAH.
  • [MeSH-minor] Adult. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20377591.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 96
  •  go-up   go-down


63. Marzano AV, Vezzoli P, Fanoni D, Venegoni L, Berti E: Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells. J Am Acad Dermatol; 2009 Aug;61(2):348-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells.
  • Regulatory T (Treg) cells, which represent 5% to 10% of peripheral T cells, regulate the activities of T-cell subsets by performing immunosuppressive functions and thus preventing the development of autoimmune responses.
  • Recently, it has been demonstrated that the tumor cells in adult T-cell leukemia lymphomas can function as Treg, raising the question of whether any variant of primary cutaneous T-cell lymphoma may also express a regulatory phenotype.
  • We describe an extraordinary case of primary cutaneous T-cell lymphoma clinically characterized by protean cutaneous manifestations and histologically showing a pattern consistent with epidermotropic pleomorphic medium-/large-cell primary cutaneous T-cell lymphoma.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Forkhead Transcription Factors / immunology. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Regulatory / immunology


64. Hishiki T, Ohshima T, Ego T, Shimotohno K: BCL3 acts as a negative regulator of transcription from the human T-cell leukemia virus type 1 long terminal repeat through interactions with TORC3. J Biol Chem; 2007 Sep 28;282(39):28335-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCL3 acts as a negative regulator of transcription from the human T-cell leukemia virus type 1 long terminal repeat through interactions with TORC3.
  • By associating with cyclic AMP-responsive element-binding protein (CREB), the human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates transcription from the HTLV-1 long terminal repeat (LTR), which contains multiple cyclic AMP-responsive elements.
  • In this study, we performed a yeast two-hybrid screen using the N-terminal region of TORC3 as bait and identified B-cell chronic lymphatic leukemia protein 3 (BCL3) as a protein interacting with TORC3.
  • By using a luciferase assay, we determined that BCL3 inhibited transcription from the HTLV-1 LTR in a manner dependent on TORC3.
  • These results suggest that BCL3 functions as a repressor of HTLV-1 LTR-mediated transcription through interactions with TORC3.
  • In addition to stimulating transcription from the HTLV-1 LTR, Tax also enhances BCL3 expression; thus, transcription from the LTR is regulated by both positive and negative feedback mechanisms.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism. Terminal Repeat Sequences / physiology. Transcription Factors / metabolism. Transcription, Genetic / physiology

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17644518.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREB1 protein, human; 0 / CRTC3 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Enzyme Inhibitors; 0 / Gene Products, tax; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3; 3X2S926L3Z / trichostatin A
  •  go-up   go-down


65. Liu M, Yang L, Zhang L, Liu B, Merling R, Xia Z, Giam CZ: Human T-cell leukemia virus type 1 infection leads to arrest in the G1 phase of the cell cycle. J Virol; 2008 Sep;82(17):8442-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia virus type 1 infection leads to arrest in the G1 phase of the cell cycle.
  • Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma.
  • Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission.
  • Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene.
  • HTLV-1-infected HeLa cells, like their tax-transduced counterparts, expressed high levels of p21(CIP1/WAF1) and p27(KIP1), developed mitotic abnormalities, and became arrested in G(1) in senescence.
  • In contrast, cells of a human osteosarcoma lineage (HOS) continued to divide after HTLV-1 infection or Tax expression, albeit at a reduced growth rate and with mitotic aberrations.
  • Unique to HOS cells is the dramatic reduction of p21(CIP1/WAF1) and p27(KIP1) expression, which is in part associated with the constitutive activation of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway.
  • The loss of p21(CIP1/WAF1) and p27(KIP1) in HOS cells apparently allows HTLV-1- and Tax-induced G(1) arrest to be bypassed.
  • Finally, HTLV-1 infection and Tax expression also cause human SupT1 T cells to arrest in the G(1) phase of the cell cycle.
  • These results suggest that productive HTLV-1 infection ordinarily leads to Tax-mediated G(1) arrest.
  • However, T cells containing somatic mutations that inactivate p21(CIP1/WAF1) and p27(KIP1) may continue to proliferate after HTLV-1 infection and Tax expression.


66. Pumfery A, de la Fuente C, Kashanchi F: HTLV-1 Tax: centrosome amplification and cancer. Retrovirology; 2006 Aug 09;3:50
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1 Tax: centrosome amplification and cancer.
  • During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis.
  • Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the proper complement of the genome.
  • The controls that ensure that centrosomes are duplicated exactly once in the cell cycle are not well understood.
  • These phenotypes are also observed in cancers induced by viruses, including adult T cell lymphoma which is caused by the human T cell lymphotrophic virus Type 1 (HTLV-1).
  • Several reports have indicated that the HTLV-1 transactivator, Tax, is directly responsible for the centrosomal abnormalities observed in ATL cells.
  • A recent paper in Nature Cell Biology by Ching et al. has shed some new light into how Tax may be inducing centrosome abnormalities.
  • The authors demonstrated that 30% of ATL cells contained more than two centrosomes and expression of Tax alone induced supernumerary centrosomes.
  • These results suggest that Tax1BP2 may be an important block to centrosome re-duplication that is observed in normal cells.
  • Presently, a specific cellular protein that prevents centrosome re-duplication has not been identified.
  • This paper has provided further insight into how Tax induces centrosome abnormalities that lead to ATL.
  • Lastly, additional work on Tax1BP2 will also provide insight into how the cell suppresses centrosome re-duplication during the cell cycle and the role that Tax1BP2 plays in this important cellular pathway.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 1999 Dec;73(12):9917-27 [10559304.001]
  • [Cites] Cancer Sci. 2006 Sep;97(9):836-41 [16805820.001]
  • [Cites] J Cell Biol. 2000 Nov 13;151(4):837-46 [11076968.001]
  • [Cites] Genes Dev. 2001 May 15;15(10):1167-81 [11358861.001]
  • [Cites] J Biol Chem. 2001 Jun 22;276(25):22797-803 [11287420.001]
  • [Cites] Curr Biol. 2001 Sep 4;11(17):R698-701 [11553343.001]
  • [Cites] Mol Cell Biol. 2002 May;22(10):3327-38 [11971966.001]
  • [Cites] Int J Cancer. 2002 May 20;99(3):378-85 [11992406.001]
  • [Cites] J Biomed Sci. 2002 Jul-Aug;9(4):292-8 [12145525.001]
  • [Cites] Oncogene. 2002 Sep 9;21(40):6222-7 [12214252.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):7075-82 [12460929.001]
  • [Cites] Mutagenesis. 2003 May;18(3):221-33 [12714687.001]
  • [Cites] Nat Cell Biol. 2003 Jun;5(6):539-44 [12766773.001]
  • [Cites] Biochemistry. 2003 Jun 10;42(22):6921-8 [12779347.001]
  • [Cites] Mol Biol Cell. 2003 May;14(5):1993-2004 [12802070.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2003;13(1):9-23 [12839094.001]
  • [Cites] J Cell Sci. 2003 Aug 15;116(Pt 16):3399-411 [12840069.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(15):5282-92 [12861014.001]
  • [Cites] Mol Cancer Res. 2004 Mar;2(3):159-69 [15037655.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4064-8 [15205312.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] DNA Cell Biol. 2004 Aug;23(8):475-89 [15307950.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2347-72 [15353292.001]
  • [Cites] Virology. 1993 Mar;193(1):456-9 [8438579.001]
  • [Cites] Oncogene. 1996 Apr 18;12(8):1645-52 [8622884.001]
  • [Cites] J Virol. 1998 Jan;72(1):633-40 [9420268.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3620-32 [9584203.001]
  • [Cites] J Virol. 1998 Nov;72(11):8852-60 [9765430.001]
  • [Cites] J Cell Sci. 1999 Jul;112 ( Pt 14):2453-61 [10381400.001]
  • [Cites] Front Biosci. 2005 Jan 1;10:919-30 [15569630.001]
  • [Cites] Oncogene. 2005 Jan 20;24(4):525-40 [15580311.001]
  • [Cites] Nat Cell Biol. 2005 Jun;7(6):626-32 [15908946.001]
  • [Cites] Cell Biol Int. 2005 May;29(5):375-83 [15996491.001]
  • [Cites] Retrovirology. 2004;1:6 [15169570.001]
  • [Cites] Retrovirology. 2005;2:45 [16014171.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6719-28 [16007163.001]
  • [Cites] Annu Rev Cell Dev Biol. 2005;21:411-34 [16212501.001]
  • [Cites] Retrovirology. 2005;2:54 [16164752.001]
  • [Cites] Cancer Lett. 2005 Dec 8;230(1):6-19 [16253756.001]
  • [Cites] Trends Cell Biol. 2005 Nov;15(11):589-98 [16214339.001]
  • [Cites] J Virol. 2006 Jan;80(2):697-709 [16378973.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18974-9 [16365316.001]
  • [Cites] Carcinogenesis. 2006 Apr;27(4):673-81 [16308315.001]
  • [Cites] Nat Cell Biol. 2006 Jul;8(7):717-24 [16767081.001]
  • [Cites] J Biol Chem. 2000 Oct 20;275(42):32906-10 [10969065.001]
  • (PMID = 16899128.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI44357; United States / NIAID NIH HHS / AI / R01 AI043894; United States / PHS HHS / / 13969; United States / NIAID NIH HHS / AI / AI43894; United States / NIAID NIH HHS / AI / R29 AI044357
  • [Publication-type] Editorial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / VAC14 protein, human
  • [Other-IDs] NLM/ PMC1555608
  •  go-up   go-down


67. Gualco G, Chioato L, Harrington WJ Jr, Weiss LM, Bacchi CE: Primary and secondary T-cell lymphomas of the breast: clinico-pathologic features of 11 cases. Appl Immunohistochem Mol Morphol; 2009 Jul;17(4):301-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary and secondary T-cell lymphomas of the breast: clinico-pathologic features of 11 cases.
  • Breast involvement by non-Hodgkin lymphomas is rare, and exceptional for T-cell lymphomas; we studied the morphologic, immunophenotypic, and clinical features of 11 patients with T-cell non-Hodgkin lymphomas involving the breast.
  • Four cases fulfilled the definition criteria for primary breast lymphomas, 3 females and 1 male, with a median age of 51 years.
  • One primary breast lymphomas was T-cell lymphoma unspecified, other was subcutaneous panniculitis-like T-cell lymphoma, and 2 cases were anaplastic large cell lymphomas.
  • One of the anaplastic large cell lymphoma cases was found surrounding a silicone breast implant and presented as clinically as mastitis; whereas the other case occurred in a man.
  • T-cell lymphoma secondarily involved the breast in 7 patients, all women and 1 bilateral, with a median age of 29 years.
  • These secondary breast lymphomas occurred as part of widespread nodal or leukemic disease.
  • Three patients had adult T-cell leukemia/lymphoma, including the patient with bilateral lesions, 3 others had precursor T-lymphoblastic lymphoma/leukemia, and the other presented with a peripheral-T-cell lymphoma non otherwise specified type.
  • Breast T-cell lymphomas are very infrequent and are morphologically and clinically heterogeneous.

  • MedlinePlus Health Information. consumer health - Male Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Surg Pathol. 2008 Oct;16(4):407-13 [18480397.001]
  • [Cites] Mod Pathol. 2000 Jun;13(6):599-605 [10874662.001]
  • [Cites] Breast J. 2002 Sep-Oct;8(5):294-304 [12199758.001]
  • [Cites] Rev Soc Bras Med Trop. 2002 Sep-Oct;35(5):499-508 [12621671.001]
  • [Cites] Arch Pathol Lab Med. 2003 Mar;127(3):e115-8 [12653596.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] Haematologica. 2004 Apr;89(4):ELT01 [15075114.001]
  • [Cites] Leuk Lymphoma. 2004 Apr;45(4):833-6 [15160967.001]
  • [Cites] Ann Oncol. 2004 Oct;15(10):1467-75 [15367405.001]
  • [Cites] Cancer. 1972 Jun;29(6):1705-12 [4555557.001]
  • [Cites] Cancer. 1990 Dec 15;66(12):2602-11 [2249200.001]
  • [Cites] Cancer. 1991 Mar 1;67(5):1359-69 [1991299.001]
  • [Cites] Diagn Mol Pathol. 1993 Jun;2(2):99-107 [8269284.001]
  • [Cites] Am J Surg Pathol. 1994 Mar;18(3):288-95 [8116797.001]
  • [Cites] JAMA. 1995 Jan 11;273(2):116 [7799490.001]
  • [Cites] Am J Surg Pathol. 1995 Jun;19(6):712-7 [7755157.001]
  • [Cites] J Am Acad Dermatol. 1995 Dec;33(6):1060-1 [7490360.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3124-8 [8874212.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] APMIS. 1997 Jun;105(6):445-8 [9236861.001]
  • [Cites] Plast Reconstr Surg. 1997 Aug;100(2):554-5 [9252643.001]
  • [Cites] Hematol Oncol. 1997 Feb;15(1):33-8 [9378471.001]
  • [Cites] Breast Cancer. 2005;12(2):154-8 [15858449.001]
  • [Cites] J Ultrasound Med. 2005 Oct;24(10):1453-60 [16179634.001]
  • [Cites] Virchows Arch. 2006 Nov;449(5):561-4 [16983530.001]
  • [Cites] Indian J Pathol Microbiol. 2007 Oct;50(4):816-8 [18306567.001]
  • [Cites] Mod Pathol. 2008 Apr;21(4):455-63 [18223553.001]
  • [Cites] Int J Hematol. 2008 Jun;87(5):491-7 [18414980.001]
  • [Cites] J Plast Reconstr Aesthet Surg. 2008 Jul;61(7):822-5 [17509956.001]
  • [Cites] Am J Surg Pathol. 2008 Sep;32(9):1299-309 [18636016.001]
  • [Cites] Leuk Lymphoma. 2002 Jan;43(1):115-9 [11908714.001]
  • [Cites] Cancer. 2002 Apr 25;96(2):110-6 [11954028.001]
  • (PMID = 19318917.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112217-03; United States / NCI NIH HHS / CA / CA121935-03; United States / NCI NIH HHS / CA / R01 CA112217-03; United States / NCI NIH HHS / CA / R01 CA121935-03; United States / NCI NIH HHS / CA / R01 CA121935
  • [Publication-type] Case Reports; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS125674; NLM/ PMC2739299
  •  go-up   go-down


68. Keramati MR, Sadeghian MH, Ayatollahi H: Clinical and laboratory features in adult T-cell leukemia/lymphoma in Khorasan, Iran. Leuk Lymphoma; 2010 Apr;51(4):727-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and laboratory features in adult T-cell leukemia/lymphoma in Khorasan, Iran.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. HTLV-I Infections / blood. HTLV-I Infections / complications. HTLV-I Infections / pathology. Humans. Iran. Male. Middle Aged. Neoplasm Staging. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20178409.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


69. Fujiwara H, Kawada H, Matsushita K, Hamada H, Ozaki A, Inoue H, Yoshimitsu M, Kukita T, Arimura K, Ohtsubo H, Uozumi K, Arima N, Tei C: Case of a patient with progressive adult T-cell leukemia/lymphoma treated successfully by reduced-intensity conditioning stem cell transplantation from an HLA-incompatible related donor. Int J Hematol; 2005 Nov;82(4):357-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case of a patient with progressive adult T-cell leukemia/lymphoma treated successfully by reduced-intensity conditioning stem cell transplantation from an HLA-incompatible related donor.
  • A 61-year-old man with progressive adult T-cell leukemia/lymphoma (ATLL) successfully received reduced-intensity conditioning stem cell transplantation (RIST) without T-cell depletion (TCD) from his HLA-incompatible son, who had negative results for human T-lymphotropic virus type 1 (HTLV-1) (1-locus, 1-allele mismatch in the graft-versus-host [GVH] direction; 2-loci, 1-allele mismatch in the host-versus-graft direction).
  • GVH disease (GVHD) prophylaxis consisted of short-term administration of methotrexate, tacrolimus, and methylprednisolone.
  • Serial analysis of HTLV-1 proviral load by quantitative polymerase chain reaction analysis using whole peripheral blood demonstrated undetectable levels from day 90.
  • The results in this case suggest the potential of non-TCD RIST from an HLA-incompatible relative donor as an alternative source of hematopoietic stem cells even for an elderly patient with advanced ATLL.
  • In addition, basiliximab combined with MMF may be effective for the treatment of steroid-refractory skin GVHD without deteriorating the graft-versus-ATL effect.
  • [MeSH-major] Histocompatibility Testing. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] B-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Graft vs Host Reaction. HLA Antigens / immunology. Humans. Male. Middle Aged. Transplantation Chimera. Treatment Outcome

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Exp Hematol. 2003 Nov;31(11):1019-25 [14585364.001]
  • [Cites] Clin Cancer Res. 2001 Oct;7(10):3120-6 [11595704.001]
  • [Cites] J Immunol Methods. 2003 Apr 1;275(1-2):133-6 [12667677.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] Br J Haematol. 2003 Oct;123(2):193-206 [14531901.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Jpn J Clin Oncol. 2004 Jul;34(7):369-78 [15342663.001]
  • [Cites] Exp Hematol. 2002 Apr;30(4):340-5 [11937269.001]
  • [Cites] Int J Hematol. 2005 Jan;81(1):13-7 [15717682.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):304-9 [12542491.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Semin Oncol. 2004 Feb;31(1):4-21 [14970932.001]
  • [Cites] Int J Oncol. 2004 Aug;25(2):437-43 [15254742.001]
  • [Cites] Bone Marrow Transplant. 2002 Dec;30(12 ):899-903 [12476283.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6977-84 [11156399.001]
  • [Cites] Leuk Lymphoma. 2000 Aug;38(5-6):533-40 [10953974.001]
  • [Cites] Virology. 1997 Oct 27;237(2):209-16 [9356333.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3821-8 [15280193.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] Leukemia. 2004 Jan;18(1):167-9 [14603340.001]
  • [Cites] Curr Opin Oncol. 1995 Mar;7(2):115-21 [7756375.001]
  • [Cites] Int J Cancer. 2005 Mar 20;114(2):257-67 [15551352.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Clin Exp Immunol. 2003 Dec;134(3):426-30 [14632747.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Curr Opin Hematol. 2004 Nov;11(6):386-91 [15548992.001]
  • [Cites] Br J Haematol. 2004 Mar;124(6):777-86 [15009066.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • (PMID = 16298831.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HLA Antigens
  •  go-up   go-down


70. Aiello A, Fattorusso E, Luciano P, Menna M, Calzado MA, Muñoz E, Bonadies F, Guiso M, Sanasi MF, Cocco G, Nicoletti R: Synthesis of structurally simplified analogues of aplidinone A, a pro-apoptotic marine thiazinoquinone. Bioorg Med Chem; 2010 Jan 15;18(2):719-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor cell lines which also inhibits the TNFalpha-induced NF-kappaB activation in a human leukemia T cell line.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Computer Simulation. Drug Screening Assays, Antitumor. Humans. Molecular Structure. NF-kappa B / metabolism. Structure-Activity Relationship. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031419.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha; 0 / aplidinone A
  •  go-up   go-down


71. Gómez-Acevedo H, Li MY: Backward bifurcation in a model for HTLV-I infection of CD4+ T cells. Bull Math Biol; 2005 Jan;67(1):101-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Backward bifurcation in a model for HTLV-I infection of CD4+ T cells.
  • Human T-cell Lymphotropic Virus Type I (HTLV-I) primarily infects CD4+ helper T cells.
  • HTLV-I infection is clinically linked to the development of Adult T-cell Leukemia/Lymphoma and of HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis, among other illnesses.
  • HTLV-I transmission can be either horizontal through cell-to-cell contact, or vertical through mitotic division of infected CD4+ T cells.
  • It has been observed that HTLV-I infection has a high proviral load but a low rate of proviral genetic variation.
  • We consider and analyze a mathematical model for HTLV-I infection of CD4+ T cells that incorporates both horizontal and vertical transmission.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Computer Simulation. Human T-lymphotropic virus 1 / growth & development. Models, Biological
  • [MeSH-minor] Algorithms. Cell Death. Cell Proliferation. Humans

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15691541.001).
  • [ISSN] 0092-8240
  • [Journal-full-title] Bulletin of mathematical biology
  • [ISO-abbreviation] Bull. Math. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


72. Yoshida M, Satou Y, Yasunaga J, Fujisawa J, Matsuoka M: Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene. J Virol; 2008 Oct;82(19):9359-68
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene.
  • The human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the HTLV-1 provirus and transcribed from the 3' long terminal repeat (LTR).
  • We compared the functions of the proteins derived from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.
  • The expression of sHBZ had a growth-promoting function in a T-cell line, while usHBZ expression did not.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / chemistry. Human T-lymphotropic virus 1 / genetics. Sp1 Transcription Factor / metabolism. Transcription, Genetic. Viral Proteins / genetics. Viral Proteins / physiology
  • [MeSH-minor] Alternative Splicing. Base Sequence. Cell Proliferation. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Humans. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Viral / metabolism. Terminal Repeat Sequences

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] Proteomics. 2008 Feb;8(4):626-49 [18203265.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):165-70 [15044019.001]
  • [Cites] Retrovirology. 2008;5:34 [18426605.001]
  • [Cites] J Virol. 2000 Sep;74(18):8277-85 [10954525.001]
  • [Cites] Oncogene. 2000 Aug 17;19(35):3988-98 [10962555.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • [Cites] Ann Hum Genet. 2000 Jan;64(Pt 1):83-6 [11246463.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Annu Rev Biochem. 2003;72:449-79 [12651739.001]
  • [Cites] Cell. 1983 Nov;35(1):79-87 [6313230.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Blood. 1987 Oct;70(4):1069-72 [3115332.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] J Virol. 1991 Aug;65(8):4525-8 [2072462.001]
  • [Cites] Mol Cell Biol. 1991 Oct;11(10):5229-43 [1922043.001]
  • [Cites] New Biol. 1991 Sep;3(9):896-906 [1931834.001]
  • [Cites] J Biol Chem. 1992 Mar 25;267(9):6450 [1348249.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] J Biol Chem. 1995 Aug 18;270(33):19487-94 [7642633.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1001-10 [15592508.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Mar;80(5):2495-505 [16474156.001]
  • [Cites] Gene. 2006 Feb 1;366(2):335-42 [16288839.001]
  • [Cites] Blood. 2006 May 15;107(10):3976-82 [16424388.001]
  • [Cites] Retrovirology. 2006;3:15 [16512901.001]
  • [Cites] J Virol. 2006 Aug;80(15):7427-38 [16840323.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • (PMID = 18653454.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2546946
  •  go-up   go-down


73. Tosi G, Pilotti E, Mortara L, De Lerma Barbaro A, Casoli C, Accolla RS: Inhibition of human T cell leukemia virus type 2 replication by the suppressive action of class II transactivator and nuclear factor Y. Proc Natl Acad Sci U S A; 2006 Aug 22;103(34):12861-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of human T cell leukemia virus type 2 replication by the suppressive action of class II transactivator and nuclear factor Y.
  • The master regulator of MHC-II gene transcription, class II transactivator (CIITA), acts as a potent inhibitor of human T cell leukemia virus type 2 (HTLV-2) replication by blocking the activity of the viral Tax-2 transactivator.
  • Furthermore, we show that Tax-2 specifically cooperates with cAMP response element binding protein-binding protein (CBP) and p300, but not with p300/CBP-associated factor, to enhance transcription from the viral promoter.
  • This finding represents a unique difference with respect to Tax-1, which uses all three coactivators to transactivate the human T cell leukemia virus type 1 LTR.
  • Interestingly, we found that the transcription factor nuclear factor Y, which interacts with CIITA to increase transcription of MHC-II genes, exerts a negative regulatory action on the Tax-2-mediated HTLV-2 LTR transactivation.
  • These findings demonstrate the dual defensive role of CIITA against pathogens: it increases the antigen-presenting function for viral determinants and suppresses HTLV-2 replication in infected cells.
  • [MeSH-major] CCAAT-Binding Factor / metabolism. Human T-lymphotropic virus 2 / physiology. Nuclear Proteins / metabolism. Trans-Activators / metabolism. Transcription Factors / metabolism. Virus Replication
  • [MeSH-minor] Animals. B-Lymphocytes / metabolism. Cell Cycle Proteins / metabolism. Cell Line. Cercopithecus aethiops. Cyclic AMP Response Element-Binding Protein / metabolism. Gene Expression Regulation. Gene Products, tax / metabolism. Histone Acetyltransferases / metabolism. Humans. Promoter Regions, Genetic / genetics. Transcriptional Activation / genetics. p300-CBP Transcription Factors / metabolism

  • Genetic Alliance. consumer health - Factor II Deficiency.
  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 2.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1999 Aug 27;285(5432):1402-5 [10464099.001]
  • [Cites] AIDS Rev. 2004 Jul-Sep;6(3):144-54 [15595431.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] J Virol. 2005 Sep;79(18):11925-34 [16140768.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5931-7 [16155600.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5965-75 [16155603.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5996-6004 [16155606.001]
  • [Cites] Gene. 1999 Oct 18;239(1):15-27 [10571030.001]
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8136-45 [10567539.001]
  • [Cites] Immunity. 2000 Jan;12(1):61-70 [10661406.001]
  • [Cites] J Virol. 2000 Mar;74(6):2655-62 [10684280.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):11852-7 [10766811.001]
  • [Cites] Genes Dev. 2000 May 1;14(9):1156-66 [10809673.001]
  • [Cites] J Virol. 2000 Aug;74(15):6866-74 [10888626.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(16):6051-61 [10913187.001]
  • [Cites] Trends Immunol. 2001 Oct;22(10):560-3 [11574280.001]
  • [Cites] J Virol. 2002 Mar;76(6):2648-53 [11861831.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5616-25 [12101253.001]
  • [Cites] Eur J Immunol. 2002 Oct;32(10):2783-91 [12355430.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5467-76 [12374747.001]
  • [Cites] J Immunol. 2003 Jan 15;170(2):922-30 [12517958.001]
  • [Cites] Int Immunol. 2003 Apr;15(4):467-75 [12663676.001]
  • [Cites] Mol Cell Biol. 2003 May;23(10):3392-404 [12724399.001]
  • [Cites] J Virol. 2003 Nov;77(22):12152-64 [14581552.001]
  • [Cites] Blood. 2004 Feb 1;103(3):995-1001 [14525769.001]
  • [Cites] J Immunol. 2004 May 1;172(9):5528-34 [15100295.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5447-58 [15156194.001]
  • [Cites] J Biol Chem. 2004 Sep 10;279(37):38577-89 [15247301.001]
  • [Cites] J Virol. 2004 Oct;78(19):10399-409 [15367606.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43307-20 [15269214.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Science. 1982 Nov 5;218(4572):571-3 [6981847.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] J Exp Med. 1986 Jul 1;164(1):369-74 [3088202.001]
  • [Cites] Cell. 1987 Sep 11;50(6):863-72 [3476205.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [Cites] J Biol Chem. 1989 Sep 15;264(26):15236-41 [2768259.001]
  • [Cites] Transfusion. 1991 Jan;31(1):67-75 [1986467.001]
  • [Cites] J Infect Dis. 1991 Mar;163(3):435-40 [1995717.001]
  • [Cites] J Clin Invest. 1991 Sep;88(3):1038-42 [1832173.001]
  • [Cites] J Exp Med. 1992 Jul 1;176(1):293-6 [1351922.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11784-8 [1465399.001]
  • [Cites] Cell. 1993 Oct 8;75(1):135-46 [8402893.001]
  • [Cites] Cell. 1994 Jan 28;76(2):287-99 [8293464.001]
  • [Cites] Virology. 1995 Feb 1;206(2):1126-8 [7531916.001]
  • [Cites] Virology. 1995 Jul 10;210(2):441-7 [7542419.001]
  • [Cites] J Virol. 1995 Sep;69(9):5806-11 [7637025.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3619-39 [7579327.001]
  • [Cites] Virology. 1996 Mar 1;217(1):373-9 [8599225.001]
  • [Cites] Nature. 1996 Apr 18;380(6575):642-6 [8602268.001]
  • [Cites] Ann Neurol. 1996 Nov;40(5):714-23 [8957012.001]
  • [Cites] J Virol. 1996 Dec;70(12):8508-17 [8970974.001]
  • [Cites] Mol Cell Biol. 1997 Mar;17(3):1236-43 [9032250.001]
  • [Cites] Cell. 1998 Feb 20;92(4):451-62 [9491887.001]
  • [Cites] Genes Dev. 1998 Jun 1;12(11):1638-51 [9620851.001]
  • [Cites] Mol Cell Biol. 1998 Sep;18(9):5052-61 [9710589.001]
  • [Cites] Mol Cell Biol. 1998 Nov;18(11):6777-83 [9774691.001]
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):34646-52 [9852138.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):941-7 [9858618.001]
  • [Cites] Immunity. 1999 Feb;10(2):163-71 [10072069.001]
  • [Cites] Mol Cell Biol. 2000 Sep;20(17):6587-99 [10938133.001]
  • [Cites] J Immunol. 2000 Sep 1;165(5):2511-7 [10946277.001]
  • [Cites] J Mol Biol. 2000 Sep 22;302(3):539-52 [10986117.001]
  • [Cites] Mol Cell Biol. 2000 Oct;20(20):7716-25 [11003667.001]
  • [Cites] Mol Cell Biol. 2000 Nov;20(22):8489-98 [11046145.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1661-8 [11080807.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):32191-7 [11413136.001]
  • [Cites] J Immunol. 2001 Oct 1;167(7):3626-34 [11564775.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(20):7078-88 [11564890.001]
  • (PMID = 16908858.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Binding Factor; 0 / Cell Cycle Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / MHC class II transactivator protein; 0 / Nuclear Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / nuclear factor Y; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors; EC 2.3.1.48 / p300-CBP-associated factor
  • [Other-IDs] NLM/ PMC1568938
  •  go-up   go-down


74. Pais-Correia AM, Sachse M, Guadagnini S, Robbiati V, Lasserre R, Gessain A, Gout O, Alcover A, Thoulouze MI: Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses. Nat Med; 2010 Jan;16(1):83-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.
  • Human T cell leukemia virus type 1 (HTLV-1) is a lymphotropic retrovirus whose cell-to-cell transmission requires cell contacts.
  • HTLV-1-infected T lymphocytes form 'virological synapses', but the mechanism of HTLV-1 transmission remains poorly understood.
  • We show here that HTLV-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the cell surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.
  • Extracellular viral assemblies rapidly adhere to other cells upon cell contact, allowing virus spread and infection of target cells.
  • Their removal strongly reduces the ability of HTLV-1-producing cells to infect target cells.
  • Our findings unveil a novel virus transmission mechanism based on the generation of extracellular viral particle assemblies whose structure, composition and function resemble those of bacterial biofilms.
  • HTLV-1 biofilm-like structures represent a major route for virus transmission from cell to cell.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Extracellular Matrix / virology. HTLV-I Infections / transmission. Human T-lymphotropic virus 1 / physiology
  • [MeSH-minor] Biofilms. Concanavalin A. Gene Products, env / metabolism. Humans. Microscopy, Electron, Transmission. Virus Assembly / physiology. Virus Attachment. Virus Internalization

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Nat Med. 2010 Jan;16(1):25-7 [20057417.001]
  • (PMID = 20023636.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, env; 11028-71-0 / Concanavalin A
  •  go-up   go-down


75. Yu Q, Minoda Y, Yoshida R, Yoshida H, Iha H, Kobayashi T, Yoshimura A, Takaesu G: HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein. Biochem Biophys Res Commun; 2008 Jan 4;365(1):189-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.
  • Human T cell leukemia virus type 1 (HTLV-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of HTLV-1-infected T lymphocytes.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. MAP Kinase Kinase Kinases / metabolism
  • [MeSH-minor] Binding Sites. Cell Line. Humans. NF-kappa B / metabolism. Ubiquitin-Protein Ligases / metabolism

  • COS Scholar Universe. author profiles.
  • 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 = 17986383.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


76. Murata K, Hayashibara T, Sugahara K, Uemura A, Yamaguchi T, Harasawa H, Hasegawa H, Tsuruda K, Okazaki T, Koji T, Miyanishi T, Yamada Y, Kamihira S: A novel alternative splicing isoform of human T-cell leukemia virus type 1 bZIP factor (HBZ-SI) targets distinct subnuclear localization. J Virol; 2006 Mar;80(5):2495-505
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel alternative splicing isoform of human T-cell leukemia virus type 1 bZIP factor (HBZ-SI) targets distinct subnuclear localization.
  • Adult T-cell leukemia (ATL) is associated with prior infection with human T-cell leukemia virus type 1 (HTLV-1); however, the mechanism by which HTLV-1 causes adult T-cell leukemia has not been fully elucidated.
  • Recently, a functional basic leucine zipper (bZIP) protein coded in the minus strand of HTLV-1 genome (HBZ) was identified.
  • We report here a novel isoform of the HTLV-1 bZIP factor (HBZ), HBZ-SI, identified by means of reverse transcription-PCR (RT-PCR) in conjunction with 5' and 3' rapid amplification of cDNA ends (RACE).
  • HBZ-SI is a 206-amino-acid-long protein and is generated by alternative splicing between part of the HBZ gene and a novel exon located in the 3' long terminal repeat of the HTLV-1 genome.
  • Duplex RT-PCR and real-time quantitative RT-PCR analyses showed that the mRNAs of these isoforms were expressed at equivalent levels in all ATL cell samples examined.
  • Nonetheless, we found by Western blotting that the HBZ-SI protein was preferentially expressed in some ATL cell lines examined.
  • A key finding was obtained from the subcellular localization analyses of these isoforms.
  • These data show the presence of a novel isoform of HBZ in ATL cells, and in addition, shed new light on the possibility that each isoform may play a unique role in distinct regions in the cell nucleus.
  • [MeSH-major] Alternative Splicing. Basic-Leucine Zipper Transcription Factors / genetics. Basic-Leucine Zipper Transcription Factors / metabolism. Cell Nucleus / metabolism. Human T-lymphotropic virus 1 / genetics. RNA Processing, Post-Transcriptional. RNA, Messenger / metabolism. RNA, Viral / metabolism. Viral Proteins / genetics. Viral Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Artificial Gene Fusion. Base Sequence. Biological Transport. Blotting, Western. Cell Line, Tumor. Green Fluorescent Proteins / analysis. Green Fluorescent Proteins / genetics. Humans. Microscopy, Fluorescence. Molecular Sequence Data. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • [Cites] J Cell Sci. 2005 Apr 1;118(Pt 7):1355-62 [15755797.001]
  • [Cites] Virus Genes. 2001;23(2):123-35 [11724264.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Nutr Cancer. 2002;44(2):193-201 [12734068.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):165-70 [15044019.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] J Biol Chem. 2004 Oct 15;279(42):43998-4004 [15308664.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Mar;78(3):1887-91 [6262827.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Crit Rev Microbiol. 1986;12(4):293-320 [3007026.001]
  • [Cites] Adv Virus Res. 1985;30:225-77 [3008524.001]
  • [Cites] Cell. 1987 Jan 30;48(2):343-50 [3026643.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5389-93 [3037548.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Biochim Biophys Acta. 1991 Dec 10;1072(2-3):129-57 [1751545.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 May 1;89(9):4042-6 [1315048.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] Jpn J Cancer Res. 1993 Jan;84(1):4-8 [8449826.001]
  • [Cites] Br J Haematol. 1994 Oct;88(2):234-41 [7803265.001]
  • [Cites] Blood. 1995 May 15;85(10):2699-704 [7742529.001]
  • [Cites] Blood. 1996 Sep 1;88(5):1551-60 [8781409.001]
  • [Cites] Leuk Lymphoma. 1996 May;21(5-6):443-7 [9172809.001]
  • [Cites] Int J Cancer. 1996 Sep 27;68(1):102-8 [8895548.001]
  • [Cites] J Virol. 1997 Apr;71(4):3188-96 [9060682.001]
  • [Cites] J Virol. 1998 Jan;72(1):388-95 [9420237.001]
  • [Cites] EMBO J. 1998 Mar 2;17(5):1476-86 [9482744.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3620-32 [9584203.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1001-10 [15592508.001]
  • [Cites] J Biol Chem. 2001 May 25;276(21):17920-31 [11279020.001]
  • (PMID = 16474156.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB219938
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ PMC1395368
  •  go-up   go-down


77. Kanazawa S, Yamaguchi K, Kinoshita Y, Nomura S: Adult T-cell leukaemia and strongyloidiasis. Eur J Cancer Care (Engl); 2008 Mar;17(2):209-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukaemia and strongyloidiasis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / parasitology. Lung Diseases, Parasitic / parasitology. Opportunistic Infections / parasitology. Strongyloidiasis / complications
  • [MeSH-minor] Anthelmintics / therapeutic use. Female. Human T-lymphotropic virus 1. Humans. Middle Aged. Thiabendazole / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Strongyloidiasis.
  • Hazardous Substances Data Bank. THIABENDAZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18302660.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthelmintics; N1Q45E87DT / Thiabendazole
  •  go-up   go-down


78. Ishitsuka K, Fukushima T, Tsukasaki K, Tobinai K: Is zidovudine and interferon-alfa the gold standard for adult T-cell leukemia-lymphoma? J Clin Oncol; 2010 Dec 20;28(36):e765; author reply e766
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is zidovudine and interferon-alfa the gold standard for adult T-cell leukemia-lymphoma?
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Zidovudine / therapeutic use
  • [MeSH-minor] Adult. Humans

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. ZIDOVUDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] J Clin Oncol. 2010 Sep 20;28(27):4177-83 [20585095.001]
  • (PMID = 20921454.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine
  •  go-up   go-down


79. Mizobe T, Tsukada J, Higashi T, Mouri F, Matsuura A, Tanikawa R, Minami Y, Yoshida Y, Tanaka Y: Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells. Exp Hematol; 2007 Dec;35(12):1812-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells.
  • OBJECTIVE: Constitutive activation of nuclear factor (NF)-kappaB is a common feature of human T-cell leukemia virus type I (HTLV-I)-transformed T cells.
  • Inhibition of NF-kappaB activity reduces cell growth and induces apoptosis of HTLV-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.
  • In this study, we investigated whether MyD88, an adaptor protein of Toll-like receptor (TLR) signaling, contributes to constitutive NF-kappaB activation in HTLV-I-transformed T cells.
  • MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-associated kinase 1 (IRAK1) in HTLV-I-transformed human T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.
  • An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in HTLV-I-transformed T cells.
  • RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of HTLV-I-transformed T cells, but not in HTLV-I-negative T cells, such as Jurkat, HUT78, and MOLT4.
  • HTLV-I Tax enhanced TLR expression and synergistically activated NF-kappaB with wild-type MyD88.
  • CONCLUSION: Our results show a novel pathway in NF-kappaB activation in HTLV-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Interleukin-1 Receptor-Associated Kinases / metabolism. Myeloid Differentiation Factor 88 / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Transformed. Cell Transformation, Viral. DNA Primers. Humans. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / metabolism

  • 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 = 17920759.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
  •  go-up   go-down


80. Silic-Benussi M, Cannizzaro E, Venerando A, Cavallari I, Petronilli V, La Rocca N, Marin O, Chieco-Bianchi L, Di Lisa F, D'Agostino DM, Bernardi P, Ciminale V: Modulation of mitochondrial K(+) permeability and reactive oxygen species production by the p13 protein of human T-cell leukemia virus type 1. Biochim Biophys Acta; 2009 Jul;1787(7):947-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of mitochondrial K(+) permeability and reactive oxygen species production by the p13 protein of human T-cell leukemia virus type 1.
  • Human T-cell leukemia virus type-1 (HTLV-1) expresses an 87-amino acid protein named p13 that is targeted to the inner mitochondrial membrane.
  • The downstream consequences of p13-induced mitochondrial K(+) permeability are likely to have an important influence on the redox state and turnover of HTLV-1-infected cells.
  • [MeSH-major] Human T-lymphotropic virus 1. Mitochondria / metabolism. Mitochondrial Membrane Transport Proteins / metabolism. Potassium / metabolism. Reactive Oxygen Species / metabolism

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • MedlinePlus Health Information. consumer health - Potassium.
  • Hazardous Substances Data Bank. VALINOMYCIN .
  • Hazardous Substances Data Bank. POTASSIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19366603.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ionophores; 0 / Mitochondrial Membrane Transport Proteins; 0 / Potassium Channels; 0 / Reactive Oxygen Species; 0 / mitochondrial permeability transition pore; 2001-95-8 / Valinomycin; 370-86-5 / Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; RWP5GA015D / Potassium; SY7Q814VUP / Calcium
  •  go-up   go-down


81. Takeuchi S, Matsushita M, Tsukasaki K, Takeuchi N, Tomonaga M, Komatsu N, Ikezoe T, Uehara Y, Koeffler HP: P53 codon 72 polymorphism is associated with disease progression in adult T-cell leukaemia/lymphoma. Br J Haematol; 2005 Nov;131(4):552-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P53 codon 72 polymorphism is associated with disease progression in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Genes, p53. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Codon. Disease Progression. Humans. Polymorphism, Genetic

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16281948.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon
  •  go-up   go-down


82. Bolinger C, Yilmaz A, Hartman TR, Kovacic MB, Fernandez S, Ye J, Forget M, Green PL, Boris-Lawrie K: RNA helicase A interacts with divergent lymphotropic retroviruses and promotes translation of human T-cell leukemia virus type 1. Nucleic Acids Res; 2007;35(8):2629-42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RNA helicase A interacts with divergent lymphotropic retroviruses and promotes translation of human T-cell leukemia virus type 1.
  • Here, stringent RNA and protein analyses determined the 5' UTR of spleen necrosis virus (SNV), reticuloendotheliosis virus A (REV-A) and human T-cell leukemia virus type 1 (HTLV-1) exhibit PCE activity, but not IRES activity.
  • Experiments with siRNAs identified that REV-A and HTLV-1 PCE modulate post-transcriptional gene expression through interaction with host RNA helicase A (RHA).
  • Analysis of hybrid SNV/HTLV-1 proviruses determined SNV PCE facilitates Rex/Rex responsive element-independent Gag production and interaction with RHA is necessary.
  • Ribosomal profile analyses determined that RHA is necessary for polysome association of HTLV-1 gag and provide direct evidence that RHA is necessary for efficient HTLV-1 replication.
  • We conclude that PCE/RHA is an important translation regulatory axis of multiple lymphotropic retroviruses.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Dec 1;102(12):3963-9 [12907436.001]
  • [Cites] J Virol. 2003 Nov;77(22):11973-84 [14581534.001]
  • [Cites] Mol Cell Biol. 2000 Jan;20(2):496-506 [10611228.001]
  • [Cites] J Virol. 2000 Jan;74(2):846-50 [10623747.001]
  • [Cites] J Biotechnol. 2000 Feb 17;77(2-3):179-89 [10682278.001]
  • [Cites] Oncogene. 2000 Feb 17;19(7):899-905 [10702798.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):11899-906 [10766817.001]
  • [Cites] RNA. 2004 Mar;10(3):469-81 [14970392.001]
  • [Cites] RNA. 2004 Apr;10(4):720-30 [15037781.001]
  • [Cites] Mol Cell Biol. 2004 Jun;24(12):5595-605 [15169918.001]
  • [Cites] J Biol Chem. 2004 Jul 9;279(28):29066-74 [15123638.001]
  • [Cites] Mol Cell Biol. 1984 Apr;4(4):743-8 [6325894.001]
  • [Cites] Cell. 1985 Mar;40(3):515-26 [2982496.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 May;83(9):2850-4 [3458245.001]
  • [Cites] J Virol. 1988 Aug;62(8):2636-43 [2839690.001]
  • [Cites] Nature. 1988 Jul 28;334(6180):320-5 [2839775.001]
  • [Cites] EMBO J. 1988 Sep;7(9):2831-7 [3181141.001]
  • [Cites] J Cell Biol. 1989 Feb;108(2):229-41 [2645293.001]
  • [Cites] EMBO J. 1990 Nov;9(11):3753-9 [2170120.001]
  • [Cites] Genes Dev. 1990 Sep;4(9):1560-72 [2174810.001]
  • [Cites] Nature. 1991 Sep 5;353(6339):90-4 [1652694.001]
  • [Cites] Nucleic Acids Res. 1992 Aug 25;20(16):4291-7 [1354856.001]
  • [Cites] Virology. 1994 May 1;200(2):632-42 [8178449.001]
  • [Cites] J Virol. 1995 Mar;69(3):1920-4 [7853535.001]
  • [Cites] J Virol. 1995 Apr;69(4):2214-22 [7884868.001]
  • [Cites] J Biol Chem. 1995 Sep 1;270(35):20376-83 [7657611.001]
  • [Cites] J Virol. 1995 Oct;69(10):6400-7 [7666541.001]
  • [Cites] J Biol Chem. 1996 Jan 12;271(2):623-6 [8557663.001]
  • [Cites] J Virol. 1996 Feb;70(2):944-51 [8551634.001]
  • [Cites] FEBS Lett. 1996 Sep 2;392(3):220-4 [8774848.001]
  • [Cites] J Virol. 1997 Feb;71(2):1514-20 [8995677.001]
  • [Cites] Hum Gene Ther. 1997 Nov 1;8(16):1855-65 [9382952.001]
  • [Cites] J Biol Chem. 1997 Dec 19;272(51):32061-6 [9405401.001]
  • [Cites] Oncogene. 1998 Jan 22;16(3):423-8 [9467968.001]
  • [Cites] J Virol. 1999 Jun;73(6):4847-55 [10233946.001]
  • [Cites] J Biol Chem. 2005 Feb 11;280(6):4144-53 [15525641.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5996-6004 [16155606.001]
  • [Cites] Nat Struct Mol Biol. 2005 Nov;12(11):1001-7 [16244661.001]
  • [Cites] Retrovirology. 2006;3:13 [16480517.001]
  • [Cites] Curr HIV Res. 2006 Apr;4(2):131-9 [16611053.001]
  • [Cites] J Biol Chem. 2006 May 5;281(18):12625-35 [16527808.001]
  • [Cites] Nat Struct Mol Biol. 2006 Jun;13(6):509-16 [16680162.001]
  • [Cites] J Virol. 2000 Jul;74(13):5796-801 [10846058.001]
  • [Cites] J Virol. 2000 Sep;74(17):8111-8 [10933721.001]
  • [Cites] Curr Opin Microbiol. 2000 Aug;3(4):366-70 [10972496.001]
  • [Cites] J Virol. 2000 Dec;74(24):11581-8 [11090156.001]
  • [Cites] J Virol. 2001 Jan;75(1):181-91 [11119587.001]
  • [Cites] J Virol. 2001 Aug;75(15):6817-24 [11435560.001]
  • [Cites] Life Sci. 2001 Oct 26;69(23):2697-709 [11720075.001]
  • [Cites] J Virol. 2002 Apr;76(7):3292-300 [11884554.001]
  • [Cites] J Virol. 2002 Oct;76(20):10211-8 [12239296.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 15;31(2):639-46 [12527772.001]
  • [Cites] J Virol. 2003 Apr;77(7):3939-49 [12634354.001]
  • [Cites] J Biol Chem. 2003 Oct 10;278(41):39330-6 [12857733.001]
  • [Cites] Virology. 2003 Dec 5;317(1):146-54 [14675633.001]
  • (PMID = 17426138.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / P01CA16058; United States / NCI NIH HHS / CA / P30CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / Gene Products, gag; 0 / RNA, Viral; EC 3.6.4.13 / RNA Helicases
  • [Other-IDs] NLM/ PMC1885656
  •  go-up   go-down


83. Patronas M, Smith JA, Levy-Clarke GA, Reed GF, Buggage RR: Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1. Am J Ophthalmol; 2006 Dec;142(6):1088-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1.
  • PURPOSE: To investigate the relationship between serum immunoglobulin levels and corneal opacities in a cohort of patients with human T-cell lymphotrophic virus type-1 (HTLV-1).
  • METHODS: Complete ophthalmologic examination was performed on 44 patients with HTLV-1 infection (25 patients with adult T-cell leukemia/lymphoma [ATL], 18 patients with HTLV-1 that was associated myelopathy/tropical spastic paraparesis [HAM/TSP], and one patient who was asymptomatic).
  • RESULTS: Corneal opacities were identified in 15 of 25 patients (60%) with ATL and five of 18 patients (28%) with HAM/TSP.
  • The prevalence of corneal opacities was associated statistically with elevated IgG level (P = .023) in patients with ATL, but not in patients with HAM/TSP (P > .99).
  • CONCLUSION: Although the mechanism remains unclear, hypergammaglobulinemia is associated with the development of the corneal opacities in patients of African descent with ATL.
  • [MeSH-major] Corneal Opacity / etiology. HTLV-I Infections / complications. Hypergammaglobulinemia / etiology
  • [MeSH-minor] Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunoglobulin A / blood. Immunoglobulin G / blood. Immunoglobulin M / blood. Nephelometry and Turbidimetry. Prevalence. Retrospective Studies

  • 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 = 17157606.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M
  •  go-up   go-down


84. Okamura J, Uike N, Utsunomiya A, Tanosaki R: Allogeneic stem cell transplantation for adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Aug;86(2):118-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic stem cell transplantation for adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) develops in elderly individuals who have been infected with human T-cell leukemia virus type 1 (HTLV-1), and the prognosis for patients with ATLL has been extremely poor.
  • Retrospective studies of allogeneic stem cell transplantation (alloSCT) for selected populations of patients have achieved several encouraging results; however, the reported incidence of transplantation-related mortality (TRM) have been high, even though more than 80% of patients received stem cells from related donors and the patients were relatively young for ATLL.
  • This report documents a prospective feasibility study of alloSCT with reduced-intensity conditioning (RIST) for elderly ATLL patients (>50 years).
  • The HTLV-1 proviral load became undetectable in 8 of 15 patients, suggesting that RIST has potential as an antiviral treatment.
  • It is clear that a graft-versus-ATLL effect is present after alloSCT, regardless of the conditioning regimen or the stem cell source.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy

  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Hematol. 2002 Jul;76(1):91-3 [12138903.001]
  • [Cites] Bone Marrow Transplant. 1987 Dec;2(4):441-4 [3332192.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1):90-9 [17222757.001]
  • [Cites] Int J Hematol. 2005 Nov;82(4):357-61 [16298831.001]
  • [Cites] Cancer Sci. 2005 May;96(5):249-55 [15904464.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):304-9 [12542491.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Cancer Sci. 2004 Jul;95(7):596-601 [15245597.001]
  • [Cites] Bone Marrow Transplant. 2006 Jan;37(1):41-4 [16247419.001]
  • [Cites] N Engl J Med. 2006 Apr 20;354(16):1758-9 [16625020.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2817-24 [9704734.001]
  • [Cites] Blood. 1998 Feb 1;91(3):756-63 [9446633.001]
  • [Cites] Bone Marrow Transplant. 1999 Jan;23(1):87-9 [10037056.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • (PMID = 17875524.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Number-of-references] 19
  •  go-up   go-down


85. Tabata R, Tabata C, Namiuchi S, Terada M, Yasumizu R, Okamoto T, Nagai T: Adult T-cell lymphoma mimicking Henoch-Schönlein purpura. Mod Rheumatol; 2007;17(1):57-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell lymphoma mimicking Henoch-Schönlein purpura.
  • We report a male patient with adult T-cell lymphoma, who was initially diagnosed clinically as having Henoch-Schönlein purpura (HSP) with abdominal pain and specific purpura.
  • Adult T-cell lymphoma-like cells were minimal and abdominal lymph nodes were transiently swollen, and the symptoms were improved by supportive management.
  • Although the clinical course was compatible with HSP, the histological examination revealed infiltration of lymphocytes rather than neutrophils.
  • Later he developed lymphoma and was treated with chemotherapy.
  • This rare case suggests the importance of skin biopsies to seek the underlying pathology in adult HSP.

  • Genetic Alliance. consumer health - Henoch-Schonlein purpura.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17278024.001).
  • [ISSN] 1439-7595
  • [Journal-full-title] Modern rheumatology
  • [ISO-abbreviation] Mod Rheumatol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


86. Ohno H, Nagata N, Isoda K: Epstein-Barr virus-associated T-cell lymphoma in an adult patient: prominent infiltrates within the liver portal area revealed by autopsy. Int J Hematol; 2008 Jul;88(1):88-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epstein-Barr virus-associated T-cell lymphoma in an adult patient: prominent infiltrates within the liver portal area revealed by autopsy.
  • In situ hybridization detected Epstein-Barr virus (EBV)-encoded RNA-positive cells in the liver and spleen as well as the bone marrow obtained before his death.
  • These observations indicate that EBV-associated T-cell lymphoma expressing cytotoxic proteins was the underlying disorder.
  • Prominent portal involvement was most likely responsible for the fatal clinical outcome of this patient.
  • [MeSH-major] Epstein-Barr Virus Infections / metabolism. Epstein-Barr Virus Infections / pathology. Herpesvirus 4, Human / metabolism. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Lymphoma, T-Cell / metabolism. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Antigens, Differentiation / metabolism. Autopsy. Fatal Outcome. Humans. Liver / metabolism. Liver / pathology. Liver Failure, Acute / metabolism. Liver Failure, Acute / pathology. Liver Failure, Acute / virology. Male

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Dec 15;102(13):4261-9 [12907441.001]
  • [Cites] Haematologica. 1997 Sep-Oct;82(5):572-6 [9407723.001]
  • [Cites] Br J Haematol. 1995 May;90(1):48-55 [7786795.001]
  • [Cites] Blood. 2001 Jul 15;98(2):280-6 [11435294.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:317-22 [17124078.001]
  • [Cites] Histopathology. 2000 Feb;36(2):127-35 [10672057.001]
  • [Cites] Histopathology. 1998 Apr;32(4):310-6 [9602326.001]
  • [Cites] Blood. 1990 Nov 15;76(10):2163-4 [2242437.001]
  • [Cites] Blood. 1990 Jan 15;75(2):434-44 [2153036.001]
  • [Cites] Radiology. 2004 Mar;230(3):685-9 [14990835.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:260-6 [16304390.001]
  • [Cites] Cancer Sci. 2007 Sep;98(9):1281-7 [17627615.001]
  • [Cites] Blood. 2000 Jul 15;96(2):443-51 [10887104.001]
  • [Cites] Blood. 1991 Feb 15;77(4):799-808 [1847084.001]
  • [Cites] Int J Oncol. 2004 May;24(5):1165-74 [15067338.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2085-91 [9490694.001]
  • [Cites] Pathol Int. 1998 Dec;48(12):934-43 [9952337.001]
  • (PMID = 18597053.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Differentiation
  •  go-up   go-down


87. Rice KL, Izon DJ, Ford J, Boodhoo A, Kees UR, Greene WK: Overexpression of stem cell associated ALDH1A1, a target of the leukemogenic transcription factor TLX1/HOX11, inhibits lymphopoiesis and promotes myelopoiesis in murine hematopoietic progenitors. Leuk Res; 2008 Jun;32(6):873-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of stem cell associated ALDH1A1, a target of the leukemogenic transcription factor TLX1/HOX11, inhibits lymphopoiesis and promotes myelopoiesis in murine hematopoietic progenitors.
  • TLX1/HOX11 is an oncogenic transcription factor in human T-cell leukemia, however, the molecular basis for its transforming activity has remained elusive.
  • Together, these data demonstrate that ALDH1A1 plays a key role in normal hematopoiesis, and confirm ALDH1A1 as a TLX1 transcriptional target that may contribute to the ability of this homeoprotein to alter cell fate and induce tumor growth.
  • [MeSH-major] Aldehyde Dehydrogenase / genetics. Hematopoietic Stem Cells / metabolism. Homeodomain Proteins / physiology. Leukemia, Erythroblastic, Acute / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Lymphopoiesis / physiology. Myelopoiesis / physiology. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Differentiation. Cell Proliferation. Cells, Cultured. DNA Primers. Female. Flow Cytometry. Gene Expression Regulation. Humans. Mice. Mice, Inbred C57BL. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Spleen / cytology. Spleen / metabolism

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18082256.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 143275-75-6 / TLX1 protein, human; EC 1.2.1.3 / ALDH1A1 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  •  go-up   go-down


88. Masutani H, Ueda S, Yodoi J: The thioredoxin system in retroviral infection and apoptosis. Cell Death Differ; 2005 Aug;12 Suppl 1:991-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Human thioredoxin (TRX) was first identified in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and is associated with the pathophysiology of retroviral infections.
  • Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in HTLV-I-transformed cells.
  • Studies of these molecules of the TRX system provide novel insights into the apoptosis associated with retroviral diseases.
  • [MeSH-minor] Animals. Glutathione / metabolism. HIV Infections / metabolism. HTLV-I Infections / metabolism. Humans. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Proteins / metabolism. Peroxidases / metabolism. Peroxiredoxins

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15818395.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 52500-60-4 / Thioredoxins; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; GAN16C9B8O / Glutathione
  • [Number-of-references] 93
  •  go-up   go-down


89. Kawai K, Uchida Y, Yonekura K, Virtanen S, Tähtinen M, Krohn K, Ranki A, Kanekura T: Cutaneous-type adult T-cell leukemia/lymphoma does not primarily show deletion of NAV3 gene. J Invest Dermatol; 2010 Jan;130(1):316-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous-type adult T-cell leukemia/lymphoma does not primarily show deletion of NAV3 gene.
  • [MeSH-major] Gene Deletion. Leukemia-Lymphoma, Adult T-Cell / genetics. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics. Skin Neoplasms / genetics

  • Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19626031.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / NAV3 protein, human; 0 / Nerve Tissue Proteins
  •  go-up   go-down


90. Chiba K, Hashino S, Izumiyama K, Toyoshima N, Suzuki S, Kurosawa M, Asaka M: Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia. Int J Lab Hematol; 2009 Jun;31(3):368-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia.
  • A 37-year-old woman was diagnosed as having chronic adult T-cell leukemia (ATL) of the skin by a skin biopsy and human T-cell leukemia virus type-1 serology at our hospital in August 1992.
  • The skin lesions of ATL were improved by treatment with psoralen ultraviolet ray A.
  • [MeSH-major] Chemokines / blood. Interleukin-6 / blood. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / complications. Osteolysis / blood. Osteolysis / etiology
  • [MeSH-minor] Adult. Chronic Disease. Fatal Outcome. Female. Humans

  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18177436.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Interleukin-6
  •  go-up   go-down


91. Kinpara S, Hasegawa A, Utsunomiya A, Nishitsuji H, Furukawa H, Masuda T, Kannagi M: Stromal cell-mediated suppression of human T-cell leukemia virus type 1 expression in vitro and in vivo by type I interferon. J Virol; 2009 May;83(10):5101-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stromal cell-mediated suppression of human T-cell leukemia virus type 1 expression in vitro and in vivo by type I interferon.
  • Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL), HTLV-1-associated myelopathy/tropical spastic paraparesis, and other inflammatory diseases.
  • Despite such severe outcomes of HTLV-1 infection, the level of HTLV-1 expression in vivo is very low and rapidly increases after transfer of cells to culture conditions.
  • In the present study, we found that human and mouse stromal cells, such as epithelial cells and fibroblasts, suppressed HTLV-1 expression in ATL and non-ATL HTLV-1-infected cells.
  • HTLV-1 mRNA and proteins in HTLV-1-infected cells markedly decreased upon coculture with human epithelial-like cells (HEK293T) or mouse embryo fibroblasts (NIH 3T3).
  • Spontaneous induction of HTLV-1 expression in primary ATL cells in the first 24 h of culture was also inhibited by coculture with HEK293T cells.
  • Coculture of HTLV-1-infected cells and HEK293T cells induced type I interferon responses, as detected by beta interferon (IFN-beta) promoter activation and IFN-stimulated gene upregulation.
  • HEK293T-mediated suppression of HTLV-1 expression was partly inhibited by antibodies to human IFN-alpha/beta receptor.
  • Furthermore, viral expression in HTLV-1-infected cells was significantly suppressed when the infected cells were intraperitoneally injected into wild-type mice but not IFN regulatory factor 7 knockout mice that are deficient of type I IFN responses.
  • These findings indicate that the innate immune system suppresses HTLV-1 expression in vivo, at least through type I IFN.
  • [MeSH-major] Human T-lymphotropic virus 1 / immunology. Interferon-beta / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Stromal Cells / immunology

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • COS Scholar Universe. author profiles.
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Feb 15;95(4):1386-92 [10666215.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):207-17 [11325603.001]
  • [Cites] J Virol. 2002 Mar;76(6):2703-13 [11861837.001]
  • [Cites] J Neurovirol. 2003 Oct;9(5):530-8 [13129767.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] J Virol. 2004 Apr;78(8):3827-36 [15047798.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):568-75 [15147371.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6035-46 [16155610.001]
  • [Cites] Virology. 2006 Feb 20;345(2):457-67 [16297951.001]
  • [Cites] Am J Pathol. 2006 Jul;169(1):189-99 [16816372.001]
  • [Cites] J Immunol Methods. 2006 Jun 30;313(1-2):61-73 [16723135.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] FEBS Lett. 2007 Nov 13;581(27):5207-12 [17950728.001]
  • [Cites] Virology. 2008 Sep 30;379(2):306-13 [18678383.001]
  • [Cites] Int J Hematol. 2008 Dec;88(5):551-64 [19043810.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Gan. 1981 Dec;72(6):978-81 [6281119.001]
  • [Cites] Gan. 1982 Apr;73(2):341-4 [6981536.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2277-81 [2986109.001]
  • [Cites] Science. 1985 Jun 21;228(4706):1430-4 [2990028.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Microbiol Immunol. 1986;30(4):373-88 [2425230.001]
  • [Cites] J Clin Invest. 1988 Jan;81(1):52-61 [2891729.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5620-4 [2787512.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Arch Virol. 1990;115(1-2):63-73 [1701080.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3536-41 [8622971.001]
  • [Cites] J Biochem. 1996 Jul;120(1):160-9 [8864859.001]
  • [Cites] Nature. 2005 Apr 7;434(7034):772-7 [15800576.001]
  • [Cites] J Med Virol. 2000 Oct;62(2):286-92 [11002260.001]
  • (PMID = 19264779.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 156986-95-7 / Receptor, Interferon alpha-beta; 77238-31-4 / Interferon-beta
  • [Other-IDs] NLM/ PMC2682107
  •  go-up   go-down


92. Sheleg SV, Peloponese JM, Chi YH, Li Y, Eckhaus M, Jeang KT: Evidence for cooperative transforming activity of the human pituitary tumor transforming gene and human T-cell leukemia virus type 1 Tax. J Virol; 2007 Aug;81(15):7894-901
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for cooperative transforming activity of the human pituitary tumor transforming gene and human T-cell leukemia virus type 1 Tax.
  • Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that primarily infects CD4+ T lymphocytes and causes adult T-cell leukemia.
  • Here, we report that overexpression of human PTTG cooperated with the HTLV-I Tax oncoprotein in cellular transformation.
  • [MeSH-major] Cell Transformation, Neoplastic. Gene Products, tax / metabolism. Neoplasm Proteins
  • [MeSH-minor] Adult. Animals. Cell Line. Female. Gene Expression Regulation. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Nude. Neoplasms / genetics. Neoplasms / metabolism. Neoplasms / pathology. Securin

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Retrovirology. 2005;2:54 [16164752.001]
  • [Cites] J Virol. 2005 Dec;79(23):14473-81 [16282446.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18974-9 [16365316.001]
  • [Cites] Oncogene. 1991 Jun;6(6):1023-9 [1906155.001]
  • [Cites] Virology. 1993 Mar;193(1):456-9 [8438579.001]
  • [Cites] Oncogene. 1993 Nov;8(11):3029-36 [8414503.001]
  • [Cites] Oncogene. 2006 Apr 6;25(15):2137-47 [16288203.001]
  • [Cites] Clin Med Res. 2006 Jun;4(2):130-7 [16809406.001]
  • [Cites] Nat Cell Biol. 2006 Jul;8(7):717-24 [16767081.001]
  • [Cites] Cancer Sci. 2006 Sep;97(9):836-41 [16805820.001]
  • [Cites] Retrovirology. 2006;3:50 [16899128.001]
  • [Cites] J Clin Invest. 2006 Nov;116(11):2972-84 [17039256.001]
  • [Cites] Oncogene. 2000 Mar 16;19(12):1491-9 [10734308.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1633-8 [11080803.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):36502-5 [11013229.001]
  • [Cites] J Virol. 2001 Jan;75(1):396-407 [11119608.001]
  • [Cites] Brain Pathol. 2001 Jul;11(3):328-41 [11414475.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] Nat Cell Biol. 2001 Sep;3(9):771-7 [11533655.001]
  • [Cites] Cell. 2002 Jan 25;108(2):207-20 [11832211.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5187-93 [11729202.001]
  • [Cites] Mol Cell Biol. 2002 May;22(10):3327-38 [11971966.001]
  • [Cites] Science. 2002 Jul 26;297(5581):559-65 [12142526.001]
  • [Cites] J Biomed Sci. 2002 Jul-Aug;9(4):292-8 [12145525.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):222-4 [12355078.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):306-11 [12355087.001]
  • [Cites] Histol Histopathol. 2003 Jan;18(1):245-51 [12507303.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Endocrinology. 2000 Feb;141(2):763-71 [10650958.001]
  • [Cites] Curr Opin Oncol. 2000 Jan;12(1):82-8 [10687734.001]
  • [Cites] Lancet. 2000 Feb 26;355(9205):716-9 [10703804.001]
  • [Cites] Semin Cancer Biol. 1999 Dec;9(6):405-11 [10712887.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7459-61 [10713046.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(15):5269-81 [12861013.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Cancer Lett. 2003 Dec 30;202(2):213-8 [14643451.001]
  • [Cites] Oncogene. 2003 Dec 4;22(55):8912-23 [14654787.001]
  • [Cites] J Virol Methods. 2004 Mar 15;116(2):195-202 [14738988.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4539-46 [15231664.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Cell. 1974 Dec;3(4):355-9 [4442124.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Science. 1990 Mar 2;247(4946):1082-4 [2309119.001]
  • [Cites] Intern Med. 1996 Sep;35(9):677-8 [8915690.001]
  • [Cites] Genes Dev. 1996 Dec 15;10(24):3081-93 [8985178.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795.001]
  • [Cites] Nature. 1997 Apr 10;386(6625):623-7 [9121588.001]
  • [Cites] FEBS Lett. 1997 Apr 14;406(3):263-6 [9136898.001]
  • [Cites] J Virol. 1997 Jun;71(6):4445-51 [9151835.001]
  • [Cites] Oncogene. 1997 Sep;15(11):1295-302 [9315097.001]
  • [Cites] Virology. 1997 Dec 8;239(1):97-107 [9426450.001]
  • [Cites] J Virol. 1998 Feb;72(2):1165-70 [9445014.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3620-32 [9584203.001]
  • [Cites] J Virol. 1998 Nov;72(11):8852-60 [9765430.001]
  • [Cites] Science. 1998 Nov 20;282(5393):1497-501 [9822382.001]
  • [Cites] Nature. 1998 Dec 17;396(6712):643-9 [9872311.001]
  • [Cites] Mol Endocrinol. 1999 Jan;13(1):156-66 [9892021.001]
  • [Cites] Nature. 1999 Jul 1;400(6739):37-42 [10403247.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • [Cites] Oncogene. 1999 Sep 23;18(39):5473-6 [10498901.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):338-41 [15549096.001]
  • [Cites] Semin Cancer Biol. 2005 Feb;15(1):1 [15613282.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):63-8 [15623561.001]
  • [Cites] J Virol. 2005 Jul;79(14):9346-50 [15994832.001]
  • [Cites] Retrovirology. 2004;1:6 [15169570.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5965-75 [16155603.001]
  • (PMID = 17507465.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human
  • [Other-IDs] NLM/ PMC1951308
  •  go-up   go-down


93. Miyatake Y, Ikeda H, Ishizu A, Baba T, Ichihashi T, Suzuki A, Tomaru U, Kasahara M, Yoshiki T: Role of neuronal interferon-gamma in the development of myelopathy in rats infected with human T-cell leukemia virus type 1. Am J Pathol; 2006 Jul;169(1):189-99
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of neuronal interferon-gamma in the development of myelopathy in rats infected with human T-cell leukemia virus type 1.
  • Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of not only adult T-cell leukemia but also HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
  • Among the rat strains infected with HTLV-1, chronic progressive myelopathy, named HAM rat disease, occurs exclusively in WKAH rats.
  • In the present study, we found that HTLV-1 infection induces interferon (IFN)-gamma production in the spinal cords of HAM-resistant strains but not in those of WKAH rats.
  • Neurons were the major cells that produced IFN-gamma in HTLV-1-infected, HAM-resistant strains.
  • Administration of IFN-gamma suppressed expression of pX, the gene critically involved in the onset of HAM rat disease, in an HTLV-1-immortalized rat T-cell line, indicating that IFN-gamma protects against the development of HAM rat disease.
  • Specifically, WKAH-derived spinal cord cells were unable to up-regulate the IL-12 receptor beta2 gene in response to IL-12 stimulation.
  • We suggest that the failure of spinal cord neurons to produce IFN-gamma through the IL-12 pathway is involved in the development of HAM rat disease.
  • [MeSH-major] HTLV-I Infections / physiopathology. Interferon-gamma / biosynthesis. Interleukin-12 / metabolism. Neurons / secretion. Spinal Cord Diseases / virology
  • [MeSH-minor] Animals. Base Sequence. Brain / metabolism. Cell Line. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Gene Expression / physiology. Genes, pX. Human T-lymphotropic virus 1. Microscopy, Confocal. Molecular Sequence Data. RNA, Messenger / analysis. Rats. Rats, Inbred Strains. Receptors, Interleukin / biosynthesis. Receptors, Interleukin / genetics. Receptors, Interleukin-12. Reverse Transcriptase Polymerase Chain Reaction. Spinal Cord / chemistry. Spinal Cord / metabolism. Spinal Cord / pathology. T-Lymphocytes / metabolism. T-Lymphocytes / virology

  • MedlinePlus Health Information. consumer health - Spinal Cord Diseases.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurol Sci. 2003 Nov 15;215(1-2):95-103 [14568135.001]
  • [Cites] Tissue Antigens. 2004 Jun;63(6):538-46 [15140029.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Lancet. 1987 Apr 18;1(8538):893-5 [2882294.001]
  • [Cites] Lancet. 1987 Nov 21;2(8569):1220 [2890850.001]
  • [Cites] Lancet. 1988 Jan 23;1(8578):177 [2893008.001]
  • [Cites] Scand J Immunol. 2000 Jan;51(1):29-35 [10632973.001]
  • [Cites] J Neurocytol. 1998 Oct;27(10):749-59 [10640190.001]
  • [Cites] J Neuroimmunol. 2000 Jul 1;106(1-2):105-13 [10814788.001]
  • [Cites] APMIS. 2000 Jun;108(6):459-66 [11028810.001]
  • [Cites] Mol Cell Neurosci. 2000 Oct;16(4):338-49 [11085872.001]
  • [Cites] J Neurotrauma. 2001 Mar;18(3):351-9 [11284554.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34509-16 [11438525.001]
  • [Cites] Trends Immunol. 2001 Oct;22(10):556-60 [11574279.001]
  • [Cites] J Biol Rhythms. 2001 Oct;16(5):444-56 [11669418.001]
  • [Cites] J Interferon Cytokine Res. 2002 Jan;22(1):5-14 [11846971.001]
  • [Cites] J Virol. 2002 May;76(9):4497-506 [11932415.001]
  • [Cites] J Infect Dis. 2002 Dec 1;186 Suppl 2:S187-92 [12424696.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Oct;14(5):361-8 [12948519.001]
  • [Cites] J Neurovirol. 2003 Oct;9(5):530-8 [13129767.001]
  • [Cites] Lancet. 1989 Feb 25;1(8635):441 [2563817.001]
  • [Cites] Lancet. 1989 Nov 18;2(8673):1184-7 [2572904.001]
  • [Cites] Brain Res. 1990 May 7;515(1-2):347-50 [2113417.001]
  • [Cites] Lancet. 1990 Dec 1;336(8727):1345-7 [1978165.001]
  • [Cites] Dev Biol. 1991 Apr;144(2):412-23 [1901286.001]
  • [Cites] Neuroscience. 1991;45(3):551-60 [1775233.001]
  • [Cites] Jpn J Cancer Res. 1992 Mar;83(3):236-9 [1582883.001]
  • [Cites] J Neurosci Res. 1992 Mar;31(3):487-93 [1322463.001]
  • [Cites] J Exp Med. 1992 Oct 1;176(4):981-9 [1402668.001]
  • [Cites] Int J Immunopharmacol. 1992 Aug;14(6):1069-79 [1428362.001]
  • [Cites] N Engl J Med. 1993 Apr 22;328(16):1173-82 [8455685.001]
  • [Cites] Eur J Immunol. 1994 Feb;24(2):308-14 [8299680.001]
  • [Cites] J Neuroimmunol. 1994 Jun;52(1):79-86 [8207121.001]
  • [Cites] J Virol. 1995 Sep;69(9):5469-74 [7636992.001]
  • [Cites] Acta Neuropathol. 1995;89(6):483-90 [7676804.001]
  • [Cites] Eur J Immunol. 1996 Jul;26(7):1641-6 [8766573.001]
  • [Cites] J Infect Dis. 1996 Aug;174(2):318-23 [8699061.001]
  • [Cites] J Exp Med. 1997 Dec 15;186(12):2023-31 [9396771.001]
  • [Cites] Virology. 1997 Nov 24;238(2):189-97 [9400592.001]
  • [Cites] J Neurol Sci. 1998 Apr 15;157(1):1-12 [9600670.001]
  • [Cites] Neuroreport. 1998 May 11;9(7):1487-90 [9631453.001]
  • [Cites] Mol Cell Neurosci. 1998 Dec;12(6):376-89 [9888990.001]
  • [Cites] Acta Neuropathol. 1999 Feb;97(2):107-12 [9928820.001]
  • [Cites] Immunol Rev. 2004 Dec;202:139-56 [15546391.001]
  • [Cites] Immunol Rev. 2005 Feb;203:38-47 [15661020.001]
  • (PMID = 16816372.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ399740/ DQ399741/ DQ399742
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL12RB2 protein, human; 0 / Il12rb2 protein, rat; 0 / RNA, Messenger; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-12; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1698768
  •  go-up   go-down


94. Ohsugi T: Increased production of viral proteins by a 3'-LTR-deleted infectious clone of human T-cell leukemia virus type 1. Virol J; 2009;6:229
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased production of viral proteins by a 3'-LTR-deleted infectious clone of human T-cell leukemia virus type 1.
  • We previously reported that a full-length provirus of HTLV-1 was directly constructed from the HTLV-1-transformed cell line MT-2 using overlapping polymerase chain reaction (PCR) and cloned into a plasmid vector (pFL-MT2).
  • 293T cells transfected with pFL-MT2 alone did not produce virus particles because there was no expression of the viral transactivator protein Tax, whereas cells transfected with pFL-MT2 plus a Tax expression vector produced virus-like particles.
  • In the process of constructing the HTLV-1 provirus by overlapping PCR, we also constructed an incomplete molecular clone, in which the 3' long terminal repeat (LTR) was replaced with the endogenous human gene, which resulted in the expression of a tax gene shorter by 43 bp.
  • [MeSH-major] Human T-lymphotropic virus 1 / metabolism. Terminal Repeat Sequences / genetics. Viral Proteins / metabolism. Virion / metabolism
  • [MeSH-minor] Cell Line. Cell Line, Transformed. Cloning, Molecular / methods. Gene Products, tax / genetics. Gene Products, tax / metabolism. Humans. Sequence Deletion. Transfection

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 3.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] J Virol. 1987 Jul;61(7):2175-81 [3035218.001]
  • [Cites] J Virol. 1988 Dec;62(12):4499-509 [3263510.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Blood. 1995 Apr 1;85(7):1865-70 [7703492.001]
  • [Cites] Annu Rev Immunol. 1997;15:15-37 [9143680.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11612-6 [9326658.001]
  • [Cites] Int J Hematol. 1997 Oct;66(3):257-78 [9401272.001]
  • [Cites] Oncogene. 1998 Feb 5;16(5):643-54 [9482110.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • [Cites] Biochimie. 2006 Feb;88(2):147-50 [16139410.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] Retrovirology. 2006;3:71 [17042961.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] J Virol. 2007 Jun;81(11):6089-98 [17376895.001]
  • [Cites] Int Rev Immunol. 2008;27(4):225-53 [18574738.001]
  • [Cites] J Virol. 2009 Jun;83(11):5339-52 [19321601.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5967-72 [10557085.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):207-17 [11325603.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Virology. 2003 Feb 1;306(1):60-7 [12620798.001]
  • [Cites] Virology. 2004 Jan 5;318(1):327-36 [14972558.001]
  • [Cites] Virology. 2004 Mar 1;320(1):52-62 [15003862.001]
  • [Cites] Anal Biochem. 2004 Jun 15;329(2):281-8 [15158488.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • (PMID = 20034388.001).
  • [ISSN] 1743-422X
  • [Journal-full-title] Virology journal
  • [ISO-abbreviation] Virol. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2804614
  •  go-up   go-down


95. Nascimento MC, Primo J, Bittencourt A, Siqueira I, de Fátima Oliveira M, Meyer R, Schriefer A, Santos SB, Carvalho EM: Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis. Clin Exp Immunol; 2009 Jun;156(3):455-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
  • Human T lymphotropic virus-type 1 (HTLV-1) is the causal agent of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), adult T cell leukaemia/lymphoma and infective dermatitis associated with HTLV-1 (IDH).
  • Over-production of proinflammatory cytokines and an increase in HTLV-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established.
  • In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the HTLV-1 proviral load.
  • HTLV-1 carriers and patients with HAM/TSP served as controls.
  • TNF-alpha and IFN-gamma levels were higher in IDH than in HTLV-1 carriers.
  • There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in HTLV-1 carriers, but the difference did not reach statistical significance.
  • The HTLV-1 proviral load was significantly higher in IDH patients than in HTLV-1 carriers.
  • IDH is characterized by an exaggerated Th1 immune response and high HTLV-1 proviral load.

  • Genetic Alliance. consumer health - Spastic paraparesis.
  • Genetic Alliance. consumer health - Tropical spastic paraparesis.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Infect Dis. 2001 Jan 15;183(2):197-205 [11120926.001]
  • [Cites] J Exp Med. 2007 Feb 19;204(2):285-97 [17283207.001]
  • [Cites] J Acquir Immune Defic Syndr. 2001 May 1;27(1):1-6 [11404513.001]
  • [Cites] Am J Trop Med Hyg. 2001 Aug;65(2):87-9 [11508396.001]
  • [Cites] J Neurovirol. 2001 Jun;7(3):228-34 [11517397.001]
  • [Cites] Ann Neurol. 2001 Dec;50(6):807-12 [11761481.001]
  • [Cites] J Virol Methods. 2002 Apr;102(1-2):37-51 [11879691.001]
  • [Cites] Dermatol Nurs. 2003 Aug;Suppl:6-9 [14520891.001]
  • [Cites] Ann Dermatol Venereol. 2004 Feb;131(2):191-3 [15026748.001]
  • [Cites] BMC Infect Dis. 2004 Mar 2;4:7 [15070424.001]
  • [Cites] Br J Dermatol. 2004 May;150(5):958-65 [15149509.001]
  • [Cites] J Infect Dis. 2004 Nov 15;190(10):1797-803 [15499536.001]
  • [Cites] Br J Dermatol. 1967 Apr;79(4):229-36 [6024739.001]
  • [Cites] Br J Dermatol. 1974 May;90(5):525-30 [4601016.001]
  • [Cites] Neurology. 1983 Nov;33(11):1444-52 [6685237.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Ann Neurol. 1990 Feb;27(2):149-56 [2317010.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5218-22 [2367534.001]
  • [Cites] J Acquir Immune Defic Syndr. 1990;3(12):1199-200 [2243322.001]
  • [Cites] Ann Neurol. 1991 Feb;29(2):194-201 [2012389.001]
  • [Cites] Lancet. 1991 Dec 21-28;338(8782-8783):1593-4 [1683991.001]
  • [Cites] Br J Rheumatol. 1992 May;31(5):293-8 [1581770.001]
  • [Cites] J Neuropathol Exp Neurol. 1994 Jan;53(1):72-7 [8301322.001]
  • [Cites] Lancet. 1995 Sep 9;346(8976):710 [7658857.001]
  • [Cites] J Clin Invest. 1995 Nov;96(5):2339-47 [7593621.001]
  • [Cites] Neurology. 1996 Apr;46(4):1016-21 [8780082.001]
  • [Cites] Transfusion. 1997 Feb;37(2):242-3 [9051104.001]
  • [Cites] J Immunol. 1997 Aug 15;159(4):2018-25 [9257869.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):439-44 [9554295.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):487-8 [9554302.001]
  • [Cites] J Invest Dermatol. 1999 Feb;112(2):171-6 [9989792.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):586-93 [10065900.001]
  • [Cites] J Immunol. 1999 Jul 1;163(1):466-75 [10384150.001]
  • [Cites] Eur J Dermatol. 2005 Jan-Feb;15(1):26-30 [15701589.001]
  • [Cites] Clin Infect Dis. 2005 Jun 1;40(11):e90-6 [15889351.001]
  • [Cites] Clin Infect Dis. 2005 Aug 15;41(4):535-41 [16028164.001]
  • [Cites] Clin Exp Immunol. 2006 Aug;145(2):296-301 [16879249.001]
  • [Cites] Clin Infect Dis. 2006 Nov 15;43(10):1257-63 [17051489.001]
  • [Cites] Neuroimmunomodulation. 2006;13(3):145-51 [17119343.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • (PMID = 19438598.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2691974
  •  go-up   go-down


96. Pezeshkpoor F, Yazdanpanah MJ, Shirdel A: Specific cutaneous manifestations in adult T-cell leukemia/lymphoma. Int J Dermatol; 2008 Apr;47(4):359-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific cutaneous manifestations in adult T-cell leukemia/lymphoma.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is an aggressive malignancy which may occur in individuals infected with human T-cell lymphotropic virus type-I (HTLV-I).
  • HTLV-I is endemic in Khorasan, with a frequency of 2.3% in the general population.
  • As specific cutaneous manifestations of lymphoma may occur in a significant number of patients, we studied these manifestations in ATLL patients admitted to the Hematology and Dermatology Departments of Ghaem Hospital, Mashhad, Iran, during 1995-2004.
  • METHODS: In this descriptive study, demographic and clinical information was obtained from 23 patients suffering from ATLL with specific cutaneous lesions (atypical lymphocytes on histopathology of cutaneous lesions), and was analyzed statistically.
  • CONCLUSION: The most common type of specific skin lesion in ATLL was maculopapular eruption, especially with a generalized distribution.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Skin / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Iran. Male. Middle Aged

  • Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18377598.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


97. Biasiotto R, Aguiari P, Rizzuto R, Pinton P, D'Agostino DM, Ciminale V: The p13 protein of human T cell leukemia virus type 1 (HTLV-1) modulates mitochondrial membrane potential and calcium uptake. Biochim Biophys Acta; 2010 Jun-Jul;1797(6-7):945-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The p13 protein of human T cell leukemia virus type 1 (HTLV-1) modulates mitochondrial membrane potential and calcium uptake.
  • Human T cell leukemia virus type 1 (HTLV-1) encodes p13, an 87-amino-acid protein that accumulates in the inner mitochondrial membrane.
  • These observations suggest that p13 might control key processes regulated through Ca2+ signaling such as activation and death of T cells, the major targets of HTLV-1 infection.
  • [MeSH-major] Calcium / metabolism. Human T-lymphotropic virus 1 / metabolism. Membrane Potential, Mitochondrial. Retroviridae Proteins / metabolism

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20188695.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP09128
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Recombinant Fusion Proteins; 0 / Retroviridae Proteins; SY7Q814VUP / Calcium
  •  go-up   go-down


98. Mesnard JM, Barbeau B, Devaux C: HBZ, a new important player in the mystery of adult T-cell leukemia. Blood; 2006 Dec 15;108(13):3979-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HBZ, a new important player in the mystery of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) was first described in 1977.
  • A link between ATL and human T-cell leukemia virus type 1 (HTLV-1) was clearly established in the early 1980s.
  • Over the years, many aspects of HTLV-1-induced cellular dysfunctions have been clarified.
  • However, the detailed mechanism behind ATL occurrence remains unsolved.
  • Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-cell transformation) in more than 50% of ATL cells.
  • A novel HTLV-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology.
  • Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both ATL cells or animal models.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. Cell Transformation, Viral / genetics. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Viral Proteins / genetics. Virus Replication / genetics
  • [MeSH-minor] Animals. Cell Proliferation. Disease Models, Animal. Gene Products, tax / deficiency. Gene Products, tax / immunology. Humans. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / immunology. RNA, Viral / genetics. RNA, Viral / immunology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / virology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16917009.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
  • [Number-of-references] 102
  •  go-up   go-down


99. Ariumi Y, Trono D: Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function. J Virol; 2006 Mar;80(5):2445-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function.
  • The ataxia-telangiectasia-mutated (ATM) kinase plays a central role in responses to various forms of DNA damage and has been suggested to facilitate human immunodeficiency virus type 1 (HIV-1) integration.
  • Notably, ATM overexpression did not stimulate the HIV-1 late gene expression within the context of Rev-independent constructs or the Rex-dependent production of capsid from human T-cell leukemia virus type 1 proviral constructs.
  • [MeSH-major] Cell Cycle Proteins / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Viral. Gene Products, rev / physiology. HIV-1 / physiology. Protein-Serine-Threonine Kinases / physiology. Tumor Suppressor Proteins / physiology. Virus Replication
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Caffeine. Cell Line. Gene Silencing. Genes, Reporter. HIV Core Protein p24 / analysis. Humans. Luciferases / analysis. Luciferases / genetics. rev Gene Products, Human Immunodeficiency Virus

  • Genetic Alliance. consumer health - Ataxia.
  • Genetic Alliance. consumer health - Ataxia Telangiectasia.
  • Addgene Non-profit plasmid repository. clones/clone libraries - Get Article's Plasmids - Addgene (subscription/membership/fee required).
  • Hazardous Substances Data Bank. CAFFEINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • eagle-i research resources. PMID 16474151 (Special Collections) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Biol. 1997 Oct 1;7(10):767-75 [9368759.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1051-60 [9323133.001]
  • [Cites] J Virol. 1998 Aug;72(8):6602-7 [9658105.001]
  • [Cites] Mol Cell. 1998 Apr;1(5):649-59 [9660949.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10146-51 [9707615.001]
  • [Cites] Science. 1998 Sep 11;281(5383):1677-9 [9733515.001]
  • [Cites] Oncogene. 1999 Apr 1;18(13):2261-71 [10327072.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4375-82 [10485486.001]
  • [Cites] Virology. 2004 Dec 20;330(2):471-80 [15567440.001]
  • [Cites] J Virol. 2005 Feb;79(3):1389-96 [15650165.001]
  • [Cites] J Virol. 2005 Feb;79(4):2058-65 [15681408.001]
  • [Cites] J Virol. 2005 Mar;79(5):2973-8 [15709017.001]
  • [Cites] Nat Cell Biol. 2005 May;7(5):493-500 [15834407.001]
  • [Cites] J Biol Chem. 1999 Nov 26;274(48):34277-82 [10567403.001]
  • [Cites] Nucleic Acids Res. 2000 Feb 15;28(4):901-10 [10648781.001]
  • [Cites] J Biol Chem. 2000 Apr 7;275(14):10342-8 [10744722.001]
  • [Cites] J Virol. 2000 May;74(10):4839-52 [10775623.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 21;287(2):556-61 [11554765.001]
  • [Cites] Science. 2002 Apr 19;296(5567):550-3 [11910072.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):155-68 [12612651.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4778-83 [12679521.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] Nat Cell Biol. 2003 Aug;5(8):754-61 [12883554.001]
  • [Cites] Trends Biochem Sci. 2003 Aug;28(8):419-24 [12932730.001]
  • [Cites] Virology. 2003 Sep 15;314(1):460-7 [14517098.001]
  • [Cites] EMBO J. 2003 Dec 15;22(24):6610-20 [14657032.001]
  • [Cites] Science. 2004 Apr 2;304(5667):93-6 [15064416.001]
  • [Cites] EMBO J. 2004 Jul 7;23(13):2632-40 [15201866.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:3187-208 [15353349.001]
  • [Cites] Cell. 2004 Oct 29;119(3):381-92 [15507209.001]
  • [Cites] J Gen Virol. 1987 Feb;68 ( Pt 2):499-506 [3029287.001]
  • [Cites] EMBO J. 1990 Dec;9(12):4155-60 [2249669.001]
  • [Cites] J Mol Biol. 1994 Sep 2;241(5):651-62 [7520946.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1480-4 [7878004.001]
  • [Cites] J Virol. 1995 Apr;69(4):2024-30 [7884847.001]
  • [Cites] J Virol. 1995 Aug;69(8):5048-56 [7541845.001]
  • [Cites] Virology. 1996 Mar 1;217(1):293-300 [8599214.001]
  • [Cites] Leuk Res. 2005 Aug;29(8):933-42 [15978944.001]
  • [Cites] Science. 1996 Apr 12;272(5259):263-7 [8602510.001]
  • [Cites] Nat Biotechnol. 1997 Sep;15(9):871-5 [9306402.001]
  • [Cites] EMBO J. 1997 Dec 15;16(24):7500-10 [9405378.001]
  • (PMID = 16474151.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Gene Products, rev; 0 / HIV Core Protein p24; 0 / Tumor Suppressor Proteins; 0 / rev Gene Products, Human Immunodeficiency Virus; 3G6A5W338E / Caffeine; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC1395391
  •  go-up   go-down


100. Ohsugi T, Koito A: Human T cell leukemia virus type I is resistant to the antiviral effects of APOBEC3. J Virol Methods; 2007 Jan;139(1):93-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T cell leukemia virus type I is resistant to the antiviral effects of APOBEC3.
  • The objective of this study was to investigate whether the anti-retroviral cellular cytidine deaminase, APOBEC3, inhibits the infectivity of human T cell leukemia virus type I (HTLV-I).
  • Sufficient quantities of cell-free HTLV-I virion for infection were obtained by cotransfecting cells with HTLV-I and human or murine APOBEC3 expression vectors along with a plasmid expressing Tax.
  • HTLV-I viruses containing these deaminases were still capable of infecting 293T and MOLT-4 cells.
  • No G-to-A mutations, which are characteristic of cytidine deaminases, were observed in the HTLV-I genome.
  • These results suggest that the enzymatic activity of APOBEC3 may not contribute substantially to antiviral responses to HTLV-I.
  • [MeSH-major] Antiviral Agents / pharmacology. Cytidine Deaminase / pharmacology. Cytosine Deaminase / pharmacology. Human T-lymphotropic virus 1 / drug effects
  • [MeSH-minor] Animals. Cell Line. Drug Resistance, Viral. Transfection

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17123636.001).
  • [ISSN] 0166-0934
  • [Journal-full-title] Journal of virological methods
  • [ISO-abbreviation] J. Virol. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 3.5.4.1 / APOBEC3 protein, human; EC 3.5.4.1 / Cytosine Deaminase; EC 3.5.4.5 / Apobec3 protein, mouse; EC 3.5.4.5 / Cytidine Deaminase
  •  go-up   go-down






Advertisement