[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
1. Osborne GE, Pagliuca A, Ho A, du Vivier AW: Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody). Br J Dermatol; 2006 Sep;155(3):617-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody).
  • We describe a patient with erythrodermic adult T-cell leukaemia/lymphoma resistant to multiple systemic therapies who, on the commencement of daclizumab, a humanized anti-interleukin-2 receptor antibody, developed a rapid and sustained complete response with resolution of previously debilitating erythroderma, suggesting significant activity of this agent in this disease process.

  • Genetic Alliance. consumer health - Sezary syndrome.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16911291.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; CUJ2MVI71Y / daclizumab
  •  go-up   go-down


2. Saito K, Saito M, Taniura N, Okuwa T, Ohara Y: Activation of the PI3K-Akt pathway by human T cell leukemia virus type 1 (HTLV-1) oncoprotein Tax increases Bcl3 expression, which is associated with enhanced growth of HTLV-1-infected T cells. Virology; 2010 Aug 1;403(2):173-80
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] Activation of the PI3K-Akt pathway by human T cell leukemia virus type 1 (HTLV-1) oncoprotein Tax increases Bcl3 expression, which is associated with enhanced growth of HTLV-1-infected T cells.
  • Bcl3 is a member of the IkappaB family that regulates genes involved in cell proliferation and apoptosis.
  • Recent reports indicated that Bcl3 is overexpressed in HTLV-1-infected T cells via Tax-mediated transactivation, and acts as a negative regulator of viral transcription.
  • However, the role of Bcl3 in cellular signal transduction and the growth of HTLV-1-infected T cells have not been reported.
  • In this study, we showed that the knockdown of Bcl3 by short hairpin RNA inhibited the growth of HTLV-1-infected T cells.
  • Although phosphatidylinositol-3 kinase (PI3K) inhibitor reduced Bcl3 expression, inactivation of glycogen synthase kinase 3 (GSK3), an effector kinase of the PI3K/Akt signaling pathway, restored Bcl3 expression in Tax-negative but not in Tax-positive T cells.
  • Our results indicate that the overexpression of Bcl3 in HTLV-1-infected T cells is regulated not only by transcriptional but also by post-transcriptional mechanisms, and is involved in overgrowth of HTLV-1-infected T cells.
  • [MeSH-major] Gene Products, tax / physiology. Human T-lymphotropic virus 1 / pathogenicity. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins / biosynthesis. T-Lymphocytes / virology. Transcription Factors / biosynthesis. Virulence Factors / physiology
  • [MeSH-minor] Cell Line. Cell Proliferation. Gene Knockdown Techniques. Humans. RNA, Small Interfering / genetics

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • 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 = 20471052.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [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 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Virulence Factors; 0 / proto-oncogene protein bcl-3; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
  •  go-up   go-down


3. Kress AK, Schneider G, Pichler K, Kalmer M, Fleckenstein B, Grassmann R: Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1. J Virol; 2010 Sep;84(17):8732-42
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] Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.
  • Human T-cell lymphotropic virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), transforms CD4(+) T cells to permanent growth through its transactivator Tax.
  • HTLV-1-transformed cells share phenotypic properties with memory and regulatory T cells (T-reg).
  • This led us to determine cAMP levels in HTLV-1-transformed cells.
  • We found elevated cAMP concentrations as a consistent feature of all HTLV-1-transformed cell lines, including in vitro-HTLV-1-transformed, Tax-transformed, and patient-derived cells.
  • We found specific downregulation of the cAMP-degrading phosphodiesterase 3B (PDE3B) in HTLV-1-transformed cells, which was independent of Tax in transient expression experiments.
  • Overexpression of PDE3B led to a decrease of cAMP in HTLV-1-transformed cells.
  • Decreased expression of PDE3B was associated with inhibitory histone modifications at the PDE3B promoter and the PDE3B locus.
  • This shows that HTLV-1-transformed cells assume biological features of long-lived T-cell populations that potentially contribute to viral persistence.
  • [MeSH-major] Cell Transformation, Viral. Cyclic AMP / metabolism. HTLV-I Infections / metabolism. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism
  • [MeSH-minor] Cell Line, Transformed. Cells, Cultured. Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics. Cyclic Nucleotide Phosphodiesterases, Type 3 / metabolism. Gene Products, tax / genetics. Gene Products, tax / metabolism. Humans. T-Lymphocytes / metabolism. T-Lymphocytes / virology

  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Pharmacol. 1999 Sep 15;58(6):935-50 [10509746.001]
  • [Cites] Cancer Res. 1986 Sep;46(9):4458-62 [2873886.001]
  • [Cites] Cancer Sci. 2005 Aug;96(8):527-33 [16108835.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6035-46 [16155610.001]
  • [Cites] Int Immunol. 2006 Feb;18(2):269-77 [16361311.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4491-9 [16467195.001]
  • [Cites] Pharmacol Rev. 2006 Sep;58(3):488-520 [16968949.001]
  • [Cites] J Leukoc Biol. 2006 Oct;80(4):880-8 [16888088.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] J Virol. 2007 Mar;81(5):2524-30 [17151105.001]
  • [Cites] Nature. 2007 Feb 15;445(7129):771-5 [17220874.001]
  • [Cites] Nature. 2007 Feb 22;445(7130):936-40 [17237761.001]
  • [Cites] Cell. 2007 Feb 23;128(4):669-81 [17320505.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1303-10 [17502663.001]
  • [Cites] J Biol Chem. 2007 Jun 29;282(26):18750-7 [17449469.001]
  • [Cites] J Immunol. 2008 Jan 15;180(2):931-9 [18178833.001]
  • [Cites] J Gen Physiol. 2008 Apr;131(4):293-305 [18378798.001]
  • [Cites] Blood. 2008 May 1;111(9):4741-51 [18276843.001]
  • [Cites] Blood. 2000 Jan 1;95(1):30-8 [10607681.001]
  • [Cites] FEBS Lett. 2001 Sep 7;505(1):136-40 [11557056.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] Mol Cell Biol. 1985 Dec;5(12):3610-6 [3915782.001]
  • [Cites] Nature. 1988 Oct 20;335(6192):738-40 [3262832.001]
  • [Cites] J Virol. 1989 Apr;63(4):1604-11 [2538645.001]
  • [Cites] J Virol. 1989 Aug;63(8):3220-6 [2501514.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] AIDS Res Hum Retroviruses. 1994 Oct;10(10):1259-68 [7531462.001]
  • [Cites] J Exp Med. 1995 Mar 1;181(3):985-92 [7532686.001]
  • [Cites] Clin Diagn Lab Immunol. 1995 May;2(3):349-55 [7545080.001]
  • [Cites] J Virol. 1998 Jan;72(1):633-40 [9420268.001]
  • [Cites] Retrovirology. 2008;5:76 [18702816.001]
  • [Cites] FEBS Lett. 2008 Oct 29;582(25-26):3614-8 [18835269.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3788-97 [18689544.001]
  • [Cites] Retrovirology. 2008;5:100 [19014482.001]
  • [Cites] Int J Cancer. 2009 Nov 15;125(10):2375-82 [19544530.001]
  • [Cites] Virus Genes. 2001 Dec;23(3):263-71 [11778694.001]
  • [Cites] Blood. 2002 May 1;99(9):3383-9 [11964307.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Sep;3(9):710-8 [12209131.001]
  • [Cites] Virology. 2003 Dec 5;317(1):136-45 [14675632.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2039-46 [15026341.001]
  • [Cites] J Virol. 2004 Sep;78(18):9814-9 [15331715.001]
  • [Cites] J Immunol. 1971 Nov;107(5):1489-92 [4330163.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] Gan. 1984 Sep;75(9):752-5 [6094296.001]
  • [Cites] J Gen Virol. 1985 Aug;66 ( Pt 8):1825-9 [2991447.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 1;332(2):569-84 [15896717.001]
  • (PMID = 20573814.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE17718
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; E0399OZS9N / Cyclic AMP; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 3; EC 3.1.4.17 / PDE3B protein, human
  • [Other-IDs] NLM/ PMC2918996
  •  go-up   go-down


Advertisement
4. Heidecker G, Lloyd PA, Soheilian F, Nagashima K, Derse D: The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1. J Virol; 2007 Sep;81(18):9769-77
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 role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1.
  • The PPPY motif in the matrix (MA) domain of human T-cell leukemia virus type 1 (HTLV-1) Gag associates with WWP1, a member of the HECT domain containing family of E3 ubiquitin ligases.
  • Virus-like particles produced by the K74R mutant did not contain ubiquitinated MA and showed a fourfold reduction in the release of infectious particles.
  • This finding indicates that the interaction between Gag and WWP1 is required for functions other than Gag ubiquitination.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 1994 Oct;68(10):6605-18 [8083996.001]
  • [Cites] J Virol. 2003 Feb;77(3):1812-9 [12525615.001]
  • [Cites] J Virol. 1995 Nov;69(11):6810-8 [7474093.001]
  • [Cites] Biochem Soc Trans. 1996 Feb;24(1):274-9 [8674685.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11382-8 [8876144.001]
  • [Cites] J Mol Biol. 1996 Dec 20;264(5):1117-31 [9000634.001]
  • [Cites] J Virol. 1997 Sep;71(9):6541-6 [9261374.001]
  • [Cites] J Virol. 1998 Apr;72(4):2962-8 [9525617.001]
  • [Cites] J Virol. 1998 May;72(5):4095-103 [9557699.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):2982-93 [9606181.001]
  • [Cites] J Virol. 1999 Mar;73(3):1860-7 [9971764.001]
  • [Cites] EMBO J. 1999 Sep 1;18(17):4700-10 [10469649.001]
  • [Cites] Virology. 1999 Sep 30;262(2):442-51 [10502522.001]
  • [Cites] J Virol. 2004 Dec;78(24):13943-53 [15564502.001]
  • [Cites] Virus Res. 2004 Dec;106(2):87-102 [15567490.001]
  • [Cites] J Cell Biol. 2005 Jan 3;168(1):89-101 [15623582.001]
  • [Cites] J Virol. 2006 Oct;80(19):9876-88 [16973592.001]
  • [Cites] Biochem J. 2006 Nov 1;399(3):361-72 [17034365.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2915-20 [17299050.001]
  • [Cites] J Virol. 2007 May;81(9):4422-8 [17287279.001]
  • [Cites] J Membr Biol. 2000 Jul 1;176(1):1-17 [10882424.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):12945-7 [11087848.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13063-8 [11087860.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13069-74 [11087861.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13871-6 [11095724.001]
  • [Cites] Virology. 2000 Dec 5;278(1):111-21 [11112487.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Mar;2(3):195-201 [11265249.001]
  • [Cites] J Virol. 2001 Jun;75(11):5277-87 [11333909.001]
  • [Cites] Biochem Soc Trans. 2001 Aug;29(Pt 4):472-5 [11498011.001]
  • [Cites] J Virol. 2001 Sep;75(18):8461-8 [11507191.001]
  • [Cites] J Mol Biol. 2003 Feb 14;326(2):493-502 [12559917.001]
  • [Cites] J Virol. 2003 Mar;77(6):3384-93 [12610113.001]
  • [Cites] Nat Cell Biol. 2003 May;5(5):461-6 [12717448.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3381-5 [12824332.001]
  • [Cites] J Cell Biol. 2003 Aug 4;162(3):435-42 [12900395.001]
  • [Cites] J Virol. 2003 Sep;77(17):9474-85 [12915562.001]
  • [Cites] Cell. 2003 Sep 19;114(6):689-99 [14505569.001]
  • [Cites] Cell. 2003 Sep 19;114(6):701-13 [14505570.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12414-9 [14519844.001]
  • [Cites] J Virol. 2003 Nov;77(22):11882-95 [14581525.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 31;102(22):7994-9 [15911757.001]
  • [Cites] J Virol. 2005 Jul;79(14):9134-44 [15994808.001]
  • [Cites] Essays Biochem. 2005;41:81-98 [16250899.001]
  • [Cites] J Virol. 2006 Jul;80(13):6267-75 [16775314.001]
  • [Cites] J Virol. 2004 Feb;78(3):1503-12 [14722305.001]
  • [Cites] Microbes Infect. 2004 Feb;6(2):150-6 [14998512.001]
  • [Cites] Oncogene. 2004 Mar 15;23(11):1972-84 [15021885.001]
  • [Cites] Oncogene. 2004 Mar 15;23(11):2057-70 [15021893.001]
  • [Cites] J Cell Sci. 2004 May 1;117(Pt 11):2357-67 [15126635.001]
  • [Cites] J Virol. 2004 Jun;78(12):6636-48 [15163754.001]
  • [Cites] J Virol. 2004 Oct;78(19):10606-16 [15367628.001]
  • [Cites] Annu Rev Cell Dev Biol. 2004;20:395-425 [15473846.001]
  • [Cites] Annu Rev Biochem. 1989;58:913-49 [2528323.001]
  • [Cites] J Virol. 1995 Sep;69(9):5455-60 [7636991.001]
  • [Cites] Cell. 2001 Oct 5;107(1):55-65 [11595185.001]
  • [Cites] Nat Med. 2001 Dec;7(12):1313-9 [11726971.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 22;99(2):955-60 [11805336.001]
  • [Cites] J Virol. 2002 Mar;76(6):3038-44 [11861870.001]
  • [Cites] EMBO Rep. 2002 Jul;3(7):636-40 [12101095.001]
  • [Cites] J Virol. 2002 Oct;76(19):10024-9 [12208980.001]
  • [Cites] J Virol. 2002 Dec;76(24):13101-5 [12438640.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Dec;3(12):893-905 [12461556.001]
  • [Cites] Trends Cell Biol. 2002 Dec;12(12):569-79 [12495845.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3195-9 [2014240.001]
  • (PMID = 17609263.001).
  • [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 / PHS HHS / / N01 C0 12400; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, gag; 0 / Ubiquitin; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / WWP1 protein, human
  • [Other-IDs] NLM/ PMC2045422
  •  go-up   go-down


5. Kashima K, Daa T, Yokoyama S: Detection of HTLV-1 gene on cytologic smear slides. Methods Mol Biol; 2005;304:183-9
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] Detection of HTLV-1 gene on cytologic smear slides.
  • In this chapter we describe a method for the detection of human T-cell leukemia virus type 1 (HTLV-1) genes in cytologic smears by polymerase chain reaction (PCR).
  • We use two sets of primers for detection of HTLV-1 genes, and the products of amplification by PCR that correspond to the pX and tax regions are expected to be 127 and 159 base pairs long, respectively.
  • Although this method does not provide proof of the monoclonal integration of HTLV-1 genes, it can be applied when adult T-cell leukemia/lymphoma is suspected cytologically but fresh samples for Southern blotting are unavailable.
  • [MeSH-major] Cytodiagnosis / methods. Genes, Viral. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Polymerase Chain Reaction / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16061975.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
  •  go-up   go-down


6. Yasunami T, Wang YH, Tsuji K, Takanashi M, Yamada Y, Motoji T: Multidrug resistance protein expression of adult T-cell leukemia/lymphoma. Leuk Res; 2007 Apr;31(4):465-70
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] Multidrug resistance protein expression of adult T-cell leukemia/lymphoma.
  • In adult T-cell leukemia/lymphoma (ATL), it is difficult to achieve remission and the reason for the resistance to chemotherapeutic agents may be linked to the presence of multidrug resistance (MDR) proteins.
  • Lung resistance-related protein (LRP), multidrug resistance-associated protein and P-glycoprotein are three MDR proteins which we examined in ATL cells using multiparametric flow cytometry and real-time RT-PCR.
  • This indicates LRP may be contributing to drug resistance in ATL patients, and the suppression of LRP function could be a new strategy for ATL treatment.
  • [MeSH-major] Drug Resistance, Multiple. Gene Expression Regulation, Leukemic. Gene Expression Regulation, Neoplastic. Leukemia-Lymphoma, Adult T-Cell / metabolism. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Adult. Aged. Antibiotics, Antineoplastic / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17134750.001).
  • [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 / Antibiotics, Antineoplastic; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 80168379AG / Doxorubicin
  •  go-up   go-down


7. Coskun AK, Sutton RE: Expression of glucose transporter 1 confers susceptibility to human T-cell leukemia virus envelope-mediated fusion. J Virol; 2005 Apr;79(7):4150-8
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] Expression of glucose transporter 1 confers susceptibility to human T-cell leukemia virus envelope-mediated fusion.
  • Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus identified and causes both adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy, among other disorders.
  • In vitro, HTLV-1 has an extremely broad host cell tropism in that it is capable of infecting most mammalian cell types, although at the same time viral titers remain relatively low.
  • Although glut-1 was shown to bind specifically to the ectodomain of HTLV-1 and HTLV-2 envelope glycoproteins, which was reversible with small interfering RNA directed against glut-1, cellular susceptibility to HTLV upon expression of glut-1 was not established.
  • Here we show that expression of glut-1 in relatively resistant MDBK cells conferred increased susceptibility to both HTLV-1- and HTLV-2-pseudotyped particles. glut-1 also markedly increased syncytium formation in MDBK cells after exposure to HTLV-1.
  • Another assay also demonstrated HTLV-1 envelope-cell fusion in the presence of glut-1.
  • Taken together, these results provide additional evidence that glut-1 is a receptor for HTLV.
  • [MeSH-major] Cell Fusion. Giant Cells / physiology. Human T-lymphotropic virus 1 / physiology. Human T-lymphotropic virus 2 / physiology. Monosaccharide Transport Proteins / biosynthesis. Receptors, Virus / biosynthesis
  • [MeSH-minor] Animals. Cattle. Cell Line. Cells, Cultured. Flow Cytometry. Glucose Transporter Type 1. Microscopy, Fluorescence. Staining and Labeling

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Tissue Res. 1996 Jun;284(3):355-65 [8646755.001]
  • [Cites] Int J Cancer. 1984 Jun 15;33(6):745-9 [6329966.001]
  • [Cites] Science. 1984 Sep 28;225(4669):1473-6 [6089348.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Oct;81(19):6202-6 [6091139.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7588-90 [6095308.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7591-5 [6095309.001]
  • [Cites] Curr Top Microbiol Immunol. 1985;115:235-46 [2983944.001]
  • [Cites] Int J Cancer. 1985 Jul 15;36(1):37-41 [2862109.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Am J Hematol. 1985 Oct;20(2):129-37 [2994470.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] J Infect. 1986 May;12(3):205-12 [3014007.001]
  • [Cites] Ann Neurol. 1987 Feb;21(2):117-22 [2881513.001]
  • [Cites] Nature. 1987 Apr 16-22;326(6114):714-7 [3031513.001]
  • [Cites] J Virol. 1996 Oct;70(10):7322-6 [8794391.001]
  • [Cites] Nat Genet. 1998 Feb;18(2):188-91 [9462754.001]
  • [Cites] Cell. 1998 Feb 20;92(4):451-62 [9491887.001]
  • [Cites] J Virol. 1998 Jul;72(7):5781-8 [9621037.001]
  • [Cites] Lancet. 1999 Jun 5;353(9168):1951-8 [10371587.001]
  • [Cites] J Histochem Cytochem. 1999 Aug;47(8):1021-30 [10424886.001]
  • [Cites] Hum Mutat. 2000 Sep;16(3):224-31 [10980529.001]
  • [Cites] J Emerg Med. 2000 Jan;18(1):109-19 [10645850.001]
  • [Cites] Infect Dis Clin North Am. 2000 Mar;14(1):211-39, x-xi [10738680.001]
  • [Cites] J Biol Chem. 2000 Aug 4;275(31):23417-20 [10851227.001]
  • [Cites] Hum Gene Ther. 2002 Jul 20;13(11):1293-303 [12162812.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1913-8 [12393496.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3085-92 [12506039.001]
  • [Cites] Brain Dev. 2003 Oct;25(7):477-80 [13129590.001]
  • [Cites] Cell. 2003 Nov 14;115(4):449-59 [14622599.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15613-8 [14673082.001]
  • [Cites] Virology. 2004 Feb 20;319(2):343-52 [14980494.001]
  • [Cites] Science. 2004 Jul 2;305(5680):61-6 [15166316.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] J Virol. 1981 Jun;38(3):906-15 [6264163.001]
  • [Cites] Nature. 1981 Nov 19;294(5838):268-71 [6272125.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(5):1653-7 [6951204.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Int J Cancer. 1982 Jun 15;29(6):631-5 [6980846.001]
  • [Cites] Int J Cancer. 1982 Sep 15;30(3):257-64 [6290401.001]
  • [Cites] Science. 1982 Feb 19;215(4535):975-8 [6760397.001]
  • [Cites] Gan. 1982 Dec;73(6):893-901 [6984401.001]
  • [Cites] J Infect Dis. 1983 Mar;147(3):406-16 [6300254.001]
  • [Cites] Nature. 1983 Apr 14;302(5909):626-8 [6835396.001]
  • [Cites] JAMA. 1983 Aug 26;250(8):1048-52 [6308290.001]
  • [Cites] Int J Cancer. 1983 Sep 15;32(3):321-8 [6604033.001]
  • [Cites] Science. 1983 Dec 9;222(4628):1125-7 [6316502.001]
  • [Cites] Virology. 1984 Feb;133(1):238-41 [6322435.001]
  • [Cites] Vox Sang. 1984;46(5):245-53 [6328765.001]
  • [Cites] Int J Cancer. 1984 Jun 15;33(6):717-20 [6329964.001]
  • [Cites] Int J Cancer. 1987 Dec 15;40(6):741-6 [2891624.001]
  • [Cites] Science. 1988 Dec 16;242(4885):1557-9 [3201246.001]
  • [Cites] Ann N Y Acad Sci. 1988;540:636-8 [3207295.001]
  • [Cites] Ann Intern Med. 1989 Oct 1;111(7):555-60 [2789009.001]
  • [Cites] Virology. 1990 May;176(1):58-69 [1691887.001]
  • [Cites] Nucleic Acids Res. 1990 Jun 25;18(12):3587-96 [2194165.001]
  • [Cites] J Acquir Immune Defic Syndr. 1992;5(1):12-8 [1738083.001]
  • [Cites] Nucleic Acids Res. 1995 Feb 25;23(4):628-33 [7899083.001]
  • [Cites] J Biol Chem. 1990 Oct 15;265(29):18035-40 [2211679.001]
  • [Cites] J Virol. 1990 Nov;64(11):5270-6 [2214018.001]
  • [Cites] EMBO J. 1990 Dec;9(13):4243-8 [2124968.001]
  • [Cites] J Immunol. 1991 Jul 1;147(1):354-60 [1711082.001]
  • [Cites] N Engl J Med. 1992 Feb 6;326(6):375-80 [1729620.001]
  • [Cites] Nucleic Acids Res. 1996 Mar 15;24(6):1171-2 [8604354.001]
  • (PMID = 15767416.001).
  • [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 / Glucose Transporter Type 1; 0 / Monosaccharide Transport Proteins; 0 / Receptors, Virus
  • [Other-IDs] NLM/ PMC1061550
  •  go-up   go-down


8. Heraud JM, Mortreux F, Merien F, Contamin H, Mahieux R, Pouliquen JF, Wattel E, Gessain A, de Thé H, Bazarbachi A, Hermine O, Kazanji M: The efficacy of combined therapy of arsenic trioxide and alpha interferon in human T-cell leukemia virus type-1-infected squirrel monkeys (Saimiri sciureus). Antiviral Res; 2006 Jul;70(3):132-9
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] The efficacy of combined therapy of arsenic trioxide and alpha interferon in human T-cell leukemia virus type-1-infected squirrel monkeys (Saimiri sciureus).
  • Human T-cell lymphotropic virus type 1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATLL) has a poor prognosis owing to its intrinsic resistance to chemotherapy.
  • Although zidovudine (AZT) and alpha interferon (IFN-alpha) give rise to some response and improve the prognosis of ATLL, alternative therapies are needed.
  • Arsenic trioxide (As(2)O(3)) has been shown to synergize with IFN-alpha in arresting cell growth and inducing apoptosis of ATLL cells in vitro.
  • In this study, we evaluated the toxicity and the efficacy of this combined treatment in HTLV-1-infected squirrel monkeys (Saimiri sciureus) and HTLV-1 infected cell lines derived therefrom.
  • We first show that treatment with As(2)O(3) and IFN-alpha can induce growth arrest in HTLV-1-transformed monkey T-cell lines in vitro.
  • Although the combination of As(2)O(3) and IFN-alpha did not affect significantly the HTLV-1 proviral load in infected monkeys, it reduced the absolute numbers of CD3(+), CD4(+) and CD8(+) cells during treatment, with a significant reduction in the total number of circulating HTLV-1 flower cells in the infected monkeys with chronic ATLL-like disease.
  • [MeSH-major] Antiviral Agents / therapeutic use. Arsenicals / therapeutic use. HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1 / drug effects. Interferon-alpha / therapeutic use. Oxides / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Transformed. Drug Therapy, Combination. Humans. Male. Saimiri. Treatment Outcome

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16540180.001).
  • [ISSN] 0166-3542
  • [Journal-full-title] Antiviral research
  • [ISO-abbreviation] Antiviral Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Arsenicals; 0 / Interferon-alpha; 0 / Oxides; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


9. Chuang SS, Ichinohasama R, Chu JS, Ohshima K: Differential diagnosis of angioimmunoblastic T-cell lymphoma with seropositivity for anti-HTLV antibody from adult T-cell leukemia/lymphoma. Int J Hematol; 2010 May;91(4):687-91
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] Differential diagnosis of angioimmunoblastic T-cell lymphoma with seropositivity for anti-HTLV antibody from adult T-cell leukemia/lymphoma.
  • Angioimmunoblastic lymphoma (AITL) is a nodal peripheral T-cell lymphoma characterized by a proliferation of arborizing vessels and hyperplastic follicular dendritic cells as well as a polymorphous lymphoid infiltrate including neoplastic cells with clear cytoplasm.
  • Adult T-cell leukemia/lymphoma (ATLL) is caused by the retrovirus human T-cell leukemia virus type I (HTLV-I), and the neoplastic cells are usually large and pleomorphic.
  • Recently, a rare morphologic variant of ATLL with AITL-like features has been reported.
  • Here, we presented a case of peripheral T-cell lymphoma with morphological features of AITL in Taiwan, a country non-endemic for HTLV, and the patient was seropositive for anti-HTLV antibody, which raised the possibility of ATLL with AITL-like features.
  • Furthermore, Southern blot analysis using DNA extracted from the nodal tissue was negative for HTLV-I proviral integration.
  • Our investigations indicated that in an HTLV-I non-endemic area, a peripheral T-cell lymphoma with typical morphologic and immunophenotypic features of AITL could be confidently diagnosed as AITL even if the patient was seropositive for anti-HTLV antibody.
  • [MeSH-major] HTLV-I Antibodies / blood. HTLV-I Infections / complications. HTLV-I Infections / immunology. Immunoblastic Lymphadenopathy. Lymphoma, T-Cell
  • [MeSH-minor] Aged, 80 and over. Biopsy. Diagnosis, Differential. Female. Humans. Lymph Nodes / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2003 Jun;121(5):681-91 [12780782.001]
  • [Cites] Br J Haematol. 1991 Oct;79(2):156-61 [1958472.001]
  • [Cites] Int J Cancer. 1997 Aug 7;72(4):592-8 [9259396.001]
  • [Cites] Blood. 2004 Jan 1;103(1):236-41 [12958063.001]
  • [Cites] Histopathology. 1995 Jun;26(6):539-46 [7665144.001]
  • [Cites] Hum Pathol. 2008 Jul;39(7):1050-8 [18479731.001]
  • [Cites] Int J Hematol. 2003 May;77(4):412-3 [12774934.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):232-9 [15726602.001]
  • [Cites] Int J Oncol. 2004 Sep;25(3):605-13 [15289861.001]
  • [Cites] Am J Surg Pathol. 2006 Apr;30(4):490-4 [16625095.001]
  • [Cites] Blood. 2002 Jan 15;99(2):627-33 [11781247.001]
  • [Cites] Am J Surg Pathol. 2007 Feb;31(2):216-23 [17255766.001]
  • [Cites] Am J Surg Pathol. 2007 Jul;31(7):1077-88 [17592275.001]
  • [Cites] Hum Pathol. 1995 Jun;26(6):614-9 [7774890.001]
  • [Cites] Cancer. 1985 Nov 1;56(9):2217-20 [2864999.001]
  • [Cites] Leuk Lymphoma. 2009 Sep;50(9):1540-2 [19603347.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Am J Surg Pathol. 2006 Jul;30(7):802-10 [16819321.001]
  • (PMID = 20198459.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
  •  go-up   go-down


10. Taniguchi Y, Nosaka K, Yasunaga J, Maeda M, Mueller N, Okayama A, Matsuoka M: Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms. Retrovirology; 2005;2:64
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] Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms.
  • BACKGROUND: Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) after a long latent period.
  • Among accessory genes encoded by HTLV-I, the tax gene is thought to play a central role in oncogenesis.
  • To clarify the role of epigenetic changes, we analyzed DNA methylation and histone modification in the whole HTLV-I provirus genome.
  • RESULTS: The gag, pol and env genes of HTLV-I provirus were more methylated than pX region, whereas methylation of 5'-LTR was variable and 3'-LTR was not methylated at all.
  • In ATL cell lines, complete DNA methylation of 5'-LTR was associated with transcriptional silencing of viral genes.
  • HTLV-I provirus was more methylated in primary ATL cells than in carrier state, indicating the association with disease progression.
  • Analysis of histone modification in the HTLV-I provirus showed that the methylated provirus was associated with hypoacetylation.
  • However, the tax gene transcript could not be detected in fresh ATL cells regardless of hyperacetylated histone H3 in 5'-LTR.
  • The transcription rapidly recovered after in vitro culture in such ATL cells.
  • CONCLUSION: These results showed that epigenetic changes of provirus facilitated ATL cells to evade host immune system by suppressing viral gene transcription.
  • [MeSH-major] Epigenesis, Genetic. Gene Silencing. Human T-lymphotropic virus 1 / genetics. Transcription, Genetic
  • [MeSH-minor] Carrier State / virology. Cell Line. DNA Methylation. Histones / metabolism. Humans. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. Terminal Repeat Sequences

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 2003 Apr;77(7):4025-32 [12634362.001]
  • [Cites] EMBO J. 2003 Apr 15;22(8):1868-77 [12682019.001]
  • [Cites] Ann N Y Acad Sci. 2003 Mar;983:170-80 [12724222.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):280-96 [14686485.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):297-303 [14686486.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] Gene Ther. 2004 May;11(10):819-28 [14985785.001]
  • [Cites] J Virol. 2004 Jun;78(12):6122-33 [15163705.001]
  • [Cites] Trends Microbiol. 2004 Jul;12(7):346-52 [15223062.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(14):6117-26 [15226416.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6002-9 [15342380.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Nature. 1983 Sep 1-7;305(5929):60-2 [6888550.001]
  • [Cites] Nature. 1984 Jun 14-20;309(5969):640-2 [6328324.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7124-8 [3174625.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4862-7 [9354450.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Science. 1999 Jan 29;283(5402):682-6 [9924027.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • [Cites] Nature. 2001 Jan 11;409(6817):207-11 [11196646.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):1043-8 [10706122.001]
  • [Cites] Blood. 2005 Aug 1;106(3):1048-53 [15840694.001]
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Blood. 2001 May 15;97(10):3177-83 [11342446.001]
  • [Cites] Hum Gene Ther. 2001 Jun 10;12(9):1079-89 [11399229.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] J Virol. 2002 Mar;76(6):2703-13 [11861837.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3740-5 [11891299.001]
  • [Cites] J Virol. 2002 Sep;76(18):9389-97 [12186921.001]
  • [Cites] Cell. 2002 Aug 23;110(4):521-9 [12202041.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Cancer Cell. 2003 Jan;3(1):89-95 [12559178.001]
  • (PMID = 16242045.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histones
  • [Other-IDs] NLM/ PMC1289293
  •  go-up   go-down


11. Higuchi M, Tsubata C, Kondo R, Yoshida S, Takahashi M, Oie M, Tanaka Y, Mahieux R, Matsuoka M, Fujii M: Cooperation of NF-kappaB2/p100 activation and the PDZ domain binding motif signal in human T-cell leukemia virus type 1 (HTLV-1) Tax1 but not HTLV-2 Tax2 is crucial for interleukin-2-independent growth transformation of a T-cell line. J Virol; 2007 Nov;81(21):11900-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperation of NF-kappaB2/p100 activation and the PDZ domain binding motif signal in human T-cell leukemia virus type 1 (HTLV-1) Tax1 but not HTLV-2 Tax2 is crucial for interleukin-2-independent growth transformation of a T-cell line.
  • Human T-cell leukemia virus type 1 (HTLV-1) but not HTLV-2 is associated with adult T-cell leukemia, and the distinct pathogenicity of these two closely related viruses is thought to stem from the distinct biological functions of the respective transforming proteins, HTLV-1 Tax1 and HTLV-2 Tax2.
  • Using RNA interference methods, we further show that NF-kappaB2/p100 is required for the transformation induced by Tax1, as determined by the ability to convert a T-cell line (CTLL-2) from interleukin-2 (IL-2)-dependent to -independent growth.
  • These results reveal that the activation of NF-kappaB2/p100 plays a crucial role in the Tax1-mediated transformation of T cells and that NF-kappaB2/p100 activation and PBM function are both responsible for the augmented transforming activity of Tax1 relative to Tax2, thus suggesting that these Tax1-specific functions play crucial roles in HTLV-1 leukemogenesis.
  • [MeSH-major] Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Human T-lymphotropic virus 2 / metabolism. Interleukin-2 / metabolism. Leukemia / pathology. NF-kappa B p52 Subunit / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Amino Acid Motifs. Animals. Cell Line, Transformed. Cell Line, Tumor. Cell Transformation, Viral. Humans. Mice. Protein Structure, Tertiary


12. Wielgosz MM, Rauch DA, Jones KS, Ruscetti FW, Ratner L: Cholesterol dependence of HTLV-I infection. AIDS Res Hum Retroviruses; 2005 Jan;21(1):43-50
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] Cholesterol dependence of HTLV-I infection.
  • Cholesterol-rich plasma membrane microdomains are important for entry of many viruses, including retroviruses.
  • Depletion of cholesterol with 2-hydroxypropyl-beta-cyclodextrin inhibits entry of human T cell leukemia virus type I (HTLV-1) and HTLV-I envelope pseudotyped lentivirus particles.
  • Using a soluble fusion protein of the HTLV-I surface envelope protein with the immunoglobulin Fc domain, the HTLV-I receptor was found to colocalize with a raft-associated marker and to cluster in specific plasma membrane microdomains.
  • Depletion of cholesterol did not alter receptor binding activity, suggesting a requirement for cholesterol in a postbinding virus entry step.

  • MedlinePlus Health Information. consumer health - Cholesterol.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 2002 Sep;76(18):9307-22 [12186914.001]
  • [Cites] J Virol. 2002 May;76(10):4709-22 [11967288.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2546-53 [12239168.001]
  • [Cites] Virology. 2002 Sep 1;300(2):244-54 [12350355.001]
  • [Cites] J Virol. 2002 Dec;76(24):12723-34 [12438598.001]
  • [Cites] J Virol. 2003 Feb;77(3):1977-83 [12525631.001]
  • [Cites] J Biol Chem. 2003 Jan 31;278(5):3153-61 [12431990.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] J Lipid Res. 2003 Apr;44(4):655-67 [12562849.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3085-92 [12506039.001]
  • [Cites] Virus Res. 2003 May;93(1):31-9 [12727340.001]
  • [Cites] J Virol. 2003 Sep;77(17):9542-52 [12915568.001]
  • [Cites] Cell. 2003 Nov 14;115(4):449-59 [14622599.001]
  • [Cites] J Virol. 2003 Dec;77(24):13389-95 [14645593.001]
  • [Cites] Virology. 2003 Dec 5;317(1):128-35 [14675631.001]
  • [Cites] J Cell Biol. 2004 Jan 5;164(1):145-55 [14709546.001]
  • [Cites] Biochem J. 2004 Mar 1;378(Pt 2):343-51 [14616090.001]
  • [Cites] J Virol. 2004 May;78(10):5279-87 [15113909.001]
  • [Cites] Medicine (Baltimore). 1988 Nov;67(6):401-22 [3054420.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] Virology. 1994 Nov 1;204(2):656-64 [7941334.001]
  • [Cites] Mol Biol Cell. 1996 Nov;7(11):1825-34 [8930903.001]
  • [Cites] EMBO J. 1997 Sep 15;16(18):5501-8 [9312009.001]
  • [Cites] J Cell Biol. 1998 May 18;141(4):929-42 [9585412.001]
  • [Cites] Exp Cell Res. 1999 Jan 10;246(1):83-90 [9882517.001]
  • [Cites] J Biol Chem. 1999 Jan 22;274(4):2038-44 [9890962.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7289-304 [10523618.001]
  • [Cites] J Virol. 2000 Jan;74(1):305-11 [10590118.001]
  • [Cites] Virology. 2000 Mar 1;268(1):41-8 [10683325.001]
  • [Cites] J Virol. 2000 Apr;74(7):3264-72 [10708443.001]
  • [Cites] J Virol. 2000 May;74(10):4634-44 [10775599.001]
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17221-4 [10770957.001]
  • [Cites] J Virol. 2000 Jul;74(14):6538-45 [10864667.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3304-13 [10880443.001]
  • [Cites] Mol Biol Cell. 2000 Aug;11(8):2775-91 [10930469.001]
  • [Cites] Virology. 2000 Oct 25;276(2):251-8 [11040117.001]
  • [Cites] J Biol Chem. 2000 Oct 27;275(43):33197-200 [10973945.001]
  • [Cites] EMBO Rep. 2000 Aug;1(2):190-6 [11265761.001]
  • [Cites] Traffic. 2001 Mar;2(3):160-6 [11260521.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4675-80 [11296297.001]
  • [Cites] Semin Immunol. 2001 Apr;13(2):89-97 [11308292.001]
  • [Cites] Nat Cell Biol. 2001 May;3(5):473-83 [11331875.001]
  • [Cites] J Virol. 2001 Aug;75(16):7351-61 [11462007.001]
  • [Cites] J Virol. 2001 Sep;75(17):7913-24 [11483736.001]
  • [Cites] AIDS Res Hum Retroviruses. 2001 Jul 20;17(11):1009-19 [11485618.001]
  • [Cites] Science. 2001 Aug 24;293(5534):1447-8 [11520975.001]
  • [Cites] J Virol. 2001 Oct;75(19):9553-9 [11533220.001]
  • [Cites] J Clin Virol. 2001 Oct;22(3):217-27 [11564586.001]
  • [Cites] J Exp Med. 2002 Mar 4;195(5):593-602 [11877482.001]
  • [Cites] J Virol. 2002 Apr;76(7):3267-75 [11884551.001]
  • [Cites] J Virol. 2002 May;76(9):4591-602 [11932424.001]
  • [Cites] Adv Virus Res. 2002;58:1-28 [12205777.001]
  • (PMID = 15665643.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA093062-02; United States / NCI NIH HHS / CA / R21 CA093062; United States / NCI NIH HHS / CA / P01 CA100730-02; United States / NCI NIH HHS / CA / CA093062-02; United States / NCI NIH HHS / CA / CA063417-09; None / None / / P01 CA100730-01; United States / NCI NIH HHS / CA / P01 CA100730-01; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / R01 CA063417-09
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HTLV-I receptor; 0 / Receptors, Virus; 0 / Viral Envelope Proteins; 0 / beta-Cyclodextrins; 94035-02-6 / 2-hydroxypropyl-beta-cyclodextrin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ NIHMS94161; NLM/ PMC2671014
  •  go-up   go-down


13. Nagasaki A, Miyagi T, Taira T, Shinhama A, Kojya S, Suzuki M, Aonahata M, Yoshimi N, Takasu N: Adult T-cell leukemia/lymphoma with multiple integration of HTLV-1 provirus presenting as an isolated paranasal sinus tumor: a case report. Head Neck; 2008 Jun;30(6):815-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma with multiple integration of HTLV-1 provirus presenting as an isolated paranasal sinus tumor: a case report.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoma and etiologically associated with human T-lymphotropic virus type 1 (HTLV-1).
  • Patients with ATLL commonly present with leukemic changes, systemic lymphadenopathy, and/or extranodal lesion and have very poor prognosis.
  • METHODS AND RESULTS: We describe a rare case of ATLL presenting as an isolated paranasal mass.
  • Southern blot analysis of the biopsied specimens demonstrated multiple integration bands of HTLV-1 provirus of different intensities.
  • Thereafter, the patient showed an indolent clinical course with leukemic changes and pulmonary and cutaneous ATLL lesions and remains alive more than 5 years from diagnosis.
  • CONCLUSION: ATLL should be included in the differential diagnosis of sinonasal lymphoma, although the event is rare.
  • Multiple HTLV-1 provirus integrations of different intensities may be indicative of good prognosis for ATLL.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Proviruses / physiology
  • [MeSH-minor] Adult. Humans. Male. Virus Integration

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18023035.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Ohshima K: Pathological features of diseases associated with human T-cell leukemia virus type I. Cancer Sci; 2007 Jun;98(6):772-8
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] Pathological features of diseases associated with human T-cell leukemia virus type I.
  • In the early 1980s, the first human retrovirus, human T-cell leukemia virus type I (HTLV-I), was isolated and its characterization opened up the new field of human viral oncology.
  • Adult T-cell leukemia/lymphoma (ATLL), which is associated with HTLV-I, is characterized clinically by the appearance of characteristic flower cells, a rapid clinical course, occasional skin lesions, lymphadenopathy and hepatosplenomegaly.
  • In addition, HTLV-I infection is associated with autoimmune and reactive disorders, such as HTLV-I-associated myelopathy and uveitis, and is also related to immunodeficient infectious diseases.
  • Pathological findings of ATLL in the lymph nodes, skin, liver and other organs have been described.
  • In addition to ATLL, non-neoplastic organopathies have been documented in many organs, such as the central nerve system, lung, skin, lymph nodes and gastrointestinal tract.
  • To clarify the HTLV-I-associated diseases, it is important to understand the pathological variations.
  • [MeSH-major] HTLV-I Infections / pathology. Human T-lymphotropic virus 1
  • [MeSH-minor] Bronchiolitis / pathology. Bronchiolitis / virology. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Lymph Nodes. Lymphadenitis / pathology. Lymphadenitis / virology. Paraparesis, Tropical Spastic / pathology. Skin Neoplasms / pathology. Stomach Neoplasms / pathology. Uveitis / pathology. Uveitis / virology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17388788.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 37
  •  go-up   go-down


15. Foucar K: Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome. Am J Clin Pathol; 2007 Apr;127(4):496-510
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] Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The 2005 Society for Hematopathology/European Association for Haematopathology Workshop Session 1 was devoted to case presentations with discussions of 3 types of mature T-cell leukemias--T-cell prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The application of clinical, morphologic, immunophenotypic, and genetic studies to the assessment and characterization of these 3 disorders is presented, along with specific diagnostic recommendations and differential diagnostic considerations.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis. Leukemia, T-Cell / diagnosis. Sezary Syndrome / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD / metabolism. Chromosome Aberrations. Diagnosis, Differential. Humans. Immunophenotyping

  • Genetic Alliance. consumer health - Sezary syndrome.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17369126.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
  •  go-up   go-down


16. Wang SS, Carreon JD, Hanchard B, Chanock S, Hisada M: Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica. Int J Cancer; 2009 Sep 15;125(6):1479-82
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] Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica.
  • We evaluated whether risk of non-Hodgkin lymphoma (NHL), particularly adult T-cell leukemia/lymphoma (ATL) related to human T-lymphotropic virus (HTLV) infection was associated with 63 single nucleotide polymorphisms (SNPs) from 38 candidate genes.
  • The 395 NHL cases registered in Jamaica were matched by age, sex, calendar-year and HTLV serostatus to 309 controls from the same population.
  • Interleukin 13 (IL13) Ex4+98A>G SNP (rs20541) was associated with decreased NHL risk (OR(AG/AA) = 0.62,95% CI = 0.44-0.87, p = 0.006), as was vascular cell adhesion molecule-1, VCAM1 Ex9+149G>A SNP (rs1041163) (OR(CT) = 0.77, 95% CI = 0.54-1.10, OR(CC) = 0.35, 95% CI = 0.16-0.76, p-trend = 0.007).
  • Both results were stronger in analyses restricted to ATL cases and HTLV-positive controls, suggesting a role for these genes in ATL etiology (IL13 OR(AG/AA) = 0.54, 95% CI = 0.36-0.84, p = 0.005; VCAM1 OR(CT) = 0.65, 95% CI = 0.42-1.01, OR(CC) = 0.20, 95% CI = 0.08-0.54, p-trend = 0.001).
  • [MeSH-major] HTLV-I Infections / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Polymorphism, Single Nucleotide / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Genetic Predisposition to Disease. Human T-lymphotropic virus 1 / immunology. Humans. Interleukin-13 / genetics. Interleukin-5 / genetics. Jamaica / epidemiology. Male. Middle Aged. Vascular Cell Adhesion Molecule-1 / genetics. Young Adult

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2009 UICC
  • (PMID = 19533685.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL5 protein, human; 0 / Interleukin-13; 0 / Interleukin-5; 0 / Vascular Cell Adhesion Molecule-1
  •  go-up   go-down


17. Zimmerman EI, Huang M, Leisewitz AV, Wang Y, Yang J, Graves LM: Identification of a novel point mutation in ENT1 that confers resistance to Ara-C in human T cell leukemia CCRF-CEM cells. FEBS Lett; 2009 Jan 22;583(2):425-9
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] Identification of a novel point mutation in ENT1 that confers resistance to Ara-C in human T cell leukemia CCRF-CEM cells.
  • The genetic basis for the Ara-C resistance of CCRF-CEM Ara-C/8C leukemia cells was investigated.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. GLYCINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2000 Mar 24;275(12):8375-81 [10722669.001]
  • [Cites] Biochem J. 2008 Sep 1;414(2):291-300 [18462193.001]
  • [Cites] J Biol Chem. 2001 Nov 30;276(48):45270-5 [11584005.001]
  • [Cites] Biochemistry. 2002 Feb 5;41(5):1512-9 [11814344.001]
  • [Cites] J Exp Ther Oncol. 2002 Jul-Aug;2(4):200-12 [12416024.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Feb;304(2):753-60 [12538831.001]
  • [Cites] Pflugers Arch. 2004 Feb;447(5):735-43 [12838422.001]
  • [Cites] Leukemia. 2004 Mar;18(3):385-93 [14737075.001]
  • [Cites] Biochem Pharmacol. 2004 Feb 1;67(3):453-8 [15037197.001]
  • [Cites] J Biol Chem. 1988 Sep 5;263(25):12391-6 [2842332.001]
  • [Cites] Adv Exp Med Biol. 1989;253B:415-20 [2558543.001]
  • [Cites] Curr Probl Cancer. 1997 Jan-Feb;21(1):1-64 [9058027.001]
  • [Cites] Blood. 1997 Jul 1;90(1):346-53 [9207471.001]
  • [Cites] Leukemia. 2005 Jan;19(1):64-8 [15510196.001]
  • [Cites] J Biochem. 2004 Nov;136(5):733-40 [15632314.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):11025-34 [15649894.001]
  • [Cites] J Biol Chem. 2005 Apr 22;280(16):15880-7 [15701636.001]
  • [Cites] Mol Pharmacol. 2005 Nov;68(5):1397-407 [16099839.001]
  • [Cites] Haematologica. 2006 Jul;91(7):895-902 [16818276.001]
  • [Cites] J Biol Chem. 2007 Feb 2;282(5):3188-95 [17121826.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2349-57 [18381442.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2000 Apr;361(4):373-82 [10763851.001]
  • (PMID = 19116148.001).
  • [ISSN] 1873-3468
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM069976-04; United States / NIGMS NIH HHS / GM / R01 GM069976; United States / NIGMS NIH HHS / GM / R01-GM069976; United States / NIGMS NIH HHS / GM / GM069976-01A1; United States / NIGMS NIH HHS / GM / R01 GM069976-01A1; United States / NIGMS NIH HHS / GM / GM069976-03; United States / NIGMS NIH HHS / GM / R01 GM069976-02; United States / NIGMS NIH HHS / GM / GM069976-02; United States / NIGMS NIH HHS / GM / R01 GM069976-03; United States / NIGMS NIH HHS / GM / R01 GM069976-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine; 38048-32-7 / 4-nitrobenzylthioinosine; 46S541971T / Thioinosine; TE7660XO1C / Glycine
  • [Other-IDs] NLM/ NIHMS92165; NLM/ PMC2647365
  •  go-up   go-down


18. Takeuchi S, Hofmann WK, Tsukasaki K, Takeuchi N, Ikezoe T, Matsushita M, Uehara Y, Phillip Koeffler H: Loss of H19 imprinting in adult T-cell leukaemia/lymphoma. Br J Haematol; 2007 May;137(4):380-1
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] Loss of H19 imprinting in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Genes, Tumor Suppressor. Leukemia-Lymphoma, Adult T-Cell / genetics. RNA, Untranslated
  • [MeSH-minor] Adult. Gene Deletion. Genomic Imprinting. Humans. RNA, Long Noncoding

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17408396.001).
  • [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 / H19 long non-coding RNA; 0 / RNA, Long Noncoding; 0 / RNA, Untranslated
  •  go-up   go-down


19. Toulza F, Nosaka K, Takiguchi M, Pagliuca T, Mitsuya H, Tanaka Y, Taylor GP, Bangham CR: FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia. Int J Cancer; 2009 Nov 15;125(10):2375-82
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] FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL).
  • It has been postulated that ATLL cells might act as regulatory T cells (T(regs)) which, in common with ATLL cells, express both CD25 and FoxP3, and so contribute to the severe immune suppression typical of ATLL.
  • We report here that the frequency of CD25(+) cells varied independently of the frequency of FoxP3(+) cells in both a cross-sectional study and in a longitudinal study of 2 patients with chronic ATLL.
  • Furthermore, the capacity of ATLL cells to suppress proliferation of heterologous CD4(+)CD25(-) cells correlated with the frequency of CD4(+) FoxP3(+) cells but was independent of CD25 expression.
  • Finally, the frequency of CD4(+)FoxP3(+) cells was inversely correlated with the lytic activity of HTLV-1-specific CTLs in patients with ATLL.
  • We conclude that ATLL is not a tumor of FoxP3(+) regulatory T cells, and that a population of FoxP3(+) cells distinct from ATLL cells has regulatory functions and may impair the cell-mediated immune response to HTLV-1 in patients with ATLL.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Proliferation. Chronic Disease. Female. Flow Cytometry. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19544530.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
  •  go-up   go-down


20. Nyborg JK, Egan D, Sharma N: The HTLV-1 Tax protein: revealing mechanisms of transcriptional activation through histone acetylation and nucleosome disassembly. Biochim Biophys Acta; 2010 Mar-Apr;1799(3-4):266-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The HTLV-1 Tax protein: revealing mechanisms of transcriptional activation through histone acetylation and nucleosome disassembly.
  • The human T-cell leukemia virus, type-1 (HTLV-1)-encoded Tax protein is required for high-level transcription of the virus.
  • Tax expression in vivo recruits p300 to the HTLV-1 promoter and correlates with depletion of nucleosomes from the integrated provirus.
  • We recently developed a novel in vitro, chromatin-based experimental system that recapitulates the eviction of nucleosomes from the HTLV-1 promoter observed in vivo.
  • In this review, we will discuss HTLV-1, Tax transactivation, and our recent findings that uncover the critical role of Tax in promoting chromatin transitions that accompany activation of viral transcription.

  • 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
  • [Copyright] 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19782779.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA055035-16; United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA055035; United States / NCI NIH HHS / CA / R01 CA055035-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Histones; 0 / Nucleosomes
  • [Number-of-references] 116
  •  go-up   go-down


21. Akimoto M, Kozako T, Sawada T, Matsushita K, Ozaki A, Hamada H, Kawada H, Yoshimitsu M, Tokunaga M, Haraguchi K, Uozumi K, Arima N, Tei C: Anti-HTLV-1 tax antibody and tax-specific cytotoxic T lymphocyte are associated with a reduction in HTLV-1 proviral load in asymptomatic carriers. J Med Virol; 2007 Jul;79(7):977-86
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] Anti-HTLV-1 tax antibody and tax-specific cytotoxic T lymphocyte are associated with a reduction in HTLV-1 proviral load in asymptomatic carriers.
  • Previous studies have suggested that higher anti-human T-lymphotropic virus 1 (HTLV-1) antibody titer and lower anti-HTLV-1 Tax antibody reactivity are risk factors for adult T-cell leukemia/lymphoma.
  • Forty-five carriers were examined for anti-HTLV-1 and anti-Tax antibody by ELISA.
  • In addition, 43 of the 45 carriers with HLA-A*0201 and/or A*2402 were examined for frequency of Tax-specific cytotoxic T lymphocytes (CTLs) using HTLV-1/HLA tetramers, and 44 were examined for proviral load by real-time PCR.
  • The frequencies of Tax11-19 and Tax301-309-specific CTLs were significantly higher in the anti-Tax antibody-positive group as compared with the antibody-negative group (P = 0.002 and 0.033, respectively).
  • Anti-HTLV-1 antibody titer had a positive correlation with proviral load (P = 0.019), whereas anti-Tax antibody did not show a significant correlation.
  • Synergistic interactions of humoral and cellular immunity against Tax protein were demonstrated in HTLV-1 carriers.
  • Tax-specific CTL may reduce HTLV-1 proviral load to prevent asymptomatic carriers from developing adult T-cell leukemia/lymphoma.
  • [MeSH-major] Carrier State / immunology. Carrier State / virology. Gene Products, tax / immunology. HTLV-I Antibodies / blood. HTLV-I Infections / immunology. HTLV-I Infections / virology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Sequence. Female. Human T-lymphotropic virus 1 / immunology. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Peptide Fragments / genetics. Peptide Fragments / immunology. Proviruses / immunology. Proviruses / isolation & purification. T-Lymphocytes, Cytotoxic / immunology

  • COS Scholar Universe. author profiles.
  • Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17516523.001).
  • [ISSN] 0146-6615
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. 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 / HTLV-I Antibodies; 0 / Peptide Fragments
  •  go-up   go-down


22. Appert A, Nam CH, Lobato N, Priego E, Miguel RN, Blundell T, Drynan L, Sewell H, Tanaka T, Rabbitts T: Targeting LMO2 with a peptide aptamer establishes a necessary function in overt T-cell neoplasia. Cancer Res; 2009 Jun 01;69(11):4784-90
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] Targeting LMO2 with a peptide aptamer establishes a necessary function in overt T-cell neoplasia.
  • LMO2 is a transcription regulator involved in human T-cell leukemia, including some occurring in X-SCID gene therapy trials, and in B-cell lymphomas and prostate cancer.
  • LMO2 functions in transcription complexes via protein-protein interactions involving two LIM domains and causes a preleukemic T-cell development blockade followed by clonal tumors.
  • The peptide inhibits Lmo2 function in a mouse T-cell tumor transplantation assay by preventing Lmo2-dependent T-cell neoplasia.
  • Lmo2 is, therefore, required for sustained T-cell tumor growth, in addition to its preleukemic effect.
  • [MeSH-major] Aptamers, Peptide / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. DNA-Binding Proteins / physiology. Drug Delivery Systems / methods. Metalloproteins / antagonists & inhibitors. Metalloproteins / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2004 Feb;24(4):1439-52 [14749362.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):320-4 [10618416.001]
  • [Cites] N Engl J Med. 2004 Feb 26;350(9):913-22 [14985489.001]
  • [Cites] N Engl J Med. 2004 Apr 29;350(18):1828-37 [15115829.001]
  • [Cites] EMBO J. 2004 Sep 15;23(18):3589-98 [15343268.001]
  • [Cites] EMBO J. 1988 Feb;7(2):385-94 [3259177.001]
  • [Cites] Oncogene. 1990 Jul;5(7):1103-5 [2115645.001]
  • [Cites] Nature. 1990 Aug 2;346(6283):418 [2142998.001]
  • [Cites] Blood. 1991 Feb 1;77(3):599-606 [1703797.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4367-71 [2034676.001]
  • [Cites] Oncogene. 1991 Oct;6(10):1887-93 [1923511.001]
  • [Cites] Gene. 1992 Sep 1;118(1):137-41 [1511877.001]
  • [Cites] Oncogene. 1992 Dec;7(12):2389-97 [1461647.001]
  • [Cites] Mol Cell Biol. 2000 Jul;20(14):5330-42 [10866689.001]
  • [Cites] Gene Ther. 2000 Jun;7(12):1063-6 [10871756.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2003 Aug;59(Pt 8):1484-6 [12876360.001]
  • [Cites] Science. 2003 Oct 17;302(5644):415-9 [14564000.001]
  • [Cites] Semin Hematol. 2003 Oct;40(4):274-80 [14582078.001]
  • [Cites] Cell. 1994 Jul 15;78(1):45-57 [8033210.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8617-21 [8078932.001]
  • [Cites] Cell. 1994 Oct 21;79(2):211-9 [7954790.001]
  • [Cites] EMBO J. 1994 Oct 17;13(20):4831-9 [7957052.001]
  • [Cites] Nature. 1994 Nov 10;372(6502):143-9 [7969446.001]
  • [Cites] Oncogene. 1994 Dec;9(12):3675-81 [7970726.001]
  • [Cites] Oncogene. 1995 Sep 7;11(5):853-62 [7545805.001]
  • [Cites] Methods Enzymol. 1995;255:331-42 [8524119.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3060-71 [7579400.001]
  • [Cites] EMBO J. 1996 Mar 1;15(5):1021-7 [8605871.001]
  • [Cites] Nature. 1996 Apr 11;380(6574):548-50 [8606778.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:289-90 [9209368.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13707-12 [9391090.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3890-5 [9520463.001]
  • [Cites] EMBO J. 1998 Aug 17;17(16):4594-605 [9707419.001]
  • [Cites] Immunity. 1999 Sep;11(3):281-8 [10514006.001]
  • [Cites] Mol Ther. 2006 Jan;13(1):15-25 [16260184.001]
  • [Cites] Nature. 2006 Sep 21;443(7109):E5-6; discussion E6-7 [16988659.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3520-9 [16873670.001]
  • [Cites] J Pathol. 2007 Feb;211(3):278-85 [17167821.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1636-42 [17038524.001]
  • [Cites] EMBO J. 2007 Jul 11;26(13):3250-9 [17568777.001]
  • [Cites] Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz. 2007 Dec;50(12):1507-17 [18046520.001]
  • [Cites] Nature. 2007 Dec 13;450(7172):1001-9 [18075579.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):447-54 [18086797.001]
  • [Cites] Proteins. 2008 Mar;70(4):1461-74 [17910069.001]
  • [Cites] Oncogene. 2008 Aug 21;27(36):4962-8 [18438427.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3143-50 [18688286.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • (PMID = 19487290.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0600914; United Kingdom / Medical Research Council / / MC/ U105178807; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Aptamers, Peptide; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins
  • [Other-IDs] NLM/ PMC2690635; NLM/ UKMS4469
  •  go-up   go-down


23. Silic-Benussi M, Biasiotto R, Andresen V, Franchini G, D'Agostino DM, Ciminale V: HTLV-1 p13, a small protein with a busy agenda. Mol Aspects Med; 2010 Oct;31(5):350-8
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] HTLV-1 p13, a small protein with a busy agenda.
  • Human T-cell leukemia virus type 1 (HTLV-1) infection is characterized by life-long persistence of the virus in the host.
  • While most infected individuals remain asymptomatic, 3-5% will eventually develop adult T-cell leukemia/lymphoma (ATLL) or tropical spastic paraparesis/HTLV-associated myelopathy (TSP/HAM) after a clinical latency that can span years (TSP/HAM) to decades (ATLL).
  • The major oncogenic determinant among HTLV-1 proteins is the Tax transactivator, which influences the expression and function of a great number of cellular proteins, drives cell proliferation, reduces cell death, and induces genetic instability.
  • The present review is focused on the current knowledge of p13, an HTLV-1 accessory protein targeted to the inner mitochondrial membrane and, under certain conditions, to the nucleus.
  • These effects are linked to the protein's effects on cell turnover which include activation of primary T-cells and reduced proliferation/sensitization to death of tumor cells.

  • COS Scholar Universe. author profiles.
  • 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 Ltd. All rights reserved.
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1765-70 [11080824.001]
  • [Cites] Retrovirology. 2009;6:102 [19903329.001]
  • [Cites] J Virol. 2001 Aug;75(16):7672-82 [11462039.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1150-9 [11493464.001]
  • [Cites] J Virol. 2002 Feb;76(3):1400-14 [11773414.001]
  • [Cites] Mol Immunol. 2002 Feb;38(10):723-32 [11841832.001]
  • [Cites] J Virol. 2002 Apr;76(7):3493-501 [11884573.001]
  • [Cites] Nat Genet. 2002 Apr;30(4):352-3 [11925557.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3562-71 [12068005.001]
  • [Cites] J Virol. 2002 Aug;76(15):7843-54 [12097596.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):34424-33 [12093802.001]
  • [Cites] J Virol. 2002 Oct;76(20):10374-82 [12239314.001]
  • [Cites] Annu Rev Immunol. 2004;22:745-63 [15032595.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6629-34 [15100416.001]
  • [Cites] Arch Biochem Biophys. 2004 Sep 15;429(2):123-33 [15313215.001]
  • [Cites] Free Radic Biol Med. 2004 Oct 15;37(8):1144-51 [15451054.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] Adv Cancer Res. 1991;57:381-411 [1659124.001]
  • [Cites] J Virol. 1993 Apr;67(4):2360-6 [8445734.001]
  • [Cites] Immunol Lett. 1996 Dec;54(2-3):67-71 [9052856.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):3050-5 [9743370.001]
  • [Cites] Oncogene. 1999 Feb 11;18(6):1341-9 [10022816.001]
  • [Cites] Oncogene. 1999 Aug 5;18(31):4505-14 [10442641.001]
  • [Cites] Cell Death Differ. 2005 Aug;12 Suppl 1:871-7 [15846376.001]
  • [Cites] J Virol. 2005 Aug;79(15):9449-57 [16014908.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Oncogene. 2006 Apr 6;25(15):2181-91 [16314839.001]
  • [Cites] Blood. 2006 May 15;107(10):3933-9 [16403915.001]
  • [Cites] J Biol Chem. 2006 Dec 1;281(48):37150-8 [17008317.001]
  • [Cites] Science. 2007 Jan 12;315(5809):201-5 [17218518.001]
  • [Cites] Leukemia. 2007 Feb;21(2):261-9 [17122865.001]
  • [Cites] Apoptosis. 2007 May;12(5):815-33 [17294078.001]
  • [Cites] Nat Rev Cancer. 2007 Jun;7(6):409-13 [17508027.001]
  • [Cites] Cell Death Differ. 2007 Jul;14(7):1267-74 [17431419.001]
  • [Cites] Nat Rev Immunol. 2007 Jul;7(7):532-42 [17589543.001]
  • [Cites] Free Radic Biol Med. 2007 Sep 15;43(6):861-8 [17697931.001]
  • [Cites] Nature. 2008 Jan 31;451(7178):591-5 [18235503.001]
  • [Cites] Nat Med. 2008 Apr;14(4):429-36 [18376405.001]
  • [Cites] Front Biosci (Landmark Ed). 2009;14:3338-51 [19273278.001]
  • [Cites] Biochim Biophys Acta. 2009 Jul;1787(7):947-54 [19366603.001]
  • [Cites] Nat Rev Drug Discov. 2009 Jul;8(7):579-91 [19478820.001]
  • [Cites] J Virol. 2001 Jul;75(13):6086-94 [11390610.001]
  • (PMID = 20332002.001).
  • [ISSN] 1872-9452
  • [Journal-full-title] Molecular aspects of medicine
  • [ISO-abbreviation] Mol. Aspects Med.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Viral Proteins
  • [Other-IDs] NLM/ NIHMS198167; NLM/ PMC2941701
  •  go-up   go-down


24. Hara S, Yokote T, Akioka T, Oka S, Yamano T, Tsuji M, Hanafusa T: [Graft-versus-ATLL effect induced by abrupt discontinuation of immunosuppression following allogeneic bone marrow transplantation]. Gan To Kagaku Ryoho; 2005 Jun;32(6):867-71
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] [Graft-versus-ATLL effect induced by abrupt discontinuation of immunosuppression following allogeneic bone marrow transplantation].
  • A 46-year-old man was admitted to our hospital with swelling of a neck lymph node in June, 2002, and was diagnosed with adult T-cell leukemia/lymphoma (ATLL).
  • As ATLL cells were detected in the peripheral blood after two courses of multi-agent chemotherapy (LSG 15), the treatment was changed to biweekly CHOP therapy.
  • Allogeneic bone marrow transplant (allo-BMT) from HTLV- negative and HLA-matched sibling donor was performed (conditioned with cyclophosphamide 60 mg/kg x 2 and total body irradiation 12 Gy).
  • Cyclosporine A (CsA) and short-term methotrexate (MTX) were used for graft-versus-host disease prevention.
  • Though the HTLV- provirus DNA (Southern blot) disappeared, HTLV-I provirus DNA (real-time PCR) T-cell receptor ygammachain gene rearrangement DNA (Southern blot) were detected in bone marrow after allo-BMT.
  • After the allo-BMT transplant, a graft-versus-ATLL (GVATLL) effect may be induced by abrupt discontinuation of immunosuppression.
  • [MeSH-major] Bone Marrow Transplantation. Graft vs Leukemia Effect. Immunosuppression. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Cyclosporine / administration & dosage. DNA, Viral / analysis. Doxorubicin / administration & dosage. Human T-lymphotropic virus 1 / genetics. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Neoplasm, Residual. Prednisone / administration & dosage. Remission Induction. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • 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 = 15984534.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Viral; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CHOP protocol
  •  go-up   go-down


25. McGirr KM, Buehuring GC: Tax & rex: overlapping genes of the Deltaretrovirus group. Virus Genes; 2006 Jun;32(3):229-39
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.
  • Bovine leukemia virus and human T-cell leukemia viruses I and II, members of the Deltaretrovirus group, have two regulatory genes, tax and rex, that are coded in overlapping reading frames.
  • We found that sequence variations in the rex gene of each virus result in amino acid differences significantly more often than variations in the tax gene.
  • For all three viruses the highest ratio of non-synonymous to synonymous changes was found in the rex gene.
  • Nucleotide C was present in all genes of the three viruses at the highest frequency and this bias was most pronounced in the rex gene.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cattle. Codon. Computational Biology. Consensus Sequence. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 2 / genetics. Humans. Leukemia Virus, Bovine / genetics. Sequence Alignment. Software

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Virology. 1985 Apr 30;142(2):357-77 [2997990.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12588-91 [15314228.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Dec;87(24):10015-8 [2263602.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7328-32 [6938980.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9489-93 [1329098.001]
  • [Cites] J Virol. 2001 Sep;75(17):7966-72 [11483741.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 May;82(10):3101-5 [2582407.001]
  • [Cites] J Virol. 1991 Jul;65(7):3721-7 [1904103.001]
  • [Cites] J Virol. 1999 May;73(5):4299-304 [10196328.001]
  • [Cites] Int J Cancer. 1995 Mar 3;60(5):701-6 [7860146.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] J Natl Cancer Inst. 1999 Jun 2;91(11):933-42 [10359545.001]
  • [Cites] J Mol Evol. 1994 May;38(5):506-32 [8028030.001]
  • [Cites] Jpn J Genet. 1994 Oct;69(5):481-8 [7999369.001]
  • [Cites] J Virol. 1998 May;72(5):4327-40 [9557723.001]
  • [Cites] Science. 2004 Jan 16;303(5656):327-32 [14726583.001]
  • [Cites] Virology. 1993 Sep;196(1):57-69 [8356807.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Feb;82(3):677-81 [2983308.001]
  • [Cites] AIDS Res Hum Retroviruses. 2003 Aug;19(8):689-97 [13678471.001]
  • [Cites] J Vet Med B Infect Dis Vet Public Health. 2005 Feb;52(1):8-16 [15702995.001]
  • [Cites] J Gen Virol. 1998 Feb;79 ( Pt 2):269-77 [9472611.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] J Virol. 1997 Nov;71(11):8912-7 [9343258.001]
  • [Cites] Trends Genet. 2002 May;18(5):228-32 [12047938.001]
  • [Cites] J Virol. 2000 Dec;74(23):10939-49 [11069988.001]
  • [Cites] AIDS Res Hum Retroviruses. 1991 Nov;7(11):923-41 [1760230.001]
  • [Cites] Virus Genes. 2001 Jan;22(1):47-52 [11210938.001]
  • [Cites] Virology. 1999 Jan 20;253(2):155-61 [9918874.001]
  • [Cites] J Virol. 1996 Sep;70(9):6442-5 [8709278.001]
  • [Cites] J Gen Virol. 1988 Jul;69 ( Pt 7):1695-710 [2899128.001]
  • [Cites] J Virol. 1993 Aug;67(8):4659-64 [8331724.001]
  • [Cites] Proc Natl Acad Sci U S A. 1961 Aug;47(8):1141-9 [16590864.001]
  • [Cites] Virology. 1999 Jan 20;253(2):181-92 [9918877.001]
  • [Cites] J Mol Evol. 1997;44 Suppl 1:S83-90 [9071016.001]
  • [Cites] Virology. 1993 Jul;195(1):271-4 [8317104.001]
  • [Cites] Bioinformatics. 2003 Dec 12;19(18):2496-7 [14668244.001]
  • [Cites] J Virol. 1993 Feb;67(2):1015-23 [8419636.001]
  • [Cites] Virology. 1993 Mar;193(1):41-9 [8438577.001]
  • [Cites] J Clin Virol. 2002 Aug;25(2):97-106 [12367644.001]
  • [Cites] Virology. 1984 Oct 15;138(1):82-93 [6093363.001]
  • [Cites] Nature. 1978 Apr 6;272(5653):532-5 [692657.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] AIDS Res Hum Retroviruses. 1998 Sep 1;14(13):1199-203 [9737591.001]
  • [Cites] Oncogene. 1991 Jan;6(1):159-63 [1846955.001]
  • [Cites] J Gen Virol. 1996 Jun;77 ( Pt 6):1193-201 [8683207.001]
  • [Cites] J Virol. 1991 Nov;65(11):6001-7 [1920623.001]
  • [Cites] Mol Biol Evol. 2001 May;18(5):763-76 [11319261.001]
  • [Cites] Virology. 2000 Nov 25;277(2):379-86 [11080485.001]
  • [Cites] Mol Biol Evol. 2000 Mar;17(3):374-86 [10723738.001]
  • [Cites] J Virol. 2000 Mar;74(5):2178-85 [10666247.001]
  • [Cites] J Gen Virol. 1991 Oct;72 ( Pt 10):2527-31 [1655959.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] Virology. 2000 May 25;271(1):142-54 [10814579.001]
  • [Cites] Mol Biol Evol. 1986 Sep;3(5):418-26 [3444411.001]
  • [Cites] Int J Cancer. 1995 Nov 15;63(4):494-9 [7591256.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Jun 10;16(9):921-3 [10875617.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 May 1;89(9):3957-61 [1315045.001]
  • [Cites] AIDS Res Hum Retroviruses. 2002 Jan 20;18(2):133-41 [11839146.001]
  • [Cites] J Vet Med Sci. 1998 May;60(5):599-605 [9637294.001]
  • (PMID = 16732475.001).
  • [ISSN] 0920-8569
  • [Journal-full-title] Virus genes
  • [ISO-abbreviation] Virus Genes
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32GM07127
  • [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 / Codon
  •  go-up   go-down


26. Kondo R, Higuchi M, Takahashi M, Oie M, Tanaka Y, Gejyo F, Fujii M: Human T-cell leukemia virus type 2 Tax protein induces interleukin 2-independent growth in a T-cell line. Retrovirology; 2006;3:88
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 2 Tax protein induces interleukin 2-independent growth in a T-cell line.
  • BACKGROUND: While human T-cell leukemia virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia, HTLV type 2 (HTLV-2) is not associated with this malignancy.
  • Accumulating evidence suggests that Tax, a transforming protein of HTLV-1 or HTLV-2, plays a crucial role in the distinctive pathogenesis of these two infections.
  • We herein examined whether Tax2 by itself has a growth promoting activity in a mouse T-cell line CTLL-2, and compared the activity with that of Tax1.
  • RESULTS: We found that Tax2 converts the cell growth of CTLL-2 from an interleukin(IL)-2-dependent growth into an independent one.
  • While the HTLV-2-transformed human T-cell lines produce a significant amount of IL-2, Tax2-transformed CTLL-2 cells only produced a minimal amount of IL-2.
  • These results thus suggest that NFAT-inducible gene(s) other than IL-2 play a role in the cell growth of Tax2-transformed CTLL-2 cells.
  • CONCLUSION: These results show that HTLV-2 Tax2 by itself has a growth promoting activity toward a T-cell line CTLL-2, and the CTLL-2 assay used in this study may therefore be a useful tool for comparing the activity of Tax2 with that of Tax1 in T-cells, thereby elucidating the mechanism of HTLV-1 specific leukemogenesis.
  • [MeSH-major] Cell Transformation, Viral. Gene Products, tax / physiology. Human T-lymphotropic virus 2 / physiology. Interleukin-2 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / virology
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Proliferation. Humans. Mice

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 2.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Virology. 2000 May 25;271(1):142-54 [10814579.001]
  • [Cites] Virology. 2001 Jan 5;279(1):38-46 [11145887.001]
  • [Cites] J Virol. 2002 Mar;76(6):2648-53 [11861831.001]
  • [Cites] Virology. 2004 Jan 5;318(1):327-36 [14972558.001]
  • [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] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Science. 1982 Aug 20;217(4561):737-9 [6980467.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Nature. 1983 Oct 6-12;305(5934):502-5 [6312323.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Nov;80(22):7006-9 [6316341.001]
  • [Cites] Science. 1984 Oct 5;226(4670):61-5 [6089351.001]
  • [Cites] EMBO J. 1986 Mar;5(3):561-5 [3011413.001]
  • [Cites] Cell. 1987 Jan 30;48(2):343-50 [3026643.001]
  • [Cites] Cell. 1987 Apr 10;49(1):47-56 [3030566.001]
  • [Cites] Int J Cancer. 1991 Jun 19;48(4):623-30 [1710610.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):7070-4 [1386673.001]
  • [Cites] Genes Dev. 1992 Nov;6(11):2066-76 [1427072.001]
  • [Cites] J Virol. 1993 Mar;67(3):1211-7 [8437212.001]
  • [Cites] Virology. 1996 Mar 1;217(1):373-9 [8599225.001]
  • [Cites] J Virol. 1996 Aug;70(8):5194-202 [8764028.001]
  • [Cites] J Virol. 1996 Dec;70(12):8508-17 [8970974.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] J Virol. 2005 Sep;79(18):11925-34 [16140768.001]
  • [Cites] Retrovirology. 2005;2:46 [16042787.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5965-75 [16155603.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5996-6004 [16155606.001]
  • [Cites] J Virol. 2005 Nov;79(22):14069-78 [16254341.001]
  • [Cites] Blood. 2006 Mar 1;107(5):1980-8 [16263794.001]
  • [Cites] Retrovirology. 2006;3:20 [16551350.001]
  • [Cites] J Virol. 1999 Feb;73(2):1271-7 [9882331.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • (PMID = 17140451.001).
  • [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 / Interleukin-2
  • [Other-IDs] NLM/ PMC1697825
  •  go-up   go-down


27. Yokote T, Akioka T, Hara S, Oka S, Miyamoto H, Yamano T, Sugino M, Tsuji M, Hanafusa T: Patients with malignancy requiring urgent therapy: CASE 2. Bilateral renal swelling induced by adult T-cell leukemia/lymphoma. J Clin Oncol; 2005 Sep 20;23(27):6793-4
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] Patients with malignancy requiring urgent therapy: CASE 2. Bilateral renal swelling induced by adult T-cell leukemia/lymphoma.
  • [MeSH-major] Acute Kidney Injury / etiology. Bone Marrow / pathology. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Biopsy, Needle. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. Male. Middle Aged. Rare Diseases. Risk Assessment. Severity of Illness Index

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16170187.001).
  • [ISSN] 0732-183X
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


28. Michael B, Nair AM, Datta A, Hiraragi H, Ratner L, Lairmore MD: Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity. Virology; 2006 Oct 25;354(2):225-39
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] Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity.
  • Human T-lymphotropic virus type-1 (HTLV-1) is a deltaretrovirus that causes adult T cell leukemia/lymphoma, and is implicated in a variety of lymphocyte-mediated inflammatory disorders.
  • HTLV-1 provirus has regulatory and accessory genes in four pX open reading frames.
  • HTLV-1 pX ORF-II encodes two proteins, p13II and p30II, which are incompletely defined in virus replication or pathogenesis.
  • We have demonstrated that pX ORF-II mutations block virus replication in vivo and that ORF-II encoded p30II, a nuclear-localizing protein that binds with CREB-binding protein (CBP)/p300, represses CREB and Tax responsive element (TRE)-mediated transcription.
  • Herein, we have identified p30II motifs important for p300 binding and in regulating TRE-mediated transcription in the absence and presence of HTLV-1 provirus.
  • Collectively, our data indicate that HTLV-1 p30II modulates viral gene expression in a cooperative manner with p300-mediated acetylation.

  • COS Scholar Universe. author profiles.
  • 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
  • [Cites] J Virol. 2000 Feb;74(3):1094-100 [10627519.001]
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8136-45 [10567539.001]
  • [Cites] J Exp Med. 2000 Feb 7;191(3):567-72 [10662802.001]
  • [Cites] Oncogene. 2000 Mar 16;19(12):1491-9 [10734308.001]
  • [Cites] Microbiol Mol Biol Rev. 2000 Jun;64(2):435-59 [10839822.001]
  • [Cites] Genes Dev. 2000 Jul 1;14(13):1553-77 [10887150.001]
  • [Cites] Virology. 2000 Aug 15;274(1):86-93 [10936091.001]
  • [Cites] Cell Mol Life Sci. 2000 Aug;57(8-9):1184-92 [11028911.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • [Cites] J Biol Chem. 2001 Apr 27;276(17):13505-8 [11279224.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7241-6 [12370815.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49459-65 [12386157.001]
  • [Cites] Adv Cancer Res. 2003;89:69-132 [14587871.001]
  • [Cites] Virology. 2003 Dec 5;317(1):136-45 [14675632.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] J Virol. 2004 Apr;78(8):3837-45 [15047799.001]
  • [Cites] Rev Clin Exp Hematol. 2003 Dec;7(4):336-61 [15129647.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2556-76 [15358581.001]
  • [Cites] J Virol. 2004 Oct;78(20):11077-83 [15452228.001]
  • [Cites] J Virol. 1992 Mar;66(3):1737-45 [1310774.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8813-7 [1528897.001]
  • [Cites] J Virol. 1993 Apr;67(4):2360-6 [8445734.001]
  • [Cites] Nature. 1995 Mar 2;374(6517):81-4 [7870178.001]
  • [Cites] Nature. 1995 Mar 2;374(6517):85-8 [7870179.001]
  • [Cites] Nature. 1995 Jul 27;376(6538):348-51 [7630403.001]
  • [Cites] EMBO J. 1995 Oct 2;14(19):4758-62 [7588605.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3619-39 [7579327.001]
  • [Cites] J Virol. 1996 Apr;70(4):2101-6 [8642630.001]
  • [Cites] Nature. 1996 Apr 18;380(6575):642-6 [8602268.001]
  • [Cites] Cell. 1996 May 3;85(3):403-14 [8616895.001]
  • [Cites] EMBO J. 1996 May 1;15(9):2236-48 [8641289.001]
  • [Cites] Nature. 1996 Sep 5;383(6595):22-3 [8779707.001]
  • [Cites] Curr Biol. 1996 Aug 1;6(8):951-4 [8805328.001]
  • [Cites] Leukemia. 1997 Jun;11(6):866-70 [9177442.001]
  • [Cites] Cell. 1997 Jun 27;89(7):1175-84 [9215639.001]
  • [Cites] Nature. 1997 Sep 25;389(6649):349-52 [9311776.001]
  • [Cites] Mol Cell Biol. 1997 Oct;17(10):6139-46 [9315674.001]
  • [Cites] J Virol. 1998 Apr;72(4):3495-500 [9525690.001]
  • [Cites] J Virol. 1998 May;72(5):4458-62 [9557741.001]
  • [Cites] J Virol. 1998 Nov;72(11):9396-9 [9765496.001]
  • [Cites] Methods. 1998 Sep;16(1):83-94 [9774518.001]
  • [Cites] J Biol Chem. 1998 Dec 18;273(51):34646-52 [9852138.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4137-43 [10435595.001]
  • [Cites] AIDS Res Hum Retroviruses. 1999 Oct 10;15(15):1351-63 [10515151.001]
  • [Cites] Front Biosci. 2005 Jan 1;10:431-45 [15574380.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):6178-98 [15988028.001]
  • [Cites] Arch Immunol Ther Exp (Warsz). 2005 Jul-Aug;53(4):283-96 [16088313.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5986-95 [16155605.001]
  • [Cites] J Virol. 2006 Jan;80(1):181-91 [16352542.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):3005-9 [1348363.001]
  • [Cites] Blood. 2000 Feb 1;95(3):745-55 [10648382.001]
  • (PMID = 16890266.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-70529; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCI NIH HHS / CA / CA92009; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / R01 CA092009; 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 / Cell Cycle Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Retroviridae Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Viral Proteins; 0 / tof protein, Human T-lymphotropic virus 1; EC 2.3.1.48 / CREB-Binding Protein; 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/ NIHMS183540; NLM/ PMC3044896
  •  go-up   go-down


29. Li K, Zhang S, Kronqvist M, Wallin M, Ekström M, Derse D, Garoff H: Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. J Virol; 2008 Jul;82(14):7135-43
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] Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env.
  • Human T-cell leukemia virus (HTLV-1) Env carries a typical disulfide isomerization motif, C(225)XXC, in the C-terminal domain SU.
  • The importance of the CXXC-mediated disulfide isomerization for infection was studied using murine leukemia virus vectors pseudotyped with wild-type or C225A HTLV-1 Env.
  • We conclude that the fusion activity of HTLV-1 Env is controlled by an SU CXXC-mediated isomerization of the intersubunit disulfide.
  • [MeSH-major] Disulfides / metabolism. Gene Products, env / metabolism. Human T-lymphotropic virus 1 / physiology. Virus Internalization
  • [MeSH-minor] Amino Acid Substitution / genetics. Animals. Cell Line. Cricetinae. Dithiothreitol / pharmacology. Humans. Mutation, Missense. Rats. Reducing Agents / pharmacology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 1981 Jun;89(3):674-9 [6265470.001]
  • [Cites] J Virol. 1976 Jun;18(3):956-68 [178931.001]
  • [Cites] Science. 1983 Feb 18;219(4586):856-9 [6600519.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Int J Cancer. 1983 Sep 15;32(3):321-8 [6604033.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Dec;80(23):7337-41 [6316359.001]
  • [Cites] Virology. 1984 Jan 15;132(1):1-11 [6320527.001]
  • [Cites] Int J Cancer. 1984 Jun 15;33(6):721-5 [6329965.001]
  • [Cites] Virology. 1984 Jul 30;136(2):338-47 [6087548.001]
  • [Cites] Virology. 1984 Oct 15;138(1):82-93 [6093363.001]
  • [Cites] Princess Takamatsu Symp. 1984;15:241-9 [6100642.001]
  • [Cites] Biotechnology (N Y). 1991 Dec;9(12):1356-61 [1370252.001]
  • [Cites] J Virol. 1993 Jan;67(1):67-74 [8416389.001]
  • [Cites] Virology. 1994 Jul;202(1):61-9 [8009867.001]
  • [Cites] Nature. 1994 Sep 1;371(6492):37-43 [8072525.001]
  • [Cites] Virology. 1995 Feb 1;206(2):885-93 [7856101.001]
  • [Cites] J Virol. 2005 Feb;79(3):1678-85 [15650193.001]
  • [Cites] Retrovirology. 2004;1:41 [15575958.001]
  • [Cites] Virology. 2006 Mar 1;346(1):194-204 [16325219.001]
  • [Cites] J Virol. 2006 Jul;80(14):6844-54 [16809290.001]
  • [Cites] J Virol. 2006 Oct;80(19):9876-88 [16973592.001]
  • [Cites] Virology. 2007 Apr 25;361(1):149-60 [17182074.001]
  • [Cites] Virology. 1994 Mar;199(2):331-8 [8122365.001]
  • [Cites] Curr Biol. 1995 Dec 1;5(12):1377-83 [8749390.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11658-63 [8876192.001]
  • [Cites] J Virol. 1997 Mar;71(3):2092-9 [9032341.001]
  • [Cites] J Virol. 1997 Oct;71(10):8073-7 [9311907.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14306-13 [9405608.001]
  • [Cites] J Virol. 1998 Aug;72(8):6537-45 [9658097.001]
  • [Cites] Protein Sci. 1998 Jul;7(7):1612-9 [9684894.001]
  • [Cites] J Virol. 1998 Dec;72(12):9955-65 [9811733.001]
  • [Cites] Biochem J. 1999 Apr 1;339 ( Pt 1):1-10 [10085220.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4319-24 [10200260.001]
  • [Cites] J Virol. 1999 Nov;73(11):9683-9 [10516085.001]
  • [Cites] J Virol. 2000 Jan;74(1):295-304 [10590117.001]
  • [Cites] J Virol. 2000 Jul;74(14):6614-21 [10864675.001]
  • [Cites] J Biol Chem. 2000 Aug 4;275(31):23417-20 [10851227.001]
  • [Cites] Annu Rev Biochem. 2000;69:531-69 [10966468.001]
  • [Cites] Cell. 2000 Nov 10;103(4):679-89 [11106737.001]
  • [Cites] J Virol. 2001 Apr;75(8):3685-95 [11264358.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4113-8 [11274436.001]
  • [Cites] J Virol. 2001 Sep;75(18):8461-8 [11507191.001]
  • [Cites] J Virol. 2001 Oct;75(19):9096-105 [11533173.001]
  • [Cites] J Virol. 2001 Nov;75(21):10472-8 [11581416.001]
  • [Cites] J Virol. 2003 Mar;77(5):3281-90 [12584351.001]
  • [Cites] J Virol. 2003 Sep;77(18):9922-30 [12941902.001]
  • [Cites] Cell. 2003 Nov 14;115(4):449-59 [14622599.001]
  • [Cites] J Virol. 2004 Jan;78(1):473-81 [14671127.001]
  • [Cites] J Virol. 2004 Feb;78(3):1403-10 [14722295.001]
  • [Cites] EMBO J. 2004 Jan 14;23(1):54-65 [14685283.001]
  • [Cites] Science. 1982 Aug 20;217(4561):737-9 [6980467.001]
  • (PMID = 18480461.001).
  • [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 / Disulfides; 0 / Gene Products, env; 0 / Reducing Agents; T8ID5YZU6Y / Dithiothreitol
  • [Other-IDs] NLM/ PMC2446982
  •  go-up   go-down


30. Silic-Benussi M, Cavallari I, Vajente N, Vidali S, Chieco-Bianchi L, Di Lisa F, Saggioro D, D'Agostino DM, Ciminale V: Redox regulation of T-cell turnover by the p13 protein of human T-cell leukemia virus type 1: distinct effects in primary versus transformed cells. Blood; 2010 Jul 8;116(1):54-62
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] Redox regulation of T-cell turnover by the p13 protein of human T-cell leukemia virus type 1: distinct effects in primary versus transformed cells.
  • The present study investigated the function of p13, a mitochondrial protein of human T-cell leukemia virus type 1 (HTLV-1).
  • In transformed cells (Jurkat, HeLa), p13 did not affect ROS unless the cells were subjected to glucose deprivation, which led to a p13-dependent increase in ROS and cell death.
  • Using RNA interference we confirmed that expression of p13 also influences glucose starvation-induced cell death in the context of HTLV-1-infected cells.
  • These findings suggest that p13 may have a distinct impact on cell turnover depending on the inherent ROS levels; in the context of the HTLV-1 propagation strategy, p13 could increase the pool of "normal" infected cells while culling cells acquiring a transformed phenotype, thus favoring lifelong persistence of the virus in the host.
  • [MeSH-major] Human T-lymphotropic virus 1 / metabolism. Reactive Oxygen Species / metabolism. Retroviridae Proteins / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Cell Line. Cells, Cultured. Gene Expression Regulation, Viral. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HeLa Cells. Host-Pathogen Interactions. Humans. Jurkat Cells. Lentivirus / genetics. Microscopy, Confocal. Mitochondria / metabolism. Oxidation-Reduction. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transduction, Genetic

  • 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 = 20395415.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 147336-22-9 / Green Fluorescent Proteins
  •  go-up   go-down


31. Kim YM, Ramírez JA, Mick JE, Giebler HA, Yan JP, Nyborg JK: Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation. J Biol Chem; 2007 Jun 29;282(26):18750-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.
  • Transcriptional activation of human T-cell leukemia virus type 1 (HTLV-1) is mediated by the viral oncoprotein Tax, which utilizes cellular transcriptional machinery to perform this function.
  • The coactivator CREB-binding protein (CBP)/p300 binds to this promoter-bound ternary complex, which promotes the initiation of HTLV-1 transcription.
  • Consonant with a fundamental role for CREB phosphorylation in Tax recruitment to the complex, we found that CREB is highly phosphorylated in a panel of HTLV-1-infected human T-cell lines.
  • Because pCREB has been implicated in leukemogenesis, enhancement of CREB phosphorylation by the virus may play a role in the etiology of adult T-cell leukemia.

  • 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
  • (PMID = 17449469.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA55035; United States / NCI NIH HHS / CA / CA055035-14S1; United States / NCI NIH HHS / CA / CA055035-14; United States / NCI NIH HHS / CA / R01 CA055035-14S1; United States / NCI NIH HHS / CA / CA55035-S1; United States / NCI NIH HHS / CA / R01 CA055035-14
  • [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 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein
  •  go-up   go-down


32. Norris PJ, Hirschkorn DF, DeVita DA, Lee TH, Murphy EL: Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells. Virulence; 2010 Jan-Feb;1(1):19-28
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 drives spontaneous proliferation of natural killer cells.
  • Most human T cell leukemia virus type 1 (HTLV-1) infected subjects remain asymptomatic throughout their lives, with a few individuals developing HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia.
  • Lymphocytes from about half of HTLV-1 infected subjects spontaneously proliferate in vitro, and how this phenomenon relates to symptomatic disease outcome and viral burden is poorly understood.
  • Spontaneous proliferation was measured in lymphocyte subsets, and these findings were correlated with HTLV-1 proviral load and Tax expression in PBMCs.
  • We found that in addition to previously described vigorous CD8+ T cell spontaneous proliferation, natural killer (NK) cells spontaneously proliferated to a similar high level, resulting in expansion of CD56-expressing NK cells.
  • Spontaneous NK cell proliferation positively correlated with HTLV-1 proviral load but not with Tax expression or the presence of HAM/TSP.
  • The strongest correlate with clinical outcome in this cohort was the ability of cells to express Tax, while HTLV-1 proviral load was more closely related to spontaneous NK cell proliferation.
  • These results demonstrate that spontaneous proliferation, Tax expression, and proviral load are inter-related but not equivalent, and that spontaneous lymphocyte proliferation is not restricted to T cells, the targets of HTLV-1 infection.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • 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] J Virol. 2007 Sep;81(18):9707-17 [17609265.001]
  • [Cites] Int Rev Immunol. 2007 Sep-Dec;26(5-6):249-68 [18027200.001]
  • [Cites] Neurol Clin. 2008 Aug;26(3):781-97, ix-x [18657726.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3788-97 [18689544.001]
  • [Cites] Retrovirology. 2009;6:19 [19228429.001]
  • [Cites] Immunology. 2009 Apr;126(4):458-65 [19278419.001]
  • [Cites] J Exp Med. 2009 Mar 16;206(3):515-23 [19255146.001]
  • [Cites] Arch Intern Med. 1999 Jul 12;159(13):1485-91 [10399901.001]
  • [Cites] J Clin Invest. 2006 Apr;116(4):974-83 [16585963.001]
  • [Cites] Immunology. 2007 Jun;121(2):258-65 [17346281.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):586-93 [10065900.001]
  • [Cites] J Virol Methods. 1998 Nov;75(2):123-40 [9870588.001]
  • [Cites] J Infect Dis. 1997 Dec;176(6):1468-75 [9395356.001]
  • [Cites] J Virol. 1997 Feb;71(2):1181-90 [8995640.001]
  • [Cites] Clin Infect Dis. 1996 Jul;23(1):138-45 [8816143.001]
  • [Cites] Thorax. 2000 May;55(5):388-92 [10770820.001]
  • [Cites] Eur J Immunol. 2000 May;30(5):1356-63 [10820382.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1506-11 [11520801.001]
  • [Cites] Trends Immunol. 2001 Nov;22(11):633-40 [11698225.001]
  • [Cites] Blood. 2002 Jan 1;99(1):88-94 [11756157.001]
  • [Cites] Neurology. 2003 Dec 9;61(11):1588-94 [14663047.001]
  • [Cites] Chest. 2003 Dec;124(6):2283-92 [14665512.001]
  • [Cites] Emerg Infect Dis. 2004 Jan;10(1):109-16 [15078605.001]
  • [Cites] J Clin Virol. 2004 Dec;31(4):275-82 [15494269.001]
  • [Cites] Science. 1984 Oct 26;226(4673):459-62 [6093248.001]
  • [Cites] Jpn J Clin Oncol. 1985 Jun;15(2):423-30 [2991627.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] J Exp Med. 1985 Dec 1;162(6):2089-106 [2415663.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Ann Neurol. 1988;23 Suppl:S143-50 [2894806.001]
  • [Cites] Int J Cancer. 1989 Feb 15;43(2):250-3 [2917802.001]
  • [Cites] Am Rev Respir Dis. 1989 Jun;139(6):1329-35 [2786358.001]
  • [Cites] J Exp Med. 1990 May 1;171(5):1509-26 [1692080.001]
  • [Cites] J Exp Med. 1990 May 1;171(5):1527-33 [2139697.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5218-22 [2367534.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] J Neuroimmunol. 1991 Aug;33(2):121-8 [2066395.001]
  • [Cites] Blood. 1991 Jul 1;78(1):169-74 [1676916.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2110-4 [1549569.001]
  • [Cites] Clin Immunol Immunopathol. 1992 Dec;65(3):201-6 [1360340.001]
  • [Cites] J Immunol. 1992 Dec 15;149(12):4101-8 [1460293.001]
  • [Cites] J Virol. 1993 Jun;67(6):3134-41 [7684460.001]
  • [Cites] Clin Immunol Immunopathol. 1994 Sep;72(3):312-20 [8062446.001]
  • [Cites] J Virol. 1995 May;69(5):2863-8 [7707509.001]
  • [Cites] Clin Diagn Lab Immunol. 1994 May;1(3):273-82 [7496962.001]
  • [Cites] Virology. 1996 Jul 15;221(2):375-81 [8661450.001]
  • [Cites] J Immunol. 1996 Aug 1;157(3):1288-96 [8757637.001]
  • [CommentIn] Virulence. 2010 Jan-Feb;1(1):8-9 [21178408.001]
  • (PMID = 20640055.001).
  • [ISSN] 2150-5608
  • [Journal-full-title] Virulence
  • [ISO-abbreviation] Virulence
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL062235-04; United States / NHLBI NIH HHS / HL / R01 HL062235; United States / NHLBI NIH HHS / HL / HL-062235; United States / NHLBI NIH HHS / HL / R01 HL062235-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Gene Products, tax; 0 / NCAM1 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Keywords] NOTNLM ; HAM/TSP / HTLV / NK cell / T cell / Tax
  •  go-up   go-down


33. Morris JC, Waldmann TA: Antibody-based therapy of leukaemia. Expert Rev Mol Med; 2009;11:e29
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] Antibody-based therapy of leukaemia.
  • Over the past decade, monoclonal antibodies have dramatically impacted the treatment of haematological malignancies, as evidenced by the effect of rituximab on the response rate and survival of patients with follicular and diffuse large B cell non-Hodgkin's lymphoma.
  • Currently, only two monoclonal antibodies - the anti-CD33 immunotoxin gemtuzumab ozogamicin and the CD52-directed antibody alemtuzumab - are approved for treatment of relapsed acute myeloid leukaemia in older patients and B cell chronic lymphocytic leukaemia, respectively.
  • Although not approved for such treatment, alemtuzumab is also active against T cell prolymphocytic leukaemia, cutaneous T cell lymphoma and Sézary syndrome, and adult T cell leukaemia and lymphoma.
  • In addition, rituximab has demonstrated activity against B cell chronic lymphocytic and hairy cell leukaemia.
  • Monoclonal antibodies targeting CD4, CD19, CD20, CD22, CD23, CD25, CD45, CD66 and CD122 are now being studied in the clinic for the treatment of leukaemia.
  • Improved interactions with Fc receptors on immune effector cells can enhance destruction of target cells through antibody-dependent cellular cytotoxicity and complement-mediated cell lysis.
  • The antibodies can also be armed with cellular toxins or radionuclides to enhance the destruction of leukaemia cells.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematologic Neoplasms / therapy. Immunologic Factors / therapeutic use. Immunotoxins / therapeutic use. Leukemia / therapy
  • [MeSH-minor] Adult. Antigens, CD / immunology. Clinical Trials as Topic. Humans

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • (PMID = 19788782.001).
  • [ISSN] 1462-3994
  • [Journal-full-title] Expert reviews in molecular medicine
  • [ISO-abbreviation] Expert Rev Mol Med
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Immunologic Factors; 0 / Immunotoxins
  • [Number-of-references] 193
  •  go-up   go-down


34. Laugel B, Boulter JM, Lissin N, Vuidepot A, Li Y, Gostick E, Crotty LE, Douek DC, Hemelaar J, Price DA, Jakobsen BK, Sewell AK: Design of soluble recombinant T cell receptors for antigen targeting and T cell inhibition. J Biol Chem; 2005 Jan 21;280(3):1882-92
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] Design of soluble recombinant T cell receptors for antigen targeting and T cell inhibition.
  • The use of recombinant T cell receptors (TCRs) to target therapeutic interventions has been hindered by the naturally low affinity of TCR interactions with peptide major histocompatibility complex ligands.
  • Here, we use multimeric forms of soluble heterodimeric alphabeta TCRs for specific detection of target cells pulsed with cognate peptide, discrimination of quantitative changes in antigen display at the cell surface, identification of virus-infected cells, inhibition of antigen-specific cytotoxic T lymphocyte activation, and identification of cross-reactive peptides.
  • Notably, the A6 TCR specific for the immunodominant HLA A2-restricted human T cell leukemia virus type 1 Tax(11-19) epitope bound to HLA A2-HuD(87-95) (K(D) 120 microm by surface plasmon resonance), an epitope implicated as a causal antigen in the paraneoplastic neurological degenerative disorder anti-Hu syndrome.
  • [MeSH-major] Antigens / immunology. Receptors, Antigen, T-Cell / immunology. T-Lymphocytes / immunology

  • COS Scholar Universe. author profiles.
  • Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15531581.001).
  • [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 / Antigens; 0 / Receptors, Antigen, T-Cell; 0 / Recombinant Proteins
  •  go-up   go-down


35. Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N: Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature. Leuk Lymphoma; 2009 Feb;50(2):187-95
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] Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
  • Extranodal adult T-cell leukemia/lymphoma (ATLL) of the head and neck is a rare disease.
  • We studied the clinicopathological features of nine patients with ATLL involving extranodal head and neck sites and conducted a literature review.
  • Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large cell-type.
  • Five patients with localised disease showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
  • Patients with localised disease documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
  • ATLL should be included in the differential diagnosis of extranodal head and neck lymphoma.
  • Localised extranodal ATLL of the head and neck may exhibit indolent clinical behaviours.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):148-9 [19235009.001]
  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):150-1 [19235010.001]
  • (PMID = 19197730.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
  •  go-up   go-down


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


44. 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
  •  <