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1. 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
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  • [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.

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  • (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
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2. Pais-Correia AM, Sachse M, Guadagnini S, Robbiati V, Lasserre R, Gessain A, Gout O, Alcover A, Thoulouze MI: Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses. Nat Med; 2010 Jan;16(1):83-9
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  • [Title] Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.
  • Human T cell leukemia virus type 1 (HTLV-1) is a lymphotropic retrovirus whose cell-to-cell transmission requires cell contacts.
  • HTLV-1-infected T lymphocytes form 'virological synapses', but the mechanism of HTLV-1 transmission remains poorly understood.
  • We show here that HTLV-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the cell surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.
  • Extracellular viral assemblies rapidly adhere to other cells upon cell contact, allowing virus spread and infection of target cells.
  • Their removal strongly reduces the ability of HTLV-1-producing cells to infect target cells.
  • Our findings unveil a novel virus transmission mechanism based on the generation of extracellular viral particle assemblies whose structure, composition and function resemble those of bacterial biofilms.
  • HTLV-1 biofilm-like structures represent a major route for virus transmission from cell to cell.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Extracellular Matrix / virology. HTLV-I Infections / transmission. Human T-lymphotropic virus 1 / physiology
  • [MeSH-minor] Biofilms. Concanavalin A. Gene Products, env / metabolism. Humans. Microscopy, Electron, Transmission. Virus Assembly / physiology. Virus Attachment. Virus Internalization

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  • [CommentIn] Nat Med. 2010 Jan;16(1):25-7 [20057417.001]
  • (PMID = 20023636.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, env; 11028-71-0 / Concanavalin A
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3. Yu Q, Minoda Y, Yoshida R, Yoshida H, Iha H, Kobayashi T, Yoshimura A, Takaesu G: HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein. Biochem Biophys Res Commun; 2008 Jan 4;365(1):189-94
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  • [Title] HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter protein.
  • Human T cell leukemia virus type 1 (HTLV-1) Tax is an oncoprotein that plays a crucial role in the proliferation and transformation of HTLV-1-infected T lymphocytes.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. MAP Kinase Kinase Kinases / metabolism
  • [MeSH-minor] Binding Sites. Cell Line. Humans. NF-kappa B / metabolism. Ubiquitin-Protein Ligases / metabolism

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  • (PMID = 17986383.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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4. 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
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  • [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

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  • (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
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5. Toulza F, Nosaka K, Tanaka Y, Schioppa T, Balkwill F, Taylor GP, Bangham CR: Human T-lymphotropic virus type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells. J Immunol; 2010 Jul 01;185(1):183-9
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  • [Title] Human T-lymphotropic virus type 1-induced CC chemokine ligand 22 maintains a high frequency of functional FoxP3+ regulatory T cells.
  • We recently reported that human T-lymphotropic virus type 1 (HTLV-1) infection is accompanied by a high frequency of CD4(+)FoxP3(+) cells in the circulation.
  • In asymptomatic carriers of HTLV-1 and in patients with HTLV-1-associated inflammatory and malignant diseases, a high FoxP3(+) cell frequency correlated with inefficient cytotoxic T cell-mediated killing of HTLV-1-infected cells.
  • In adult T cell leukemia/lymphoma (ATLL), the FoxP3(+) population was distinct from the leukemic T cell clones.
  • However, the cause of the increase in FoxP3(+) cell frequency in HTLV-1 infection was unknown.
  • In this study, we report that the plasma concentration of the chemokine CCL22 is abnormally high in HTLV-1-infected subjects and that the concentration is strongly correlated with the frequency of FoxP3(+) cells, which express the CCL22 receptor CCR4.
  • Further, we show that CCL22 is produced by cells that express the HTLV-1 transactivator protein Tax, and that the increased CCL22 enhances the migration and survival of FoxP3(+) cells in vitro.
  • Finally, we show that FoxP3(+) cells inhibit the proliferation of ex vivo, autologous leukemic clones from patients with ATLL.
  • We conclude that HTLV-1-induced CCL22 causes the high frequency of FoxP3(+) cells observed in HTLV-1 infection; these FoxP3(+) cells may both retard the progression of ATLL and HTLV-1-associated inflammatory diseases and contribute to the immune suppression seen in HTLV-1 infection, especially in ATLL.
  • [MeSH-major] Cell Proliferation. Chemokine CCL22 / physiology. Forkhead Transcription Factors / physiology. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes, Regulatory / cytology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] CD4 Lymphocyte Count. Cell Survival / immunology. Cytotoxicity Tests, Immunologic. HTLV-I Infections / immunology. HTLV-I Infections / pathology. Humans. Jurkat Cells. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / pathology. T-Lymphocytes, Cytotoxic / cytology. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / virology

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  • [Cites] Blood. 2000 Feb 15;95(4):1386-92 [10666215.001]
  • [Cites] Int J Cancer. 2009 Nov 15;125(10):2375-82 [19544530.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1505-11 [11861261.001]
  • [Cites] J Infect Dis. 2002 Oct 1;186(7):932-9 [12232833.001]
  • [Cites] Nat Rev Immunol. 2003 Mar;3(3):189-98 [12658267.001]
  • [Cites] J Neurovirol. 2003 Apr;9(2):228-35 [12707853.001]
  • [Cites] J Immunol. 2004 Oct 15;173(8):5121-9 [15470056.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [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] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Cell. 1987 Apr 10;49(1):47-56 [3030566.001]
  • [Cites] Tohoku J Exp Med. 1989 Jan;157(1):1-11 [2711372.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] J Virol. 1994 Oct;68(10):6778-81 [8084014.001]
  • [Cites] J Biol Chem. 1998 Jan 16;273(3):1764-8 [9430724.001]
  • [Cites] J Virol Methods. 1998 Nov;75(1):21-6 [9820571.001]
  • [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] Nat Immunol. 2005 Apr;6(4):331-7 [15785758.001]
  • [Cites] J Exp Med. 2005 Apr 4;201(7):1037-44 [15809349.001]
  • [Cites] J Gen Virol. 2005 May;86(Pt 5):1515-23 [15831965.001]
  • [Cites] Clin Infect Dis. 2005 Jun 1;40(11):e90-6 [15889351.001]
  • [Cites] Cancer Sci. 2005 Aug;96(8):527-33 [16108835.001]
  • [Cites] Nat Rev Immunol. 2006 Apr;6(4):295-307 [16557261.001]
  • [Cites] Blood. 2006 May 1;107(9):3639-46 [16403912.001]
  • [Cites] Immunity. 2006 Jul;25(1):129-41 [16860762.001]
  • [Cites] J Immunol. 2006 Oct 1;177(7):4488-94 [16982885.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1139-46 [16952304.001]
  • [Cites] Leukemia. 2006 Dec;20(12):2162-8 [17039235.001]
  • [Cites] J Immunol. 2008 Jan 15;180(2):931-9 [18178833.001]
  • [Cites] Immunology. 2008 Feb;123(2):157-63 [18067556.001]
  • [Cites] Int J Cancer. 2008 May 15;122(10):2286-93 [18224687.001]
  • [Cites] Blood. 2008 May 15;111(10):5047-53 [18094326.001]
  • [Cites] J Immunol. 2008 Jun 1;180(11):7681-6 [18490771.001]
  • [Cites] J Acquir Immune Defic Syndr. 2008 Aug 15;48(5):607-10 [18645510.001]
  • [Cites] Eur J Haematol. 2008 Sep;81(3):209-17 [18510697.001]
  • [Cites] Cancer Immunol Immunother. 2009 Mar;58(3):441-7 [18685848.001]
  • [Cites] Cancer Res. 2009 Mar 1;69(5):2000-9 [19244125.001]
  • [Cites] Clin Cancer Res. 2009 Apr 1;15(7):2231-7 [19318474.001]
  • [Cites] J Immunol. 2009 May 1;182(9):5723-9 [19380819.001]
  • [Cites] PLoS Negl Trop Dis. 2009;3(6):e456 [19513105.001]
  • [Cites] Eur J Immunol. 2009 Jul;39(7):1700-12 [19582737.001]
  • [Cites] Blood. 2001 Aug 1;98(3):721-6 [11468172.001]
  • (PMID = 20525891.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 080871; United Kingdom / Medical Research Council / / G0501974; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL22 protein, human; 0 / Chemokine CCL22; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
  • [Other-IDs] NLM/ EMS51736; NLM/ PMC3575032
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6. Saito M, Mori A, Irie T, Tanaka M, Morioka M, Uchiyama Y, Taukamoto E: [Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ]. Rinsho Ketsueki; 2009 Dec;50(12):1669-70
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  • [Title] [Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ].
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / radiography. Leukemia-Lymphoma, Adult T-Cell / radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed

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  • (PMID = 20068272.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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7. Shiratori S, Yasumoto A, Tanaka J, Shigematsu A, Yamamoto S, Nishio M, Hashino S, Morita R, Takahata M, Onozawa M, Kahata K, Kondo T, Ota S, Wakasa K, Sugita J, Koike T, Asaka M, Kasai M, Imamura M: A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect. Biol Blood Marrow Transplant; 2008 Jul;14(7):817-23
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  • [Title] A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect.
  • Adult T cell leukemia/lymphoma (ATL) is a highly aggressive T cell malignancy, and has a poor prognosis.
  • Recently, allogeneic-hematopoietic stem cell transplantation (allo-HSCT) has been suggested to improve the outcome.
  • We retrospectively analyzed 15 patients with ATL who had received allo-HSCT in 2 institutions in Hokkaido, Japan.
  • Calcineurin inhibitor dosage was reduced and administration was discontinued abruptly in 6 of the 15 patients for disease control; as a result, 4 (66.7%) of the 6 patients achieved complete response (CR) or partial response.
  • Therefore, a graft-versus-leukemia/lymphoma (GVL) effect might be induced by discontinuation of immunosuppression.
  • Thirteen of the 15 patients were followed up by monitoring HTLV-1 proviral DNA levels.
  • In 10 of the 11 patients with positive HTLV-1 proviral DNA before allo-HSCT, HTLV-1 proviral DNA became undetectable at least once after allo-HSCT, and only 1 of the 5 patients in whom HTLV-1 proviral DNA became detectable after allo-HSCT relapsed.
  • Compared to the results of past studies, these results show that allo-HSCT greatly improved the prognosis of ATL and suggest a contribution of the induction of a GVL effect.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Follow-Up Studies. HTLV-I Infections / blood. HTLV-I Infections / therapy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Retrospective Studies. Transplantation, Homologous. Viral Load

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  • [ErratumIn] Biol Blood Marrow Transplant. 2008 Sep;14(9):1079
  • (PMID = 18541202.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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8. Uphoff CC, Denkmann SA, Steube KG, Drexler HG: Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines. J Biomed Biotechnol; 2010;2010:904767
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  • [Title] Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines.
  • The high prevalence of contaminated cell cultures suggests that viral contaminations might be distributed among cultures.
  • We investigated more than 460 primate cell lines for Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV), human immunodeficiency virus type 1 (HIV-1), human T-cell leukemia/lymphoma virus I and II (HTLV-I/-II), and squirrel monkey retrovirus (SMRV) infections for risk assessment.
  • None of the cell lines were infected with HCV, HIV-1, or HTLV-I/-II.
  • However, one cell line displayed reverse transcriptase activity.
  • Thirty-nine cell lines harbored EBV DNA sequences.
  • Studies on the lytic phase of EBV revealed that five cell lines produce EBV particles and six further cell lines produced EBV upon stimulation.
  • One cell line contained an integrated HBV genome fragment but showed no virus production.
  • Six cell lines were SMRV-infected.
  • Newly established cell lines should be tested for EBV infections to detect B-lymphoblastoid cell lines (B-LCL).
  • B-LCLs established with EBV from cell line B95-8 should be tested for SMRV infections.
  • [MeSH-major] Primates / virology. Viruses / genetics. Viruses / isolation & purification
  • [MeSH-minor] Animals. Blotting, Southern. Cell Line. DNA, Circular / analysis. HIV-1 / genetics. HIV-1 / isolation & purification. Hepacivirus / genetics. Hepacivirus / isolation & purification. Hepatitis B virus / genetics. Hepatitis B virus / isolation & purification. Herpesvirus 4, Human / genetics. Herpesvirus 4, Human / isolation & purification. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / genetics. Human T-lymphotropic virus 2 / isolation & purification. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Retroviruses, Simian / genetics. Retroviruses, Simian / isolation & purification. Saimiri / virology. Viral Proteins / analysis

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  • [Cites] Genes Chromosomes Cancer. 1992 Apr;4(3):205-10 [1382560.001]
  • [Cites] ALTEX. 2005;22(2):103-9 [15953965.001]
  • [Cites] J Virol Methods. 1992 Sep;39(3):259-68 [1430070.001]
  • [Cites] J Virol Methods. 1992 Dec 1;40(3):347-56 [1282132.001]
  • [Cites] Gastroenterology. 1993 Nov;105(5):1529-33 [8224658.001]
  • [Cites] Leukemia. 1994 Apr;8(4):652-8 [8152260.001]
  • [Cites] Leukemia. 1994 Aug;8(8):1385-91 [8057678.001]
  • [Cites] Leukemia. 1994 Sep;8(9):1510-26 [8090031.001]
  • [Cites] Int J Cancer. 1997 Nov 14;73(4):562-9 [9389573.001]
  • [Cites] J Hepatol. 1998 Mar;28(3):396-403 [9551676.001]
  • [Cites] DNA Cell Biol. 1998 May;17(5):415-25 [9628585.001]
  • [Cites] Br J Haematol. 1998 Sep;102(4):1081-9 [9734661.001]
  • [Cites] Leukemia. 1998 Nov;12(11):1806-9 [9823957.001]
  • [Cites] Eur J Haematol. 1999 Jan;62(1):1-18 [9918306.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Oct 14;264(1):33-6 [10527836.001]
  • [Cites] J Hepatol. 1999 Nov;31(5):967-8 [10580600.001]
  • [Cites] Eur J Cancer. 1999 Dec;35(14):1878-85 [10711230.001]
  • [Cites] Leuk Res. 2002 Apr;26(4):329-33 [11839374.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 2002 Feb;38(2):79-85 [11928999.001]
  • [Cites] J Virol. 2002 Jun;76(11):5612-26 [11991990.001]
  • [Cites] Haemophilia. 2002 May;8(3):236-43 [12010417.001]
  • [Cites] Leuk Lymphoma. 2004 Mar;45(3):567-74 [15160920.001]
  • [Cites] Nature. 1973 Mar 2;242(5392):44-7 [4348458.001]
  • [Cites] Int J Cancer. 1974 Mar 15;13(3):363-76 [4362611.001]
  • [Cites] Neoplasma. 1974;21(6):619-27 [4141066.001]
  • [Cites] J Virol Methods. 2006 Sep;136(1-2):193-9 [16806502.001]
  • [Cites] Adv Cancer Res. 2007;97:81-109 [17419942.001]
  • [Cites] Beitr Pathol. 1975 May;155(1):72-8 [168861.001]
  • [Cites] Science. 1977 Jan 21;195(4275):289-92 [63993.001]
  • [Cites] Virology. 1980 Mar;101(2):553-7 [6244705.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Int J Cancer. 1982 Jul 15;30(1):93-9 [6288581.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Apr;80(7):1987-91 [6300885.001]
  • [Cites] J Virol. 1984 Apr;50(1):248-54 [6321792.001]
  • [Cites] Gene. 1984 Mar;27(3):279-88 [6329907.001]
  • [Cites] Cell Mol Biol. 1986;32(3):343-50 [3017561.001]
  • [Cites] Int J Cancer. 1987 Jan 15;39(1):89-93 [3098690.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Feb;84(4):1005-9 [3029758.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1332-6 [3029778.001]
  • [Cites] Eur J Biochem. 1987 Jun 1;165(2):393-401 [2439332.001]
  • [Cites] Blood. 1987 Nov;70(5):1665-72 [3478106.001]
  • [Cites] Clin Exp Immunol. 1988 Jul;73(1):23-8 [3262465.001]
  • [Cites] J Infect Dis. 1988 Dec;158(6):1193-7 [3198935.001]
  • [Cites] Virology. 1988 Dec;167(2):468-76 [3201749.001]
  • [Cites] J Exp Med. 1989 Jun 1;169(6):2191-8 [2543732.001]
  • [Cites] J Virol. 1990 Mar;64(3):1143-55 [2154599.001]
  • [Cites] Leuk Res. 1990;14(4):381-7 [2159091.001]
  • [Cites] J Med Virol. 1990 Apr;30(4):266-71 [2164560.001]
  • [Cites] Leukemia. 1991 Mar;5(3):221-4 [1849602.001]
  • [Cites] Leukemia. 1991 May;5(5):399-407 [1851909.001]
  • [Cites] Braz J Med Biol Res. 2004 Nov;37(11):1707-12 [15517087.001]
  • [Cites] Int J Cancer. 1992 Sep 30;52(3):451-4 [1339415.001]
  • (PMID = 20454443.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Circular; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2861168
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9. Okudaira T, Hirashima M, Ishikawa C, Makishi S, Tomita M, Matsuda T, Kawakami H, Taira N, Ohshiro K, Masuda M, Takasu N, Mori N: A modified version of galectin-9 suppresses cell growth and induces apoptosis of human T-cell leukemia virus type I-infected T-cell lines. Int J Cancer; 2007 May 15;120(10):2251-61
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  • [Title] A modified version of galectin-9 suppresses cell growth and induces apoptosis of human T-cell leukemia virus type I-infected T-cell lines.
  • ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.
  • Galectins are a family of animal lectins that function both extracellularly (by interacting with cell surface and extracellular matrix glycoproteins and glycolipids) and intracellularly (by interacting with cytoplasmic and nuclear proteins) to modulate signaling pathways.
  • We found that protease-resistant galectin-9 by modification of its linker peptide, hG9NC(null), prevented cell growth of HTLV-I-infected T-cell lines and primary ATL cells.
  • The suppression of cell growth was inhibited by lactose, but not by sucrose, indicating that beta-galactoside binding is essential for hG9NC(null)-induced cell growth suppression. hG9NC(null) induced cell cycle arrest by reducing the expression of cyclin D1, cyclin D2, cyclin B1, Cdk1, Cdk4, Cdk6, Cdc25C and c-Myc, and apoptosis by reducing the expression of XIAP, c-IAP2 and survivin.
  • Most of these genes are regulated by NF-kappaB, which plays a critical role in oncogenesis by HTLV-I. hG9NC(null) suppressed IkappaBalpha phosphorylation, resulting in suppression of NF-kappaB.
  • Most importantly, treatment with hG9NC(null) (6.7 mg/kg injected intraperitoneally every day) reduced tumor formation from an HTLV-I-infected T-cell line when these cells were inoculated subcutaneously into SCID mice.
  • Our results suggest that hG9NC(null) could be a suitable agent for the management of ATL.
  • [MeSH-major] Apoptosis / drug effects. Galectins / pharmacology. HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1 / growth & development. Leukemia-Lymphoma, Adult T-Cell / therapy. T-Lymphocytes / pathology. T-Lymphocytes / virology
  • [MeSH-minor] Animals. Caspases / metabolism. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Female. Galactosides / metabolism. Growth Inhibitors / pharmacology. Humans. Membrane Proteins. Mice. Mice, SCID. NF-kappa B / genetics. NF-kappa B / immunology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Virus / biosynthesis. beta-Galactosidase / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [RetractionIn] Int J Cancer. 2011 Dec 1;129(11):2762-3 [21960263.001]
  • (PMID = 17278100.001).
  • [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 / Galactosides; 0 / Galectins; 0 / Growth Inhibitors; 0 / HAVCR2 protein, human; 0 / LGALS8 protein, human; 0 / LGALS9 protein, human; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Virus; 0 / beta-galactoside; EC 3.2.1.23 / beta-Galactosidase; EC 3.4.22.- / Caspases
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10. Peloponese JM, Yeung ML, Jeang KT: Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation. Immunol Res; 2006;34(1):1-12
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  • [Title] Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.
  • Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).
  • HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.
  • [MeSH-major] Cell Transformation, Neoplastic / immunology. Gene Products, tax / immunology. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Inflammation / immunology. NF-kappa B / immunology

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  • (PMID = 16720895.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B
  • [Number-of-references] 102
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11. Sargent JT, Smith OP: Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders. Br J Haematol; 2010 May;149(4):465-77
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  • 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

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  • (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
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12. 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
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  • [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


13. Miyano-Kurosaki N, Kira J, Barnor JS, Maeda N, Misawa N, Kawano Y, Tanaka Y, Yamamoto N, Koyanagi Y: Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients. Microbiol Immunol; 2007;51(2):235-42
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  • [Title] Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients.
  • That HTLV-I infects CD4(+) T cells and enhances their cell growth has been shown as successful long-term in vitro proliferation in the presence of IL-2.
  • It is known that T cells isolated from HAM patients possess strong ability for cell proliferation in vitro and mRNA of various cytokines are abundantly expressed in CNS tissues of HAM patients.
  • In this study, we examined the relationship between cell proliferation and ability of in vitro cytokine production of CD4(+) T cell clones isolated from HAM patients.
  • We started a culture from a single cell to isolate cell clones immediately after drawing blood from the patients using limiting dilution method, which could allow the cell to avoid in vitro HTLV-I infection after initiation of culture.
  • Many cell clones were obtained and the rate of proliferation efficiency from a single cell was as high as 80%, especially in the 4 weeks' culture cells from HAM patients.
  • Our results indicate that the ability of cell proliferation in HAM patients is not restricted in HTLV-I-infected T cells.
  • HTLV-Iuninfected CD4(+) T cells, mainly Th0 cells, also have a strong ability to respond to IL-2-stimulation, showing that unusual immune activation on T cells has been observed in HAM patients.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / immunology. Paraparesis, Tropical Spastic / immunology
  • [MeSH-minor] Adult. Aged. Clone Cells. Cytokines / genetics. Cytokines / immunology. DNA, Viral / chemistry. DNA, Viral / genetics. Female. Humans. Lymphocyte Activation. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Antigen, T-Cell / immunology

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  • (PMID = 17310092.001).
  • [ISSN] 0385-5600
  • [Journal-full-title] Microbiology and immunology
  • [ISO-abbreviation] Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA, Viral; 0 / Receptors, Antigen, T-Cell
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14. Wang YY, Zhou GB, Yin T, Chen B, Shi JY, Liang WX, Jin XL, You JH, Yang G, Shen ZX, Chen J, Xiong SM, Chen GQ, Xu F, Liu YW, Chen Z, Chen SJ: AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec. Proc Natl Acad Sci U S A; 2005 Jan 25;102(4):1104-9
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  • [Title] AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.
  • To explore the genetic abnormalities that cooperate with AML1-ETO (AE) fusion gene to cause acute myeloid leukemia (AML) with t(8;21), we screened a number of candidate genes and identified 11 types of mutations in C-KIT gene (mC-KIT), including 6 previously undescribed ones among 26 of 54 (48.1%) cases with t(8;21).
  • To address a possible chronological order between AE and mC-KIT, we showed that, among patients with AE and mC-KIT, most leukemic cells at disease presentation harbored both genetic alteration, whereas in three such cases investigated during complete remission, only AE, but not mC-KIT, could be detected by allele-specific PCR.
  • This may lead to an alternative way of C-KIT activation and may explain the significantly higher C-KIT expression in 81.3% of patients with t(8;21) than in patients with other leukemias.
  • These data strongly suggest that t(8;21) AML follows a stepwise model in leukemogenesis, i.e., AE represents the first, fundamental genetic hit to initiate the disease, whereas activation of the C-KIT pathway may be a second but also crucial hit for the development of a full-blown leukemia.
  • Gleevec also exerted a synergic effect in apoptosis induction with cytarabine, thus providing a potential therapeutic for t(8;21) leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Piperazines / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Apoptosis / drug effects. Benzamides. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Female. Humans. Imatinib Mesylate. Male. Middle Aged

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  • [Cites] Genome Res. 2003 Feb;13(2):287-93 [12566407.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1359-68 [11516096.001]
  • [Cites] Br J Haematol. 2003 Jun;121(5):775-7 [12780793.001]
  • [Cites] J Clin Microbiol. 2003 Jul;41(7):3306-11 [12843079.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9506-11 [12881486.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5646-57 [12944913.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4369-76 [12946995.001]
  • [Cites] Blood. 2004 May 15;103(10):3644-54 [14726395.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4255-62 [15156181.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Blood. 1993 Aug 1;82(3):712-5 [8338940.001]
  • [Cites] Cancer Res. 1993 Aug 1;53(15):3638-42 [7687925.001]
  • [Cites] Leukemia. 1994 Feb;8(2):258-63 [7508533.001]
  • [Cites] Blood. 1995 Apr 1;85(7):1769-80 [7535588.001]
  • [Cites] Leukemia. 1996 Feb;10(2):288-96 [8637238.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4789-96 [8639850.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11895-900 [8876234.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14059-64 [8943060.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Oncogene. 1999 Mar 4;18(9):1701-10 [10208431.001]
  • [Cites] Mol Cell Biol. 1999 May;19(5):3635-44 [10207087.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14882-7 [10611307.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] Blood. 2000 Jul 15;96(2):655-63 [10887131.001]
  • [Cites] Blood. 2000 Jul 1;96(1):288-96 [10891464.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Oct;295(1):139-45 [10991971.001]
  • [Cites] J Biol Chem. 2000 Dec 22;275(51):40282-7 [11032826.001]
  • [Cites] Biochem J. 2001 Mar 15;354(Pt 3):481-4 [11237851.001]
  • [Cites] EMBO Rep. 2000 Aug;1(2):133-9 [11265752.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Nature. 2001 May 17;411(6835):355-65 [11357143.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6470-83 [11533236.001]
  • [Cites] Blood. 2002 Jan 1;99(1):15-23 [11756147.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):744-57 [11886377.001]
  • [Cites] Hematol J. 2001;2(5):330-40 [11920269.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Hematol J. 2002;3(3):157-63 [12111653.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:179-98 [12194988.001]
  • [Cites] Mol Cancer Ther. 2002 Oct;1(12):1115-24 [12481435.001]
  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • [Cites] Blood. 2003 Jan 15;101(2):624-32 [12393523.001]
  • [Cites] Leukemia. 2003 Feb;17(2):471-2 [12592353.001]
  • (PMID = 15650049.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC545849
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15. Rizack T, Mega A, Legare R, Castillo J: Management of hematological malignancies during pregnancy. Am J Hematol; 2009 Dec;84(12):830-41
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  • The management of hematological malignancies during pregnancy is a challenging endeavor, which not only requires technical skills and knowledge by the clinicians but also requires sound clinical judgment and compassion, keeping in mind the patient and family preferences and, ultimately, the wellbeing of the neonate.
  • The purpose of this review is to evaluate the limited existing data and make useful suggestions in the management of acute and chronic leukemias, Hodgkin and non-Hodgkin lymphomas, plasma cell myeloma, and other hematological malignancies, such as myelodysplastic syndromes and hairy cell leukemia, during pregnancy.
  • [MeSH-minor] Abnormalities, Drug-Induced / etiology. Abnormalities, Drug-Induced / prevention & control. Abortion, Induced. Adult. Antiemetics / therapeutic use. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / contraindications. Antineoplastic Agents / therapeutic use. Cesarean Section. Clinical Protocols. Combined Modality Therapy. Disease Management. Female. Humans. Incidence. Infant, Newborn. Infant, Newborn, Diseases / chemically induced. Infant, Newborn, Diseases / prevention & control. Leukapheresis. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19844988.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiemetics; 0 / Antineoplastic Agents
  • [Number-of-references] 179
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16. Tanaka Y, Nakasone H, Yamazaki R, Sato K, Sato M, Terasako K, Kimura S, Okuda S, Kako S, Oshima K, Tanihara A, Nishida J, Yoshikawa T, Nakatsura T, Sugiyama H, Kanda Y: Single-cell analysis of T-cell receptor repertoire of HTLV-1 Tax-specific cytotoxic T cells in allogeneic transplant recipients with adult T-cell leukemia/lymphoma. Cancer Res; 2010 Aug 1;70(15):6181-92
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  • [Title] Single-cell analysis of T-cell receptor repertoire of HTLV-1 Tax-specific cytotoxic T cells in allogeneic transplant recipients with adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia (ATL) is a lymphoproliferative malignancy associated with human T-cell lymphotropic virus type 1 (HTLV-1) infection.
  • Recently, it has been shown that allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an effective treatment for ATL, and that HTLV-1 Tax-specific CD8(+) cytotoxic T cells (CTL) contribute to the graft-versus-ATL effect.
  • In the present study, we, for the first time, analyzed the T-cell receptor (TCR) repertoire of isolated Tax(301-309) (SFHSLHLLF)-specific CTLs in HLA-A*2402(+) ATL patients before and after allo-HSCT by single-cell reverse transcription-PCR.
  • In addition, a unique conserved amino acid motif of "P-D/P-R" in TCR-beta complementarity-determining region 3 in either BV7- or BV18-expressing CTLs was observed not only in all of the samples from ATL patients, but also in samples from the same patient before and after HSCT.
  • Furthermore, the P-D/P-R motif-bearing CTL clones established from peripheral blood samples after HSCT exhibited strong killing activity against the HTLV-1-infected T cells of the patient.
  • Hence, Tax(301-309)-specific CTLs in ATL patients might have a preference for TCR construction and induce strong immune responses against the HTLV-1-infected T cells of patients, which contribute to the graft-versus-ATL effects after allo-HSCT.
  • [MeSH-major] Gene Products, tax / immunology. Hematopoietic Stem Cell Transplantation. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Amino Acid Motifs. HLA-A Antigens / immunology. HLA-A24 Antigen. Humans. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology

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  • (PMID = 20647322.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [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 / HLA-A Antigens; 0 / HLA-A*24:02 antigen; 0 / HLA-A24 Antigen; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / tax protein, Human T-lymphotrophic virus 1
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17. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Title] [Effects of proteasome inhibitors on leukemias].
  • The abnormality of its activity is sign of tumorigenesis.
  • Bortezomib, the first proteasome inhibitor, obtained permission of clinical trial and on sale.
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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18. 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
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  • [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.

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  • [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
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19. Tözsér J, Weber IT: The protease of human T-cell leukemia virus type-1 is a potential therapeutic target. Curr Pharm Des; 2007;13(12):1285-94
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  • [Title] The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.
  • Human T-cell leukemia virus type-1 (HTLV-1) is associated with a number of human diseases.
  • Although the mechanism by which the virus causes diseases is still not known, studies indicate that viral replication is critical for the development of HTLV-1 associated myelopathy, and initial studies suggested that blocking replication with reverse transcriptase inhibitors had a therapeutic effect.
  • Therefore, based on the success of HIV-1 protease inhibitors, the HTLV-1 protease is also a potential target for chemotherapy.
  • Furthermore, mutated residues in HIV-1 protease that confer drug resistance are frequently seen in equivalent positions of other retroviral proteases, like HTLV-1 protease.
  • Therefore, comparison of HTLV-1 and HIV-1 proteases is expected to aid the rational design of broad spectrum inhibitors effective against various retroviral proteases, including the mutant HIV-1 enzymes appearing in drug resistance.
  • This review describes the characteristics of HTLV-1 protease, makes comparison with HIV-1 protease, and discusses the status of inhibitor development for the HTLV-1 protease.

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  • (PMID = 17504236.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM062920; United States / NIGMS NIH HHS / GM / GM 062920; United States / FIC NIH HHS / TW / TW01001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HTLV-1 protease
  • [Number-of-references] 45
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20. Sucić M, Batinić D, Zadro R, Mrsić S, Labar B: [Cytomorphology of acute mixed leukemia]. Acta Med Croatica; 2008 Oct;62(4):379-85
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  • [Title] [Cytomorphology of acute mixed leukemia].
  • Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.
  • RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).
  • These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.
  • Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology
  • [MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19205415.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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21. Aiello A, Fattorusso E, Luciano P, Menna M, Calzado MA, Muñoz E, Bonadies F, Guiso M, Sanasi MF, Cocco G, Nicoletti R: Synthesis of structurally simplified analogues of aplidinone A, a pro-apoptotic marine thiazinoquinone. Bioorg Med Chem; 2010 Jan 15;18(2):719-27
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  • The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor cell lines which also inhibits the TNFalpha-induced NF-kappaB activation in a human leukemia T cell line.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Computer Simulation. Drug Screening Assays, Antitumor. Humans. Molecular Structure. NF-kappa B / metabolism. Structure-Activity Relationship. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031419.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha; 0 / aplidinone A
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22. Gómez-Acevedo H, Li MY: Backward bifurcation in a model for HTLV-I infection of CD4+ T cells. Bull Math Biol; 2005 Jan;67(1):101-14
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  • [Title] Backward bifurcation in a model for HTLV-I infection of CD4+ T cells.
  • Human T-cell Lymphotropic Virus Type I (HTLV-I) primarily infects CD4+ helper T cells.
  • HTLV-I infection is clinically linked to the development of Adult T-cell Leukemia/Lymphoma and of HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis, among other illnesses.
  • HTLV-I transmission can be either horizontal through cell-to-cell contact, or vertical through mitotic division of infected CD4+ T cells.
  • It has been observed that HTLV-I infection has a high proviral load but a low rate of proviral genetic variation.
  • We consider and analyze a mathematical model for HTLV-I infection of CD4+ T cells that incorporates both horizontal and vertical transmission.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Computer Simulation. Human T-lymphotropic virus 1 / growth & development. Models, Biological
  • [MeSH-minor] Algorithms. Cell Death. Cell Proliferation. Humans

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  • (PMID = 15691541.001).
  • [ISSN] 0092-8240
  • [Journal-full-title] Bulletin of mathematical biology
  • [ISO-abbreviation] Bull. Math. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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23. Mahieux R, Gessain A: Adult T-cell leukemia/lymphoma and HTLV-1. Curr Hematol Malig Rep; 2007 Oct;2(4):257-64
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  • [Title] Adult T-cell leukemia/lymphoma and HTLV-1.
  • Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) was the first oncogenic human retrovirus to be discovered, more than 25 years ago.
  • HTLV-1 infects 15 to 20 million individuals worldwide.
  • HTLV-1 causes two major diseases: adult T-cell leukemia/lymphoma (ATLL) and tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM).
  • ATLL can be classified into four major subtypes: a smoldering type, a chronic type, a lymphoma type, and a leukemic type.
  • Because of intrinsic chemoresistance and severe immunosuppression, the survival rate of ATLL patients, especially those who develop the acute leukemic or lymphoma forms, is very poor, and such clonal malignant CD4 expansion remains one of the most severe lymphoproliferations.
  • [MeSH-major] Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. CD4-Positive T-Lymphocytes / virology. Clinical Trials as Topic. Drug Resistance, Neoplasm. Endemic Diseases. Female. Gene Products, tax / physiology. Genes, pX. Humans. Immunoglobulin G / therapeutic use. Immunophenotyping. Immunotherapy. Infant, Newborn. Infectious Disease Transmission, Vertical. Interferon-alpha / therapeutic use. Male. Oxides / therapeutic use. Paraparesis, Tropical Spastic / epidemiology. Paraparesis, Tropical Spastic / virology. Pregnancy. Pregnancy Complications, Infectious. Zidovudine / therapeutic use

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  • [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] Br J Haematol. 1998 Dec;103(3):721-8 [9858223.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] Blood. 1992 Jan 15;79(2):477-80 [1730092.001]
  • [Cites] Blood. 1991 Feb 15;77(4):896-905 [1993227.001]
  • [Cites] Leuk Lymphoma. 2005 Nov;46(11):1553-9 [16236609.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Cancer Sci. 2005 May;96(5):249-55 [15904464.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Immunity. 2000 Nov;13(5):657-64 [11114378.001]
  • [Cites] Retrovirology. 2007 Apr 14;4:27 [17433108.001]
  • [Cites] Int J Cancer. 1995 Mar 16;60(6):773-6 [7896443.001]
  • [Cites] Int J Cancer. 2007 May 1;120(9):2052-7 [17278106.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1386-92 [10666215.001]
  • [Cites] Cancer. 1995 Apr 1;75(7):1598-607 [8826916.001]
  • [Cites] Clin Lab Haematol. 2005 Aug;27(4):235-41 [16048490.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3060-8 [17138822.001]
  • [Cites] Blood. 1999 Jan 1;93(1):278-83 [9864171.001]
  • [Cites] Blood. 2006 May 15;107(10 ):3976-82 [16424388.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1838-45 [14592824.001]
  • [Cites] Blood. 1983 Oct;62(4):758-66 [6224522.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Int J Cancer. 1994 Nov 15;59(4):491-3 [7960218.001]
  • [Cites] Blood. 2001 Dec 15;98 (13):3762-9 [11739184.001]
  • [Cites] Hematol Oncol. 1986 Jan-Mar;4(1):59-65 [3009298.001]
  • [Cites] J Clin Immunol. 2007 Jan;27(1):1-18 [17216565.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2462-71 [15956280.001]
  • [Cites] J Virol. 1995 May;69(5):2863-8 [7707509.001]
  • [Cites] Int J Cancer. 1988 Apr 15;41(4):505-12 [2895748.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • [Cites] Int Immunol. 2006 Feb;18(2):269-77 [16361311.001]
  • [Cites] Rev Clin Exp Hematol. 2003 Dec;7(4):336-61 [15129647.001]
  • [Cites] Lancet Infect Dis. 2007 Apr;7(4):266-81 [17376384.001]
  • [Cites] Cancer. 1985 Feb 1;55(3):615-9 [2981152.001]
  • [Cites] Int J Cancer. 1989 Feb 15;43(2):250-3 [2917802.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Br J Haematol. 1999 Jun;105(3):743-51 [10354140.001]
  • [Cites] Int J Cancer. 1999 Sep 9;82(6):832-6 [10446450.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] J Infect Dis. 2005 May 1;191(9):1490-7 [15809908.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • (PMID = 20425378.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Gene Products, tax; 0 / Immunoglobulin G; 0 / Interferon-alpha; 0 / Oxides; 0 / tax protein, Human T-lymphotrophic virus 1; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine; CUJ2MVI71Y / daclizumab; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 63
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24. Yoshie O: Expression of CCR4 in adult T-cell leukemia. Leuk Lymphoma; 2005 Feb;46(2):185-90
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  • [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

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  • (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
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25. Hieshima K, Nagakubo D, Nakayama T, Shirakawa AK, Jin Z, Yoshie O: Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells. J Immunol; 2008 Jan 15;180(2):931-9
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  • [Title] Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells.
  • Adult T cell leukemia is a mature CD4+ T cell malignancy which predominantly expresses CCR4 and is etiologically associated with human T cell leukemia virus type 1 (HTLV-1).
  • Because HTLV-1 transmission depends on close cell-cell contacts, HTLV-1-infected T cells may preferentially interact with CCR4+CD4+ T cells for efficient viral transmission.
  • In terms of gene expression and protein secretion, we found a strong correlation between HTLV-1 Tax oncoprotein and CCL22, a CCR4 ligand, in HTLV-1-infected T cells.
  • Transient Tax expression in an HTLV-1-negative T cell line activated the CCL22 promoter and induced CCL22.
  • In chemotaxis assays, the culture supernatants of HTLV-1-infected T cells selectively attracted CCR4+CD4+ T cells in PBMCs.
  • Finally, anti-CCL22 Ab treatment also blocked HTLV-1 transmission to primary CD4+ T cells in coculture experiments with HTLV-1 producer cells.
  • Thus, HTLV-1-infected T cells produce CCL22 through Tax and selectively interact with CCR4+CD4+ T cells, resulting in preferential transmission of HTLV-1 to CCR4+CD4+ T cells.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Chemokine CCL22 / genetics. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / physiology. Virus Internalization
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Adhesion / genetics. Cell Line. Humans. Pertussis Toxin / pharmacology. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Receptors, CCR4 / antagonists & inhibitors. Receptors, CCR4 / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / virology

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  • [ErratumIn] J Immunol. 2008 Jun 15;180(12):8470
  • (PMID = 18178833.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL22 protein, human; 0 / CCR4 protein, human; 0 / Chemokine CCL22; 0 / Gene Products, tax; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, CCR4; EC 2.4.2.31 / Pertussis Toxin
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26. D'Agostino DM, Silic-Benussi M, Hiraragi H, Lairmore MD, Ciminale V: The human T-cell leukemia virus type 1 p13II protein: effects on mitochondrial function and cell growth. Cell Death Differ; 2005 Aug;12 Suppl 1:905-15
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  • [Title] The human T-cell leukemia virus type 1 p13II protein: effects on mitochondrial function and cell growth.
  • p13(II) of human T-cell leukemia virus type 1 (HTLV-1) is an 87-amino-acid protein that is targeted to the inner mitochondrial membrane. p13(II) alters mitochondrial membrane permeability, producing a rapid, membrane potential-dependent influx of K(+).
  • At the cellular level, p13(II) has been found to interfere with cell proliferation and transformation and to promote apoptosis induced by ceramide and Fas ligand.
  • Assays carried out in T cells (the major targets of HTLV-1 infection in vivo) demonstrate that p13(II)-mediated sensitization to Fas ligand-induced apoptosis can be blocked by an inhibitor of Ras farnesylation, thus implicating Ras signaling as a downstream target of p13(II) function.

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  • [Cites] Nat Rev Mol Cell Biol. 2003 May;4(5):373-84 [12728271.001]
  • [Cites] Biochem Biophys Res Commun. 2003 May 9;304(3):575-81 [12729592.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 13;100(10):6104-8 [12719519.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5141-9 [12910251.001]
  • [Cites] J Biol Chem. 2003 Aug 22;278(34):31745-55 [12799372.001]
  • [Cites] FEBS Lett. 2003 Sep 18;552(1):28-34 [12972148.001]
  • [Cites] Hematol J. 2003;4(5):328-35 [14502257.001]
  • [Cites] Mol Genet Metab. 2003 Sep-Oct;80(1-2):11-26 [14567954.001]
  • [Cites] Adv Cancer Res. 2003;89:69-132 [14587871.001]
  • [Cites] J Virol. 2004 Feb;78(4):2142-51 [14747580.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] J Gen Virol. 2004 Feb;85(Pt 2):451-61 [14769903.001]
  • [Cites] J Virol. 2004 Apr;78(8):3837-45 [15047799.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15460-71 [14724286.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):14473-6 [14973134.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6629-34 [15100416.001]
  • [Cites] DNA Cell Biol. 2004 Apr;23(4):193-205 [15142377.001]
  • [Cites] J Virol. 2004 Jul;78(13):7199-207 [15194796.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] J Biol Chem. 2004 Aug 27;279(35):36803-8 [15201276.001]
  • [Cites] J Virol. 2004 Oct;78(20):11077-83 [15452228.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] J Gen Virol. 1988 Jul;69 ( Pt 7):1695-710 [2899128.001]
  • [Cites] J Virol. 1992 Mar;66(3):1737-45 [1310774.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):3005-9 [1348363.001]
  • [Cites] Virology. 1992 Jun;188(2):618-27 [1585637.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8813-7 [1528897.001]
  • [Cites] J Virol. 1993 Feb;67(2):1015-23 [8419636.001]
  • [Cites] J Virol. 1993 Mar;67(3):1218-26 [8437213.001]
  • [Cites] J Virol. 1993 Apr;67(4):2360-6 [8445734.001]
  • [Cites] J Virol. 1994 Oct;68(10):6778-81 [8084014.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11532-6 [7972096.001]
  • [Cites] J Virol. 1995 Mar;69(3):1907-12 [7853532.001]
  • [Cites] Int J Cancer. 1995 Mar 3;60(5):701-6 [7860146.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):111-5 [8552585.001]
  • [Cites] J Virol. 1997 Jan;71(1):75-83 [8985325.001]
  • [Cites] Int J Cancer. 1997 Apr 10;71(2):196-202 [9139842.001]
  • [Cites] Leukemia. 1997 Jun;11(6):866-70 [9177442.001]
  • [Cites] J Virol. 1997 Jul;71(7):5579-92 [9188632.001]
  • [Cites] Virology. 1997 Oct 13;237(1):123-8 [9344914.001]
  • [Cites] Virology. 1997 Oct 27;237(2):397-403 [9356350.001]
  • [Cites] Oncogene. 1997 Oct 16;15(16):1895-901 [9365235.001]
  • [Cites] J Virol. 1998 Mar;72(3):2554-9 [9499124.001]
  • [Cites] J Virol. 1998 May;72(5):4458-62 [9557741.001]
  • [Cites] Science. 1998 Jul 10;281(5374):266-9 [9657723.001]
  • [Cites] Acta Neuropathol. 1999 Feb;97(2):107-12 [9928820.001]
  • [Cites] Oncogene. 1999 Aug 5;18(31):4505-14 [10442641.001]
  • [Cites] Oncogene. 1999 Sep 2;18(35):4930-9 [10490827.001]
  • [Cites] Physiol Rev. 1999 Oct;79(4):1127-55 [10508231.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):12039-43 [10518572.001]
  • [Cites] J Exp Med. 2001 Feb 19;193(4):509-19 [11181702.001]
  • [Cites] J Gen Virol. 1999 Dec;80 ( Pt 12):3257-65 [10567659.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):33-46 [10620603.001]
  • [Cites] J Virol. 2000 Feb;74(3):1094-100 [10627519.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):E23-5 [10655597.001]
  • [Cites] J Exp Med. 2000 Feb 7;191(3):567-72 [10662802.001]
  • [Cites] J Virol. 2000 Mar;74(6):2840-6 [10684300.001]
  • [Cites] Virology. 2000 Nov 10;277(1):127-35 [11062043.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1787-95 [11080828.001]
  • [Cites] Cell Death Differ. 2000 Dec;7(12):1146-54 [11175251.001]
  • [Cites] Biochemistry. 2001 Apr 24;40(16):4893-903 [11305904.001]
  • [Cites] EMBO J. 2001 Aug 1;20(15):4107-21 [11483514.001]
  • [Cites] J Neurovirol. 2001 Feb;7(1):61-5 [11519484.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] Clin Cancer Res. 2001 Nov;7(11):3567-73 [11705878.001]
  • [Cites] J Virol. 2002 Feb;76(3):1400-14 [11773414.001]
  • [Cites] Trends Immunol. 2002 Jan;23(1):1-4 [11801441.001]
  • [Cites] Biochim Biophys Acta. 2002 Mar 19;1561(1):27-45 [11988179.001]
  • [Cites] J Virol. 2002 Aug;76(15):7843-54 [12097596.001]
  • [Cites] Eur J Biochem. 2002 Jul;269(14):3339-54 [12135472.001]
  • [Cites] Biochim Biophys Acta. 2002 Sep 2;1592(1):79-87 [12191770.001]
  • [Cites] J Virol. 2002 Oct;76(19):9806-18 [12208959.001]
  • [Cites] Microbiol Mol Biol Rev. 2002 Sep;66(3):396-406, table of contents [12208996.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):34424-33 [12093802.001]
  • [Cites] J Virol. 2002 Nov;76(21):10914-20 [12368334.001]
  • [Cites] Biochim Biophys Acta. 2002 Oct 11;1565(2):347-63 [12409206.001]
  • [Cites] FEBS Lett. 2003 Jan 30;535(1-3):34-8 [12560074.001]
  • [Cites] J Biol Chem. 2003 Feb 21;278(8):5775-85 [12477721.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Mar 28;303(1):1-7 [12646157.001]
  • [Cites] Virology. 2003 Mar 30;308(1):1-12 [12706085.001]
  • (PMID = 15761473.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 100730; United States / FIC NIH HHS / TW / TW005705-03; United States / FIC NIH HHS / TW / TW 05705; United States / FIC NIH HHS / TW / R03 TW005705; United States / FIC NIH HHS / TW / R03 TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-02; United States / FIC NIH HHS / TW / R03 TW005705-03; United States / FIC NIH HHS / TW / R03 TW005705-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; SY7Q814VUP / Calcium
  • [Number-of-references] 84
  • [Other-IDs] NLM/ NIHMS183534; NLM/ PMC3057663
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27. Lyell V, Khatamzas E, Allain T: Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report. J Med Case Rep; 2007;1:56
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  • [Title] Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
  • Human T cell lymphotrophic virus type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.
  • Although there is a long latency, carriers have a 1-5% chance of developing adult T cell leukaemia/lymphoma, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.
  • We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have lymphoma and was positive for HTLV-1.

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  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3545-50 [10522993.001]
  • [Cites] BMJ. 2000 Mar 4;320(7235):611-2 [10698878.001]
  • [Cites] Endocr Relat Cancer. 2003 Sep;10(3):403-7 [14503917.001]
  • [Cites] Clin Lymphoma. 2004 Jun;5(1):29-36 [15245605.001]
  • [Cites] Am J Med Sci. 1995 Jun;309(6):312-4 [7771500.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):232-9 [15726602.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4467-70 [15930259.001]
  • [Cites] Endocr Relat Cancer. 2005 Sep;12(3):549-83 [16172192.001]
  • [Cites] J Natl Med Assoc. 1995 Oct;87(10):746-8 [7473848.001]
  • [Cites] Anticancer Res. 2004 Sep-Oct;24(5A):2665-73 [15517871.001]
  • (PMID = 17651486.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1950877
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28. 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
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  • 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

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  • [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
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29. Miyamura F, Kako S, Yamagami H, Sato K, Sato M, Terasako K, Kimura S, Nakasone H, Aoki S, Okuda S, Yamazaki R, Oshima K, Yoshinaga K, Higuchi T, Nishida J, Demitsu T, Kakehashi A, Kanda Y: Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Oct;90(3):397-401
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  • [Title] Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation.
  • Only some carriers of human T cell lymphotropic virus type I (HTLV-1) develop adult T cell leukemia/lymphoma (ATLL) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset ATLL.
  • A 25-year-old female developed ATLL and underwent allogeneic hematopoietic stem cell transplantation (HSCT) in non-remission.
  • She had chronic refractory eczema and corneal injury at the onset of ATLL.
  • Remission of ATLL was achieved, and the HTLV-1 proviral load decreased after HSCT.
  • More than a year has passed since the transplantation was performed, and she has had no recurrence of either ATLL or lesions in the skin and eye.
  • Her clinical course suggests a possible association between skin and eye lesions and HTLV-1 infection.
  • Special attention is needed when HTLV-1 carriers develop eye or skin lesions.
  • [MeSH-major] Corneal Diseases / therapy. Eczema / therapy. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Chronic Disease. Female. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Humans. Transplantation, Homologous. Treatment Outcome. Viral Load


30. Nicot C, Harrod RL, Ciminale V, Franchini G: Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions. Oncogene; 2005 Sep 5;24(39):6026-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.
  • The human T-cell leukemia/lymphoma virus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.
  • To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).
  • [MeSH-major] Human T-lymphotropic virus 1 / genetics. Viral Nonstructural Proteins / genetics

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  • (PMID = 16155609.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI058944; United States / NCI NIH HHS / CA / R01 CA106258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viral Nonstructural Proteins
  • [Number-of-references] 54
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31. Figueroa ME, Wouters BJ, Skrabanek L, Glass J, Li Y, Erpelinck-Verschueren CA, Langerak AW, Löwenberg B, Fazzari M, Greally JM, Valk PJ, Melnick A, Delwel R: Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features. Blood; 2009 Mar 19;113(12):2795-804
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  • [Title] Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features.
  • Acute myeloid leukemia is a heterogeneous disease from the molecular and biologic standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity.
  • We studied the epigenetic profiles of a cohort of patients who shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, whereas the rest presented with silencing of this gene and coexpression of certain T-cell markers.
  • Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group.
  • CEBPA-silenced leukemias also displayed marked hypermethylation compared with normal CD34(+) hematopoietic cells, whereas CEBPA mutant cases showed only mild changes in DNA methylation compared with these normal progenitors.
  • Biologically, CEBPA-silenced leukemias presented with a decreased response to myeloid growth factors in vitro.

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  • [Cites] Blood. 2000 Apr 1;95(7):2364-71 [10733508.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3142-51 [18451139.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Blood. 2001 May 1;97(9):2823-9 [11313277.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1079-82 [11834837.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26293-9 [11978795.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Science. 2002 Nov 1;298(5595):1039-43 [12351676.001]
  • [Cites] Hematol J. 2003;4(1):31-40 [12692518.001]
  • [Cites] Leukemia. 2003 May;17(5):910-8 [12750705.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):394-400 [15122210.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2445-51 [10498617.001]
  • [Cites] Immunity. 2004 Dec;21(6):853-63 [15589173.001]
  • [Cites] J Exp Med. 2005 Mar 21;201(6):881-90 [15781580.001]
  • [Cites] Leuk Res. 2005 Jun;29(6):653-9 [15863205.001]
  • [Cites] Bioinformatics. 2005 Jun 1;21(11):2789-90 [15797915.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):653-8 [16423993.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] J Natl Cancer Inst. 2006 Mar 15;98(6):396-406 [16537832.001]
  • [Cites] Oncogene. 2006 Apr 20;25(17):2477-88 [16331260.001]
  • [Cites] Genomics. 2006 May;87(5):572-9 [16487676.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nat Rev Immunol. 2007 Feb;7(2):105-17 [17259967.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3462-9 [17148581.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4657-64 [17510391.001]
  • [Cites] BMC Cancer. 2007;7:126 [17626620.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5680-91 [17353908.001]
  • [Cites] Nature. 2007 Oct 11;449(7163):731-4 [17713478.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6697-714 [17934479.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6829-37 [17934489.001]
  • [Cites] Mol Cell. 2007 Oct 26;28(2):337-50 [17964271.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3706-14 [17671232.001]
  • [Cites] Nucleic Acids Res. 2007;35(20):6798-807 [17932072.001]
  • [Cites] J Clin Invest. 2008 Mar;118(3):853-67 [18246201.001]
  • [Cites] PLoS One. 2008;3(3):e1882 [18365023.001]
  • [Cites] Bioinformatics. 2008 May 1;24(9):1161-7 [18353789.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • (PMID = 19168792.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE14417
  • [Grant] United States / NIGMS NIH HHS / GM / GM007288; United States / NCI NIH HHS / CA / R01 CA118316; United States / NCI NIH HHS / CA / CA118316; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / R01 CA104348
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Interleukin-3; 0 / Neoplasm Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2945920
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32. Patronas M, Smith JA, Levy-Clarke GA, Reed GF, Buggage RR: Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1. Am J Ophthalmol; 2006 Dec;142(6):1088-9
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  • [Title] Hypergammaglobulinemia and corneal opacities in patients with human T-cell lymphotrophic virus type-1.
  • PURPOSE: To investigate the relationship between serum immunoglobulin levels and corneal opacities in a cohort of patients with human T-cell lymphotrophic virus type-1 (HTLV-1).
  • METHODS: Complete ophthalmologic examination was performed on 44 patients with HTLV-1 infection (25 patients with adult T-cell leukemia/lymphoma [ATL], 18 patients with HTLV-1 that was associated myelopathy/tropical spastic paraparesis [HAM/TSP], and one patient who was asymptomatic).
  • RESULTS: Corneal opacities were identified in 15 of 25 patients (60%) with ATL and five of 18 patients (28%) with HAM/TSP.
  • The prevalence of corneal opacities was associated statistically with elevated IgG level (P = .023) in patients with ATL, but not in patients with HAM/TSP (P > .99).
  • CONCLUSION: Although the mechanism remains unclear, hypergammaglobulinemia is associated with the development of the corneal opacities in patients of African descent with ATL.
  • [MeSH-major] Corneal Opacity / etiology. HTLV-I Infections / complications. Hypergammaglobulinemia / etiology
  • [MeSH-minor] Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunoglobulin A / blood. Immunoglobulin G / blood. Immunoglobulin M / blood. Nephelometry and Turbidimetry. Prevalence. Retrospective Studies

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  • (PMID = 17157606.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A; 0 / Immunoglobulin G; 0 / Immunoglobulin M
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33. Wada T, Yoshinaga E, Oiso N, Kawara S, Kawada A, Kozuka T: Adult T-cell leukemia-lymphoma associated with follicular mucinosis. J Dermatol; 2009 Dec;36(12):638-42
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  • [Title] Adult T-cell leukemia-lymphoma associated with follicular mucinosis.
  • Follicular mucinosis (alopecia mucinosa) is often associated with malignancies including mycosis fungoides and Sézary syndrome, but not adult T-cell leukemia-lymphoma (ATLL).
  • The patient showed 11% of flower-shaped atypical lymphocytes in blood examination and positive human T-cell leukemia virus type 1 antibody in serology, consistent with the chronic type of ATLL.
  • This case seems to be a very rare association of follicular mucinosis and chronic ATLL, suggesting that malignant T cells may have a feature of folliculotropism as well as epidermotropism.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Mucinosis, Follicular / complications
  • [MeSH-minor] DNA, Viral / genetics. DNA, Viral / isolation & purification. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged

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  • (PMID = 19958447.001).
  • [ISSN] 1346-8138
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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34. Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J: HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia. J Gen Intern Med; 2007 Mar;22(3):420-3
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  • [Title] HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
  • BACKGROUND: Since the initial description of human T cell lymphotropic virus (HTLV-1), clusters of this infection have been detected globally.
  • Unlike HIV infection, most patients infected with HTLV-1 remain asymptomatic throughout their lifetime.
  • CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with HTLV-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.
  • HTLV-1-associated adult T cell leukemia lymphoma (ATLL) was diagnosed in this patient by bone marrow and lymph node biopsy.
  • This is believed to be the first description of this type of reaction to pneumocystis jiroveci in a HTLV-1-infected ATLL patient.
  • [MeSH-major] HTLV-I Infections / diagnosis. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pneumocystis jirovecii. Pneumonia, Pneumocystis / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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  • [Cites] Leuk Lymphoma. 1994 Aug;14(5-6):395-400 [7812198.001]
  • [Cites] Leuk Lymphoma. 1994 Feb;12(5-6):471-6 [8180610.001]
  • [Cites] Clin Infect Dis. 1996 Jun;22(6):1111-2 [8783726.001]
  • [Cites] J Clin Invest. 1996 Oct 1;98(7):1544-9 [8833902.001]
  • [Cites] Leukemia. 1997 Mar;11(3):453-4 [9067590.001]
  • [Cites] Int J Hematol. 1997 Oct;66(3):257-78 [9401272.001]
  • [Cites] Aust N Z J Med. 1999 Feb;29(1):102-3 [10200829.001]
  • [Cites] Intern Med. 1999 Feb;38(2):83-5 [10225661.001]
  • [Cites] Semin Neurol. 2005 Sep;25(3):315-27 [16170744.001]
  • [Cites] Eur Respir J. 2000 Jan;15(1):213-6 [10678649.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):435-8 [11378559.001]
  • [Cites] Am J Kidney Dis. 2002 Feb;39(2):E8 [11840399.001]
  • [Cites] Thorax. 2002 May;57(5):435-7 [11978921.001]
  • [Cites] J R Soc Med. 2003 Mar;96(3):126-7 [12612113.001]
  • [Cites] Am J Clin Pathol. 1975 Mar;63(3):384-90 [1090147.001]
  • [Cites] J Clin Invest. 1986 Aug;78(2):592-6 [3016032.001]
  • [Cites] Cancer Res. 1989 Jul 15;49(14):3849-52 [2544261.001]
  • [Cites] Semin Diagn Pathol. 1989 Aug;6(3):273-86 [2678337.001]
  • [Cites] Arch Pathol Lab Med. 1989 Nov;113(11):1281-4 [2684091.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Br J Cancer. 1991 Oct;64(4):745-8 [1911223.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] J La State Med Soc. 1992 Jan;144(1):35-8 [1538186.001]
  • [Cites] J Biol Chem. 1993 Jan 15;268(2):1174-9 [8380405.001]
  • [Cites] Blood. 1993 Feb 15;81(4):1017-24 [8427983.001]
  • [Cites] Endocrinology. 1993 Jun;132(6):2551-6 [8099324.001]
  • [Cites] J Biol Chem. 1993 Aug 5;268(22):16730-6 [8393873.001]
  • [Cites] Clin Infect Dis. 1995 Oct;21(4):1014-6 [8645790.001]
  • (PMID = 17356979.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1824742
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35. Ohkura S, Yamashita M, Ishida T, Babu PG, Koyanagi Y, Yamamoto N, Miura T, Hayami M: Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A. AIDS Res Hum Retroviruses; 2005 Apr;21(4):325-30
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  • [Title] Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A.
  • Seven isolates of human T cell leukemia virus type 1 (HTLV-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of HTLV-1 in the subcontinent.
  • The new Indian HTLV-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.
  • These results demonstrate that Indian HTLV-1s are genetically heterogeneous and include the most divergent strain of subgroup A.
  • On the basis of these results, we speculate that subgroup A HTLV- 1s may have been present for thousands of years in India.
  • [MeSH-major] HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Child. DNA, Viral / chemistry. Female. Humans. India. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics

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  • (PMID = 15943577.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY607576/ AY607577/ AY607578/ AY607579/ AY607580/ AY607581/ AY607582
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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36. Phillips AA, Shapira I, Willim RD, Sanmugarajah J, Solomon WB, Horwitz SM, Savage DG, Bhagat G, Soff G, Zain JM, Alobeid B, Seshan VE, O'Connor OA: A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score. Cancer; 2010 Jul 15;116(14):3438-46
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  • [Title] A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score.
  • BACKGROUND: To define the clinicopathologic and prognostic features of patients with human T-cell lymphotropic virus type-1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATLL) in North America, standard criteria were used to identify patients with ATLL.
  • The acute subtype predominated (68.5%).
  • Although the International Prognostic Index and Prognostic Index for peripheral T-cell lymphoma unspecified identified subsets of patients, these models were not completely predictive.
  • A recursive partitioning analysis was performed on the data, which successfully identified 3 prognostic categories based on Eastern Cooperative Oncology Group performance status, stage, age, and calcium level at diagnosis.
  • CONCLUSIONS: This series proposed a new prognostic model for patients with HTLV-1-associated ATLL and confirmed a poor outcome for these patients in North America.
  • [MeSH-major] Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Male. Middle Aged. Prognosis. United States

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  • [Copyright] Copyright (c) 2010 American Cancer Society.
  • (PMID = 20564100.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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37. Hidaka T, Nakahata S, Hatakeyama K, Hamasaki M, Yamashita K, Kohno T, Arai Y, Taki T, Nishida K, Okayama A, Asada Y, Yamaguchi R, Tsubouchi H, Yokota J, Taniwaki M, Higashi Y, Morishita K: Down-regulation of TCF8 is involved in the leukemogenesis of adult T-cell leukemia/lymphoma. Blood; 2008 Jul 15;112(2):383-93
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  • [Title] Down-regulation of TCF8 is involved in the leukemogenesis of adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) is caused by latent human T-lymphotropic virus-1 (HTLV-1) infection.
  • To clarify the molecular mechanism underlying leukemogenesis after viral infection, we precisely mapped 605 chromosomal breakpoints in 61 ATLL cases by spectral karyotyping and identified frequent chromosomal breakpoints in 10p11, 14q11, and 14q32.
  • Single nucleotide polymorphism (SNP) array-comparative genomic hybridization (CGH), genetic, and expression analyses of the genes mapped within a common breakpoint cluster region in 10p11.2 revealed that in ATLL cells, transcription factor 8 (TCF8) was frequently disrupted by several mechanisms, including mainly epigenetic dysregulation.
  • TCF8 mutant mice frequently developed invasive CD4(+) T-cell lymphomas in the thymus or in ascitic fluid in vivo.
  • Down-regulation of TCF8 expression in ATLL cells in vitro was associated with resistance to transforming growth factor beta1 (TGF-beta1), a well-known characteristic of ATLL cells, suggesting that escape from TGF-beta1-mediated growth inhibition is important in the pathogenesis of ATLL.
  • These findings indicate that TCF8 has a tumor suppressor role in ATLL.
  • [MeSH-major] Homeodomain Proteins / physiology. Leukemia-Lymphoma, Adult T-Cell / etiology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
  • [MeSH-minor] Animals. Chromosome Breakage. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 14. Down-Regulation / genetics. Humans. Karyotyping. Mice. Tumor Cells, Cultured

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  • (PMID = 18467597.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / ZEB1 protein, human
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38. Javier RT: Cell polarity proteins: common targets for tumorigenic human viruses. Oncogene; 2008 Nov 24;27(55):7031-46
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  • [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

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  • [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


39. Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y: CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells. J Biol Chem; 2010 May 14;285(20):15511-22
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  • [Title] CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
  • CADM1 encodes a multifunctional immunoglobulin-like cell adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
  • Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in adult T-cell leukemia-lymphoma (ATL) cells.
  • It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent clinical manifestations of ATL.
  • Amino acid sequence alignment revealed that Tiam1 (T-lymphoma invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-associated guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
  • In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as ATL cell lines.
  • Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in ATL patients.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Immunoglobulins / metabolism. Leukemia, T-Cell / pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Adhesion Molecules. Cell Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid

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  • [Cites] Genomics. 1999 Dec 1;62(2):139-46 [10610705.001]
  • [Cites] Retrovirology. 2006;3:71 [17042961.001]
  • [Cites] Nat Genet. 2001 Apr;27(4):427-30 [11279526.001]
  • [Cites] Annu Rev Neurosci. 2001;24:1-29 [11283303.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Mol Reprod Dev. 2001 Oct;60(2):158-64 [11553913.001]
  • [Cites] Neuroreport. 2001 Oct 29;12(15):3217-21 [11711859.001]
  • [Cites] Nature. 2002 Jun 20;417(6891):867-71 [12075356.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):31014-9 [12050160.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1525-31 [12202822.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5129-33 [12234973.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2601-8 [12456501.001]
  • [Cites] Biol Reprod. 2003 May;68(5):1755-63 [12606335.001]
  • [Cites] FEBS Lett. 2003 Jul 3;546(1):11-6 [12829230.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Lab Invest. 2003 Aug;83(8):1175-83 [12920246.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35421-7 [12826663.001]
  • [Cites] Oncogene. 2003 Sep 18;22(40):6160-5 [13679854.001]
  • [Cites] Curr Opin Cell Biol. 2003 Oct;15(5):583-9 [14519393.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7979-85 [14633730.001]
  • [Cites] J Biol Chem. 2004 Jan 2;279(1):495-508 [14530271.001]
  • [Cites] Cell. 2004 Jan 23;116(2):167-79 [14744429.001]
  • [Cites] Trends Cell Biol. 2007 Jan;17(1):36-43 [17126549.001]
  • [Cites] Hepatology. 2007 Mar;45(3):684-94 [17326163.001]
  • [Cites] J Cell Biol. 2007 Mar 12;176(6):863-75 [17353362.001]
  • [Cites] J Biol Chem. 2007 May 4;282(18):13864-74 [17339315.001]
  • [Cites] Rev Med Virol. 2007 Sep-Oct;17(5):301-11 [17621367.001]
  • [Cites] J Neurosci. 2007 Nov 14;27(46):12516-30 [18003830.001]
  • [Cites] Retrovirology. 2008;5:76 [18702816.001]
  • [Cites] J Virol. 2008 Dec;82(23):11958-63 [18922876.001]
  • [Cites] Breast Cancer Res Treat. 2004 Mar;84(1):21-32 [14999151.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Oct;80(19):6061-5 [6193528.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):237-43 [2303290.001]
  • [Cites] Cell. 1994 May 20;77(4):537-49 [7999144.001]
  • [Cites] Nature. 1995 May 25;375(6529):338-40 [7753201.001]
  • [Cites] Science. 1997 Jan 3;275(5296):73-7 [8974395.001]
  • [Cites] J Cell Biol. 1997 Apr 21;137(2):387-98 [9128250.001]
  • [Cites] Science. 1997 Nov 21;278(5342):1464-6 [9367959.001]
  • [Cites] EMBO J. 1998 Jul 15;17(14):4066-74 [9670021.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):501-11 [9927410.001]
  • [Cites] Leuk Lymphoma. 2005 Feb;46(2):185-90 [15621800.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1204-13 [15471956.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):6934-42 [15905536.001]
  • [Cites] J Biol Chem. 2005 Jun 10;280(23):21955-64 [15781451.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Blood. 2005 Aug 1;106(3):779-86 [15811952.001]
  • [Cites] Int Immunol. 2005 Sep;17(9):1227-37 [16091383.001]
  • [Cites] Cancer Sci. 2005 Sep;96(9):543-52 [16128739.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42164-71 [16223734.001]
  • [Cites] Trends Cell Biol. 2006 Oct;16(10):522-9 [16949823.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1139-46 [16952304.001]
  • [Cites] Int J Cancer. 2000 Nov 1;88(3):369-76 [11054665.001]
  • (PMID = 20215110.001).
  • [ISSN] 1083-351X
  • [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 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2865322
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40. Sugita S, Takase H, Yoshida T, Sugamoto Y, Watanabe T, Mochizuki M: Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion. Br J Ophthalmol; 2006 Sep;90(9):1204-6
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  • [Title] Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion.
  • [MeSH-major] Biomarkers, Tumor / analysis. Eye / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / immunology. Receptors, Interleukin-2 / analysis

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  • [Cites] Am J Ophthalmol. 2002 Oct;134(4):616-8 [12383828.001]
  • [Cites] J Lab Clin Med. 1989 Oct;114(4):407-10 [2794753.001]
  • [Cites] J Clin Invest. 1995 Feb;95(2):852-8 [7860769.001]
  • [Cites] Arch Ophthalmol. 1994 Jul;112(7):954-9 [8031276.001]
  • [Cites] Rinsho Ketsueki. 1992 Apr;33(4):537-41 [1318431.001]
  • (PMID = 16929066.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / IL2RA protein, human; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2
  • [Other-IDs] NLM/ PMC1857395
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41. Zhang J, Yamada O, Matsushita Y, Chagan-Yasutan H, Hattori T: Transactivation of human osteopontin promoter by human T-cell leukemia virus type 1-encoded Tax protein. Leuk Res; 2010 Jun;34(6):763-8
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  • [Title] Transactivation of human osteopontin promoter by human T-cell leukemia virus type 1-encoded Tax protein.
  • We report here that OPN gene is transactivated by Tax protein of human T-cell leukemia virus type 1 (HTLV-1).
  • This study suggests that OPN is one of the downstream mediators of aberrantly activated PI3K/AKT signaling by Tax, which may partially contribute to HTLV-1-associated leukemogenesis.
  • [MeSH-minor] Base Sequence. Binding Sites. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Cell Transformation, Viral / genetics. Gene Expression Regulation, Neoplastic. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / physiology. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Phosphatidylinositol 3-Kinases / metabolism. Phosphatidylinositol 3-Kinases / physiology. Promoter Regions, Genetic / physiology. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-akt / physiology. Signal Transduction / genetics. Transcription Factor AP-1 / metabolism

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19767100.001).
  • [ISSN] 1873-5835
  • [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 / Gene Products, tax; 0 / Transcription Factor AP-1; 0 / tax protein, Human T-lymphotrophic virus 1; 106441-73-0 / Osteopontin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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42. Peloponese JM Jr, Yeung ML, Jeang KT: Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation. Immunol Res; 2006 Jan;34(1):1-12
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  • [Title] Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation.
  • Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).
  • HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.

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  • [Cites] Immunity. 1999 Nov;11(5):547-54 [10591180.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • [Cites] Science. 1997 Oct 31;278(5339):860-6 [9346484.001]
  • [Cites] Curr Biol. 1999 Jun 3;9(11):601-4 [10359702.001]
  • [Cites] J Virol. 1992 Dec;66(12):7183-92 [1433511.001]
  • [Cites] Nature. 1998 Jan 22;391(6665):410-3 [9450761.001]
  • [Cites] Science. 1997 Oct 31;278(5339):866-9 [9346485.001]
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Annu Rev Immunol. 1994;12:141-79 [8011280.001]
  • [Cites] Retrovirology. 2005 Mar 02;2:16 [15743528.001]
  • [Cites] J Biol Chem. 2004 Jul 16;279(29):30099-105 [15140882.001]
  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34060-7 [10906125.001]
  • [Cites] Cell. 1997 Jul 25;90(2):373-83 [9244310.001]
  • [Cites] Mol Cell. 2001 Feb;7(2):401-9 [11239468.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5926-30 [16155599.001]
  • [Cites] Immunity. 2002 Oct;17 (4):525-35 [12387745.001]
  • [Cites] Genes Dev. 2001 Sep 15;15(18):2321-42 [11562344.001]
  • [Cites] Biochim Biophys Acta. 1992 Dec 16;1114(2-3):223-33 [1333808.001]
  • [Cites] J Exp Med. 1997 Oct 6;186(7):999-1014 [9314550.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6938-47 [10602468.001]
  • [Cites] Retrovirology. 2005 Mar 02;2:17 [15743526.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] J Biol Chem. 2004 Apr 30;279(18):18137-45 [14963024.001]
  • [Cites] Retrovirology. 2005 Apr 26;2:27 [15854229.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5965-75 [16155603.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] Annu Rev Immunol. 1998;16:225-60 [9597130.001]
  • [Cites] Cell. 1992 Mar 20;68(6):1121-33 [1547506.001]
  • [Cites] EMBO J. 1996 Feb 15;15(4):873-87 [8631308.001]
  • [Cites] Annu Rev Cell Biol. 1994;10:405-55 [7888182.001]
  • [Cites] Genes Dev. 2000 Jul 15;14 (14 ):1729-33 [10898787.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):10983-5 [11572954.001]
  • [Cites] Oncogene. 2003 Dec 4;22(55):8912-23 [14654787.001]
  • [Cites] Mol Cell Biol. 1994 Feb;14(2):1374-82 [8289813.001]
  • [Cites] Oncogene. 1994 Jul;9(7):1931-7 [8208540.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):36005-12 [12840022.001]
  • [Cites] J Exp Med. 2003 Sep 1;198(5):771-81 [12939342.001]
  • [Cites] Science. 1999 May 21;284(5418):1313-8 [10334979.001]
  • [Cites] J Biol Chem. 1999 May 28;274(22):15297-300 [10336413.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6853-66 [10602461.001]
  • [Cites] Oncogene. 2000 Oct 26;19(45):5198-203 [11064457.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6948-58 [10602469.001]
  • [Cites] Nature. 2001 May 31;411(6837):603-6 [11385577.001]
  • [Cites] Retrovirology. 2005 Feb 01;2:4 [15686595.001]
  • [Cites] Acta Paediatr Jpn. 1992 Jun;34(3):358-64 [1509882.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23 ):6805-15 [11726516.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] J Exp Med. 1998 Jan 19;187(2):147-59 [9432973.001]
  • [Cites] Oncogene. 2000 Mar 9;19(11):1448-56 [10723136.001]
  • [Cites] Science. 2001 Mar 16;291(5511):2162-5 [11251123.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5375-85 [12374738.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6137-46 [8413215.001]
  • [Cites] Cell. 1996 Oct 4;87(1):13-20 [8858144.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6719-28 [16007163.001]
  • [Cites] Retrovirology. 2005 Dec 09;2:75 [16336683.001]
  • [Cites] Oncogene. 1993 Oct;8(10):2839-45 [8378093.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):2994-9 [10077625.001]
  • [Cites] Oncogene. 1994 Aug;9(8):2335-44 [8036016.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2493-503 [11971184.001]
  • [Cites] Cell. 1997 Oct 17;91(2):243-52 [9346241.001]
  • [Cites] Retrovirology. 2005 May 06;2:29 [15876358.001]
  • [Cites] Nature. 1997 Aug 7;388(6642):548-54 [9252186.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6888-95 [10602464.001]
  • [Cites] Immunol Today. 1998 Feb;19(2):80-8 [9509763.001]
  • [Cites] Oncogene. 2003 Jul 31;22(31):4868-74 [12894228.001]
  • [Cites] J Exp Med. 1988 Mar 1;167(3):1259-64 [2832508.001]
  • [Cites] Science. 1999 Sep 24;285(5436):2122-5 [10497129.001]
  • [Cites] Annu Rev Immunol. 1997;15:15-37 [9143680.001]
  • [Cites] J Biol Chem. 2004 Oct 22;279(43):44563-72 [15310758.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Nov 27;181(1):80-6 [1958222.001]
  • [Cites] Expert Rev Anticancer Ther. 2004 Jun;4(3):369-76 [15161436.001]
  • [Cites] EMBO J. 2004 Oct 27;23 (21):4202-10 [15470505.001]
  • [Cites] Oncogene. 1994 Mar;9(3):841-52 [8108127.001]
  • [Cites] Cell. 1998 Jun 26;93(7):1231-40 [9657155.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6005-15 [16155607.001]
  • [Cites] J Virol. 2005 Jul;79(14 ):9346-50 [15994832.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):22911-4 [10438454.001]
  • [Cites] Science. 1999 Apr 9;284(5412):316-20 [10195896.001]
  • [Cites] J Biol Chem. 2005 Dec 9;280(49):40965-73 [16207722.001]
  • [Cites] Semin Cancer Biol. 1997 Apr;8(2):75-82 [9299585.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] EMBO J. 1997 Dec 1;16(23):7078-90 [9384586.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5931-7 [16155600.001]
  • [Cites] J Cell Physiol. 2002 Feb;190(2):133-59 [11807819.001]
  • [Cites] J Cell Mol Med. 2005 Jan-Mar;9(1):59-71 [15784165.001]
  • [Cites] Cell Signal. 2002 May;14(5):381-95 [11882383.001]
  • [Cites] J Biol Chem. 2005 Jan 7;280(1):18-27 [15485830.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18827-35 [10373501.001]
  • [Cites] J Theor Biol. 2000 Nov 7;207(1):65-79 [11027480.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12 (2-3):207-17 [11325603.001]
  • [Cites] J Biol Chem. 2005 Oct 21;280(42):35713-22 [16105841.001]
  • [Cites] Genes Dev. 1995 Nov 15;9(22):2736-46 [7590249.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • [Cites] Nature. 1995 Jan 26;373(6512):303-10 [7530332.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6035-46 [16155610.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] J Exp Med. 1998 Jan 19;187(2):185-96 [9432976.001]
  • (PMID = 27519575.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Adult T cell leukemia (ATL) / HTLV-1 Tax / Human T cell leukemia virus (HTLV-1) / IKK / Inflammation / NF-ϰB / NIK
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43. Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R: Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut. CMAJ; 2006 Sep 12;175(6):579
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  • [Title] Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / ethnology
  • [MeSH-minor] Adult. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic

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  • [Cites] Tissue Antigens. 1998 Nov;52(5):444-51 [9864034.001]
  • [Cites] CMAJ. 2006 Jan 17;174(2):150-1 [16415454.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):232-9 [15726602.001]
  • (PMID = 16966657.001).
  • [ISSN] 1488-2329
  • [Journal-full-title] CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
  • [ISO-abbreviation] CMAJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1559419
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44. Mesnard JM, Barbeau B, Devaux C: HBZ, a new important player in the mystery of adult T-cell leukemia. Blood; 2006 Dec 15;108(13):3979-82
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  • [Title] HBZ, a new important player in the mystery of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) was first described in 1977.
  • A link between ATL and human T-cell leukemia virus type 1 (HTLV-1) was clearly established in the early 1980s.
  • Over the years, many aspects of HTLV-1-induced cellular dysfunctions have been clarified.
  • However, the detailed mechanism behind ATL occurrence remains unsolved.
  • Presently, we are still unable to explain the absence of viral Tax protein (thought to play a central role in T-cell transformation) in more than 50% of ATL cells.
  • A novel HTLV-1 HBZ protein, encoded on the negative strand, was characterized by our group and is currently the subject of intensive research efforts to determine its function in viral replication and/or pathophysiology.
  • Recently, 4 studies reported on the existence of different HBZ isoforms and have investigated on their function in both ATL cells or animal models.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. Cell Transformation, Viral / genetics. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Viral Proteins / genetics. Virus Replication / genetics
  • [MeSH-minor] Animals. Cell Proliferation. Disease Models, Animal. Gene Products, tax / deficiency. Gene Products, tax / immunology. Humans. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / immunology. RNA, Viral / genetics. RNA, Viral / immunology. T-Lymphocytes / immunology. T-Lymphocytes / pathology. T-Lymphocytes / virology

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  • (PMID = 16917009.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
  • [Number-of-references] 102
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45. Ariumi Y, Trono D: Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function. J Virol; 2006 Mar;80(5):2445-52
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  • [Title] Ataxia-telangiectasia-mutated (ATM) protein can enhance human immunodeficiency virus type 1 replication by stimulating Rev function.
  • The ataxia-telangiectasia-mutated (ATM) kinase plays a central role in responses to various forms of DNA damage and has been suggested to facilitate human immunodeficiency virus type 1 (HIV-1) integration.
  • Notably, ATM overexpression did not stimulate the HIV-1 late gene expression within the context of Rev-independent constructs or the Rex-dependent production of capsid from human T-cell leukemia virus type 1 proviral constructs.
  • [MeSH-major] Cell Cycle Proteins / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Viral. Gene Products, rev / physiology. HIV-1 / physiology. Protein-Serine-Threonine Kinases / physiology. Tumor Suppressor Proteins / physiology. Virus Replication
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Caffeine. Cell Line. Gene Silencing. Genes, Reporter. HIV Core Protein p24 / analysis. Humans. Luciferases / analysis. Luciferases / genetics. rev Gene Products, Human Immunodeficiency Virus

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  • [Cites] Curr Biol. 1997 Oct 1;7(10):767-75 [9368759.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1051-60 [9323133.001]
  • [Cites] J Virol. 1998 Aug;72(8):6602-7 [9658105.001]
  • [Cites] Mol Cell. 1998 Apr;1(5):649-59 [9660949.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10146-51 [9707615.001]
  • [Cites] Science. 1998 Sep 11;281(5383):1677-9 [9733515.001]
  • [Cites] Oncogene. 1999 Apr 1;18(13):2261-71 [10327072.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4375-82 [10485486.001]
  • [Cites] Virology. 2004 Dec 20;330(2):471-80 [15567440.001]
  • [Cites] J Virol. 2005 Feb;79(3):1389-96 [15650165.001]
  • [Cites] J Virol. 2005 Feb;79(4):2058-65 [15681408.001]
  • [Cites] J Virol. 2005 Mar;79(5):2973-8 [15709017.001]
  • [Cites] Nat Cell Biol. 2005 May;7(5):493-500 [15834407.001]
  • [Cites] J Biol Chem. 1999 Nov 26;274(48):34277-82 [10567403.001]
  • [Cites] Nucleic Acids Res. 2000 Feb 15;28(4):901-10 [10648781.001]
  • [Cites] J Biol Chem. 2000 Apr 7;275(14):10342-8 [10744722.001]
  • [Cites] J Virol. 2000 May;74(10):4839-52 [10775623.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 21;287(2):556-61 [11554765.001]
  • [Cites] Science. 2002 Apr 19;296(5567):550-3 [11910072.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):155-68 [12612651.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4778-83 [12679521.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] Nat Cell Biol. 2003 Aug;5(8):754-61 [12883554.001]
  • [Cites] Trends Biochem Sci. 2003 Aug;28(8):419-24 [12932730.001]
  • [Cites] Virology. 2003 Sep 15;314(1):460-7 [14517098.001]
  • [Cites] EMBO J. 2003 Dec 15;22(24):6610-20 [14657032.001]
  • [Cites] Science. 2004 Apr 2;304(5667):93-6 [15064416.001]
  • [Cites] EMBO J. 2004 Jul 7;23(13):2632-40 [15201866.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:3187-208 [15353349.001]
  • [Cites] Cell. 2004 Oct 29;119(3):381-92 [15507209.001]
  • [Cites] J Gen Virol. 1987 Feb;68 ( Pt 2):499-506 [3029287.001]
  • [Cites] EMBO J. 1990 Dec;9(12):4155-60 [2249669.001]
  • [Cites] J Mol Biol. 1994 Sep 2;241(5):651-62 [7520946.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1480-4 [7878004.001]
  • [Cites] J Virol. 1995 Apr;69(4):2024-30 [7884847.001]
  • [Cites] J Virol. 1995 Aug;69(8):5048-56 [7541845.001]
  • [Cites] Virology. 1996 Mar 1;217(1):293-300 [8599214.001]
  • [Cites] Leuk Res. 2005 Aug;29(8):933-42 [15978944.001]
  • [Cites] Science. 1996 Apr 12;272(5259):263-7 [8602510.001]
  • [Cites] Nat Biotechnol. 1997 Sep;15(9):871-5 [9306402.001]
  • [Cites] EMBO J. 1997 Dec 15;16(24):7500-10 [9405378.001]
  • (PMID = 16474151.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Gene Products, rev; 0 / HIV Core Protein p24; 0 / Tumor Suppressor Proteins; 0 / rev Gene Products, Human Immunodeficiency Virus; 3G6A5W338E / Caffeine; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC1395391
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46. Yoshida M, Satou Y, Yasunaga J, Fujisawa J, Matsuoka M: Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene. J Virol; 2008 Oct;82(19):9359-68
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  • [Title] Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene.
  • The human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the HTLV-1 provirus and transcribed from the 3' long terminal repeat (LTR).
  • We compared the functions of the proteins derived from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.
  • The expression of sHBZ had a growth-promoting function in a T-cell line, while usHBZ expression did not.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / chemistry. Human T-lymphotropic virus 1 / genetics. Sp1 Transcription Factor / metabolism. Transcription, Genetic. Viral Proteins / genetics. Viral Proteins / physiology
  • [MeSH-minor] Alternative Splicing. Base Sequence. Cell Proliferation. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Humans. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Viral / metabolism. Terminal Repeat Sequences

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  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] Proteomics. 2008 Feb;8(4):626-49 [18203265.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):165-70 [15044019.001]
  • [Cites] Retrovirology. 2008;5:34 [18426605.001]
  • [Cites] J Virol. 2000 Sep;74(18):8277-85 [10954525.001]
  • [Cites] Oncogene. 2000 Aug 17;19(35):3988-98 [10962555.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • [Cites] Ann Hum Genet. 2000 Jan;64(Pt 1):83-6 [11246463.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Annu Rev Biochem. 2003;72:449-79 [12651739.001]
  • [Cites] Cell. 1983 Nov;35(1):79-87 [6313230.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Blood. 1987 Oct;70(4):1069-72 [3115332.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] J Virol. 1991 Aug;65(8):4525-8 [2072462.001]
  • [Cites] Mol Cell Biol. 1991 Oct;11(10):5229-43 [1922043.001]
  • [Cites] New Biol. 1991 Sep;3(9):896-906 [1931834.001]
  • [Cites] J Biol Chem. 1992 Mar 25;267(9):6450 [1348249.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] J Biol Chem. 1995 Aug 18;270(33):19487-94 [7642633.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1001-10 [15592508.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5938-51 [16155601.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Mar;80(5):2495-505 [16474156.001]
  • [Cites] Gene. 2006 Feb 1;366(2):335-42 [16288839.001]
  • [Cites] Blood. 2006 May 15;107(10):3976-82 [16424388.001]
  • [Cites] Retrovirology. 2006;3:15 [16512901.001]
  • [Cites] J Virol. 2006 Aug;80(15):7427-38 [16840323.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • (PMID = 18653454.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2546946
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47. 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
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  • [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

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  • [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
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48. Malyukova A, Dohda T, von der Lehr N, Akhoondi S, Corcoran M, Heyman M, Spruck C, Grandér D, Lendahl U, Sangfelt O: The tumor suppressor gene hCDC4 is frequently mutated in human T-cell acute lymphoblastic leukemia with functional consequences for Notch signaling. Cancer Res; 2007 Jun 15;67(12):5611-6
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  • [Title] The tumor suppressor gene hCDC4 is frequently mutated in human T-cell acute lymphoblastic leukemia with functional consequences for Notch signaling.
  • Notch signaling is of crucial importance in normal T-cell development and Notch 1 is frequently mutated in T-cell acute lymphoblastic leukemias (T-ALL), leading to aberrantly high Notch signaling.
  • We show that the hCDC4 gene is mutated in leukemic cells from more than 30% of patients with pediatric T-ALL and derived cell lines.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptor, Notch1 / metabolism. Signal Transduction / physiology. Ubiquitin-Protein Ligases / genetics

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  • [ErratumIn] Cancer Res. 2008 Mar 15;68(6):2051. Akhondi, Shahab [corrected to Akhoondi, Shahab]
  • (PMID = 17575125.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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49. Suzuki R, Nakamura S, Suzumiya J, Ichimura K, Ichikawa M, Ogata K, Kura Y, Aikawa K, Teshima H, Sako M, Kojima H, Nishio M, Yoshino T, Sugimori H, Kawa K, Oshimi K, NK-cell Tumor Study Group: Blastic natural killer cell lymphoma/leukemia (CD56-positive blastic tumor): prognostication and categorization according to anatomic sites of involvement. Cancer; 2005 Sep 1;104(5):1022-31
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  • [Title] Blastic natural killer cell lymphoma/leukemia (CD56-positive blastic tumor): prognostication and categorization according to anatomic sites of involvement.
  • BACKGROUND: Blastic natural killer (NK) cell lymphoma/leukemia (BNKL) is an immature CD56-positive neoplasm, which was recognized recently and characterized by systemic proliferation of tumor cells including skin, lymph node, and bone marrow.
  • METHODS: The current study analyzed 47 patients with BNKL (27 had leukemias and 20 had lymphomas).
  • Patient data were collected for the survey of the NK-Cell Tumor Study Group.
  • There were few clinicopathologic differences between the leukemia and lymphoma types.
  • Cutaneous involvement was noted at diagnosis in 28 patients, who presented a tendency for older age of onset (median: 56 vs. 46 years, P = 0.11) than patients with noncutaneous BNKL.
  • Both groups responded well to chemotherapy for lymphoid malignancies, but disease recurrence was frequent.
  • CONCLUSIONS: These findings suggested that BNKL is a heterogeneous disease and contains at least two subtypes.
  • [MeSH-major] Antigens, CD56 / analysis. Killer Cells, Natural / pathology. Leukemia, Lymphoid / mortality. Lymphoma, T-Cell / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. DNA Nucleotidylexotransferase / analysis. Female. Gene Rearrangement, T-Lymphocyte. Humans. Immunophenotyping. Interleukin-3 Receptor alpha Subunit. Karyotyping. Male. Middle Aged. Prognosis. Receptors, Interleukin-3 / analysis. Skin Neoplasms / immunology. Skin Neoplasms / mortality. Skin Neoplasms / therapy

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  • (PMID = 15999368.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, Interleukin-3; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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50. Masutani H, Ueda S, Yodoi J: The thioredoxin system in retroviral infection and apoptosis. Cell Death Differ; 2005 Aug;12 Suppl 1:991-8
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  • Human thioredoxin (TRX) was first identified in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and is associated with the pathophysiology of retroviral infections.
  • Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in HTLV-I-transformed cells.
  • Studies of these molecules of the TRX system provide novel insights into the apoptosis associated with retroviral diseases.
  • [MeSH-minor] Animals. Glutathione / metabolism. HIV Infections / metabolism. HTLV-I Infections / metabolism. Humans. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Proteins / metabolism. Peroxidases / metabolism. Peroxiredoxins

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  • (PMID = 15818395.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; 52500-60-4 / Thioredoxins; EC 1.11.1.- / Peroxidases; EC 1.11.1.15 / Peroxiredoxins; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; GAN16C9B8O / Glutathione
  • [Number-of-references] 93
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51. Mukherjee S, Negi VS, Keitany G, Tanaka Y, Orth K: In vitro activation of the IkappaB kinase complex by human T-cell leukemia virus type-1 Tax. J Biol Chem; 2008 May 30;283(22):15127-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro activation of the IkappaB kinase complex by human T-cell leukemia virus type-1 Tax.
  • Human T-cell leukemia virus type-I expresses Tax, a 40-kDa oncoprotein that activates IkappaB kinase (IKK), resulting in constitutive activation of NFkappaB.

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  • [Cites] J Biol Chem. 2000 Nov 3;275(44):34060-7 [10906125.001]
  • [Cites] Trends Biochem Sci. 2007 May;32(5):210-6 [17412595.001]
  • [Cites] Science. 2000 Nov 24;290(5496):1594-7 [11090361.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):1487-93 [12419799.001]
  • [Cites] Exp Biol Med (Maywood). 2003 Feb;228(2):111-33 [12563018.001]
  • [Cites] J Biol Chem. 2003 Dec 5;278(49):48903-6 [14514672.001]
  • [Cites] Oncogene. 2004 Jul 8;23(31):5378-86 [15077173.001]
  • [Cites] Tohoku J Exp Med. 1989 Jan;157(1):1-11 [2711372.001]
  • [Cites] Nature. 1997 Aug 7;388(6642):548-54 [9252186.001]
  • [Cites] Cell. 1998 May 29;93(5):875-84 [9630230.001]
  • [Cites] J Biol Chem. 1999 May 28;274(22):15297-300 [10336413.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • [Cites] Science. 1999 Sep 17;285(5435):1920-3 [10489373.001]
  • [Cites] IUBMB Life. 2005 Feb;57(2):83-91 [16036567.001]
  • [Cites] J Biol Chem. 2005 Aug 19;280(33):29653-60 [15975923.001]
  • [Cites] Annu Rev Microbiol. 2005;59:69-89 [15847602.001]
  • [Cites] J Biol Chem. 2005 Oct 28;280(43):35974-82 [16126728.001]
  • [Cites] Science. 2006 May 26;312(5777):1211-4 [16728640.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 5;103(49):18574-9 [17116858.001]
  • [Cites] Cell. 2000 Oct 13;103(2):351-61 [11057907.001]
  • (PMID = 18223255.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI 056404; United States / NIDDK NIH HHS / DK / R21 DK 072134
  • [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 / Bacterial Proteins; 0 / Gene Products, tax; 0 / HSP90 Heat-Shock Proteins; 0 / Multiprotein Complexes; 0 / NF-kappa B; 0 / Recombinant Proteins; 0 / YopP protein, Yersinia; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.3.16 / Phosphoprotein Phosphatases
  • [Other-IDs] NLM/ PMC2397464
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52. Chiba K, Hashino S, Izumiyama K, Toyoshima N, Suzuki S, Kurosawa M, Asaka M: Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia. Int J Lab Hematol; 2009 Jun;31(3):368-71
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  • [Title] Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia.
  • A 37-year-old woman was diagnosed as having chronic adult T-cell leukemia (ATL) of the skin by a skin biopsy and human T-cell leukemia virus type-1 serology at our hospital in August 1992.
  • The skin lesions of ATL were improved by treatment with psoralen ultraviolet ray A.
  • [MeSH-major] Chemokines / blood. Interleukin-6 / blood. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / complications. Osteolysis / blood. Osteolysis / etiology
  • [MeSH-minor] Adult. Chronic Disease. Fatal Outcome. Female. Humans

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  • (PMID = 18177436.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Interleukin-6
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53. Fan J, Ma G, Nosaka K, Tanabe J, Satou Y, Koito A, Wain-Hobson S, Vartanian JP, Matsuoka M: APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo. J Virol; 2010 Jul;84(14):7278-87
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  • [Title] APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo.
  • Human T-cell leukemia virus type 1 (HTLV-1) induces cell proliferation after infection, leading to efficient transmission by cell-to-cell contact.
  • After a long latent period, a fraction of carriers develop adult T-cell leukemia (ATL).
  • Genetic changes in the tax gene in ATL cells were reported in about 10% of ATL cases.
  • To determine genetic changes that may occur throughout the provirus, we determined the entire sequence of the HTLV-1 provirus in 60 ATL cases.
  • Abortive genetic changes, including deletions, insertions, and nonsense mutations, were frequent in all viral genes except the HBZ gene, which is transcribed from the minus strand of the virus.
  • G-to-A base substitutions were the most frequent mutations in ATL cells.
  • The sequence context of G-to-A mutations was in accordance with the preferred target sequence of human APOBEC3G (hA3G).
  • The target sequences of hA3G were less frequent in the plus strand of the HBZ coding region than in other coding regions of the HTLV-1 provirus.
  • HTLV-1-infected cells likely take advantage of hA3G to escape from the host immune system by losing expression of viral proteins.
  • [MeSH-major] Cytidine Deaminase / metabolism. Genome, Viral. HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Mutation. Proviruses / genetics
  • [MeSH-minor] Base Sequence. Cell Line. Genes, Reporter. Genetic Variation. Genetic Vectors. Humans. Molecular Sequence Data. Mutagenesis

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  • [Cites] J Virol. 2000 Oct;74(20):9525-31 [11000222.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1061-5 [15718460.001]
  • [Cites] Virus Genes. 2001;23(2):123-35 [11724264.001]
  • [Cites] J Virol. 2002 Sep;76(18):9389-97 [12186921.001]
  • [Cites] Virology. 2005 Mar 15;333(2):374-86 [15721369.001]
  • [Cites] Nat Immunol. 2005 Jul;6(7):655-61 [15970938.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Retrovirology. 2005;2:32 [15943885.001]
  • [Cites] J Gen Virol. 2005 Sep;86(Pt 9):2489-94 [16099907.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6005-15 [16155607.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):381-7 [16052518.001]
  • [Cites] Retrovirology. 2005;2:64 [16242045.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] EMBO J. 2006 Apr 19;25(8):1741-52 [16601696.001]
  • [Cites] J Virol. 2006 Nov;80(21):10683-91 [16943297.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2915-20 [17299050.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Nat Med. 2007 Apr;13(4):470-6 [17401375.001]
  • [Cites] J Virol. 2007 May;81(9):4422-8 [17287279.001]
  • [Cites] J Virol. 2007 Jun;81(11):5714-23 [17344291.001]
  • [Cites] Annu Rev Immunol. 2008;26:317-53 [18304004.001]
  • [Cites] Cell Host Microbe. 2008 Jun 12;3(6):388-98 [18541215.001]
  • [Cites] J Virol. 2008 Sep;82(17):8442-55 [18596104.001]
  • [Cites] J Virol. 2008 Oct;82(19):9359-68 [18653454.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Nat Med. 2003 Nov;9(11):1404-7 [14528300.001]
  • [Cites] Science. 2003 Nov 7;302(5647):1056-60 [14564014.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):280-96 [14686485.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] Nat Struct Mol Biol. 2004 May;11(5):435-42 [15098018.001]
  • [Cites] EMBO J. 2004 Jun 16;23(12):2451-8 [15152192.001]
  • [Cites] EMBO Rep. 2004 Jul;5(7):679-80 [15229643.001]
  • [Cites] J Biol Chem. 2004 Aug 6;279(32):33177-84 [15159405.001]
  • [Cites] Curr Biol. 2004 Aug 10;14(15):1385-91 [15296757.001]
  • [Cites] J Virol. 2004 Nov;78(21):11841-52 [15479826.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [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 Virol. 1995 Apr;69(4):2611-6 [7884912.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4243-9 [7492783.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] J Neurovirol. 1995 Sep;1(3-4):286-94 [9222367.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4862-7 [9354450.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Nat Rev Immunol. 2004 Nov;4(11):868-77 [15516966.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):63-8 [15623561.001]
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • (PMID = 20463074.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / APOBEC3G protein, human; EC 3.5.4.5 / Cytidine Deaminase
  • [Other-IDs] NLM/ PMC2898234
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54. Mizobe T, Tsukada J, Higashi T, Mouri F, Matsuura A, Tanikawa R, Minami Y, Yoshida Y, Tanaka Y: Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells. Exp Hematol; 2007 Dec;35(12):1812-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells.
  • OBJECTIVE: Constitutive activation of nuclear factor (NF)-kappaB is a common feature of human T-cell leukemia virus type I (HTLV-I)-transformed T cells.
  • Inhibition of NF-kappaB activity reduces cell growth and induces apoptosis of HTLV-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.
  • In this study, we investigated whether MyD88, an adaptor protein of Toll-like receptor (TLR) signaling, contributes to constitutive NF-kappaB activation in HTLV-I-transformed T cells.
  • MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-associated kinase 1 (IRAK1) in HTLV-I-transformed human T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.
  • An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in HTLV-I-transformed T cells.
  • RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of HTLV-I-transformed T cells, but not in HTLV-I-negative T cells, such as Jurkat, HUT78, and MOLT4.
  • HTLV-I Tax enhanced TLR expression and synergistically activated NF-kappaB with wild-type MyD88.
  • CONCLUSION: Our results show a novel pathway in NF-kappaB activation in HTLV-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Interleukin-1 Receptor-Associated Kinases / metabolism. Myeloid Differentiation Factor 88 / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Transformed. Cell Transformation, Viral. DNA Primers. Humans. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / metabolism

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  • (PMID = 17920759.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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55. Park CW, Kim A, Cha SW, Jung SH, Yang HW, Lee YJ, Lee HIe, Kim SH, Kim YH: A case of phlegmonous gastritis associated with marked gastric distension. Gut Liver; 2010 Sep;4(3):415-8
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  • [Title] A case of phlegmonous gastritis associated with marked gastric distension.
  • Phlegmonous gastritis is an acute and severe infectious disease that is occasionally fatal if the diagnosis is delayed.
  • Alcohol consumption, an immunocompromised state (e.g., due to HIV infection, rheumatoid arthritis, diabetes mellitus, or adult T-cell lymphoma), and mucosal injury of the stomach are reported to be predisposing factors.

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  • (PMID = 20981225.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2956360
  • [Keywords] NOTNLM ; Gastric outlet obstruction / Phlegmonous gastritis
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56. Arisawa K, Soda M, Ono M, Uemura H, Hiyoshi M, Suyama A: Trends of incidence rate of adult T-cell leukemia/lymphoma in an HTLV-1 endemic area in Japan. Int J Cancer; 2009 Aug 1;125(3):737-8
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  • [Title] Trends of incidence rate of adult T-cell leukemia/lymphoma in an HTLV-1 endemic area in Japan.
  • [MeSH-major] Endemic Diseases. HTLV-I Infections / epidemiology. Leukemia-Lymphoma, Adult T-Cell / epidemiology
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Female. Humans. Incidence. Japan / epidemiology. Male. Middle Aged. Odds Ratio. Registries. Risk Assessment. Risk Factors. Time Factors

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  • (PMID = 19437534.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] United States
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57. Venkitaraman R, Sagar TG, George MK: Adult T-cell lymphoma with HTLV-I and HTLV-II infection. South Med J; 2007 Nov;100(11):1178-9
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  • [Title] Adult T-cell lymphoma with HTLV-I and HTLV-II infection.
  • [MeSH-major] HTLV-I Infections / diagnosis. HTLV-II Infections / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

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  • (PMID = 17984755.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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58. 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
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  • [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

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  • [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
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59. Janik JE, Morris JC: Survivin(g) adult T-cell leukemia/lymphoma. Oncology (Williston Park); 2009 Dec;23(14):1256, 1261, 1266
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  • [Title] Survivin(g) adult T-cell leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / genetics. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / therapy. Microtubule-Associated Proteins / genetics
  • [MeSH-minor] Adult. Female. Gene Expression Profiling. Humans. Inhibitor of Apoptosis Proteins. Male. Transplantation, Homologous

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  • [CommentOn] Oncology (Williston Park). 2009 Dec;23(14):1250-6 [20120837.001]
  • (PMID = 20120838.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins
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60. Nascimento MC, Primo J, Bittencourt A, Siqueira I, de Fátima Oliveira M, Meyer R, Schriefer A, Santos SB, Carvalho EM: Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis. Clin Exp Immunol; 2009 Jun;156(3):455-62
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  • [Title] Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
  • Human T lymphotropic virus-type 1 (HTLV-1) is the causal agent of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), adult T cell leukaemia/lymphoma and infective dermatitis associated with HTLV-1 (IDH).
  • Over-production of proinflammatory cytokines and an increase in HTLV-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established.
  • In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the HTLV-1 proviral load.
  • HTLV-1 carriers and patients with HAM/TSP served as controls.
  • TNF-alpha and IFN-gamma levels were higher in IDH than in HTLV-1 carriers.
  • There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in HTLV-1 carriers, but the difference did not reach statistical significance.
  • The HTLV-1 proviral load was significantly higher in IDH patients than in HTLV-1 carriers.
  • IDH is characterized by an exaggerated Th1 immune response and high HTLV-1 proviral load.

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  • [Cites] J Infect Dis. 2001 Jan 15;183(2):197-205 [11120926.001]
  • [Cites] J Exp Med. 2007 Feb 19;204(2):285-97 [17283207.001]
  • [Cites] J Acquir Immune Defic Syndr. 2001 May 1;27(1):1-6 [11404513.001]
  • [Cites] Am J Trop Med Hyg. 2001 Aug;65(2):87-9 [11508396.001]
  • [Cites] J Neurovirol. 2001 Jun;7(3):228-34 [11517397.001]
  • [Cites] Ann Neurol. 2001 Dec;50(6):807-12 [11761481.001]
  • [Cites] J Virol Methods. 2002 Apr;102(1-2):37-51 [11879691.001]
  • [Cites] Dermatol Nurs. 2003 Aug;Suppl:6-9 [14520891.001]
  • [Cites] Ann Dermatol Venereol. 2004 Feb;131(2):191-3 [15026748.001]
  • [Cites] BMC Infect Dis. 2004 Mar 2;4:7 [15070424.001]
  • [Cites] Br J Dermatol. 2004 May;150(5):958-65 [15149509.001]
  • [Cites] J Infect Dis. 2004 Nov 15;190(10):1797-803 [15499536.001]
  • [Cites] Br J Dermatol. 1967 Apr;79(4):229-36 [6024739.001]
  • [Cites] Br J Dermatol. 1974 May;90(5):525-30 [4601016.001]
  • [Cites] Neurology. 1983 Nov;33(11):1444-52 [6685237.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Ann Neurol. 1990 Feb;27(2):149-56 [2317010.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5218-22 [2367534.001]
  • [Cites] J Acquir Immune Defic Syndr. 1990;3(12):1199-200 [2243322.001]
  • [Cites] Ann Neurol. 1991 Feb;29(2):194-201 [2012389.001]
  • [Cites] Lancet. 1991 Dec 21-28;338(8782-8783):1593-4 [1683991.001]
  • [Cites] Br J Rheumatol. 1992 May;31(5):293-8 [1581770.001]
  • [Cites] J Neuropathol Exp Neurol. 1994 Jan;53(1):72-7 [8301322.001]
  • [Cites] Lancet. 1995 Sep 9;346(8976):710 [7658857.001]
  • [Cites] J Clin Invest. 1995 Nov;96(5):2339-47 [7593621.001]
  • [Cites] Neurology. 1996 Apr;46(4):1016-21 [8780082.001]
  • [Cites] Transfusion. 1997 Feb;37(2):242-3 [9051104.001]
  • [Cites] J Immunol. 1997 Aug 15;159(4):2018-25 [9257869.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):439-44 [9554295.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):487-8 [9554302.001]
  • [Cites] J Invest Dermatol. 1999 Feb;112(2):171-6 [9989792.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):586-93 [10065900.001]
  • [Cites] J Immunol. 1999 Jul 1;163(1):466-75 [10384150.001]
  • [Cites] Eur J Dermatol. 2005 Jan-Feb;15(1):26-30 [15701589.001]
  • [Cites] Clin Infect Dis. 2005 Jun 1;40(11):e90-6 [15889351.001]
  • [Cites] Clin Infect Dis. 2005 Aug 15;41(4):535-41 [16028164.001]
  • [Cites] Clin Exp Immunol. 2006 Aug;145(2):296-301 [16879249.001]
  • [Cites] Clin Infect Dis. 2006 Nov 15;43(10):1257-63 [17051489.001]
  • [Cites] Neuroimmunomodulation. 2006;13(3):145-51 [17119343.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • (PMID = 19438598.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2691974
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61. Mizuguchi M, Asao H, Hara T, Higuchi M, Fujii M, Nakamura M: Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells. J Biol Chem; 2009 Sep 18;284(38):25501-11
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  • [Title] Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells.
  • At the incipient stages of the development of adult T-cell leukemia, T-cells infected with human T-cell leukemia virus type 1 (HTLV-1) suffer disregulation in cell growth caused by aberrant expression of host genes by the HTLV-1 transactivator protein Tax (Tax1).
  • Tax1-mediated growth promotion is thought to result from, at least in part, up-regulation of genes for growth factors and their receptors that induce T-cell growth.
  • In the present study, we demonstrate that Tax1 transactivates the interleukin-21 (IL-21) and its receptor (IL-21R) genes in human T-cells.
  • Chromatin immunoprecipitation assay and gel mobility shift assay exhibited that the IL-21 promoter elements bound transcription factors AP-1 and NF-kappaB, and the IL-21R promoter elements were associated with AP-1 and interferon regulatory factor.
  • The related virus HTLV-2 with Tax2 similar to Tax1 is known not to be pathogenic.
  • The study suggests insights into cytokine-dependent aberrant growth of HTLV-1-infected T-cells and the molecular basis of different pathogenicity between HTLV-1 and HTLV-2.
  • [MeSH-major] CD4-Positive T-Lymphocytes / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Interleukin-21 Receptor alpha Subunit / biosynthesis. Interleukins / biosynthesis. Response Elements. Transcriptional Activation
  • [MeSH-minor] Adenoviridae. HTLV-I Infections / genetics. HTLV-I Infections / metabolism. Human T-lymphotropic virus 2 / genetics. Human T-lymphotropic virus 2 / metabolism. Human T-lymphotropic virus 2 / pathogenicity. Humans. Jurkat Cells. NF-kappa B / genetics. NF-kappa B / metabolism. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transduction, Genetic

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  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Cell. 1987 Apr 10;49(1):47-56 [3030566.001]
  • [Cites] EMBO J. 1987 Feb;6(2):389-95 [3034589.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4831-5 [2440031.001]
  • [Cites] Science. 1988 Jul 1;241(4861):89-92 [2838905.001]
  • [Cites] Nucleic Acids Res. 1989 Feb 25;17(4):1589-604 [2784206.001]
  • [Cites] Tohoku J Exp Med. 1989 Jan;157(1):1-11 [2711372.001]
  • [Cites] Science. 1989 Apr 28;244(4903):457-60 [2497518.001]
  • [Cites] J Biol Chem. 1989 Dec 5;264(34):20189-92 [2555345.001]
  • [Cites] Int J Cancer. 1991 Jun 19;48(4):623-30 [1710610.001]
  • [Cites] Oncogene. 1992 Sep;7(9):1737-42 [1501885.001]
  • [Cites] J Virol. 1993 Mar;67(3):1590-9 [8382312.001]
  • [Cites] J Biol Chem. 1995 Mar 31;270(13):7479-86 [7706294.001]
  • [Cites] Science. 1995 Jul 7;269(5220):79-81 [7604283.001]
  • [Cites] Oncogene. 1996 Apr 18;12(8):1645-52 [8622884.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3744-50 [8670878.001]
  • [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] J Virol. 1996 Aug;70(8):5194-202 [8764028.001]
  • [Cites] Immunity. 1996 Oct;5(4):365-76 [8885869.001]
  • [Cites] J Virol. 1997 Jun;71(6):4445-51 [9151835.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2452-7 [9482906.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Cell. 1999 Aug 6;98(3):295-303 [10458605.001]
  • [Cites] Br J Haematol. 2005 Jan;128(2):169-76 [15638850.001]
  • [Cites] J Exp Med. 2005 Jan 17;201(2):233-40 [15657292.001]
  • [Cites] J Virol. 2005 Sep;79(18):11925-34 [16140768.001]
  • [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] Mol Cell Biol. 2005 Nov;25(22):9741-52 [16260592.001]
  • [Cites] Blood. 2007 May 15;109(10):4135-42 [17234735.001]
  • [Cites] Nature. 2007 Jul 26;448(7152):484-7 [17581588.001]
  • [Cites] Nature. 2007 Jul 26;448(7152):480-3 [17581589.001]
  • [Cites] FEBS Lett. 2007 Aug 21;581(21):4001-9 [17673207.001]
  • [Cites] Int Immunol. 2007 Oct;19(10):1191-9 [17698559.001]
  • [Cites] J Virol. 2007 Nov;81(21):11900-7 [17715223.001]
  • [Cites] J Virol. 2008 Apr;82(7):3632-41 [18216101.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):11154-63 [10753922.001]
  • [Cites] Genes Dev. 2000 Apr 1;14(7):804-16 [10766737.001]
  • [Cites] Virology. 2000 May 25;271(1):142-54 [10814579.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3915-21 [10845928.001]
  • [Cites] Nature. 2000 Nov 2;408(6808):57-63 [11081504.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1683-8 [11080810.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • [Cites] J Immunol. 2001 Jul 1;167(1):1-5 [11418623.001]
  • [Cites] Mol Cell Biol. 2002 May;22(10):3327-38 [11971966.001]
  • [Cites] J Immunol. 2002 Jun 1;168(11):5667-74 [12023365.001]
  • [Cites] J Immunol. 2002 Sep 15;169(6):3120-30 [12218129.001]
  • [Cites] Cell. 2004 Aug 20;118(4):453-64 [15315758.001]
  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43307-20 [15269214.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Microbiol Immunol. 1986;30(4):373-88 [2425230.001]
  • (PMID = 19617351.001).
  • [ISSN] 1083-351X
  • [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 / Gene Products, tax; 0 / IL21R protein, human; 0 / Interleukin-21 Receptor alpha Subunit; 0 / Interleukins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / interleukin-21; 0 / tax protein, Human T-lymphotrophic virus 1; 0 / tax protein, Human T-lymphotrophic virus 2
  • [Other-IDs] NLM/ PMC2757951
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62. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Nair R, Sengar M, Nair C: Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia. Indian J Cancer; 2010 Apr-Jun;47(2):189-93
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  • [Title] Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia.
  • INTRODUCTION: Mature T/NK cell lymphomas (MTNKL) presenting as leukemia are rare and show considerable overlapping of clinical, morphological and immunophenotypic features.
  • MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as leukemia and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.
  • MTNKL constituted 4% (nine cases) of all mature lymphoid neoplasms presenting as leukemia.
  • It included four cases of T-large granular leukemia (T-LGL), two of T-cell prolymphocytic leukemia small cell variant (T-PLL), two of adult T-cell leukemia/lymphoma (ATLL) and one of primary cutaneous gamma delta T-cell lymphoma (PCGDTCL).
  • One case of T- PLL small cell variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.
  • Both cases of ATLL showed CD4+/CD8+/CD25+ phenotype.
  • TCRalpha/beta was performed in three cases of T-LGL and was positive in all.
  • CONCLUSION: Mature nodal T/NK cell neoplasms are rare and MTNKL presenting as leukemia are even rarer.
  • There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK cell panels are required for their evaluation.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Bone Marrow / immunology. Bone Marrow / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 20448385.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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63. Silveira-Lacerda Ede P, Vilanova-Costa CA, Hamaguchi A, Pavanin LA, Goulart LR, Homsi-Brandenburgo MI, Dos Santos WB, Soares AM, Nomizo A: The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B cell lymphoma (A-20), murine ascitic sarcoma 180 (S-180), human breast adenocarcinoma (SK-BR-3), and human T cell leukemia (Jurkat) tumor cell lines. Biol Trace Elem Res; 2010 Jun;135(1-3):98-111
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  • [Title] The ruthenium complex cis-(dichloro)tetraammineruthenium(III) chloride presents selective cytotoxicity against murine B cell lymphoma (A-20), murine ascitic sarcoma 180 (S-180), human breast adenocarcinoma (SK-BR-3), and human T cell leukemia (Jurkat) tumor cell lines.
  • The aim of present study was to verify the in vitro antitumor activity of a ruthenium complex, cis-(dichloro)tetraammineruthenium(III) chloride (cis-[RuCl(2)(NH(3))(4)]Cl) toward different tumor cell lines.
  • The antitumor studies showed that ruthenium(III) complex presents a relevant cytotoxic activity against murine B cell lymphoma (A-20), murine ascitic sarcoma 180 (S-180), human breast adenocarcinoma (SK-BR-3), and human T cell leukemia (Jurkat) cell lines and a very low cytotoxicity toward human peripheral blood mononuclear cells.
  • The cytotoxic activity of a high concentration (2 mg mL(-1)) of cis-[RuCl(2)(NH(3))(4)]Cl toward Jurkat cells correlated with an increased number of annexin V-positive cells and also the presence of DNA fragmentation, suggesting that this compound induces apoptosis in tumor cells.
  • Thus, a mechanistic understanding of how metal complexes achieve their activities is crucial to their clinical success and to the rational design of new compounds with improved potency.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cytotoxicity, Immunologic / drug effects. Female. Humans. Jurkat Cells / drug effects. Lymphoma, B-Cell / drug therapy. Mice. Ruthenium / therapeutic use. Sarcoma 180 / drug therapy

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  • (PMID = 19727575.001).
  • [ISSN] 1559-0720
  • [Journal-full-title] Biological trace element research
  • [ISO-abbreviation] Biol Trace Elem Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / (dichloro)tetraammineruthenium(III); 0 / Antineoplastic Agents; 0 / Ruthenium Compounds; 7UI0TKC3U5 / Ruthenium
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64. Lepoutre V, Jain P, Quann K, Wigdahl B, Khan ZK: Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease. Front Biosci (Landmark Ed); 2009 Jan 01;14:1152-68
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  • [Title] Role of resident CNS cell populations in HTLV-1-associated neuroinflammatory disease.
  • Human T cell leukemia virus type 1 (HTLV-1), the first human retrovirus discovered, is the etiologic agent for a number of disorders; the two most common pathologies include adult T cell leukemia (ATL) and a progressive demyelinating neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
  • The neurologic dysfunction associated with HAM/TSP is a result of viral intrusion into the central nervous system (CNS) and the generation of a hyperstimulated host response within the peripheral and central nervous system that includes expanded populations of CD4+ and CD8+ T cells and proinflammatory cytokines/chemokines in the cerebrospinal fluid (CSF).
  • The mechanisms of neurological degeneration in HAM/TSP have yet to be fully delineated in vivo and may involve the immunogenic properties of the HTLV-1 transactivator protein Tax.
  • This comprehensive review characterizes the available knowledge to date concerning the effects of HTLV-1 on CNS resident cell populations with emphasis on both viral and host factors contributing to the genesis of HAM/TSP.

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  • [Cites] J Neurovirol. 1995 Jun;1(2):145-56 [9222353.001]
  • [Cites] Mol Pharmacol. 1997 Jul;52(1):6-15 [9224806.001]
  • [Cites] J Immunol. 1997 Aug 15;159(4):2018-25 [9257869.001]
  • [Cites] J Virol. 1997 Sep;71(9):6982-9 [9261427.001]
  • [Cites] Brain. 1997 Aug;120 ( Pt 8):1461-83 [9278635.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4862-7 [9354450.001]
  • [Cites] N Engl J Med. 1998 Jan 29;338(5):278-85 [9445407.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2452-7 [9482906.001]
  • [Cites] Science. 1998 Jun 5;280(5369):1610-3 [9616125.001]
  • [Cites] Ann N Y Acad Sci. 1997 Dec 19;835:142-52 [9616769.001]
  • [Cites] Am J Pathol. 1998 Sep;153(3):767-83 [9736027.001]
  • [Cites] J Virol. 1999 Dec;73(12):9917-27 [10559304.001]
  • [Cites] J Virol. 1999 Dec;73(12):10289-95 [10559346.001]
  • [Cites] Virology. 1999 Nov 25;264(2):370-84 [10562499.001]
  • [Cites] Immunol Today. 2000 Mar;21(3):141-7 [10689302.001]
  • [Cites] J Theor Biol. 2000 Nov 7;207(1):65-79 [11027480.001]
  • [Cites] Immunity. 2000 Nov;13(5):657-64 [11114378.001]
  • [Cites] J Immunol. 2000 Dec 15;165(12):7278-84 [11120862.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2000 Aug 29;355(1400):1013-9 [11186302.001]
  • [Cites] J Immunol. 1998 Oct 1;161(7):3767-75 [9759903.001]
  • [Cites] AIDS. 1998 Oct 22;12(15):1941-55 [9814862.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Dec 15;19(5):536-41 [9859969.001]
  • [Cites] J Neurosci Res. 1999 Jan 1;55(1):1-8 [9890428.001]
  • [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] J Virol. 1999 May;73(5):4299-304 [10196328.001]
  • [Cites] J Virol. 1999 Jun;73(6):4575-81 [10233916.001]
  • [Cites] J Gen Virol. 1999 Jun;80 ( Pt 6):1429-36 [10374960.001]
  • [Cites] J Neurol. 1999 May;246(5):358-64 [10399866.001]
  • [Cites] J Infect Dis. 1999 Aug;180(2):278-84 [10395840.001]
  • [Cites] J Infect Dis. 1999 Sep;180(3):880-3 [10438385.001]
  • [Cites] Nat Rev Immunol. 2005 Jan;5(1):69-81 [15630430.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):294-6 [15654060.001]
  • [Cites] Nat Med. 2005 Mar;11(3):328-34 [15735653.001]
  • [Cites] J Neurovirol. 2004 Dec;10(6):358-71 [15765807.001]
  • [Cites] Arch Virol. 2005 Apr;150(4):743-53 [15592888.001]
  • [Cites] J Biol Chem. 2005 Apr 29;280(17):17353-62 [15659397.001]
  • [Cites] Virus Res. 2005 Aug;111(2):194-213 [15885841.001]
  • [Cites] J Biol Chem. 2005 Aug 19;280(33):29653-60 [15975923.001]
  • [Cites] J Clin Pathol. 2005 Sep;58(9):996-7 [16126888.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6035-46 [16155610.001]
  • [Cites] J Biol Chem. 2006 Feb 17;281(7):3964-71 [16368688.001]
  • [Cites] J Virol. 2006 May;80(10):4771-80 [16641270.001]
  • [Cites] Virology. 2006 May 10;348(2):354-69 [16458341.001]
  • [Cites] J Virol. 2006 Jul;80(14):6844-54 [16809290.001]
  • [Cites] Clin Exp Immunol. 2006 Aug;145(2):296-301 [16879249.001]
  • [Cites] J Leukoc Biol. 2006 Sep;80(3):640-50 [16829632.001]
  • [Cites] Lancet Neurol. 2006 Dec;5(12):1068-76 [17110288.001]
  • [Cites] J Virol. 2007 Feb;81(3):1506-10 [17108050.001]
  • [Cites] J Virol. 2007 Feb;81(4):1690-700 [17121800.001]
  • [Cites] Biomed Pharmacother. 2007 May;61(4):201-8 [17391906.001]
  • [Cites] J Leukoc Biol. 2007 Jul;82(1):44-56 [17442856.001]
  • [Cites] Ann Neurol. 1991 Feb;29(2):194-201 [2012389.001]
  • [Cites] J Virol. 1991 May;65(5):2612-21 [2016773.001]
  • [Cites] J Pediatr. 1991 May;118(5):724-30 [1673468.001]
  • [Cites] J Immunol. 1991 Sep 1;147(5):1522-9 [1908877.001]
  • [Cites] J Virol. 1991 Nov;65(11):6094-100 [1920627.001]
  • [Cites] J Exp Med. 1992 Feb 1;175(2):331-40 [1346269.001]
  • [Cites] Virology. 1992 Mar;187(1):316-20 [1736534.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] J Clin Microbiol. 1992 Apr;30(4):905-10 [1572977.001]
  • [Cites] Virology. 1992 Jun;188(2):628-36 [1374983.001]
  • [Cites] Science. 1992 Jul 10;257(5067):217-9 [1352911.001]
  • [Cites] AIDS Res Hum Retroviruses. 1992 May;8(5):724-7 [1515222.001]
  • [Cites] Ann Intern Med. 1992 Dec 1;117(11):933-46 [1443956.001]
  • [Cites] Ann Neurol. 1992 Nov;32(5):651-7 [1449245.001]
  • [Cites] AIDS Res Hum Retroviruses. 1992 Sep;8(9):1699-706 [1457215.001]
  • [Cites] J Virol. 1993 Jan;67(1):196-203 [8416368.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11784-8 [1465399.001]
  • [Cites] Cell. 1993 Feb 26;72(4):551-60 [7679952.001]
  • [Cites] J Biol Chem. 1993 Mar 5;268(7):5032-9 [8444879.001]
  • [Cites] N Engl J Med. 1993 Apr 22;328(16):1173-82 [8455685.001]
  • [Cites] Oncogene. 1993 Apr;8(4):867-75 [8455941.001]
  • [Cites] AIDS Res Hum Retroviruses. 1993 May;9(5):381-6 [8318266.001]
  • [Cites] J Neuroimmunol. 1993 Jun;45(1-2):133-6 [8331158.001]
  • [Cites] J Neuropathol Exp Neurol. 1993 Jul;52(4):424-30 [8355031.001]
  • [Cites] Virology. 1993 Sep;196(1):25-33 [8356797.001]
  • [Cites] Trends Neurosci. 1993 Jul;16(7):268-73 [7689770.001]
  • [Cites] Clin Exp Immunol. 1993 Oct;94(1):32-7 [8403513.001]
  • [Cites] Virology. 1993 Dec;197(2):778-81 [7504369.001]
  • [Cites] Neurology. 1993 Dec;43(12):2621-4 [7504797.001]
  • [Cites] Curr Opin Neurobiol. 1993 Oct;3(5):773-8 [8260828.001]
  • [Cites] J Virol. 1994 Mar;68(3):1854-63 [7906313.001]
  • [Cites] J Neuroimmunol. 1994 Aug;53(1):23-9 [7914211.001]
  • [Cites] J Exp Med. 1994 Sep 1;180(3):831-9 [8064235.001]
  • [Cites] J Biol Chem. 1994 Sep 9;269(36):22466-9 [8077190.001]
  • [Cites] J Virol. 1994 Oct;68(10):6778-81 [8084014.001]
  • [Cites] Ann Neurol. 1994 Nov;36(5):787-90 [7979225.001]
  • [Cites] Neurology. 1994 Dec;44(12):2295-9 [7991115.001]
  • [Cites] Ann Neurol. 1995 Feb;37(2):167-75 [7847858.001]
  • [Cites] J Virol. 1995 Apr;69(4):2159-67 [7884864.001]
  • [Cites] J Neurol Sci. 1995 Apr;129(2):147-51 [7608729.001]
  • [Cites] J Neurosci. 1995 Nov;15(11):7293-300 [7472483.001]
  • [Cites] J Biol Chem. 1995 Dec 1;270(48):28503-6 [7499359.001]
  • [Cites] Brain. 1996 Feb;119 ( Pt 1):239-48 [8624685.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2253-6 [8637858.001]
  • [Cites] J Virol. 1996 Jun;70(6):4038-44 [8648741.001]
  • [Cites] Glia. 1995 Dec;15(4):437-46 [8926037.001]
  • [Cites] Ann Neurol. 1996 Jul;40(1):84-90 [8687197.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3744-50 [8670878.001]
  • [Cites] Cereb Cortex. 1996 Jan-Feb;6(1):50-61 [8670638.001]
  • [Cites] Lancet. 1996 Sep 7;348(9028):649-54 [8782755.001]
  • [Cites] Neuroscience. 1996 Sep;74(1):283-92 [8843093.001]
  • [Cites] Trends Neurosci. 1996 Aug;19(8):312-8 [8843599.001]
  • [Cites] Trends Neurosci. 1996 Aug;19(8):331-8 [8843602.001]
  • [Cites] Neuroscience. 1996 Sep;74(2):599-608 [8865208.001]
  • [Cites] Blood. 1997 Jan 1;89(1):346-8 [8978312.001]
  • [Cites] J Comp Neurol. 1997 Jan 20;377(3):443-64 [8989657.001]
  • [Cites] J Virol. 1997 Feb;71(2):1173-80 [8995639.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2699-704 [9122259.001]
  • [Cites] J Neurovirol. 1997 Apr;3(2):126-40 [9111175.001]
  • [Cites] Virology. 1997 Apr 28;231(1):135-40 [9143312.001]
  • [Cites] Neuroscience. 1997 May;78(2):549-60 [9145809.001]
  • [Cites] Proc Assoc Am Physicians. 1997 May;109(3):228-36 [9154639.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:10-3 [9209281.001]
  • [Cites] J Neurovirol. 1995 Mar;1(1):50-61 [9222342.001]
  • [Cites] J Cell Physiol. 2002 Feb;190(2):133-59 [11807819.001]
  • [Cites] Annu Rev Immunol. 2002;20:621-67 [11861614.001]
  • [Cites] AIDS Res Hum Retroviruses. 1992 Nov;8(11):1845-9 [1489573.001]
  • [Cites] J Neuroimmunol. 1993 Feb;42(2):223-6 [8429106.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2717-26 [11160337.001]
  • [Cites] Brain. 2001 Mar;124(Pt 3):480-92 [11222448.001]
  • [Cites] Microbiol Mol Biol Rev. 2001 Mar;65(1):131-50 [11238989.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6295-300 [11371643.001]
  • [Cites] Proc Biol Sci. 2001 Jun 22;268(1473):1215-21 [11410146.001]
  • [Cites] Nat Immunol. 2001 Jul;2(7):585-9 [11429541.001]
  • [Cites] Blood. 2001 Aug 1;98(3):721-6 [11468172.001]
  • [Cites] J Virol. 2001 Sep;75(18):8461-8 [11507191.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1506-11 [11520801.001]
  • [Cites] Virus Res. 2001 Oct 30;78(1-2):5-16 [11520576.001]
  • [Cites] Virus Res. 2001 Oct 30;78(1-2):93-100 [11520583.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1858-61 [11535522.001]
  • [Cites] J Virol. 2000 Jul;74(13):6021-30 [10846084.001]
  • [Cites] J Virol. 2000 Jul;74(14):6433-41 [10864655.001]
  • [Cites] Nat Med. 2002 May;8(5):455-7 [11984586.001]
  • [Cites] Nat Med. 2002 May;8(5):509-13 [11984596.001]
  • [Cites] J Infect Dis. 2002 Oct 1;186(7):932-9 [12232833.001]
  • [Cites] J Neurovirol. 2002 Oct;8(5):359-64 [12402162.001]
  • [Cites] Springer Semin Immunopathol. 2002;24(2):105-25 [12503060.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Virology. 2003 Mar 30;308(1):1-12 [12706085.001]
  • [Cites] J Biol Chem. 2003 Jun 13;278(24):21814-22 [12670929.001]
  • [Cites] J Infect Dis. 2003 Aug 1;188(3):424-7 [12870124.001]
  • [Cites] Nat Rev Immunol. 2003 Jul;3(7):569-81 [12876559.001]
  • [Cites] J Neurovirol. 2003 Oct;9(5):522-9 [13129766.001]
  • [Cites] J Long Term Eff Med Implants. 2003;13(2):127-40 [14510286.001]
  • [Cites] Nat Med. 2004 Jan;10(1):20-1 [14702624.001]
  • [Cites] Virology. 2004 Jan 20;318(2):556-65 [14972524.001]
  • [Cites] Neurobiol Dis. 2004 Jun;16(1):1-13 [15207256.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2527-39 [15353305.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [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] J Infect Dis. 1983 Mar;147(3):406-16 [6300254.001]
  • [Cites] Science. 1984 Sep 28;225(4669):1473-6 [6089348.001]
  • [Cites] J Virol. 1987 Apr;61(4):1244-7 [3644020.001]
  • [Cites] Science. 1988 Jan 15;239(4837):290-2 [3276004.001]
  • [Cites] Nature. 1988 Feb 11;331(6156):540-3 [2829028.001]
  • [Cites] Am J Epidemiol. 1988 Mar;127(3):532-9 [2893539.001]
  • [Cites] Ann Neurol. 1988;23 Suppl:S143-50 [2894806.001]
  • [Cites] Ann Neurol. 1988 Apr;23(4):339-46 [3132891.001]
  • [Cites] Science. 1988 Sep 23;241(4873):1652-5 [2843985.001]
  • [Cites] J Neurol Sci. 1988 Oct;87(1):15-24 [3193123.001]
  • [Cites] J Clin Invest. 1988 Dec;82(6):1908-14 [2974045.001]
  • [Cites] Nature. 1989 Jan 26;337(6205):368-70 [2536142.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1993-7 [2564677.001]
  • [Cites] Int J Cancer. 1989 Sep 15;44(3):419-23 [2777408.001]
  • [Cites] J Gen Virol. 1989 Oct;70 ( Pt 10):2653-60 [2677235.001]
  • [Cites] J Neuropathol Exp Neurol. 1989 Nov;48(6):610-9 [2677251.001]
  • [Cites] Ann Neurol. 1989 Sep;26(3):331-5 [2802532.001]
  • [Cites] Ann Neurol. 1989 Oct;26(4):523-30 [2817828.001]
  • [Cites] J Acquir Immune Defic Syndr. 1989;2(6):550-6 [2585247.001]
  • [Cites] J Clin Invest. 1989 Dec;84(6):1892-9 [2574188.001]
  • [Cites] Blood. 1990 Jan 15;75(2):428-33 [1967218.001]
  • [Cites] J Virol. 1990 Mar;64(3):1278-82 [2304144.001]
  • [Cites] Ann Neurol. 1990 Jul;28(1):50-6 [2375633.001]
  • [Cites] J Neurol Sci. 1990 Jul;97(2-3):183-93 [2401896.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] Neurology. 1991 Apr;41(4):594-5 [2011262.001]
  • (PMID = 19273122.001).
  • [ISSN] 1093-4715
  • [Journal-full-title] Frontiers in bioscience (Landmark edition)
  • [ISO-abbreviation] Front Biosci (Landmark Ed)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA054559; United States / NCI NIH HHS / CA / CA054559-14; United States / NCI NIH HHS / CA / R01 CA054559-14; United States / NCI NIH HHS / CA / 2R1 CA054559; United States / NCI NIH HHS / CA / CA054559-15; United States / NCI NIH HHS / CA / CA054559-13A1; United States / NCI NIH HHS / CA / CA054559; United States / NIAID NIH HHS / AI / AI077414-01A2; United States / NIAID NIH HHS / AI / R01 AI077414; United States / NIAID NIH HHS / AI / R01 AI077414-01A2; United States / NCI NIH HHS / CA / R01 CA054559-13A1; United States / NCI NIH HHS / CA / R01 CA054559-15
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 181
  • [Other-IDs] NLM/ NIHMS126265; NLM/ PMC2739244
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65. Pezeshkpoor F, Yazdanpanah MJ, Shirdel A: Specific cutaneous manifestations in adult T-cell leukemia/lymphoma. Int J Dermatol; 2008 Apr;47(4):359-62
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  • [Title] Specific cutaneous manifestations in adult T-cell leukemia/lymphoma.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is an aggressive malignancy which may occur in individuals infected with human T-cell lymphotropic virus type-I (HTLV-I).
  • HTLV-I is endemic in Khorasan, with a frequency of 2.3% in the general population.
  • As specific cutaneous manifestations of lymphoma may occur in a significant number of patients, we studied these manifestations in ATLL patients admitted to the Hematology and Dermatology Departments of Ghaem Hospital, Mashhad, Iran, during 1995-2004.
  • METHODS: In this descriptive study, demographic and clinical information was obtained from 23 patients suffering from ATLL with specific cutaneous lesions (atypical lymphocytes on histopathology of cutaneous lesions), and was analyzed statistically.
  • CONCLUSION: The most common type of specific skin lesion in ATLL was maculopapular eruption, especially with a generalized distribution.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Skin / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Iran. Male. Middle Aged

  • Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.
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  • (PMID = 18377598.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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66. Tsuji Y, Hatanaka M, Maeda T, Seya T, Takenaka H, Shimizu A: Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in human T cell leukemia cell lines. Int J Mol Med; 2005 Nov;16(5):889-93
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  • [Title] Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in human T cell leukemia cell lines.
  • Caveolin-1 and -2 are expressed in most cell types, but are not expressed in normal blood cells and cell lines.
  • We previously demonstrated that caveolin-1 is expressed in a panel of human leukemia cell lines that show an activated T cell phenotype.
  • Using this method we detected caveolin-1beta, -2alpha and -2beta, but not caveolin-3 in the leukemia cell lines.
  • This modification is likely to cause the lack of reactivity of caveolin-1alpha to the mAb, and suggests a possible close relationship to cell activation.
  • [MeSH-major] Leukemia, T-Cell / metabolism. Tyrosine / metabolism
  • [MeSH-minor] Antibodies / immunology. Antibodies, Monoclonal / immunology. Cell Line, Tumor. Humans. Phosphorylation. Protein Isoforms / analysis. Protein Isoforms / immunology. Protein Isoforms / metabolism

  • Hazardous Substances Data Bank. L-TYROSINE .
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  • (PMID = 16211260.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Protein Isoforms; 42HK56048U / Tyrosine
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67. Kameda T, Shide K, Shimoda HK, Hidaka T, Kubuki Y, Katayose K, Taniguchi Y, Sekine M, Kamiunntenn A, Maeda K, Nagata K, Matsunaga T, Shimoda K: Absence of gain-of-function JAK1 and JAK3 mutations in adult T cell leukemia/lymphoma. Int J Hematol; 2010 Sep;92(2):320-5
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  • [Title] Absence of gain-of-function JAK1 and JAK3 mutations in adult T cell leukemia/lymphoma.
  • Somatic JAK1 mutations are found in 18% of adult precursor T acute lymphoblastic leukemias and somatic JAK3 mutations are found in 3.3% of cutaneous T cell lymphomas.
  • Adult T cell leukemia/lymphoma (ATLL) is a type of T cell neoplasm, and activation of JAK/STAT pathways is sometimes observed in them.
  • We investigated JAK1 and JAK3 mutations in 20 ATLL patients.
  • JAK1 and JAK3 mutations are unlikely involved in the leukemogenesis of ATLL.
  • [MeSH-major] Janus Kinase 1 / genetics. Janus Kinase 3 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adult. Cell Differentiation. Cell Proliferation. DNA Mutational Analysis. Humans. Japan. Polymorphism, Single Nucleotide

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  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Science. 1994 Nov 11;266(5187):1042-5 [7973658.001]
  • [Cites] Cell. 1987 Jan 30;48(2):343-50 [3026643.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14 (12 ):3716-21 [18559588.001]
  • [Cites] Leuk Lymphoma. 2005 Nov;46(11):1553-9 [16236609.001]
  • [Cites] Br J Haematol. 2007 May;137(4):337-41 [17456055.001]
  • [Cites] Leuk Res. 2004 Jan;28(1):71-82 [14630083.001]
  • [Cites] J Exp Med. 2008 Apr 14;205(4):751-8 [18362173.001]
  • [Cites] Cell. 1998 May 1;93(3):373-83 [9590172.001]
  • [Cites] Eur J Haematol. 2002 Jun;68(6):362-9 [12225394.001]
  • [Cites] Nature. 2005 Oct 27;437(7063):1299-320 [16255080.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):1107-9 [11697628.001]
  • [Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]
  • [Cites] Br J Haematol. 2008 May;141(5):681-8 [18397343.001]
  • [Cites] Science. 1995 Jul 7;269(5220):79-81 [7604283.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13897-902 [9391124.001]
  • [Cites] Science. 1997 Nov 14;278(5341):1309-12 [9360930.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2535-40 [9326218.001]
  • [Cites] Rev Med Virol. 2007 Sep-Oct;17 (5):301-11 [17621367.001]
  • [Cites] Science. 1995 Nov 3;270(5237):794-7 [7481767.001]
  • [Cites] Retrovirology. 2006 Apr 09;3:22 [16603085.001]
  • [Cites] Leukemia. 2003 Jan;17(1):26-38 [12529656.001]
  • [Cites] J Leukoc Biol. 2008 Jan;83(1):220-2 [17962369.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):673-83 [17721432.001]
  • [Cites] J Virol. 1998 May;72 (5):4408-12 [9557732.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3770-4 [11325850.001]
  • [Cites] Immunity. 1995 Dec;3(6):771-82 [8777722.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5389-93 [3037548.001]
  • [Cites] FEBS Lett. 1994 Oct 24;353(3):289-93 [7957877.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1484-92 [18805579.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Blood. 2008 May 1;111(9):4809-12 [18160671.001]
  • [Cites] Int Rev Immunol. 2007 Sep-Dec;26(5-6):269-81 [18027201.001]
  • [Cites] Blood. 2009 Mar 19;113(12 ):2746-54 [19139084.001]
  • [Cites] Nature. 1994 Jul 14;370(6485):153-7 [8022486.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Cancer Cell. 2006 Jul;10 (1):65-75 [16843266.001]
  • [Cites] Leuk Res. 1999 Apr;23 (4):373-84 [10229324.001]
  • [Cites] Cell. 1998 May 1;93(3):397-409 [9590174.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2623-9 [17312100.001]
  • (PMID = 20697856.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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68. Jin Q, Alkhatib B, Cornetta K, Alkhatib G: Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1. Virology; 2010 Jan 20;396(2):203-12
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  • [Title] Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1.
  • Recent studies have demonstrated that neuropilin 1 (NP-1) is involved in HTLV-1 entry; however, the role NP-1 plays in this process is not understood.
  • We demonstrated that ectopic expression of human NP-1 but not NP-2 cDNA increased susceptibility to HTLV-1.
  • SiRNA-mediated inhibition of NP-1 expression correlated with significant reduction of HTLV-1 Env-mediated fusion.
  • The vascular endothelial growth factor (VEGF(165)) caused downmodulation of surface NP-1 and inhibited HTLV-1 infection of U87 cells.
  • HTLV-1 Env forms complexes with both NP-1 and GLUT-1 in primary human astrocytes.
  • The alternate usage of these two cellular receptors may have important implications regarding HTLV-1 neuro-tropism.