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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

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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. 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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15. 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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16. 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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17. 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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18. 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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19. 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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20. 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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21. 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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22. 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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23. 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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24. 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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25. Siedlar M, Rudzki Z, Strach M, Trzyna E, Pituch-Noworolska A, Błaut-Szlósarczyk A, Bukowska-Strakova K, Lenart M, Grodzicki T, Zembala M: Familial occurrence of warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome. Arch Immunol Ther Exp (Warsz); 2008 Nov-Dec;56(6):419-25
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  • INTRODUCTION: Warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome is a rare immunodeficiency disorder with an autosomal-dominant pattern of inheritance and low fatality rate but significant lifelong morbidity.
  • MATERIALS AND METHODS: A 27-year-old mother of two children has been suffering from severe neutropenia and recurrent infections with the diagnosis of sporadic WHIM syndrome established by sequencing the CXCR4 gene and the finding of a heterozygous 1000 C-->T nonsense mutation in the second CXCR4 exon.
  • Moreover, a perinatal diagnosis of WHIM syndrome made by sequencing the CXCR4 gene should be performed in cases where either parent is known to be affected with this disease.
  • [MeSH-major] Agammaglobulinemia / diagnosis. Immunologic Deficiency Syndromes / diagnosis. Mutation. Warts / diagnosis. Warts / pathology
  • [MeSH-minor] Adult. Cell Lineage. Exons. Female. Fetal Blood / metabolism. Humans. Infant. Male. Monocytes / metabolism. Receptors, CXCR4 / genetics. Syndrome

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  • [Cites] Am J Med Genet. 2000 Apr 24;91(5):368-76 [10767001.001]
  • [Cites] J Leukoc Biol. 2007 Mar;81(3):584-92 [17135573.001]
  • [Cites] Ann Hematol. 2002 Aug;81(8):470-3 [12224006.001]
  • [Cites] Nat Genet. 2003 May;34(1):70-4 [12692554.001]
  • [Cites] Blood. 2004 Jul 15;104(2):444-52 [15026312.001]
  • [Cites] J Mol Histol. 2004 Mar;35(3):233-45 [15339043.001]
  • [Cites] Am J Dis Child. 1977 Jun;131(6):655-8 [868817.001]
  • [Cites] Br J Haematol. 1977 Jul;36(3):313-22 [889707.001]
  • [Cites] Eur J Haematol. 1989 Jan;42(1):99-102 [2914601.001]
  • [Cites] Am J Med. 1990 Nov;89(5):663-72 [2239986.001]
  • [Cites] Clin Lab Haematol. 1991;13(1):81-5 [2060265.001]
  • [Cites] J Pediatr Hematol Oncol. 1997 Sep-Oct;19(5):443-8 [9329467.001]
  • [Cites] N Engl J Med. 1964 Apr 2;270:699-704 [14101065.001]
  • [Cites] Immunol Rev. 2005 Feb;203:235-43 [15661033.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2449-57 [15536153.001]
  • [Cites] Exp Hematol. 2005 Apr;33(4):460-8 [15781337.001]
  • [Cites] J Allergy Clin Immunol. 2005 Nov;116(5):1101-5 [16275383.001]
  • [Cites] J Microbiol Immunol Infect. 2006 Apr;39(2):114-20 [16604243.001]
  • [Cites] Br J Haematol. 2006 Sep;134(6):640-4 [16899028.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1915-24 [16900209.001]
  • [Cites] Eur J Haematol. 2007 Jan;78(1):86-8 [17087743.001]
  • [Cites] J Am Acad Dermatol. 2001 Jan;44(1):124-8 [11148489.001]
  • (PMID = 19043667.001).
  • [ISSN] 1661-4917
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Receptors, CXCR4
  • [Other-IDs] NLM/ PMC2805795
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26. 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


27. 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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  • [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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28. 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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29. 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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30. 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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31. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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32. 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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33. 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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34. 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
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35. Zhu KE, Li JP, Zhang T, Zhong J, Chen J: Clinical features and risk factors of pure red cell aplasia following major ABO-incompatible allogeneic hematopoietic stem cell transplantation. Hematology; 2007 Apr;12(2):117-21
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  • [Title] Clinical features and risk factors of pure red cell aplasia following major ABO-incompatible allogeneic hematopoietic stem cell transplantation.
  • The objective of this paper was to study the incidence, risk factors, clinical outcome, management and prevention of pure red cell aplasia (PRCA) following major ABO-incompatible allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  • The following factors were associated with an increased risk of PRCA:.
  • Only blood group O/A in recipient/donor pair was identified as being significantly associated with the occurrence of PRCA by multivariate analysis.
  • Eight patients obtained spontaneous remission and in the remaining 3 patients 2 with long-lasting PRCA were successfully treated with plasma exchange with donor-type plasma replacement and the other one who was also complicated by EBV-associated lymphoproliferative disorder (EBV-PTLD) responded rapidly to anti-CD20 monoclonal antibody and achieved complete resolution of clinical finding and symptom of both EBV-PTLD and PRCA.
  • We conclude that blood group A/O in donor/recipient pair is identified as being significantly associated with the occurrence of PRCA by multivariate analysis.
  • [MeSH-major] Blood Group Incompatibility / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Red-Cell Aplasia, Pure / etiology. Transplantation, Homologous / adverse effects
  • [MeSH-minor] ABO Blood-Group System / genetics. ABO Blood-Group System / immunology. Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. Busulfan / pharmacology. Child, Preschool. Cyclosporine / therapeutic use. Epstein-Barr Virus Infections / complications. Female. Graft Survival. Graft vs Host Disease / prevention & control. Humans. Immunosuppressive Agents / therapeutic use. Leukemia / surgery. Lymphoproliferative Disorders / etiology. Lymphoproliferative Disorders / therapy. Male. Methotrexate / therapeutic use. Middle Aged. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / therapeutic use. Plasma Exchange. Remission, Spontaneous. Retrospective Studies. Risk Factors. Rituximab. Transplantation Conditioning. Vidarabine / analogs & derivatives. Vidarabine / pharmacology. Whole-Body Irradiation. beta-Thalassemia / surgery

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  • Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .
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  • (PMID = 17454192.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABO Blood-Group System; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; HU9DX48N0T / Mycophenolic Acid; P2K93U8740 / fludarabine; YL5FZ2Y5U1 / Methotrexate
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66. Bitar N, Hajj HE, Houmani Z, Sabbah A, Otrock ZK, Mahfouz R, Zaatari G, Bazarbachi A: Adult T-cell leukemia/lymphoma in the Middle East: first report of two cases from Lebanon. Transfusion; 2009 Sep;49(9):1859-64
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  • [Title] Adult T-cell leukemia/lymphoma in the Middle East: first report of two cases from Lebanon.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATL) is an aggressive lymphoproliferative disorder caused by human T-cell leukemia virus type I (HTLV-I).
  • HTLV-I is endemic in southern Japan, the Caribbean, Central and South America, certain areas of Africa, and the southeastern United States.
  • CASE REPORTS: In this report, the first two cases of ATL diagnosed in Lebanon are described.
  • The first patient of Lebanese origin presented with acute ATL.
  • The second patient of Romanian origin developed acute ATL in early relapse after autologous transplantation for ATL.
  • Both patients had lymphocytosis, severe hypercalcemia, and CD25+ T-cell immunophenotype on peripheral blood.
  • In both patients, HTLV-I serology was positive by enzyme-linked immunosorbent assay and confirmed by Western blot and HTLV-I oncoprotein Tax expression was documented in the leukemic cells.
  • Upon screening, seven direct family members of the first patient were HTLV-I positive; four of them were regular blood donors.
  • CONCLUSIONS: Screening blood donors for HTLV-I seropositivity is not currently performed in Lebanon.
  • A large screening study in Lebanon is needed to confirm whether South Lebanon is a new endemic region for HTLV-I infection and to recommend mandatory screening of blood donors for HTLV-I infection.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Bone Density Conservation Agents / therapeutic use. Diphosphonates / therapeutic use. Fatal Outcome. Female. Gene Products, tax / blood. Humans. Imidazoles / therapeutic use. Interferon-alpha / therapeutic use. Lebanon. Middle Aged. Zidovudine / therapeutic use

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  • (PMID = 19453978.001).
  • [ISSN] 1537-2995
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Gene Products, tax; 0 / Imidazoles; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine; 6XC1PAD3KF / zoledronic acid
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67. Olteanu H, Karandikar NJ, Eshoa C, Kroft SH: Laboratory findings in CD4(+) large granular lymphocytoses. Int J Lab Hematol; 2010 Feb;32(1 Pt 1):e9-16
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  • Large granular lymphocytic (LGL) leukemia is an uncommon disorder of mature T or natural killer (NK) cells.
  • We report the clinicopathologic features of eight patients with aberrant CD4(+), cytotoxic T-cell lymphocytoses.
  • Morphologic expansions of granulated lymphocytes were evident in 6/8.
  • Abnormal levels of expression of two or more T-cell antigens were seen in all cases.
  • All tested cases were Tgamma PCR positive.
  • Our results support that CD4(+) T-LGL lymphocytosis is a clonal disorder with clinicopathologic characteristics distinct from the more common CD8(+) variant.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Leukemia, Large Granular Lymphocytic / immunology
  • [MeSH-minor] Adult. Aged. Antigens, CD56 / immunology. Antigens, CD57 / immunology. Cohort Studies. Female. Flow Cytometry. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 20089001.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD57
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68. Ishikawa C, Tafuku S, Kadekaru T, Sawada S, Tomita M, Okudaira T, Nakazato T, Toda T, Uchihara JN, Taira N, Ohshiro K, Yasumoto T, Ohta T, Mori N: Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer; 2008 Dec 1;123(11):2702-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol.
  • Adult T-cell leukemia (ATL) is a fatal malignancy of T lymphocytes caused by human T-cell leukemia virus type 1 (HTLV-1) infection and remains incurable.
  • We evaluated the anti-ATL effects of fucoxanthin and its metabolite, fucoxanthinol.
  • Both carotenoids inhibited cell viability of HTLV-1-infected T-cell lines and ATL cells, and fucoxanthinol was approximately twice more potent than fucoxanthin.
  • In contrast, other carotenoids, beta-carotene and astaxanthin, had mild inhibitory effects on HTLV-1-infected T-cell lines.
  • Importantly, uninfected cell lines and normal peripheral blood mononuclear cells were resistant to fucoxanthin and fucoxanthinol.
  • Both carotenoids induced cell cycle arrest during G(1) phase by reducing the expression of cyclin D1, cyclin D2, CDK4 and CDK6, and inducing the expression of GADD45alpha, and induced apoptosis by reducing the expression of Bcl-2, XIAP, cIAP2 and survivin.
  • The induced apoptosis was associated with activation of caspase-3, -8 and -9.
  • Mice with severe combined immunodeficiency harboring tumors induced by inoculation of HTLV-1-infected T cells responded to treatment with fucoxanthinol with suppression of tumor growth, showed extensive tissue distribution of fucoxanthinol, and the presence of therapeutically effective serum concentrations of fucoxanthinol.
  • Our preclinical data suggest that fucoxanthin and fucoxanthinol could be potentially useful therapeutic agents for patients with ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Phaeophyta / chemistry. Xanthophylls / therapeutic use. beta Carotene / analogs & derivatives
  • [MeSH-minor] Acetylation. Animals. Caspases / metabolism. Cell Survival / drug effects. Female. Human T-lymphotropic virus 1 / drug effects. Humans. Mice. NF-kappa B / metabolism. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


69. Mirsaliotis A, Nurkiyanova K, Lamb D, Kuo CW, Brighty DW: An antibody that blocks human T-cell leukemia virus type 1 six-helix-bundle formation in vitro identified by a novel assay for inhibitors of envelope function. J Gen Virol; 2007 Feb;88(Pt 2):660-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An antibody that blocks human T-cell leukemia virus type 1 six-helix-bundle formation in vitro identified by a novel assay for inhibitors of envelope function.
  • Fusion of the viral and cellular membranes is a critical step in the infection of cells by the human T-cell leukemia virus type 1 (HTLV-1) and this process is catalysed by the viral envelope glycoproteins.
  • Importantly, synthetic peptides that interfere with the conformational changes of TM are potent inhibitors of membrane fusion and HTLV-1 entry, suggesting that the pre-hairpin motif is a valid target for antiviral therapy.
  • However, the mAb failed to neutralize HTLV-1 envelope-mediated membrane fusion, suggesting that, on native viral envelope, the epitope recognized by the mAb is obscured during fusion.
  • This novel mAb will be of value in the immunological characterization of fusion-active structures of HTLV-1 TM.
  • Moreover, the assay developed here will aid the search for therapeutic antibodies, peptides and small-molecule inhibitors targeting envelope and the HTLV-1 entry process.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Glycoproteins / metabolism. Human T-lymphotropic virus 1 / metabolism. Membrane Fusion / drug effects. Viral Envelope Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Cell Membrane / drug effects. Cell Membrane / metabolism. HeLa Cells. Humans. Models, Molecular. Molecular Sequence Data. Peptides / chemical synthesis. Peptides / chemistry. Peptides / metabolism. Peptides / pharmacology. Protein Conformation

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  • (PMID = 17251585.001).
  • [ISSN] 0022-1317
  • [Journal-full-title] The Journal of general virology
  • [ISO-abbreviation] J. Gen. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Glycoproteins; 0 / Peptides; 0 / Viral Envelope Proteins
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70. Cunha L, Plouzeau C, Ingrand P, Gudo JP, Ingrand I, Mondlane J, Beauchant M, Agius G: Use of replacement blood donors to study the epidemiology of major blood-borne viruses in the general population of Maputo, Mozambique. J Med Virol; 2007 Dec;79(12):1832-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of replacement blood donors to study the epidemiology of major blood-borne viruses in the general population of Maputo, Mozambique.
  • The seroprevalence rates of human immunodeficiency virus (HIV), human T-cell leukemia/lymphoma virus (HTLV), hepatitis B virus (HBV), hepatitis D virus (HDV), and hepatitis C virus (HCV) in Mozambique are poorly documented.
  • All donors attending the blood bank during the study period were interviewed and underwent serological and molecular tests for markers of virus exposure.
  • The age-standardized prevalence rates among 15- to 49-year-old men and women were, respectively, 12.3 and 15.4% for HIV and 0.9 and 1.2% for HTLV.
  • The age-adjusted prevalence rates of markers of hepatotropic virus among men and women were, respectively, 10.6 and 4.5% for hepatitis B surface antigen (HBsAg), 1.2 and 1.0% for anti-HCV, and 0 and 0% for anti-HDV.
  • HBsAg was associated with the place of birth (P = 0.011) and a history of transfusion (P = 0.069).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Viral / blood. Antigens, Viral / blood. Cross-Sectional Studies. Female. Hepacivirus / genetics. Hepatitis B virus / genetics. Humans. Male. Middle Aged. Mozambique / epidemiology. Seroepidemiologic Studies


71. Beyazit Y, Haznedaroglu IC, Aksu S, Kekilli M, Uner A, Agbaht K, Sungur A, Koca E, Goker H, Ozcebe OI: Changing clinical manifestations of a T-peripheral lymphoma: from hypereosinophilic syndrome to questionable Kimura's disease resulting in parotid mass. Leuk Lymphoma; 2006 Feb;47(2):357-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changing clinical manifestations of a T-peripheral lymphoma: from hypereosinophilic syndrome to questionable Kimura's disease resulting in parotid mass.
  • The diagnosis of low-grade lymphoproliferative disorders during a long clinical course sometimes represents a great clinical challenge.
  • Kimura's disease (KD) mimicking HES is an immune mediated inflammatory disorder that usually involves the head and neck region, primarily affecting the salivary glands, adjacent muscle and regional lymph nodes.
  • Lymphomas may uncommonly present as a parotid mass.
  • One, herein, would like to present a 35-year-old patient with changing clinical presentation patterns over a period of more than 6 years of follow-up.
  • The first clinical presentation of the patient was HES.
  • The 'diagnosis' of KD was reached after 4 years of management with HES.
  • The final manifestation was parotid gland, preauricular and cutaneous manifestations of a peripheral T-cell lymphoma.
  • This unique clinical presentation pattern of the patient may represent the distinct pathobiological progression of a clonal neoplastic lymphoproliferative disorder.
  • [MeSH-major] Angiolymphoid Hyperplasia with Eosinophilia / diagnosis. Hypereosinophilic Syndrome / diagnosis. Lymphoma, T-Cell, Peripheral / diagnosis. Parotid Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Disease Progression. Follow-Up Studies. Humans. Male

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  • (PMID = 16321872.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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72. Sales MM, Bezerra CN, Hiraki Y, Melo NB, Rebouças NA: Clonally rearranged T-cell receptor beta chain genes in HTLV-I carriers with abnormal, non-flower-like, lymphocytes. Eur J Haematol; 2005 Oct;75(4):280-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clonally rearranged T-cell receptor beta chain genes in HTLV-I carriers with abnormal, non-flower-like, lymphocytes.
  • BACKGROUND: The diagnosis of Adult T-cell leukemia/lymphoma ATLL subtypes in human T-lymphotropic virus type I (HTLV-I) carriers based in morphology and immunophenotype of lymphocytes can be challenger.
  • We propose that polymerase chain reaction (PCR) amplification of the rearranged TCR gene in HTLV-I healthy carriers would be a convenient method for establishing the nature of the circulating T lymphocytes in asymptomatic HTLV-I carriers, presenting only mild and inconclusive signals of deviation from normality.
  • METHODS: Using PCR, we analyzed the genetic recombination pattern of the T-cell beta-chain receptor gene (TCR-beta) in order to identify clonal expansion of peripheral blood T lymphocytes in 17 HTLV-I-positive healthy carriers and in nine normal HTLV-I-negative blood donors.
  • To evaluate the performance of PCR in detection of clonality, we also analyzed 18 patients with post-thymic/mature T-cell malignancies presenting circulating abnormal lymphocytes.
  • RESULTS: Seven of the 17 HTLV-I positive individuals presented circulating abnormal lymphocytes; monoclonal or oligoclonal expansion of T-cells was detected in five of the 17 HTLV-I-positive individuals, all of them presenting abnormal lymphocytes.
  • All patients in the positive control group tested positive by PCR and Southern blots.
  • CONCLUSIONS: PCR amplification of segments of rearranged TCR-beta is reliable for allowing early detection of small populations of clonal T cells in blood samples from asymptomatic HTLV-I carriers, providing an additional alert in the follow-up of carriers with abnormal circulating lymphocytes.
  • [MeSH-major] Carrier State / diagnosis. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor / genetics. HTLV-I Infections / diagnosis. HTLV-I Infections / immunology. T-Lymphocytes / pathology
  • [MeSH-minor] Adult. Blotting, Southern. Case-Control Studies. Cell Proliferation. Clone Cells. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / prevention & control. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 16146533.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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73. Vega F, Padula A, Valbuena JR, Stancu M, Jones D, Medeiros LJ: Lymphomas involving the pleura: a clinicopathologic study of 34 cases diagnosed by pleural biopsy. Arch Pathol Lab Med; 2006 Oct;130(10):1497-502
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  • [Title] Lymphomas involving the pleura: a clinicopathologic study of 34 cases diagnosed by pleural biopsy.
  • CONTEXT: Pleural involvement by lymphoma is relatively common.
  • However, there are very few clinicopathologic studies reported in the literature of lymphomas involving the pleura.
  • OBJECTIVE: To characterize the clinicopathologic features of lymphomas involving the pleura.
  • DESIGN: We reviewed the clinicopathologic features of 34 patients with lymphoma involving the pleura proven by biopsy and classified these neoplasms using the World Health Organization classification.
  • Nine (26.5%) patients had pleural involvement as the only site of disease, 22 (64.7%) had other sites of involvement, and 3 (8.8%) had inadequate staging data.
  • Eighteen (56.2%) of 32 patients with adequate clinical data had a history of lymphoma (including 3 patients with pleural involvement as the only disease site).
  • In 29 (85.3%) cases, a specific diagnosis according to the World Health Organization classification could be made: 17 (58.6%) diffuse large B-cell lymphoma, 5 (17.2%) follicular lymphoma (including a case with areas of diffuse large B-cell lymphoma), 2 (6.9%) small lymphocytic lymphomas/chronic lymphocytic leukemia, 2 (6.9%) precursor T-cell lymphoblastic lymphoma/leukemia, 1 (3.4%) mantle cell lymphoma, 1 (3.4%) posttransplant lymphoproliferative disorder, and 1 (3.4%) classical Hodgkin lymphoma.
  • The other 5 cases were B-cell lymphomas that could not be further classified.
  • Cytologic examination of pleural fluid was performed in 15 cases and was positive for lymphoma in 8 (53.3%) cases.
  • CONCLUSIONS: Most patients with lymphoma involving the pleura have simultaneous evidence of systemic involvement.
  • The most frequent type is diffuse large B-cell lymphoma, followed by follicular lymphoma.
  • Cytologic examination can have negative results in patients with pleural involvement by lymphoma.
  • [MeSH-major] Lymphoma / pathology. Pleura / pathology. Pleural Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Body Fluids / cytology. Female. Humans. Immunophenotyping. Incidence. Lymphoma, B-Cell / epidemiology. Lymphoma, Follicular / epidemiology. Lymphoma, Large B-Cell, Diffuse / epidemiology. Male. Medical Records. Middle Aged. Neoplasms, Second Primary / pathology. Retrospective Studies. World Health Organization

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  • (PMID = 17090191.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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74. Younis I, Green PL: The human T-cell leukemia virus Rex protein. Front Biosci; 2005 Jan 1;10:431-45
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  • [Title] The human T-cell leukemia virus Rex protein.
  • A critical step in the life cycle of complex retroviruses, including HTLV-1 and HTLV-2 is the ability of these viruses to adopt a mechanism by which the genome-length unspliced mRNA as well as the partially spliced mRNAs are exported from the nucleus instead of being subjected to splicing or degradation.
  • In HTLV, this is accomplished through the expression of the viral Rex, which recognizes a specific response element on the incompletely spliced mRNAs, stabilizes them, inhibits their splicing, and utilizes the CRM1-dependent cellular pathway for transporting them from the nucleus to the cytoplasm.
  • Rex itself is regulated by phosphorylation, which implies that proper activation of the protein in response to certain cellular cues is an important tool for the virus to ensure that specific viral gene expression is allowed only when the host cell can provide the best conditions for virion production.
  • Having such a critical role in HTLV life cycle, Rex is indispensable for efficient viral replication, infection and spread.
  • Indeed, Rex is considered to regulate the switch between the latent and productive phases of the HTLV life cycle.
  • Without a functional Rex, the virus would still produce regulatory and some accessory gene products; however, structural and enzymatic post-transcriptional gene expression would be severely repressed, essentially leading to non-productive viral replication.
  • More detailed understanding of the exact molecular mechanism of action of Rex will thus allow for better design of therapeutic drugs against Rex function and ultimately HTLV replication.
  • Herein we summarize the progress made towards understanding Rex function and its role in the HTLV life cycle.

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  • [Cites] Chem Biol. 1997 Feb;4(2):139-47 [9190288.001]
  • [Cites] EMBO J. 1997 Feb 17;16(4):807-16 [9049309.001]
  • [Cites] Annu Rev Neurosci. 1997;20:269-301 [9056715.001]
  • [Cites] Science. 1988 May 13;240(4854):916-9 [2834826.001]
  • [Cites] EMBO J. 1988 Feb;7(2):519-23 [2835230.001]
  • [Cites] Cell. 1988 Oct 21;55(2):197-209 [3048703.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7124-8 [3174625.001]
  • [Cites] J Virol. 1988 Dec;62(12):4445-51 [2846863.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1495-9 [2784208.001]
  • [Cites] J Cell Biol. 1989 Apr;108(4):1195-207 [2647765.001]
  • [Cites] J Virol. 1989 Apr;63(4):1569-77 [2522558.001]
  • [Cites] J Virol. 1989 May;63(5):1959-66 [2704072.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9798-802 [2602375.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1198-202 [2405396.001]
  • [Cites] Virology. 1990 May;176(1):81-6 [2330679.001]
  • [Cites] J Virol. 1990 Jun;64(6):2825-32 [2335818.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Jun 15;169(2):469-75 [2357216.001]
  • [Cites] Genes Dev. 1990 Jun;4(6):1014-22 [2116986.001]
  • [Cites] J Virol. 1990 Oct;64(10):4914-21 [2398533.001]
  • [Cites] J Virol. 1990 Oct;64(10):5226-9 [2398545.001]
  • [Cites] Genes Dev. 2004 Jan 1;18(1):23-34 [14701878.001]
  • [Cites] Mech Dev. 2004 Mar;121(3):213-24 [15003625.001]
  • [Cites] Trends Plant Sci. 2004 Apr;9(4):174-9 [15063867.001]
  • [Cites] Trends Biochem Sci. 2004 Apr;29(4):175-82 [15082311.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Science. 1982 Nov 5;218(4572):571-3 [6981847.001]
  • [Cites] Curr Top Microbiol Immunol. 1984;113:192-7 [6478866.001]
  • [Cites] J Virol. 1990 Nov;64(11):5682-7 [1976827.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7497-501 [2170981.001]
  • [Cites] J Virol. 1991 Jan;65(1):405-14 [1985205.001]
  • [Cites] J Virol. 1991 Jan;65(1):546-50 [1898667.001]
  • [Cites] New Biol. 1991 Apr;3(4):389-97 [2065024.001]
  • [Cites] J Cell Biol. 2001 Jun 25;153(7):1391-402 [11425870.001]
  • [Cites] J Virol. 2001 Sep;75(18):8440-8 [11507189.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Feb 28;175(1):98-103 [1998523.001]
  • [Cites] Virology. 1991 Apr;181(2):433-44 [2014632.001]
  • [Cites] J Virol. 1991 May;65(5):2261-72 [2016758.001]
  • [Cites] Genes Dev. 1991 May;5(5):808-19 [1827422.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5704-8 [1905815.001]
  • [Cites] Cell Mol Life Sci. 2001 Nov;58(12-13):1766-73 [11766877.001]
  • [Cites] Ann Epidemiol. 2002 Jan;12(1):46-66 [11750240.001]
  • [Cites] J Med Virol. 2002 Feb;66(2):253-7 [11782936.001]
  • [Cites] Results Probl Cell Differ. 2002;35:49-66 [11791408.001]
  • [Cites] Results Probl Cell Differ. 2002;35:67-91 [11791409.001]
  • [Cites] Trends Biochem Sci. 2002 Mar;27(3):111-2 [11893500.001]
  • [Cites] RNA. 2002 Mar;8(3):290-5 [12003489.001]
  • [Cites] J Biol Chem. 2002 May 24;277(21):18744-52 [11893730.001]
  • [Cites] J Virol. 2003 Jul;77(14):7728-35 [12829812.001]
  • [Cites] Oncogene. 2003 Jul 31;22(31):4819-30 [12894223.001]
  • [Cites] J Virol. 2003 Dec;77(23):12829-40 [14610204.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(23):8751-61 [14612415.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3963-9 [12907436.001]
  • [Cites] Virology. 2003 Dec 5;317(1):136-45 [14675632.001]
  • [Cites] EMBO J. 1991 Aug;10(8):2311-8 [2065667.001]
  • [Cites] J Virol. 1991 Aug;65(8):4408-13 [2072457.001]
  • [Cites] Cell. 1991 Jul 26;66(2):383-94 [1830244.001]
  • [Cites] J Virol. 1991 Oct;65(10):5165-73 [1716687.001]
  • [Cites] J Virol. 1991 Nov;65(11):6001-7 [1920623.001]
  • [Cites] Oncogene. 1991 Oct;6(10):1753-7 [1923501.001]
  • [Cites] J Virol. 1991 Dec;65(12):6645-53 [1942248.001]
  • [Cites] J Virol. 1992 Mar;66(3):1737-45 [1310774.001]
  • [Cites] Lancet. 1992 Mar 14;339(8794):645-6 [1347339.001]
  • [Cites] Mol Cell Biol. 1992 Mar;12(3):1375-86 [1545819.001]
  • [Cites] J Virol. 1992 Apr;66(4):2583-7 [1548784.001]
  • [Cites] Genes Dev. 1992 May;6(5):837-47 [1577277.001]
  • [Cites] J Virol. 1992 Jul;66(7):4325-30 [1602546.001]
  • [Cites] J Virol. 1992 Jul;66(7):4540-5 [1602559.001]
  • [Cites] J Exp Med. 1992 Jul 1;176(1):293-6 [1351922.001]
  • [Cites] Acta Neuropathol. 1992;84(2):147-52 [1381859.001]
  • [Cites] J Biol Chem. 1992 Oct 25;267(30):21977-81 [1400509.001]
  • [Cites] Virology. 1994 Oct;204(1):144-52 [8091649.001]
  • [Cites] J Virol. 1994 Dec;68(12):7944-52 [7966585.001]
  • [Cites] Oncogene. 1994 Dec;9(12):3535-44 [7970714.001]
  • [Cites] Cell. 1994 Dec 2;79(5):767-78 [8001116.001]
  • [Cites] J Virol. 1995 May;69(5):3125-33 [7707541.001]
  • [Cites] Cell. 1995 Apr 21;81(2):153-9 [7537634.001]
  • [Cites] Virology. 1995 Jun 1;209(2):445-56 [7539968.001]
  • [Cites] Virology. 1995 Jul 10;210(2):441-7 [7542419.001]
  • [Cites] Curr Biol. 1995 Apr 1;5(4):383-92 [7627554.001]
  • [Cites] Exp Cell Res. 1995 Jul;219(1):122-9 [7628528.001]
  • [Cites] Cell. 1995 Aug 11;82(3):463-73 [7634336.001]
  • [Cites] Cell. 1995 Aug 11;82(3):485-94 [7634337.001]
  • [Cites] Cell. 1995 Aug 11;82(3):495-506 [7634338.001]
  • [Cites] Nature. 1995 Aug 10;376(6540):530-3 [7637788.001]
  • [Cites] Clin Diagn Lab Immunol. 1994 May;1(3):273-82 [7496962.001]
  • [Cites] J Virol. 1996 Feb;70(2):1282-7 [8551596.001]
  • [Cites] J Virol. 1996 Apr;70(4):2350-9 [8642662.001]
  • [Cites] Virology. 1996 Apr 15;218(2):316-25 [8610458.001]
  • [Cites] J Virol. 1996 Jun;70(6):3834-43 [8648719.001]
  • [Cites] J Mol Biol. 1996 May 24;258(5):763-77 [8637008.001]
  • [Cites] Virology. 1996 Jun 15;220(2):502-7 [8661402.001]
  • [Cites] Mol Cell Biol. 1996 Aug;16(8):4207-14 [8754820.001]
  • [Cites] J Virol. 1996 Sep;70(9):6442-5 [8709278.001]
  • [Cites] Mol Cell Biol. 1996 Sep;16(9):5147-55 [8756672.001]
  • [Cites] J Virol. 1996 Aug;70(8):5194-202 [8764028.001]
  • [Cites] J Virol. 1997 Jan;71(1):95-101 [8985327.001]
  • [Cites] Mol Cell. 1998 Apr;1(5):649-59 [9660949.001]
  • [Cites] Oncogene. 1998 Jun 25;16(25):3309-16 [9681830.001]
  • [Cites] J Cell Biol. 2000 Mar 20;148(6):1091-5 [10725320.001]
  • [Cites] Oncogene. 2000 Aug 17;19(35):4071-4 [10962565.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1661-8 [11080807.001]
  • [Cites] J Virol. 1996 Aug;70(8):5511-8 [8764063.001]
  • [Cites] J Cell Biol. 1996 Sep;134(5):1157-68 [8794858.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5584-94 [8896452.001]
  • [Cites] Mol Cell Biol. 1996 Dec;16(12):7144-50 [8943370.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):135-44 [8972193.001]
  • [Cites] J Virol. 1998 Sep;72(9):7593-7 [9696859.001]
  • [Cites] J Virol. 1998 Nov;72(11):8627-35 [9765402.001]
  • [Cites] J Virol. 1998 Nov;72(11):8659-68 [9765406.001]
  • [Cites] J Virol. 1998 Dec;72(12):10316-22 [9811783.001]
  • [Cites] J Biol Chem. 1998 Dec 11;273(50):33414-22 [9837918.001]
  • [Cites] Mol Cell Biol. 1999 Feb;19(2):1218-25 [9891056.001]
  • [Cites] Annu Rev Microbiol. 1998;52:491-532 [9891806.001]
  • [Cites] J Biochem. 1999 Mar;125(3):574-85 [10050047.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6229-34 [10339570.001]
  • [Cites] Nat Med. 1999 Jun;5(6):635-42 [10371501.001]
  • [Cites] J Virol. 1992 Dec;66(12):7572-5 [1433531.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11784-8 [1465399.001]
  • [Cites] Virology. 1993 Mar;193(1):41-9 [8438577.001]
  • [Cites] Science. 1993 Apr 9;260(5105):219-22 [8385799.001]
  • [Cites] J Virol. 1993 May;67(5):2496-502 [8474155.001]
  • [Cites] Mol Cell Biol. 1993 Jun;13(6):3221-30 [7684491.001]
  • [Cites] J Biol Chem. 1993 Jul 5;268(19):13930-4 [8314759.001]
  • [Cites] Virology. 1993 Sep;196(1):25-33 [8356797.001]
  • [Cites] Biochemistry. 1993 Oct 5;32(39):10497-505 [8399195.001]
  • [Cites] J Cell Biol. 1993 Dec;123(6 Pt 1):1309-20 [8253832.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Feb 15;91(4):1256-60 [8108397.001]
  • [Cites] J Biol Chem. 1994 Mar 4;269(9):6320-4 [8119981.001]
  • [Cites] J Virol. 1994 Jun;68(6):3850-6 [8189522.001]
  • [Cites] J Cell Sci. 1997 Feb;110 ( Pt 3):369-78 [9057089.001]
  • [Cites] J Virol. 1997 Apr;71(4):2810-8 [9060636.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2235-46 [9121474.001]
  • [Cites] Curr Opin Cell Biol. 1997 Jun;9(3):401-11 [9159086.001]
  • [Cites] Curr Opin Cell Biol. 1997 Jun;9(3):412-9 [9159081.001]
  • [Cites] Exp Cell Res. 1997 Jun 15;233(2):363-71 [9194498.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3256-71 [9214641.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8590-5 [9238021.001]
  • [Cites] Blood Rev. 1997 Jun;11(2):91-104 [9242992.001]
  • [Cites] EMBO J. 1997 Jul 16;16(14):4276-84 [9250671.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1041-50 [9323132.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1051-60 [9323133.001]
  • [Cites] J Virol. 1997 Nov;71(11):8514-21 [9343209.001]
  • [Cites] Curr Biol. 1997 Oct 1;7(10):767-75 [9368759.001]
  • [Cites] J Biol Chem. 1998 May 8;273(19):11463-71 [9565558.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7427-32 [9636166.001]
  • [Cites] J Virol. 1998 Aug;72(8):6602-7 [9658105.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7588-90 [6095308.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] FEBS Lett. 1986 Dec 15;209(2):187-90 [3025015.001]
  • [Cites] FEBS Lett. 1986 Dec 15;209(2):289-94 [3025019.001]
  • [Cites] Science. 1987 Feb 20;235(4791):901-4 [3027896.001]
  • [Cites] J Virol. 1987 Apr;61(4):1147-54 [3029409.001]
  • [Cites] J Virol. 1987 Jul;61(7):2175-81 [3035218.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Mol Cell Biol. 1987 Jun;7(6):2201-11 [3110603.001]
  • [Cites] J Virol. 1988 Mar;62(3):680-6 [2828664.001]
  • [Cites] Genome Res. 1999 Jun;9(6):525-40 [10400920.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4080-90 [10435589.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):6276-85 [10454574.001]
  • [Cites] J Virol. 1999 Oct;73(10):8112-9 [10482560.001]
  • [Cites] J Virol. 2000 Mar;74(6):2655-62 [10684280.001]
  • (PMID = 15574380.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA77556; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCI NIH HHS / CA / CA92009; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / R01 CA077556; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / R01 CA092009
  • [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] United States
  • [Chemical-registry-number] 0 / Gene Products, rex
  • [Number-of-references] 167
  • [Other-IDs] NLM/ NIHMS94141; NLM/ PMC2659543
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75. Mitani S, Kamata H, Fujiwara M, Aoki N, Okada S, Watanabe M, Tango T, Mori S: Missense mutation with/without nonsense mutation of the p53 gene is associated with large cell morphology in human malignant lymphoma. Pathol Int; 2007 Jul;57(7):430-6
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  • [Title] Missense mutation with/without nonsense mutation of the p53 gene is associated with large cell morphology in human malignant lymphoma.
  • Mutations in p53 gene exons 5-9 were studied in 44 non-Hodgkin's lymphomas (NHL) consisting of 35 B-NHL and 9 T-NHL.
  • Missense mutations were found in two diffuse large B-cell lymphomas (DLBL) and one peripheral T-cell lymphoma (unspecified).
  • Double transversion missense and nonsense mutations were detected in one DLBL and one adult T-cell leukemia/lymphoma.
  • Cytomorphometric analysis was therefore conducted by measuring the gross area of 100 lymphoma cell nuclei in 44 cases and the results were compared between lymphomas harboring p53 missense mutation with/without nonsense mutation and lymphomas harboring p53 silent mutation or lacking mutation.
  • It was found that the lymphomas harboring p53 missense mutation with/without nonsense mutation had a highly significantly larger nuclear gross area than lymphomas with silent p53 mutation or lacking mutation (two-sample t-test, P < 0.00001; Exact Wilcoxon rank-sum test, P < 0.00001).
  • This result suggests that p53 mutation might induce enlargement of neoplastic cell nuclei by some molecular mechanism.
  • [MeSH-major] Codon, Nonsense. Genes, p53 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Mutation, Missense
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / pathology. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Male. Middle Aged

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  • (PMID = 17587242.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / DNA, Neoplasm
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76. Ejima Y: [An autopsied case of adult T-cell leukemia/lymphoma (ATLL) presenting with specific MRI findings in the cerebral cortex]. Brain Nerve; 2007 Nov;59(11):1305-13
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  • [Title] [An autopsied case of adult T-cell leukemia/lymphoma (ATLL) presenting with specific MRI findings in the cerebral cortex].
  • [MeSH-major] Cerebral Cortex. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Magnetic Resonance Imaging
  • [MeSH-minor] Aged. Cerebral Infarction / pathology. Diagnosis, Differential. Humans. Hypoxia, Brain / diagnosis. Male

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  • (PMID = 18044209.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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77. Lairmore MD, Montgomery A: Isolation and confirmation of human T-cell leukemia virus type 2 from peripheral blood mononuclear cells. Methods Mol Biol; 2005;304:113-23
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  • [Title] Isolation and confirmation of human T-cell leukemia virus type 2 from peripheral blood mononuclear cells.
  • Human T-cell leukemia virus type 2 (HTLV-2) was first isolated from leukemia patients, but has been found to be endemic among asymptomatic groups worldwide, including certain American Indian tribes.
  • The virus infection is associated with a low incidence of disease among infected subjects, but has been found in patients with neurologic disorders and contributes to bacterial sepsis in AIDS patients.
  • Polymerase chain reaction (PCR) and virus isolation techniques revealed that a high percentage of HTLV seroreactivity among intravenous drug users and blood donors in the United States is caused by HTLV-2.
  • Among serologic methods, enzyme-linked immunosorbent assays (ELISA) using whole virus preparations or in combination with recombinant and synthetic peptides are used as a primary screen for the infection.
  • Antigen-capture systems have increased the sensitivity and accuracy in verification of HTLV-2 culture systems.
  • The verification of HTLV-2 infection and detection of new strains of related viruses has been enhanced by employing virus-isolation methods using primary lymphocytes.
  • Lymphocyte culture methods have also been used to test transformation properties of the virus and create stably expressing cell lines.
  • This chapter briefly summarizes the biology of HTLV-2 infection and disease and details methods to isolate and verify the virus in lymphocyte cultures.
  • [MeSH-major] HTLV-II Infections / diagnosis. HTLV-II Infections / virology. Human T-lymphotropic virus 2 / isolation & purification. Leukocytes, Mononuclear / virology

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  • [Cites] Cancer Invest. 2003 Apr;21(2):323-4 [12743997.001]
  • [Cites] Virology. 1998 Mar 15;242(2):425-34 [9514966.001]
  • [Cites] Virology. 1996 Sep 15;223(2):362-4 [8806571.001]
  • [Cites] J Infect Dis. 1999 Dec;180(6):1777-83 [10558931.001]
  • [Cites] Transfusion. 2000 Aug;40(8):924-30 [10960518.001]
  • [Cites] J Clin Pathol. 2000 Aug;53(8):581-6 [11002759.001]
  • [Cites] J Acquir Immune Defic Syndr. 2001 Feb 1;26(2):185-90 [11242188.001]
  • [Cites] Ann Epidemiol. 2002 Jan;12(1):46-66 [11750240.001]
  • [Cites] J Med Virol. 2002 Feb;66(2):253-7 [11782936.001]
  • [Cites] AIDS Res Hum Retroviruses. 2002 Jan 1;18(1):71-7 [11804558.001]
  • [Cites] Rev Soc Bras Med Trop. 2001 Nov-Dec;34(6):519-25 [11813057.001]
  • [Cites] Transfusion. 2002 Jun;42(6):780-91 [12147033.001]
  • [Cites] Microbiol Mol Biol Rev. 2002 Sep;66(3):396-406, table of contents [12208996.001]
  • [Cites] J Acquir Immune Defic Syndr. 2002 Dec 1;31(4):440-7 [12447016.001]
  • [Cites] Leukemia. 2003 Jan;17(1):26-38 [12529656.001]
  • [Cites] J Trop Pediatr. 1999 Feb;45(1):42-7 [10191592.001]
  • [Cites] J Virol. 2003 Jul;77(14):7728-35 [12829812.001]
  • [Cites] J Acquir Immune Defic Syndr. 2003 Aug 15;33(5):655-6 [12902815.001]
  • [Cites] Science. 1982 Nov 5;218(4572):571-3 [6981847.001]
  • [Cites] Science. 1988 Apr 29;240(4852):643-6 [2896386.001]
  • [Cites] Blood. 1989 Nov 15;74(7):2585-91 [2804381.001]
  • [Cites] J Infect Dis. 1990 Jul;162(1):241-4 [2192006.001]
  • [Cites] Ann Intern Med. 1990 Sep 1;113(5):368-72 [2382919.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8840-4 [2247455.001]
  • [Cites] J Infect Dis. 1991 Feb;163(2):252-6 [1988509.001]
  • [Cites] Int J Cancer. 1993 May 8;54(2):255-60 [8486428.001]
  • [Cites] Ann Neurol. 1993 Apr;33(4):392-6 [8489210.001]
  • [Cites] J Acquir Immune Defic Syndr. 1993 Dec;6(12):1368-72 [8254477.001]
  • (PMID = 16061970.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-02
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS183536; NLM/ PMC3060566
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78. Tsukasaki K, Hermine O, Bazarbachi A, Ratner L, Ramos JC, Harrington W Jr, O'Mahony D, Janik JE, Bittencourt AL, Taylor GP, Yamaguchi K, Utsunomiya A, Tobinai K, Watanabe T: Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting. J Clin Oncol; 2009 Jan 20;27(3):453-9
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  • [Title] Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting.
  • Adult T-cell leukemia-lymphoma (ATL) is a distinct peripheral T-lymphocytic malignancy associated with a retrovirus designated human T-cell lymphotropic virus type I (HTLV-1).
  • The diversity in clinical features and prognosis of patients with this disease has led to its subclassification into the following four categories: acute, lymphoma, chronic, and smoldering types.
  • The chronic and smoldering subtypes are considered indolent and are usually managed with watchful waiting until disease progression, analogous to the management of some patients with chronic lymphoid leukemia (CLL) or other indolent histology lymphomas.
  • Patients with aggressive ATL generally have a poor prognosis because of multidrug resistance of malignant cells, a large tumor burden with multiorgan failure, hypercalcemia, and/or frequent infectious complications as a result of a profound T-cell immunodeficiency.
  • Under the sponsorship of the 13th International Conference on Human Retrovirology: HTLV, a group of ATL researchers joined to form a consensus statement based on established data to define prognostic factors, clinical subclassifications, and treatment strategies.
  • A set of response criteria specific for ATL reflecting a combination of those for lymphoma and CLL was proposed.
  • Clinical subclassification is useful but is limited because of the diverse prognosis among each subtype.
  • A treatment strategy based on the clinical subclassification and prognostic factors is suggested, including watchful waiting approach, chemotherapy, antiviral therapy, allogeneic hematopoietic stem-cell transplantation (alloHSCT), and targeted therapies.

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  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5458-64 [17968021.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3612-20 [11369658.001]
  • [Cites] Br J Haematol. 2001 Jun;113(3):779-84 [11380470.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3875-81 [11389029.001]
  • [Cites] Leuk Lymphoma. 2001 Jan;40(3-4):287-94 [11426550.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1160-5 [11493465.001]
  • [Cites] Blood. 2002 May 1;99(9):3383-9 [11964307.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2466-75 [11971181.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4576-82 [12560223.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3625-34 [14506150.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1838-45 [14592824.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2474-9 [14645001.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1987 Jul 11;2(8550):94-5 [2885585.001]
  • [Cites] Cancer. 1988 Feb 15;61(4):824-8 [3257406.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Cancer. 1990 Jan 15;65(2):327-32 [2295055.001]
  • [Cites] Cancer. 1991 May 15;67(10):2605-9 [2015561.001]
  • [Cites] Leuk Res. 1991;15(2-3):81-90 [2016910.001]
  • [Cites] Leuk Res. 1991;15(2-3):99-103 [2016911.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Leuk Res. 1993 Feb;17(2):157-66 [8429692.001]
  • [Cites] Cancer. 1994 Jun 1;73(11):2753-8 [8194016.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S186-90 [8797722.001]
  • [Cites] Blood. 1997 Feb 1;89(3):948-56 [9028326.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1778-85 [9164185.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1996;67:1-424 [9190379.001]
  • [Cites] Blood. 1999 Jan 1;93(1):278-83 [9864171.001]
  • [Cites] Br J Haematol. 1999 May;105(2):369-75 [10233406.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Cancer Lett. 2006 Mar 28;234(2):249-55 [15896902.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3054-61 [16425276.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):579-86 [17242396.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3060-8 [17138822.001]
  • [Cites] Leuk Res. 2007 Jun;31(6):751-7 [17188352.001]
  • [Cites] Leuk Res. 2007 Jul;31(7):915-20 [17123603.001]
  • [Cites] Am J Clin Pathol. 2007 Nov;128(5):875-82 [17951212.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • (PMID = 19064971.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Number-of-references] 61
  • [Other-IDs] NLM/ PMC2737379
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79. Atsumi E, Yara S, Higa F, Hirata T, Haranaga S, Tateyama M, Fujita J: Influence of human T lymphotropic virus type I infection on the etiology of community-acquired pneumonia. Intern Med; 2009;48(12):959-65
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  • [Title] Influence of human T lymphotropic virus type I infection on the etiology of community-acquired pneumonia.
  • BACKGROUND: Human T lymphotropic virus type I (HTLV-I), the cause of human T cell leukemia, is associated with a high incidence of several other infectious diseases.
  • However, the relationship between pulmonary infections and HTLV-I infection is still unclear.
  • OBJECTIVE: A large-scale retrospective study was conducted on hospital inpatients to evaluate the relationship between community-acquired pneumonia (CAP) and HTLV-I infection.
  • The presence of serum HTLV-I antibody was determined in all patients on admission.
  • Prevalence of HTLV-I infection was analyzed between CAP patients and all inpatients.
  • We also compared HTLV-I-positive CAP patients and HTLV-I-negative CAP patients for severity and manifestation of pneumonia.
  • RESULTS: The prevalence of HTLV-I was higher in CAP patients than in all inpatients (18.9%: 13.7%, p=0.011).
  • The rates of renal diseases and collagen vascular disorders were higher in the HTLV-I-positive CAP patients than in the HTLV-I-negative CAP patients.
  • Multivariate analysis revealed that HTLV-I infection, gender, COPD and collagen vascular disorders were all independent risk factors for CAP.
  • The severity indices of CAP, the PORT score and the CURB-65 score, were higher in the HTLV-I-positive patients than in the HTLV-I-negative patients.
  • CONCLUSION: This study demonstrates that HTLV-I infection might be an independent risk factor for CAP and that HTLV-I-infected patients tend to demonstrate a relatively severe form of pneumonia.
  • [MeSH-major] Community-Acquired Infections / etiology. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Pneumonia / etiology
  • [MeSH-minor] Adult. Aged. Female. HTLV-I Antibodies / blood. Humans. Male. Middle Aged. Multivariate Analysis. Prevalence. Retrospective Studies. Risk Factors. Severity of Illness Index

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  • (PMID = 19525581.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
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80. Morice WG, Jevremovic D, Hanson CA: The expression of the novel cytotoxic protein granzyme M by large granular lymphocytic leukaemias of both T-cell and NK-cell lineage: an unexpected finding with implications regarding the pathobiology of these disorders. Br J Haematol; 2007 May;137(3):237-9
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  • [Title] The expression of the novel cytotoxic protein granzyme M by large granular lymphocytic leukaemias of both T-cell and NK-cell lineage: an unexpected finding with implications regarding the pathobiology of these disorders.
  • As most T-cell granular lymphocytic leukaemias (T-LGL) are thought to be derived from the adaptive immune system it was predicted that T-LGL would be GrM negative.
  • These unexpected results suggest commonality between T- and NK-LGL, providing further support to the notion that T-LGL is a disorder of dysregulated, chronically stimulated, adaptive cytotoxic T-cells.
  • [MeSH-major] Granzymes / analysis. Killer Cells, Natural / immunology. Leukemia, Lymphoid / enzymology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Lineage. Humans. Immunohistochemistry / methods. Leukemia, T-Cell / enzymology. Leukemia, T-Cell / immunology. Middle Aged. Poly(A)-Binding Proteins / analysis

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  • (PMID = 17408463.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Poly(A)-Binding Proteins; 0 / TIA1 protein, human; EC 3.4.21.- / GZMM protein, human; EC 3.4.21.- / Granzymes
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81. Feng X, Ratner L: Human T-cell leukemia virus type 1 blunts signaling by interferon alpha. Virology; 2008 Apr 25;374(1):210-6
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  • [Title] Human T-cell leukemia virus type 1 blunts signaling by interferon alpha.
  • Although many animal viruses block the interferon (IFN) signaling pathway, this issue has not been previously investigated in retrovirus-infected cells.
  • For this purpose, an infectious molecular clone of human T-cell leukemia virus type 1 (HTLV-1) was transfected into 293T or HeLa cells and was found to reduce interferon-stimulated response element (ISRE) reporter activity.
  • HTLV-1 reduced the phosphorylation of tyrosine kinase 2 (TYK2) and signal transducer and transcriptional activator 2 (STAT2), suggesting a specific effect of HTLV-1 on the ability of an adaptor tyrosine kinase to transfer an IFN signal to the STAT-transcriptional activator complex.

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  • [Cites] EMBO J. 2001 Jan 15;20(1-2):91-100 [11226159.001]
  • [Cites] Virology. 2000 Mar 1;268(1):41-8 [10683325.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1150-9 [11493464.001]
  • [Cites] J Virol. 2001 Oct;75(19):9553-9 [11533220.001]
  • [Cites] Annu Rev Microbiol. 2001;55:255-81 [11544356.001]
  • [Cites] Microbes Infect. 2002 May;4(6):647-55 [12048034.001]
  • [Cites] J Neuroimmunol. 1999 Mar 1;95(1-2):185-9 [10229129.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] Oncogene. 1999 Oct 14;18(42):5727-37 [10523853.001]
  • [Cites] J Virol. 2005 Feb;79(3):1343-50 [15650160.001]
  • [Cites] J Immunol. 2005 Jun 15;174(12):8163-72 [15944325.001]
  • [Cites] J Virol. 2005 Oct;79(20):12828-39 [16188985.001]
  • [Cites] J Interferon Cytokine Res. 2005 Dec;25(12):733-44 [16375601.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1440-5 [16434471.001]
  • [Cites] Virology. 2006 May 10;348(2):489-97 [16480752.001]
  • [Cites] J Virol. 2006 Jun;80(12):5908-18 [16731929.001]
  • [Cites] Mol Biol Cell. 2006 Jul;17(7):2896-909 [16624862.001]
  • [Cites] J Virol. 2006 Oct;80(19):9349-60 [16973541.001]
  • [Cites] Immunity. 2006 Sep;25(3):361-72 [16979568.001]
  • [Cites] Acta Biochim Pol. 2007;54(1):27-38 [17351669.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3060-8 [17138822.001]
  • [Cites] Nat Rev Immunol. 2002 Sep;2(9):675-87 [12209136.001]
  • [Cites] J Virol. 2002 Dec;76(24):13101-5 [12438640.001]
  • [Cites] J Virol. 2003 Dec;77(24):13389-95 [14645593.001]
  • [Cites] Br J Haematol. 2004 Jun;125(5):568-75 [15147371.001]
  • [Cites] J Mol Biol. 2004 Sep 17;342(3):833-46 [15342240.001]
  • [Cites] Virology. 1994 Nov 1;204(2):656-64 [7941334.001]
  • [Cites] Virology. 1995 Feb 1;206(2):913-22 [7856104.001]
  • [Cites] Science. 1995 Jul 7;269(5220):79-81 [7604283.001]
  • [Cites] Mol Cell Biol. 1996 Apr;16(4):1283-94 [8657101.001]
  • [Cites] Microbiol Immunol. 1997;41(1):63-6 [9087969.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):143-56 [11325598.001]
  • (PMID = 18234266.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100730-010005; United States / NCI NIH HHS / CA / P50 CA094056; United States / NCI NIH HHS / CA / R21 CA109678-02; United States / NCI NIH HHS / CA / CA094056-070003; United States / NCI NIH HHS / CA / R21 CA109678; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA105218-03; United States / NCI NIH HHS / CA / P50 CA094056-070003; United States / NCI NIH HHS / CA / CA109678-02; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / P01 CA100730-010005; United States / NCI NIH HHS / CA / CA063417-09; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / CA109678; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / R01 CA105218-03; United States / NCI NIH HHS / CA / R01 CA105218; United States / NCI NIH HHS / CA / P01 CA100730; United States / NCI NIH HHS / CA / R01 CA063417-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / STAT2 Transcription Factor; 0 / STAT2 protein, human; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human
  • [Other-IDs] NLM/ NIHMS47609; NLM/ PMC2373983
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82. Richard V, Nadella MV, Green PL, Lairmore MD, Feuer G, Foley JG, Rosol TJ: Transcriptional regulation of parathyroid hormone-related protein promoter P3 by ETS-1 in adult T-cell leukemia/lymphoma. Leukemia; 2005 Jul;19(7):1175-83
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  • [Title] Transcriptional regulation of parathyroid hormone-related protein promoter P3 by ETS-1 in adult T-cell leukemia/lymphoma.
  • Parathyroid hormone-related protein (PTHrP) plays a primary role in the development of humoral hypercalcemia of malignancy seen in the majority of adult T-cell leukemia/lymphoma (ATLL) patients with human T-cell lymphotropic virus type-1 (HTLV-1) infection.
  • HTLV-1 Tax has been shown to complex with ETS-1 and SP1 to transactivate the PTHrP P3 promoter.
  • Previously, we established a SCID/bg mouse model of human ATL with RV-ATL cells and showed that PTHrP expression was independent of Tax.
  • In this study, we report an inverse correlation of PTHrP with tax/rex mRNA in multiple HTLV-1-positive cell lines and RV-ATL cells.
  • Stimulation of Jurkat T cells with PMA/ionomycin upregulated the PTHrP P3 promoter by a previously characterized Ets binding site and also induced protein/DNA complex formation identical to that observed in RV-ATL cells.
  • Further, we provide evidence that cotransfection with Ets-1 and constitutively active Mek-1 in HTLV-1-negative transformed T cells with stimulation by PMA/ionomycin not only resulted in a robust induction of PTHrP P3 but also formed a complex with ETS-1/P3 EBS similar to that in ATLL cells.
  • Our data demonstrate that transcriptional regulation of PTHrP in ATLL cells can be controlled by T-cell receptor signaling and the ETS and MAPK ERK pathway in a Tax-independent manner.

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  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Endocrinology. 2000 May;141(5):1882-92 [10803599.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3915-21 [10845928.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1583-90 [11080795.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):2219-28 [11395400.001]
  • [Cites] Rev Endocr Metab Disord. 2000 Nov;1(4):253-63 [11706739.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46661-70 [11590145.001]
  • [Cites] Gene. 2003 Jan 16;303:11-34 [12559563.001]
  • [Cites] Int J Oncol. 2003 Apr;22(4):799-805 [12632071.001]
  • [Cites] Mol Cell Endocrinol. 2003 Jun 30;204(1-2):155-68 [12850290.001]
  • [Cites] Clin Chem. 2003 Aug;49(8):1398-402 [12881458.001]
  • [Cites] Biochem J. 2003 Jun 15;372(Pt 3):787-97 [12628005.001]
  • [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 Oct;81(19):6207-11 [6091140.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):556-63 [3043221.001]
  • [Cites] Science. 1988 Sep 23;241(4873):1652-5 [2843985.001]
  • [Cites] Gene. 1989 Apr 15;77(1):95-105 [2744490.001]
  • [Cites] J Immunol. 1989 Aug 15;143(4):1283-9 [2545785.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5620-4 [2787512.001]
  • [Cites] J Endocrinol. 1989 Jul;122(1):219-27 [2788697.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Mar 30;167(3):1134-8 [2322262.001]
  • [Cites] J Virol. 1990 Jun;64(6):2825-32 [2335818.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Mol Endocrinol. 1990 Jun;4(6):851-8 [2233743.001]
  • [Cites] J Biol Chem. 1992 Jul 5;267(19):13623-8 [1618864.001]
  • [Cites] Mol Endocrinol. 1992 Oct;6(10):1642-52 [1280327.001]
  • [Cites] Curr Top Microbiol Immunol. 1992;182:421-4 [1490380.001]
  • [Cites] Blood. 1993 Feb 15;81(4):1017-24 [8427983.001]
  • [Cites] Cancer. 1993 May 1;71(9):2803-6 [8467460.001]
  • [Cites] Mol Endocrinol. 1993 Feb;7(2):273-82 [8469240.001]
  • [Cites] Endocrinology. 1993 Jun;132(6):2551-6 [8099324.001]
  • [Cites] Cancer Res. 1993 Jul 1;53(13):2980-6 [8319205.001]
  • [Cites] Blood. 1993 Aug 1;82(3):722-31 [8338942.001]
  • [Cites] J Biol Chem. 1993 Aug 5;268(22):16730-6 [8393873.001]
  • [Cites] J Virol. 1993 Oct;67(10):6087-95 [8371355.001]
  • [Cites] Urology. 1994 May;43(5):675-9 [8165768.001]
  • [Cites] J Bone Miner Res. 1994 May;9(5):639-44 [8053392.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8960-3 [8090753.001]
  • [Cites] Endocrinology. 1995 Apr;136(4):1782-9 [7895691.001]
  • [Cites] Mol Cell Biol. 1995 Aug;15(8):4064-75 [7623802.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2257-67 [7662973.001]
  • [Cites] Br J Cancer. 1995 Sep;72(3):702-7 [7669584.001]
  • [Cites] Mol Cell Endocrinol. 1995 Jun;111(2):225-32 [7556886.001]
  • [Cites] Endocrinology. 1995 Dec;136(12):5416-22 [7588290.001]
  • [Cites] J Cell Physiol. 1996 Jan;166(1):1-11 [8557757.001]
  • [Cites] Endocrinology. 1996 Apr;137(4):1349-57 [8625910.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3744-50 [8670878.001]
  • [Cites] J Biol Chem. 1997 Feb 21;272(8):4953-8 [9030555.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13897-902 [9391124.001]
  • [Cites] J Biol Chem. 1998 May 8;273(19):11463-71 [9565558.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23):14119-29 [9603911.001]
  • [Cites] Cancer Res. 1999 Dec 1;59(23):6015-22 [10606251.001]
  • [Cites] Mol Cell Endocrinol. 1999 Oct 25;156(1-2):13-23 [10612419.001]
  • (PMID = 15889157.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077911; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCRR NIH HHS / RR / RR00168; United States / NCI NIH HHS / CA / CA100730; United States / NCRR NIH HHS / RR / P51 RR000168; United States / NCRR NIH HHS / RR / K26 RR000168; United States / NCI NIH HHS / CA / CA77911; United States / NCI NIH HHS / CA / P01 CA100730-03; None / None / / P01 CA100730-01; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / P01 CA100730-01; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS1 protein, human; 0 / Ets1 protein, mouse; 0 / Gene Products, rex; 0 / Gene Products, tax; 0 / Parathyroid Hormone-Related Protein; 0 / Proto-Oncogene Protein c-ets-1; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell; 0 / Transcription Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS94146; NLM/ PMC2661941
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83. Toulza F, Nosaka K, Takiguchi M, Pagliuca T, Mitsuya H, Tanaka Y, Taylor GP, Bangham CR: FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia. Int J Cancer; 2009 Nov 15;125(10):2375-82
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  • [Title] FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL).
  • It has been postulated that ATLL cells might act as regulatory T cells (T(regs)) which, in common with ATLL cells, express both CD25 and FoxP3, and so contribute to the severe immune suppression typical of ATLL.
  • We report here that the frequency of CD25(+) cells varied independently of the frequency of FoxP3(+) cells in both a cross-sectional study and in a longitudinal study of 2 patients with chronic ATLL.
  • Furthermore, the capacity of ATLL cells to suppress proliferation of heterologous CD4(+)CD25(-) cells correlated with the frequency of CD4(+) FoxP3(+) cells but was independent of CD25 expression.
  • Finally, the frequency of CD4(+)FoxP3(+) cells was inversely correlated with the lytic activity of HTLV-1-specific CTLs in patients with ATLL.
  • We conclude that ATLL is not a tumor of FoxP3(+) regulatory T cells, and that a population of FoxP3(+) cells distinct from ATLL cells has regulatory functions and may impair the cell-mediated immune response to HTLV-1 in patients with ATLL.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Proliferation. Chronic Disease. Female. Flow Cytometry. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate

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  • (PMID = 19544530.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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84. Ohashi T, Nagai M, Okada H, Takayanagi R, Shida H: Activation and detection of HTLV-I Tax-specific CTLs by epitope expressing single-chain trimers of MHC class I in a rat model. Retrovirology; 2008;5:90
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  • [Title] Activation and detection of HTLV-I Tax-specific CTLs by epitope expressing single-chain trimers of MHC class I in a rat model.
  • BACKGROUND: Human T cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) in infected individuals after a long incubation period.
  • Immunological studies have suggested that insufficient host T cell response to HTLV-I is a potential risk factor for ATL.
  • To understand the relationship between host T cell response and HTLV-I pathogenesis in a rat model system, we have developed an activation and detection system of HTLV-I Tax-specific cytotoxic T lymphocytes (CTLs) by Epitope expressing Single-Chain Trimers (SCTs) of MHC class I.
  • Human cell lines transfected with the established expression vectors were able to induce IFN-gamma and TNF-alpha production by a Tax180-188-specific CTL line, 4O1/C8.
  • CONCLUSION: We have generated a SCT of rat MHC-I linked to Tax epitope peptide, which can be applicable for the induction of Tax-specific CTLs in rat model systems of HTLV-I infection.
  • These systems will be useful tools in understanding the role of HTLV-I specific CTLs in HTLV-I pathogenesis.
  • [MeSH-major] Epitopes, T-Lymphocyte / genetics. Gene Expression. Gene Products, tax / genetics. Genes, MHC Class I. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / genetics. T-Lymphocytes, Cytotoxic / immunology. Transcriptional Activation
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line. Cells, Cultured. Cytokines / genetics. Cytokines / immunology. Disease Models, Animal. Female. Genetic Vectors / genetics. Humans. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / virology. Molecular Sequence Data. Rats. Rats, Inbred F344. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / immunology

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  • [Cites] J Virol. 2000 Jan;74(1):428-35 [10590132.001]
  • [Cites] J Immunol. 2006 Oct 15;177(8):5718-26 [17015761.001]
  • [Cites] J Virol. 2000 Oct;74(20):9610-6 [11000233.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] J Immunol. 2002 Apr 1;168(7):3145-9 [11907065.001]
  • [Cites] J Virol. 2002 Jul;76(14):7010-9 [12072501.001]
  • [Cites] J Immunol Methods. 2002 Dec 20;271(1-2):125-35 [12445736.001]
  • [Cites] J Virol. 2003 Mar;77(5):2956-63 [12584320.001]
  • [Cites] Nat Med. 2003 Apr;9(4):469-76 [12652294.001]
  • [Cites] Leukemia. 2004 Jan;18(1):126-32 [14574331.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] J Virol. 2004 Apr;78(8):3827-36 [15047798.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] J Immunol. 1983 Jun;130(6):2942-6 [6189906.001]
  • [Cites] J Exp Med. 1984 Apr 1;159(4):1105-16 [6323614.001]
  • [Cites] J Immunol. 1984 Aug;133(2):1037-41 [6203964.001]
  • [Cites] Science. 1985 Jun 28;228(4707):1532-4 [2990031.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Science. 1987 May 29;236(4805):1103-6 [2883731.001]
  • [Cites] Lancet. 1989 Feb 25;1(8635):441 [2563817.001]
  • [Cites] Lancet. 1990 Dec 1;336(8727):1345-7 [1978165.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Science. 1991 Jul 19;253(5017):317-20 [1857968.001]
  • [Cites] Virology. 1992 Jun;188(2):628-36 [1374983.001]
  • [Cites] J Exp Med. 1992 Oct 1;176(4):981-9 [1402668.001]
  • [Cites] J Virol. 1999 Jul;73(7):6031-40 [10364355.001]
  • [Cites] Cancer Immunol Immunother. 2005 Sep;54(9):867-79 [15906027.001]
  • [Cites] Gene Ther. 2005 Aug;12(15):1180-6 [15800656.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5931-7 [16155600.001]
  • [Cites] Cancer Immunol Immunother. 2006 Feb;55(2):235-6 [16261380.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Aug;80(15):7375-81 [16840318.001]
  • [Cites] J Immunol. 2006 Sep 1;177(5):2862-72 [16920921.001]
  • [Cites] Immunogenetics. 1999 Nov;50(3-4):213-9 [10602881.001]
  • (PMID = 18840303.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Epitopes, T-Lymphocyte; 0 / Gene Products, tax; 0 / Recombinant Fusion Proteins; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Other-IDs] NLM/ PMC2579301
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85. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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86. Bremer E, Samplonius DF, Peipp M, van Genne L, Kroesen BJ, Fey GH, Gramatzki M, de Leij LF, Helfrich W: Target cell-restricted apoptosis induction of acute leukemic T cells by a recombinant tumor necrosis factor-related apoptosis-inducing ligand fusion protein with specificity for human CD7. Cancer Res; 2005 Apr 15;65(8):3380-8
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  • [Title] Target cell-restricted apoptosis induction of acute leukemic T cells by a recombinant tumor necrosis factor-related apoptosis-inducing ligand fusion protein with specificity for human CD7.
  • Current treatment of human T-cell leukemia and lymphoma is predominantly limited to conventional cytotoxic therapy and is associated with limited therapeutic response and significant morbidity.
  • Therefore, more potent and leukemia-specific therapies with favorable toxicity profiles are urgently needed.
  • Here, we report on the construction of a novel therapeutic fusion protein, scFvCD7:sTRAIL, designed to induce target antigen-restricted apoptosis in human T-cell tumors.
  • ScFvCD7:sTRAIL consists of the death-inducing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genetically linked to an scFv antibody fragment specific for the T-cell surface antigen CD7.
  • Treatment with scFvCD7:sTRAIL induced potent CD7-restricted apoptosis in a series of malignant T-cell lines, whereas normal resting leukocytes, activated T cells, and vascular endothelial cells (human umbilical vein endothelial cells) showed no detectable apoptosis.
  • In mixed culture experiments with CD7-positive and CD7-negative tumor cells, scFvCD7:sTRAIL induced very potent bystander apoptosis of CD7-negative tumor cells.
  • In vitro treatment of blood cells freshly derived from T-acute lymphoblastic leukemia patients resulted in marked apoptosis of the malignant T cells that was strongly augmented by vincristin.
  • In conclusion, scFvCD7:sTRAIL is a novel recombinant protein causing restricted apoptosis in human leukemic T cells with low toxicity for normal human blood and endothelial cells.
  • [MeSH-major] Antigens, CD7 / immunology. Apoptosis / drug effects. Immunotoxins / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Membrane Glycoproteins / pharmacology. Recombinant Fusion Proteins / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Apoptosis Regulatory Proteins. CHO Cells. Cell Line, Tumor. Cricetinae. Drug Synergism. Epitopes. Humans. Immunoglobulin Fragments / genetics. Immunoglobulin Fragments / immunology. Immunoglobulin Fragments / pharmacology. Jurkat Cells / cytology. Jurkat Cells / drug effects. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. T-Lymphocytes / pathology. TNF-Related Apoptosis-Inducing Ligand. Vincristine / pharmacology

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  • (PMID = 15833872.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD7; 0 / Apoptosis Regulatory Proteins; 0 / Epitopes; 0 / Immunoglobulin Fragments; 0 / Immunotoxins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine
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87. Kiewe P, Dallenbach FE, Fischer L, Hoecht S, Kombos T, Thiel E, Korfel A: Isolated B-cell lymphoproliferative disorder at the dura mater with B-cell chronic lymphocytic leukemia immunophenotype. Clin Lymphoma Myeloma; 2007 Nov;7(9):594-6
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  • [Title] Isolated B-cell lymphoproliferative disorder at the dura mater with B-cell chronic lymphocytic leukemia immunophenotype.
  • Lymphoma manifestations of the dura mater are extremely rare and have mostly been attributed to extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) type.
  • We report a patient with an isolated meningeal tumor, identified as a B-cell lymphoproliferative disorder with typical B-cell chronic lymphocytic leukemia immunophenotype.
  • Because of the subclinical detection of trisomy 3 in the bone marrow by cytogenetic analysis and interphase fluorescence in situ hybridization, CD5(+) MALT is an important differential diagnosis; however, to our knowledge, this entity has never been reported in the context of dural lymphoma.
  • [MeSH-major] Brain Neoplasms / pathology. Leukemia, Large Granular Lymphocytic / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Immunophenotyping. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / immunology. Lymphoma, B-Cell, Marginal Zone / pathology. Male


88. Hayase H, Ishizu A, Ikeda H, Miyatake Y, Baba T, Higuchi M, Abe A, Tomaru U, Yoshiki T: Aberrant gene expression by CD25+CD4+ immunoregulatory T cells in autoimmune-prone rats carrying the human T cell leukemia virus type-I gene. Int Immunol; 2005 Jun;17(6):677-84
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  • [Title] Aberrant gene expression by CD25+CD4+ immunoregulatory T cells in autoimmune-prone rats carrying the human T cell leukemia virus type-I gene.
  • Transgenic rats expressing the env-pX gene of human T cell leukemia virus type-I under the control of the viral long terminal repeat promoter (env-pX rats) developed systemic autoimmune diseases.
  • Prior to disease manifestation, the immunosuppressive function of CD25(+)CD4(+) T (T-reg) cells was impaired in these rats.
  • Since T cell differentiation appeared to be disordered in env-pX rats, we assumed that the impairment of T-reg cells might be caused by an abortive differentiation in the thymus.
  • However, reciprocal bone marrow transfers between env-pX and wild-type rats revealed that direct effects of the transgene unrelated to the thymus framework induced the abnormality of T-reg cells.
  • Expression of the Foxp3 gene and cell-surface markers supported a naive phenotype for env-pX T-reg cells.
  • Array analyses of gene expression showed some interesting profiles, e.g. up-regulation of genes associated with the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways in env-pX T-reg cells.
  • We suggest that investigation of the pathology of T-reg cells in our autoimmune-prone rat model may aid in understanding the roles of T-reg cells in human autoimmune diseases.
  • [MeSH-major] Autoimmune Diseases / immunology. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antigens, CD / analysis. Antigens, CD4 / genetics. Bone Marrow Transplantation. Disease Models, Animal. Forkhead Transcription Factors / biosynthesis. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / immunology. Gene Expression Regulation / immunology. Immediate-Early Proteins / immunology. Immediate-Early Proteins / metabolism. Janus Kinase 1. Male. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / immunology. Rats. Receptors, Interleukin-2 / genetics. Spleen / cytology. Spleen / immunology. Suppressor of Cytokine Signaling Proteins / biosynthesis. Suppressor of Cytokine Signaling Proteins / immunology

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  • (PMID = 15908451.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD4; 0 / Forkhead Transcription Factors; 0 / Foxp3 protein, rat; 0 / Immediate-Early Proteins; 0 / Receptors, Interleukin-2; 0 / Socs1 protein, rat; 0 / Socs2 protein, rat; 0 / Socs3 protein, rat; 0 / Suppressor of Cytokine Signaling Proteins; 0 / cytokine inducible SH2-containing protein; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Jak1 protein, rat; EC 2.7.10.2 / Janus Kinase 1
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89. Sugita K, Shimauchi T, Kabashima R, Nakashima D, Hino R, Kabashima K, Nakamura M, Tokura Y: Loss of tumor cell CCR4 expression upon leukemic change in adult T-cell leukemia/lymphoma. J Am Acad Dermatol; 2009 Jul;61(1):163-4
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  • [Title] Loss of tumor cell CCR4 expression upon leukemic change in adult T-cell leukemia/lymphoma.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / metabolism. Receptors, CCR4 / biosynthesis
  • [MeSH-minor] Aged. Fatal Outcome. Gene Expression. Humans. Leukemia / pathology. Male. Skin Neoplasms / pathology

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  • (PMID = 19539864.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4
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90. Arpin-André C, Mesnard JM: The PDZ domain-binding motif of the human T cell leukemia virus type 1 tax protein induces mislocalization of the tumor suppressor hScrib in T cells. J Biol Chem; 2007 Nov 9;282(45):33132-41
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  • [Title] The PDZ domain-binding motif of the human T cell leukemia virus type 1 tax protein induces mislocalization of the tumor suppressor hScrib in T cells.
  • In this regard, the oncogenic potential of the human T cell leukemia virus type 1 Tax protein correlates with its binding capacity to the tumor suppressor hDlg.
  • Recent results show that hDlg in T cells is associated to a network of scaffolding proteins including another PDZ domain-containing protein termed hScrib.
  • Interestingly, previous studies have revealed complementary activities of both proteins in the control of epithelial cell polarity.
  • Here, we demonstrate that Tax can bind to hScrib and that the resulting Tax/hScrib complex is present in human T cell leukemia virus type 1-infected T cells.
  • By confocal microscopy, we show that Tax modifies the localization of hScrib in transfected COS cells as well as in infected T cell lines and targets hScrib to particular spots exhibiting a granular distribution, mainly distributed in the cytoplasm.
  • Providing further support to this idea, we find that transient overexpression of hScrib attenuates T cell receptor-induced NFAT activity but that the presence of Tax counteracts this negative effect on the NFAT pathway.
  • The fact that hDlg and hScrib are both targeted by Tax underlies their importance in T cell function.
  • [MeSH-major] Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Membrane Proteins / metabolism. T-Lymphocytes / metabolism. Transcription, Genetic / genetics. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Line. Humans. PDZ Domains. Protein Binding. Protein Transport

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  • (PMID = 17855372.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Membrane Proteins; 0 / SCRIB protein, human; 0 / Tumor Suppressor Proteins
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91. Miyazato A, Sheleg S, Iha H, Li Y, Jeang KT: Evidence for NF-kappaB- and CBP-independent repression of p53's transcriptional activity by human T-cell leukemia virus type 1 Tax in mouse embryo and primary human fibroblasts. J Virol; 2005 Jul;79(14):9346-50
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  • [Title] Evidence for NF-kappaB- and CBP-independent repression of p53's transcriptional activity by human T-cell leukemia virus type 1 Tax in mouse embryo and primary human fibroblasts.
  • The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein can repress the transcriptional activity of the tumor suppressor protein p53.

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  • [Cites] Oncogene. 2000 Mar 16;19(12):1491-9 [10734308.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6948-58 [10602469.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3377-86 [10779327.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3939-44 [10845931.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1669-75 [11080808.001]
  • [Cites] J Virol. 2001 Jan;75(1):396-407 [11119608.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):594-604 [12154352.001]
  • [Cites] J Virol. 2002 Dec;76(24):12564-73 [12438582.001]
  • [Cites] J Biol Chem. 2003 Jan 17;278(3):1487-93 [12419799.001]
  • [Cites] Oncogene. 2003 Dec 4;22(55):8912-23 [14654787.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Science. 1987 Sep 11;237(4820):1324-9 [2888190.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):413-7 [2403646.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1071-5 [2300570.001]
  • [Cites] Science. 1992 May 8;256(5058):827-30 [1589764.001]
  • [Cites] J Virol. 1992 Dec;66(12):7183-92 [1433511.001]
  • [Cites] Oncogene. 1993 Nov;8(11):3029-36 [8414503.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] J Virol. 1995 Sep;69(9):5806-11 [7637025.001]
  • [Cites] FEBS Lett. 1997 Apr 14;406(3):263-6 [9136898.001]
  • [Cites] J Virol. 1998 Feb;72(2):1165-70 [9445014.001]
  • [Cites] Cell. 1998 Jun 26;93(7):1231-40 [9657155.001]
  • [Cites] J Virol. 1998 Aug;72(8):6348-55 [9658074.001]
  • [Cites] J Virol. 1998 Nov;72(11):8852-60 [9765430.001]
  • [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] Mol Cell Biol. 1999 Jul;19(7):4547-51 [10373503.001]
  • [Cites] Oncogene. 1999 Jun 24;18(25):3766-72 [10391685.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):22911-4 [10438454.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10326-32 [15611068.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):11852-7 [10766811.001]
  • (PMID = 15994832.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Crebbp protein, mouse; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.1.- / Chuk protein, mouse; EC 2.7.1.- / IKBKE protein, human; EC 2.7.1.- / Ikbke protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; EC 2.7.11.10 / Ikbkb protein, mouse
  • [Other-IDs] NLM/ PMC1168794
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92. Armstrong F, Brunet de la Grange P, Gerby B, Rouyez MC, Calvo J, Fontenay M, Boissel N, Dombret H, Baruchel A, Landman-Parker J, Roméo PH, Ballerini P, Pflumio F: NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity. Blood; 2009 Feb 19;113(8):1730-40
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  • [Title] NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity.
  • Understanding the pathways that regulate the human T-cell acute lymphoblastic leukemia (T-ALL) initiating cells (T-LiC) activity has been hampered by the lack of biologic assays in which this human disease can be studied.
  • Here we show that coculture of primary human T-ALL with a mouse stromal cell line expressing the NOTCH ligand delta-like-1 (DL1) reproducibly allowed maintenance of T-LiC and long-term growth of blast cells.
  • Human T-ALL mutated or not on the NOTCH receptor required sustained activation of the NOTCH pathway via receptor/ligand interaction for growth and T-LiC activity.
  • On the reverse, inhibition of the NOTCH pathway during primary cultures abolished in vitro cell growth and in vivo T-LiC activity.
  • Altogether, these results demonstrate the major role of the NOTCH pathway activation in human T-ALL development and in the maintenance of leukemia-initiating cells.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Receptor, Notch1 / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Cell Communication / physiology. Cell Culture Techniques / methods. Coculture Techniques. Genes, T-Cell Receptor gamma / genetics. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Oligopeptides / pharmacology. Stromal Cells / cytology. Stromal Cells / physiology. Tumor Cells, Cultured

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  • (PMID = 18984862.001).
  • [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 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / Oligopeptides; 0 / Receptor, Notch1; 0 / benzyloxycarbonyl-leucyl-leucyl-norleucinal; EC 3.4.- / Amyloid Precursor Protein Secretases
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93. Tong X, Zhang L, Zhang L, Hu M, Leng J, Yu B, Zhou B, Hu Y, Zhang Q: The mechanism of chemokine receptor 9 internalization triggered by interleukin 2 and interleukin 4. Cell Mol Immunol; 2009 Jun;6(3):181-9
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  • In previous study, we found that the chemokine receptor 9 (CCR9) was highly expressed on CD4+ T cells from patients with T-cell lineage acute lymphocytic leukemia (T-ALL) and mediated leukemia cell infiltration and metastasis.
  • Combined use of interleukin 2 (IL-2) and IL-4 promoted the internalization of CCR9 and therefore attenuated leukemia cell infiltration and metastasis.
  • In this study, we preliminarily investigated the mechanism of internalization of CCR9 on MOLT4 cell model (a human leukemia T-cell line, naturally expresses CCR9) and found that IL-2 upregulated the cell surface expression of IL-4Ralpha (CD124) greatly, whereas IL-4 had no significant influence on alpha (CD25) and beta subunits (CD122) of IL-2R.
  • Furthermore, GRK2 was upregulated and translocated to cell membrane in IL-2 and IL-4 treated cells which indicated that PKC could be a prerequisite for GRK2 activity.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / metabolism. Flow Cytometry. G-Protein-Coupled Receptor Kinase 2 / genetics. G-Protein-Coupled Receptor Kinase 2 / metabolism. G-Protein-Coupled Receptor Kinase 3 / genetics. G-Protein-Coupled Receptor Kinase 3 / metabolism. G-Protein-Coupled Receptor Kinase 5 / genetics. G-Protein-Coupled Receptor Kinase 5 / metabolism. G-Protein-Coupled Receptor Kinases / genetics. G-Protein-Coupled Receptor Kinases / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Interleukin-2 Receptor beta Subunit / metabolism. Isoquinolines / pharmacology. Leukemia, T-Cell / genetics. Leukemia, T-Cell / metabolism. Leukemia, T-Cell / pathology. Protein Kinase Inhibitors / pharmacology. RNA Interference. Receptors, Interleukin-2 / metabolism. Receptors, Interleukin-4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sulfonamides / pharmacology

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  • (PMID = 19567201.001).
  • [ISSN] 2042-0226
  • [Journal-full-title] Cellular & molecular immunology
  • [ISO-abbreviation] Cell. Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CC chemokine receptor 9; 0 / Interleukin-2; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-2 Receptor beta Subunit; 0 / Isoquinolines; 0 / Protein Kinase Inhibitors; 0 / Receptors, CCR; 0 / Receptors, Interleukin-2; 0 / Receptors, Interleukin-4; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 207137-56-2 / Interleukin-4; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.15 / ADRBK1 protein, human; EC 2.7.11.15 / ADRBK2 protein, human; EC 2.7.11.15 / G-Protein-Coupled Receptor Kinase 2; EC 2.7.11.15 / G-Protein-Coupled Receptor Kinase 3; EC 2.7.11.16 / G-Protein-Coupled Receptor Kinase 5; EC 2.7.11.16 / G-Protein-Coupled Receptor Kinases; EC 2.7.11.16 / G-protein-coupled receptor kinase 6; EC 2.7.11.16 / GRK5 protein, human
  • [Other-IDs] NLM/ PMC4003061
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94. Suzumiya J, Ohshima K, Tamura K, Karube K, Uike N, Tobinai K, Gascoyne RD, Vose JM, Armitage JO, Weisenburger DD, International Peripheral T-Cell Lymphoma Project: The International Prognostic Index predicts outcome in aggressive adult T-cell leukemia/lymphoma: analysis of 126 patients from the International Peripheral T-Cell Lymphoma Project. Ann Oncol; 2009 Apr;20(4):715-21
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  • [Title] The International Prognostic Index predicts outcome in aggressive adult T-cell leukemia/lymphoma: analysis of 126 patients from the International Peripheral T-Cell Lymphoma Project.
  • BACKGROUND: The International Peripheral T-cell Lymphoma Project was organized to better understand the T-cell and natural killer (NK) cell lymphomas, and our task is to present the clinicopathologic correlations and therapeutic results for adult T-cell leukemia/lymphoma (ATL).
  • PATIENTS AND METHODS: Among 1153 patients with T-cell or NK cell lymphomas, 126 patients (9.6%) with ATL were represented in this project.
  • All were categorized as aggressive ATL, i.e. acute or lymphoma type, and 87% fell into the lymphoma type.
  • CONCLUSION: Patients with aggressive ATL have a poor clinical outcome and the IPI is a useful model for predicting outcome in ATL of the lymphoma type.

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  • (PMID = 19150954.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Investigator] Savage K; Connors J; Gascoyne R; Chhanabhai M; Wilson W; Jaffe E; Armitage J; Vose J; Weisenburger D; Anderson J; Ullrich F; Bast M; Hochberg E; Harris N; Levine A; Nathwani B; Miller T; Rimsza L; Montserrat E; Lopez-Guillermo A; Campo E; Cuadros M; Alvarez Ferreira J; Martinez Delgado B; Holte H; Delabie J; Rüdiger T; Müller-Hermelink K; Reimer P; Adam P; Wilhelm M; Schmitz N; Nerl C; MacLennan KA; Zinzani PL; Pileri S; Federico M; Bellei M; Coiffier B; Berger F; Tanin I; Wannakrairot P; Au W; Liang R; Loong F; Rajan S; Sng I; Tobinai K; Matsuno Y; Morishima Y; Nakamura S; Seto M; Tanimoto M; Yoshino T; Suzumiya J; Ohshima K; Kim WS; Ko YH
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95. Komori K, Hasegawa A, Kurihara K, Honda T, Yokozeki H, Masuda T, Kannagi M: Reduction of human T-cell leukemia virus type 1 (HTLV-1) proviral loads in rats orally infected with HTLV-1 by reimmunization with HTLV-1-infected cells. J Virol; 2006 Aug;80(15):7375-81
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  • [Title] Reduction of human T-cell leukemia virus type 1 (HTLV-1) proviral loads in rats orally infected with HTLV-1 by reimmunization with HTLV-1-infected cells.
  • Human T-cell leukemia virus type 1 (HTLV-1) persistently infects humans, and the proviral loads that persist in vivo vary widely among individuals.
  • Elevation in the proviral load is associated with serious HTLV-1-mediated diseases, such as adult T-cell leukemia and HTLV-1-associated myelopathy/tropical spastic paraparesis.
  • However, it remains controversial whether HTLV-1-specific T-cell immunity can control HTLV-1 in vivo.
  • We previously reported that orally HTLV-1-infected rats showed insufficient HTLV-1-specific T-cell immunity that coincided with elevated levels of the HTLV-1 proviral load.
  • In the present study, we found that individual HTLV-1 proviral loads established in low-responding hosts could be reduced by the restoration of HTLV-1-specific T-cell responses.
  • Despite the T-cell unresponsiveness for HTLV-1 in orally infected rats, an allogeneic mixed lymphocyte reaction in the splenocytes and a contact hypersensitivity response in the skin of these rats were comparable with those of naive rats.
  • HTLV-1-specific T-cell response in orally HTLV-1-infected rats could be restored by subcutaneous reimmunization with mitomycin C (MMC)-treated syngeneic HTLV-1-transformed cells.
  • Similar T-cell immune conversion could be reproduced in orally HTLV-1-infected rats by subcutaneous inoculation with MMC-treated primary T cells from syngeneic orally HTLV-1-infected rats.
  • The present results indicate that, although HTLV-1-specific T-cell unresponsiveness is an underlying risk factor for the propagation of HTLV-1-infected cells in vivo, the risk may potentially be reduced by reimmunization, for which autologous HTLV-1-infected cells are a candidate immunogen.
  • [MeSH-major] HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / physiology. Immunization. Viral Load

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  • [Cites] J Virol. 1999 Dec;73(12):10289-95 [10559346.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):237-43 [2303290.001]
  • [Cites] J Immunol. 2000 Jul 1;165(1):263-70 [10861060.001]
  • [Cites] J Virol. 2000 Oct;74(20):9610-6 [11000233.001]
  • [Cites] Immunity. 2001 Jan;14(1):69-79 [11163231.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Int J Cancer. 2001 Feb 15;91(4):497-9 [11251972.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):207-17 [11325603.001]
  • [Cites] Proc Biol Sci. 2001 Jun 22;268(1473):1215-21 [11410146.001]
  • [Cites] J Neurovirol. 2001 Jun;7(3):228-34 [11517397.001]
  • [Cites] AIDS Res Hum Retroviruses. 2001 Sep 1;17(13):1273-7 [11559427.001]
  • [Cites] J Virol. 2001 Dec;75(23):11515-25 [11689633.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] J Virol. 2003 Mar;77(5):2956-63 [12584320.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Leukemia. 2004 Jan;18(1):126-32 [14574331.001]
  • [Cites] Toxicology. 2004 Apr 1;197(1):57-66 [15003334.001]
  • [Cites] Oncogene. 1996 Jun 6;12(11):2419-23 [8649783.001]
  • [Cites] J Immunol. 1996 Aug 1;157(3):1288-96 [8757637.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S199-203 [8797724.001]
  • [Cites] J Acquir Immune Defic Syndr. 1990;3(10):1006-9 [2398453.001]
  • [Cites] Arch Dermatol Res. 1990;282(5):318-24 [2121107.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] J Neurol Sci. 1990 Dec;100(1-2):211-6 [1982449.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] Virology. 1992 Jun;188(2):628-36 [1374983.001]
  • [Cites] Int J Cancer. 1993 Jun 19;54(4):582-8 [8514449.001]
  • [Cites] Lancet. 1993 Dec 11;342(8885):1447-50 [7902480.001]
  • [Cites] Int J Cancer. 1994 Feb 1;56(3):337-40 [8314320.001]
  • [Cites] Science. 1996 Apr 5;272(5258):74-9 [8600540.001]
  • [Cites] Annu Rev Immunol. 1997;15:15-37 [9143680.001]
  • [Cites] Scand J Immunol. 1997 Sep;46(3):225-9 [9315108.001]
  • [Cites] Int J Cancer. 1998 Jul 17;77(2):188-92 [9650550.001]
  • [Cites] J Virol. 1998 Sep;72(9):7289-93 [9696824.001]
  • [Cites] J Exp Med. 1999 Mar 1;189(5):779-86 [10049941.001]
  • [Cites] J Virol. 1999 Aug;73(8):6436-43 [10400737.001]
  • [Cites] Int J Cancer. 2005 Mar 20;114(2):257-67 [15551352.001]
  • [Cites] Viral Immunol. 2004;17(4):604-8 [15671758.001]
  • [Cites] Immunol Rev. 2005 Aug;206:232-59 [16048553.001]
  • [Cites] Int Immunol. 2006 Feb;18(2):269-77 [16361311.001]
  • [Cites] Int J Cancer. 2004 Jul 1;110(4):621-5 [15122598.001]
  • [Cites] J Immunol. 2004 Oct 15;173(8):5121-9 [15470056.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Gan. 1982 Apr;73(2):341-4 [6981536.001]
  • [Cites] J Immunol. 1983 Jun;130(6):2942-6 [6189906.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] J Immunol. 1984 Aug;133(2):1037-41 [6203964.001]
  • [Cites] Jpn J Cancer Res. 1985 Jun;76(6):474-80 [2991060.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Int J Cancer. 1989 Jun 15;43(6):1061-4 [2732000.001]
  • [Cites] J Neuroimmunol. 2000 Jan 24;102(2):208-15 [10636490.001]
  • (PMID = 16840318.001).
  • [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 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1563733
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96. Komuro T, Okamoto S: Pure intracerebral mass lesion of adult T-cell leukemia/lymphoma--case report. Neurol Med Chir (Tokyo); 2010;50(6):492-4
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  • [Title] Pure intracerebral mass lesion of adult T-cell leukemia/lymphoma--case report.
  • A 48-year-old female presented with a rare case of adult T-cell leukemia/lymphoma (ATL) occurring as only intracerebral mass lesion manifesting as progressively worsening headaches, transient mild weakness of the left lower extremity, bilateral papilledema, and left homonymous hemianopsia.
  • The patient underwent gross total removal, and the histological diagnosis was intracerebral ATL.
  • Intracerebral ATL should be considered in the differential diagnosis of intracerebral mass without leukemia or systemic lymphoma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Occipital Lobe / pathology

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  • (PMID = 20587977.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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97. Larousserie F, Bardel E, Pflanz S, Arnulf B, Lome-Maldonado C, Hermine O, Brégeaud L, Perennec M, Brousse N, Kastelein R, Devergne O: Analysis of interleukin-27 (EBI3/p28) expression in Epstein-Barr virus- and human T-cell leukemia virus type 1-associated lymphomas: heterogeneous expression of EBI3 subunit by tumoral cells. Am J Pathol; 2005 Apr;166(4):1217-28
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  • [Title] Analysis of interleukin-27 (EBI3/p28) expression in Epstein-Barr virus- and human T-cell leukemia virus type 1-associated lymphomas: heterogeneous expression of EBI3 subunit by tumoral cells.
  • Interleukin (IL)-27 is a novel heterodimeric cytokine of the IL-12 family that is composed of two subunits, Epstein-Barr virus (EBV)-induced gene 3 (EBI3) and p28.
  • EBI3 is expressed at high levels in EBV-transformed B-cell lines and is induced in vitro by the EBV oncogene LMP1 in a nuclear factor (NF)-kappaB-dependent manner.
  • We show here that EBI3 expression is up-regulated in human T-cell leukemia virus type 1 (HTLV-1)-infected cell lines and IL-2-dependent leukemic cells from adult T-cell leukemia/lymphoma (ATL) patients, compared to normal activated T cells.
  • EBI3 expression was decreased in HTLV-1-transformed cells after treatment with the NF-kappaB inhibitor BAY11-7082 and was induced in Jurkat cells by expression of HTLV-1 wild-type Tax oncoprotein, but not by the Tax mutant M22, which is defective for NF-kappaB activation.
  • In situ analysis of EBI3 and p28 expression in Hodgkin's lymphomas (HLs), in various EBV-associated lymphoproliferative disorders (LPDs) (including post-transplant LPDs and nasal-type NK/T-cell lymphomas), and in ATL showed that EBI3 was expressed by neoplastic cells in all cases of HL and of LMP1-positive EBV-associated LPD, at variable levels in ATL cases, but rarely in control T-cell lymphomas.
  • In contrast, in all lymphomas tested, no or few tumoral cells expressed p28.
  • Consistent with these data, no significant p28 or IL-27 expression was detected in HL-derived cell lines, or in EBV- or HTLV-1-transformed cell lines.
  • [MeSH-major] Epstein-Barr Virus Infections / metabolism. Interleukins / biosynthesis. Lymphoma / virology. Tumor Virus Infections / metabolism
  • [MeSH-minor] Blotting, Western. Deltaretrovirus / metabolism. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Herpesvirus 4, Human / metabolism. Humans. Immunohistochemistry. In Situ Hybridization. Jurkat Cells. NF-kappa B / metabolism

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  • [Cites] Cancer Cell. 2004 Apr;5(4):353-64 [15093542.001]
  • [Cites] J Virol. 2004 Apr;78(8):4108-19 [15047827.001]
  • [Cites] Genes Dev. 1990 Nov;4(11):1875-85 [2276622.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Int J Cancer. 1994 Jun 1;57(5):760-4 [8194885.001]
  • [Cites] J Virol. 1996 Feb;70(2):1143-53 [8551575.001]
  • [Cites] Int J Cancer. 1996 Mar 28;66(1):18-23 [8608960.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 28;94(22):12041-6 [9342359.001]
  • [Cites] J Virol. 1998 Oct;72(10):7900-8 [9733827.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Exp Hematol. 1999 Jul;27(7):1168-75 [10390192.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6959-64 [10602470.001]
  • [Cites] J Exp Med. 2000 Jan 17;191(2):207-12 [10637266.001]
  • [Cites] Nature. 2000 Oct 19;407(6806):916-20 [11057672.001]
  • [Cites] Hum Pathol. 2000 Dec;31(12):1482-90 [11150373.001]
  • [Cites] J Clin Invest. 2001 Jan;107(2):143-51 [11160127.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):259-70 [11325606.001]
  • [Cites] J Biol Chem. 2001 May 25;276(21):18579-90 [11279141.001]
  • [Cites] Immunity. 2001 Oct;15(4):569-78 [11672539.001]
  • [Cites] Am J Pathol. 2001 Nov;159(5):1763-76 [11696437.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1497-502 [11830667.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4283-97 [12036854.001]
  • [Cites] Immunity. 2002 Jun;16(6):779-90 [12121660.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] J Pathol. 2002 Nov;198(3):310-6 [12375263.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16951-6 [12482940.001]
  • [Cites] J Immunol. 2003 May 15;170(10):4886-90 [12734330.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Nat Rev Immunol. 2003 Oct;3(10):801-12 [14523386.001]
  • [Cites] J Interferon Cytokine Res. 2003 Sep;23(9):513-22 [14565860.001]
  • [Cites] J Immunol. 2003 Nov 15;171(10):5233-43 [14607924.001]
  • [Cites] Immunity. 2003 Nov;19(5):641-4 [14614851.001]
  • [Cites] Immunity. 2003 Nov;19(5):645-55 [14614852.001]
  • [Cites] Immunity. 2003 Nov;19(5):657-67 [14614853.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):15047-52 [14657353.001]
  • [Cites] J Pathol. 2004 Feb;202(2):164-71 [14743498.001]
  • [Cites] J Immunol. 2004 Feb 15;172(4):2225-31 [14764690.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):1152-6 [14871851.001]
  • [Cites] J Virol. 2004 Sep;78(17):9093-104 [15308705.001]
  • (PMID = 15793300.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C19orf10 protein, human; 0 / IL27 protein, human; 0 / Interleukins; 0 / NF-kappa B
  • [Other-IDs] NLM/ PMC1602381
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98. Barnes JA, Abramson JS: Adult T-cell leukemia/lymphoma: complexities in diagnosis and novel treatment strategies. Oncology (Williston Park); 2009 Dec;23(14):1267, 1270
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma: complexities in diagnosis and novel treatment strategies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Deltaretrovirus Antibodies / blood. Diagnosis, Differential. Emigrants and Immigrants. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Transplantation, Homologous. United States

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  • [CommentOn] Oncology (Williston Park). 2009 Dec;23(14):1250-6 [20120837.001]
  • (PMID = 20120839.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Deltaretrovirus Antibodies
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99. Kohno T, Yamada Y, Akamatsu N, Kamihira S, Imaizumi Y, Tomonaga M, Matsuyama T: Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells. Cancer Sci; 2005 Aug;96(8):527-33
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  • [Title] Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells.
  • Adult T-cell leukemia/lymphoma (ATLL) is a lymphoproliferative disorder caused by human T lymphotropic virus type 1 (HTLV-I).
  • Although ATLL cells display an activated helper/inducer T-cell phenotype, CD4+ and CD25+, they are known to exhibit strong immunosuppressive activity.
  • As regulatory T cells (Treg cells) express CD4+ and CD25+ molecules and possess potent immune response suppressive activity, we investigated a possible link between ATLL cells and Treg cells.
  • In primary ATLL cells, the expression levels of the Treg cell marker molecules Foxp3 and glucocorticoid-induced tumor necrosis factor receptor family related protein (GITR) were significantly higher than in those from healthy adults.
  • Furthermore, ATLL cells are unresponsive in vitro to concanavalin A stimulation and suppress the proliferation of normal T cells.
  • GITR mRNA expression was induced by the HTLV-I transactivator Tax, and GITR promoter analyses revealed that this induction depends on the kappaB site from -431 bp to -444 bp upstream of the putative transcription site.
  • Taken together, ATLL cells may originate from HTLV-I-infected Treg cells, and GITR seems to be involved in the progression to ATLL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Cell Division. Cell Line, Tumor. Concanavalin A. DNA-Binding Proteins / genetics. Forkhead Transcription Factors. Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Glucocorticoid-Induced TNFR-Related Protein. Humans. Lymphocyte Activation. Receptors, Nerve Growth Factor / genetics. Receptors, Tumor Necrosis Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16108835.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Gene Products, tax; 0 / Glucocorticoid-Induced TNFR-Related Protein; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF18 protein, human; 11028-71-0 / Concanavalin A
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100. Yang Y, Takeuchi S, Tsukasaki K, Yamada Y, Hata T, Mori N, Fukushima A, Seo H, Koeffler HP, Taguchi H: Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma. Leuk Res; 2005 Jan;29(1):47-51
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  • [Title] Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma.
  • We investigated methylation status of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma (ATL).
  • APC methylation was found in 15 of 31 (48%) primary samples, and 2 of 4 (50%) ATL cell lines.
  • Methylation of the APC gene occurred more frequently in acute ATL (12/21) (57%) than chronic ATL (1/8) (13%) (P = 0.03).
  • APC was not expressed in the APC-methylated ATL cell line ST1.
  • Demethylation with 5-azacytidine treatment restored APC expression in the ST1 cell line.
  • Our data show that hypermethylation of the APC gene is involved in the pathogenesis of ATL.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Azacitidine / pharmacology. Cell Line, Tumor. CpG Islands / genetics. Disease Progression. Humans. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Leuk Res. 2005 May;29(5):475-6 [15755498.001]
  • (PMID = 15541474.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; M801H13NRU / Azacitidine
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