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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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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. 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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  • (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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8. 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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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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11. 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


12. 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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13. 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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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes.
  • PURPOSE: Adult T-cell leukemia/lymphoma induced by human T-cell leukemia virus type 1 (HTLV-1) is usually a fatal lymphoproliferative malignant disease.
  • HTLV-1 Tax protein plays a critical role in HTLV-1-associated leukemogenesis and is an attractive target for vaccine development.
  • Although HTLV-1 Tax is the most dominant antigen for HTLV-1-specific CD8(+) CTLs in HTLV-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in HTLV-1 Tax protein have been described.
  • The aim of the present study was to study T-helper-cell responses to HTLV-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.
  • EXPERIMENTAL DESIGN: An MHC class II binding peptide algorithm was used to predict potential T-helper cell epitope peptides from HTLV-1 Tax.
  • We assessed the ability of the corresponding peptides to elicit helper T-cell responses by in vitro vaccination of purified CD4(+) T lymphocytes.
  • RESULTS: Peptides Tax(191-205) and Tax(305-319) were effective in inducing T-helper-cell responses.
  • Both these epitopes were found to be naturally processed by HTLV-1(+) T-cell lymphoma cells and by autologous antigen-presenting cells that were pulsed with HTLV-1 Tax(+) tumor lysates.
  • Notably, the two newly identified helper T-cell epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.
  • CONCLUSION: Our data suggest that HTLV-1 Tax protein could serve as tumor-associated antigen for CD4(+) helper T cells and that the present epitopes might be used for T-cell-based immunotherapy against tumors expressing HTLV-1.

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  • (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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15. 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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16. 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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17. 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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18. Nagai K, Jinnai I, Hata T, Usui T, Sasaki D, Tsukasaki K, Sugahara K, Hishikawa Y, Yamada Y, Tanaka Y, Koji T, Mano H, Kamihira S, Tomonaga M: Adhesion-dependent growth of primary adult T cell leukemia cells with down-regulation of HTLV-I p40Tax protein: a novel in vitro model of the growth of acute ATL cells. Int J Hematol; 2008 Dec;88(5):551-64
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  • [Title] Adhesion-dependent growth of primary adult T cell leukemia cells with down-regulation of HTLV-I p40Tax protein: a novel in vitro model of the growth of acute ATL cells.
  • In order to better understand the biology of adult T cell leukemia (ATL), we aimed to establish a novel method, which allows the primary growth of ATL cells using a co-culture system with murine bone marrow-derived stromal cells, MS-5.
  • ATL cells grew in close contact with MS-5 layers and formed so-called "cobblestone areas" (CAs) without the addition of IL-2.
  • In clinical samples, eight of ten (80.0%) cases of acute or lymphoma type ATL cells formed CAs.
  • The frequency of CA forming cells in ATL cells ranged from 0.03 to 1.04%.
  • The morphology, immunophenotyping, and DNA analysis indicated that cells composing CA were compatible with ATL cells, and clonally identical to primary CD4-positive ATL cells.
  • Furthermore, in ATL cells composing CA, the expression of p40Tax was down-regulated in transcriptional and translational level, while that of HTLV-I basic leucine zipper factor (HBZ) gene was comparable to the level of primary ATL cells, resembling expression pattern of proviral genes in in vivo ATL cells.
  • By microarray analysis, several genes which coded products involved in cell-cell interaction, and cellular survival and proliferation, were differentially expressed in ATL cells composing CA compared with primary samples.
  • In conclusion, our co-culture system allows for the first time the growth of primary ATL cells in vitro, and might be useful as an in vitro assay for biological and clinical studies to develop molecular targeting drugs against ATL.
  • [MeSH-major] Cell Proliferation. Down-Regulation. Gene Expression Regulation, Leukemic. Gene Products, tax / biosynthesis. Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / metabolism. Models, Biological
  • [MeSH-minor] Acute Disease. Animals. Cell Adhesion. Cell Line. Cell Survival. Coculture Techniques. Gene Expression Profiling. Humans. Interleukin-2 / pharmacology. Mice. Oligonucleotide Array Sequence Analysis. Tumor Cells, Cultured

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  • (PMID = 19043810.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / IL2 protein, human; 0 / Interleukin-2; 0 / tax protein, Human T-lymphotrophic virus 1
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19. 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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20. 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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  • (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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21. 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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  • (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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22. 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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  • (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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23. 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


24. 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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25. 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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26. 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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27. 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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  • (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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28. 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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29. 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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30. 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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31. 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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  • (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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32. Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y: CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells. J Biol Chem; 2010 May 14;285(20):15511-22
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  • [Title] CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
  • CADM1 encodes a multifunctional immunoglobulin-like cell adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
  • Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in adult T-cell leukemia-lymphoma (ATL) cells.
  • It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent clinical manifestations of ATL.
  • Amino acid sequence alignment revealed that Tiam1 (T-lymphoma invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-associated guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
  • In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as ATL cell lines.
  • Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in ATL patients.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Immunoglobulins / metabolism. Leukemia, T-Cell / pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Adhesion Molecules. Cell Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid

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  • (PMID = 20215110.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2865322
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33. Sugita S, Takase H, Yoshida T, Sugamoto Y, Watanabe T, Mochizuki M: Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion. Br J Ophthalmol; 2006 Sep;90(9):1204-6
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  • [Title] Intraocular soluble IL-2 receptor alpha in a patient with adult T cell leukaemia with intraocular invasion.
  • [MeSH-major] Biomarkers, Tumor / analysis. Eye / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / immunology. Receptors, Interleukin-2 / analysis

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

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19767100.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Transcription Factor AP-1; 0 / tax protein, Human T-lymphotrophic virus 1; 106441-73-0 / Osteopontin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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35. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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36. Peloponese JM Jr, Yeung ML, Jeang KT: Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation. Immunol Res; 2006 Jan;34(1):1-12
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  • [Title] Modulation of nuclear factor-ϰB by human T cell leukemia virus type 1 tax protein : Implications for oncogenesis and inflammation.
  • Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).
  • HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.

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  • (PMID = 27519575.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Adult T cell leukemia (ATL) / HTLV-1 Tax / Human T cell leukemia virus (HTLV-1) / IKK / Inflammation / NF-ϰB / NIK
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37. Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R: Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut. CMAJ; 2006 Sep 12;175(6):579
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  • [Title] Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / ethnology
  • [MeSH-minor] Adult. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic

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

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

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  • (PMID = 16474151.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Gene Products, rev; 0 / HIV Core Protein p24; 0 / Tumor Suppressor Proteins; 0 / rev Gene Products, Human Immunodeficiency Virus; 3G6A5W338E / Caffeine; EC 1.13.12.- / Luciferases; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC1395391
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40. Yoshida M, Satou Y, Yasunaga J, Fujisawa J, Matsuoka M: Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene. J Virol; 2008 Oct;82(19):9359-68
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  • [Title] Transcriptional control of spliced and unspliced human T-cell leukemia virus type 1 bZIP factor (HBZ) gene.
  • The human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) gene is encoded by the minus strand of the HTLV-1 provirus and transcribed from the 3' long terminal repeat (LTR).
  • We compared the functions of the proteins derived from the sHBZ and usHBZ transcripts. sHBZ showed a stronger suppression of Tax-mediated transcriptional activation through the 5' LTR than did usHBZ; the level of suppression correlated with the level of protein produced.
  • The expression of sHBZ had a growth-promoting function in a T-cell line, while usHBZ expression did not.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / chemistry. Human T-lymphotropic virus 1 / genetics. Sp1 Transcription Factor / metabolism. Transcription, Genetic. Viral Proteins / genetics. Viral Proteins / physiology
  • [MeSH-minor] Alternative Splicing. Base Sequence. Cell Proliferation. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Humans. Molecular Sequence Data. Promoter Regions, Genetic. RNA, Viral / metabolism. Terminal Repeat Sequences

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  • (PMID = 18653454.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Viral; 0 / Sp1 Transcription Factor; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2546946
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41. Sagara Y, Inoue Y, Sagara Y, Kashiwagi S: Involvement of molecular mimicry between human T-cell leukemia virus type 1 gp46 and osteoprotegerin in induction of hypercalcemia. Cancer Sci; 2009 Mar;100(3):490-6
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  • [Title] Involvement of molecular mimicry between human T-cell leukemia virus type 1 gp46 and osteoprotegerin in induction of hypercalcemia.
  • Human T-cell leukemia virus type-1 (HTLV-1) causes adult T-cell leukemia/lymphoma (ATL), frequently associated with hypercalcemia and bone destruction.
  • A positive correlation between the appearance of an antibody recognizing the central region (Asp197 to Leu216) on Gp46, gp46-197, and the severity of ATL has been demonstrated.
  • In rats, femoral growth inhibition by the gp46-197 peptide was restored by the coadministration of recombinant human OPG.
  • Improvement by OPG in the adverse effect indicates that the central region of HTLV-1 Gp46 acts as an antagonist for OPG and leads to hypercalcemia.
  • [MeSH-major] Gene Products, env / immunology. HTLV-I Antibodies / immunology. Hypercalcemia / etiology. Leukemia-Lymphoma, Adult T-Cell / immunology. Molecular Mimicry / immunology. Osteoprotegerin / immunology. Retroviridae Proteins, Oncogenic / immunology

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  • (PMID = 19134004.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, env; 0 / HTLV-I Antibodies; 0 / Osteoprotegerin; 0 / Retroviridae Proteins, Oncogenic; 0 / gp46 protein, Human T-cell leukemia virus type I
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42. Kress AK, Schneider G, Pichler K, Kalmer M, Fleckenstein B, Grassmann R: Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1. J Virol; 2010 Sep;84(17):8732-42
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  • [Title] Elevated cyclic AMP levels in T lymphocytes transformed by human T-cell lymphotropic virus type 1.
  • Human T-cell lymphotropic virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), transforms CD4(+) T cells to permanent growth through its transactivator Tax.
  • HTLV-1-transformed cells share phenotypic properties with memory and regulatory T cells (T-reg).
  • This led us to determine cAMP levels in HTLV-1-transformed cells.
  • We found elevated cAMP concentrations as a consistent feature of all HTLV-1-transformed cell lines, including in vitro-HTLV-1-transformed, Tax-transformed, and patient-derived cells.
  • We found specific downregulation of the cAMP-degrading phosphodiesterase 3B (PDE3B) in HTLV-1-transformed cells, which was independent of Tax in transient expression experiments.
  • Overexpression of PDE3B led to a decrease of cAMP in HTLV-1-transformed cells.
  • Decreased expression of PDE3B was associated with inhibitory histone modifications at the PDE3B promoter and the PDE3B locus.
  • This shows that HTLV-1-transformed cells assume biological features of long-lived T-cell populations that potentially contribute to viral persistence.
  • [MeSH-major] Cell Transformation, Viral. Cyclic AMP / metabolism. HTLV-I Infections / metabolism. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism
  • [MeSH-minor] Cell Line, Transformed. Cells, Cultured. Cyclic Nucleotide Phosphodiesterases, Type 3 / genetics. Cyclic Nucleotide Phosphodiesterases, Type 3 / metabolism. Gene Products, tax / genetics. Gene Products, tax / metabolism. Humans. T-Lymphocytes / metabolism. T-Lymphocytes / virology

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  • (PMID = 20573814.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE17718
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; E0399OZS9N / Cyclic AMP; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 3; EC 3.1.4.17 / PDE3B protein, human
  • [Other-IDs] NLM/ PMC2918996
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43. Masutani H, Ueda S, Yodoi J: The thioredoxin system in retroviral infection and apoptosis. Cell Death Differ; 2005 Aug;12 Suppl 1:991-8
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  • Human thioredoxin (TRX) was first identified in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and is associated with the pathophysiology of retroviral infections.
  • Thioredoxin binding protein-2/vitamin D(3) upregulated protein 1 is a growth suppressor and its expression is suppressed in HTLV-I-transformed cells.
  • Studies of these molecules of the TRX system provide novel insights into the apoptosis associated with retroviral diseases.
  • [MeSH-minor] Animals. Glutathione / metabolism. HIV Infections / metabolism. HTLV-I Infections / metabolism. Humans. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Proteins / metabolism. Peroxidases / metabolism. Peroxiredoxins

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

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  • (PMID = 18223255.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI 056404; United States / NIDDK NIH HHS / DK / R21 DK 072134
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Gene Products, tax; 0 / HSP90 Heat-Shock Proteins; 0 / Multiprotein Complexes; 0 / NF-kappa B; 0 / Recombinant Proteins; 0 / YopP protein, Yersinia; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.3.16 / Phosphoprotein Phosphatases
  • [Other-IDs] NLM/ PMC2397464
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45. Chiba K, Hashino S, Izumiyama K, Toyoshima N, Suzuki S, Kurosawa M, Asaka M: Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia. Int J Lab Hematol; 2009 Jun;31(3):368-71
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  • [Title] Multiple osteolytic bone lesions with high serum levels of interleukin-6 and CCL chemokines in a patient with adult T cell leukemia.
  • A 37-year-old woman was diagnosed as having chronic adult T-cell leukemia (ATL) of the skin by a skin biopsy and human T-cell leukemia virus type-1 serology at our hospital in August 1992.
  • The skin lesions of ATL were improved by treatment with psoralen ultraviolet ray A.
  • [MeSH-major] Chemokines / blood. Interleukin-6 / blood. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / complications. Osteolysis / blood. Osteolysis / etiology
  • [MeSH-minor] Adult. Chronic Disease. Fatal Outcome. Female. Humans

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

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  • (PMID = 20463074.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / APOBEC3G protein, human; EC 3.5.4.5 / Cytidine Deaminase
  • [Other-IDs] NLM/ PMC2898234
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47. Mizobe T, Tsukada J, Higashi T, Mouri F, Matsuura A, Tanikawa R, Minami Y, Yoshida Y, Tanaka Y: Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells. Exp Hematol; 2007 Dec;35(12):1812-22
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  • [Title] Constitutive association of MyD88 to IRAK in HTLV-I-transformed T cells.
  • OBJECTIVE: Constitutive activation of nuclear factor (NF)-kappaB is a common feature of human T-cell leukemia virus type I (HTLV-I)-transformed T cells.
  • Inhibition of NF-kappaB activity reduces cell growth and induces apoptosis of HTLV-I-transformed T cells, suggesting a central role of NF-kappaB in their proliferation and survival.
  • In this study, we investigated whether MyD88, an adaptor protein of Toll-like receptor (TLR) signaling, contributes to constitutive NF-kappaB activation in HTLV-I-transformed T cells.
  • MATERIALS AND METHODS: Activation status of MyD88 and interleukin (IL)-1R-associated kinase 1 (IRAK1) in HTLV-I-transformed human T cells, MT2, MT4, and HUT102 was examined by using Western blot and immunoprecipitation.
  • An expression vector encoding a dominant negative MyD88 with a deletion of its death domain (MyD88dn) was transfected into MT2 cells to evaluate roles of MyD88 in spontaneous activation of cytokine gene promoters and transcription factors, proliferation, and apoptosis in HTLV-I-transformed T cells.
  • RESULTS: Constitutive association of MyD88 with IRAK1 was observed in all three of HTLV-I-transformed T cells, but not in HTLV-I-negative T cells, such as Jurkat, HUT78, and MOLT4.
  • HTLV-I Tax enhanced TLR expression and synergistically activated NF-kappaB with wild-type MyD88.
  • CONCLUSION: Our results show a novel pathway in NF-kappaB activation in HTLV-I-transformed T cells and further demonstrate a critical role of MyD88 in their dysregulated gene activation, survival, and proliferation.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Interleukin-1 Receptor-Associated Kinases / metabolism. Myeloid Differentiation Factor 88 / metabolism
  • [MeSH-minor] Base Sequence. Cell Line, Transformed. Cell Transformation, Viral. DNA Primers. Humans. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / metabolism

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

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

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

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  • (PMID = 17984755.001).
  • [ISSN] 0038-4348
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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51. Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N: Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature. Leuk Lymphoma; 2009 Feb;50(2):187-95
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  • [Title] Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
  • Extranodal adult T-cell leukemia/lymphoma (ATLL) of the head and neck is a rare disease.
  • We studied the clinicopathological features of nine patients with ATLL involving extranodal head and neck sites and conducted a literature review.
  • Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large cell-type.
  • Five patients with localised disease showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
  • Patients with localised disease documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
  • ATLL should be included in the differential diagnosis of extranodal head and neck lymphoma.
  • Localised extranodal ATLL of the head and neck may exhibit indolent clinical behaviours.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):148-9 [19235009.001]
  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):150-1 [19235010.001]
  • (PMID = 19197730.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
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52. Janik JE, Morris JC: Survivin(g) adult T-cell leukemia/lymphoma. Oncology (Williston Park); 2009 Dec;23(14):1256, 1261, 1266
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  • [Title] Survivin(g) adult T-cell leukemia/lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / genetics. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / therapy. Microtubule-Associated Proteins / genetics
  • [MeSH-minor] Adult. Female. Gene Expression Profiling. Humans. Inhibitor of Apoptosis Proteins. Male. Transplantation, Homologous

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

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  • (PMID = 19438598.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2691974
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54. Mizuguchi M, Asao H, Hara T, Higuchi M, Fujii M, Nakamura M: Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells. J Biol Chem; 2009 Sep 18;284(38):25501-11
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  • [Title] Transcriptional activation of the interleukin-21 gene and its receptor gene by human T-cell leukemia virus type 1 Tax in human T-cells.
  • At the incipient stages of the development of adult T-cell leukemia, T-cells infected with human T-cell leukemia virus type 1 (HTLV-1) suffer disregulation in cell growth caused by aberrant expression of host genes by the HTLV-1 transactivator protein Tax (Tax1).
  • Tax1-mediated growth promotion is thought to result from, at least in part, up-regulation of genes for growth factors and their receptors that induce T-cell growth.
  • In the present study, we demonstrate that Tax1 transactivates the interleukin-21 (IL-21) and its receptor (IL-21R) genes in human T-cells.
  • Chromatin immunoprecipitation assay and gel mobility shift assay exhibited that the IL-21 promoter elements bound transcription factors AP-1 and NF-kappaB, and the IL-21R promoter elements were associated with AP-1 and interferon regulatory factor.
  • The related virus HTLV-2 with Tax2 similar to Tax1 is known not to be pathogenic.
  • The study suggests insights into cytokine-dependent aberrant growth of HTLV-1-infected T-cells and the molecular basis of different pathogenicity between HTLV-1 and HTLV-2.
  • [MeSH-major] CD4-Positive T-Lymphocytes / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Interleukin-21 Receptor alpha Subunit / biosynthesis. Interleukins / biosynthesis. Response Elements. Transcriptional Activation
  • [MeSH-minor] Adenoviridae. HTLV-I Infections / genetics. HTLV-I Infections / metabolism. Human T-lymphotropic virus 2 / genetics. Human T-lymphotropic virus 2 / metabolism. Human T-lymphotropic virus 2 / pathogenicity. Humans. Jurkat Cells. NF-kappa B / genetics. NF-kappa B / metabolism. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transduction, Genetic

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  • (PMID = 19617351.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / IL21R protein, human; 0 / Interleukin-21 Receptor alpha Subunit; 0 / Interleukins; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 0 / interleukin-21; 0 / tax protein, Human T-lymphotrophic virus 1; 0 / tax protein, Human T-lymphotrophic virus 2
  • [Other-IDs] NLM/ PMC2757951
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55. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Nair R, Sengar M, Nair C: Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia. Indian J Cancer; 2010 Apr-Jun;47(2):189-93
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  • [Title] Immunophenotyping of mature T/NK cell neoplasm presenting as leukemia.
  • INTRODUCTION: Mature T/NK cell lymphomas (MTNKL) presenting as leukemia are rare and show considerable overlapping of clinical, morphological and immunophenotypic features.
  • MATERIALS AND METHODS: We reviewed 380 consecutive cases of mature lymphoid neoplasm that presented as leukemia and were diagnosed on morphology and immunophenotyping of bone marrow and/or peripheral blood samples.
  • MTNKL constituted 4% (nine cases) of all mature lymphoid neoplasms presenting as leukemia.
  • It included four cases of T-large granular leukemia (T-LGL), two of T-cell prolymphocytic leukemia small cell variant (T-PLL), two of adult T-cell leukemia/lymphoma (ATLL) and one of primary cutaneous gamma delta T-cell lymphoma (PCGDTCL).
  • One case of T- PLL small cell variant showed CD4+/CD8- phenotype, while the other revealed CD4-/CD8+ phenotype.
  • Both cases of ATLL showed CD4+/CD8+/CD25+ phenotype.
  • TCRalpha/beta was performed in three cases of T-LGL and was positive in all.
  • CONCLUSION: Mature nodal T/NK cell neoplasms are rare and MTNKL presenting as leukemia are even rarer.
  • There is an overlap between the immunophenotypic profiles of different MTNKL subtypes and elaborate T/NK cell panels are required for their evaluation.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Prolymphocytic, T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Lymphoma, T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Bone Marrow / immunology. Bone Marrow / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 20448385.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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76. 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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77. 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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  • (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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78. 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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  • (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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79. 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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80. 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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81. 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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82. 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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83. 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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84. 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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  • (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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85. 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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86. 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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87. 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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88. 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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  • (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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89. 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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90. Kozako T, Yoshimitsu M, Fujiwara H, Masamoto I, Horai S, White Y, Akimoto M, Suzuki S, Matsushita K, Uozumi K, Tei C, Arima N: PD-1/PD-L1 expression in human T-cell leukemia virus type 1 carriers and adult T-cell leukemia/lymphoma patients. Leukemia; 2009 Feb;23(2):375-82
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  • [Title] PD-1/PD-L1 expression in human T-cell leukemia virus type 1 carriers and adult T-cell leukemia/lymphoma patients.
  • Adult T-cell leukemia/lymphoma (ATLL) develops after infection with human T-cell leukemia virus-1 (HTLV-1) after a long latency period.
  • To determine whether the PD-1/PD-L1 pathway could be involved in the establishment of persistent HTLV-1 infections and immune evasion of ATLL cells in patients, we examined PD-1/PD-L1 expression on cells from 27 asymptomatic HTLV-1 carriers (ACs) and 27 ATLL patients in comparison with cells from 18 healthy donors.
  • PD-1 expression on HTLV-1-specific CTLs from ACs and ATLL patients was dramatically elevated.
  • In addition, PD-1 expression was significantly higher on CD8+ T cells along with cytomegalovirus (CMV)- and Epstein-Barr virus (EBV)-specific CTLs in ATLL patients compared with ACs and control individuals.
  • Primary ATLL cells in 21.7% of ATLL patients expressed PD-L1, whereas elevated expression was not observed in cells from ACs.
  • Finally, in functional studies, we observed that an anti-PD-L1 antagonistic antibody upregulated HTLV-1-specific CD8+T-cell response.
  • These observations suggest that the PD-1/PD-L1 pathway plays a role in fostering persistent HTLV-1 infections, which may further ATLL development and facilitate immune evasion by ATLL cells.
  • [MeSH-major] Antigens, CD / analysis. Apoptosis Regulatory Proteins / analysis. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Antigens, CD274. CD8-Positive T-Lymphocytes / chemistry. CD8-Positive T-Lymphocytes / immunology. Case-Control Studies. Disease Progression. Human T-lymphotropic virus 1. Humans. Programmed Cell Death 1 Receptor. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18830259.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / Apoptosis Regulatory Proteins; 0 / CD274 protein, human; 0 / PDCD1 protein, human; 0 / Programmed Cell Death 1 Receptor
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91. 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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  • [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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92. 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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93. Yamamoto K, Utsunomiya A, Tobinai K, Tsukasaki K, Uike N, Uozumi K, Yamaguchi K, Yamada Y, Hanada S, Tamura K, Nakamura S, Inagaki H, Ohshima K, Kiyoi H, Ishida T, Matsushima K, Akinaga S, Ogura M, Tomonaga M, Ueda R: Phase I study of KW-0761, a defucosylated humanized anti-CCR4 antibody, in relapsed patients with adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma. J Clin Oncol; 2010 Mar 20;28(9):1591-8
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  • [Title] Phase I study of KW-0761, a defucosylated humanized anti-CCR4 antibody, in relapsed patients with adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma.
  • This phase I study assessed the safety, pharmacokinetics, recommended phase II dose and efficacy of KW-0761 in patients with relapsed CCR4-positive adult T-cell leukemia-lymphoma (ATL) or peripheral T-cell lymphoma (PTCL).
  • Other treatment-related grade 3 to 4 toxicities were lymphopenia (n = 10), neutropenia (n = 3), leukopenia (n = 2), herpes zoster (n = 1), and acute infusion reaction/cytokine release syndrome (n = 1).
  • CONCLUSION: KW-0761 was tolerated at all the dose levels tested, demonstrating potential efficacy against relapsed CCR4-positive ATL or PTCL.
  • [MeSH-major] Antibodies, Anti-Idiotypic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell, Peripheral / drug therapy. Receptors, CCR4 / antagonists & inhibitors

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  • [CommentIn] J Clin Oncol. 2010 Aug 10;28(23):e404-5; author reply e406 [20566994.001]
  • (PMID = 20177026.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Receptors, CCR4; 0 / mogamulizumab
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94. Geiger TR, Sharma N, Kim YM, Nyborg JK: The human T-cell leukemia virus type 1 tax protein confers CBP/p300 recruitment and transcriptional activation properties to phosphorylated CREB. Mol Cell Biol; 2008 Feb;28(4):1383-92
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  • [Title] The human T-cell leukemia virus type 1 tax protein confers CBP/p300 recruitment and transcriptional activation properties to phosphorylated CREB.
  • The human T-cell leukemia virus-encoded oncoprotein Tax is a potent activator of viral transcription.

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  • (PMID = 18070920.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA055035-14; United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA55035; United States / NCI NIH HHS / CA / R01 CA055035-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / Phosphoproteins; EC 2.3.1.48 / p300-CBP Transcription Factors
  • [Other-IDs] NLM/ PMC2258755
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95. Pattabiraman DR, Sun J, Dowhan DH, Ishii S, Gonda TJ: Mutations in multiple domains of c-Myb disrupt interaction with CBP/p300 and abrogate myeloid transforming ability. Mol Cancer Res; 2009 Sep;7(9):1477-86
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  • The c-myb proto-oncogene is a key regulator of hematopoietic cell proliferation and differentiation.
  • MYB mRNA is expressed at high levels in, and is required for the proliferation of, most human myeloid and acute lymphoid leukemias.
  • Recently, chromosomal translocation and genomic duplications of c-MYB have been identified in human T-cell acute leukemia.
  • Using both a novel myeloid cell line-based assay and a primary hematopoietic cell assay, we have shown that mutation of single residues in the transactivation domain important for CBP/p300 binding leads to complete loss of transforming ability.
  • Our results imply that multiple Myb domains influence its interaction with CBP/p300, highlight the importance of this interaction for myeloid transformation, and suggest an approach for molecular targeting of Myb in leukemia.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-myb / genetics. p300-CBP Transcription Factors / metabolism
  • [MeSH-minor] Animals. Cell Differentiation / genetics. Cell Growth Processes / genetics. Cell Line. Cells, Cultured. Hematopoietic Stem Cells / pathology. Hematopoietic Stem Cells / physiology. Humans. Mice. Mice, Inbred CBA. Mutagenesis. Polymerase Chain Reaction. Protein Binding. Protein Structure, Tertiary. Transcriptional Activation

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  • (PMID = 19737967.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb; EC 2.3.1.48 / p300-CBP Transcription Factors
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96. Molho-Pessach V, Lotem M: Viral carcinogenesis in skin cancer. Curr Probl Dermatol; 2007;35:39-51
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  • The skin is an organ in which direct contact with viruses, solar UV irradiation and increased susceptibility to immune suppression gather to support viral tumorigenesis.
  • Viruses transform keratinocytes by activation of cancer-promoting genes.
  • Decreased T-cell reactivity and lower number of antigen-presenting cells in the skin assist in viral escape and emergence of skin tumors.
  • Three pathogenic human viruses associated with skin neoplasms are described: human papilloma virus (HPV), Kaposi's sarcoma (KS)-associated herpesvirus and human T-cell leukemia virus type 1.
  • HPV was linked to squamous cell carcinoma (SCC) of the skin after its role in SCC of the cervix has been discovered.
  • The discovery of human herpesvirus 8 as the causative pathogen of KS was made following the AIDS epidemic, and its role in all clinical variants of this tumor was confirmed.
  • KS-associated herpesvirus exerts its tumorigenic effect through a wide repertoire of genes that regulate angiogenesis, inflammation, and cell cycle.
  • Human T-cell leukemia virus type 1 causes adult T-cell leukemia and is often associated with skin eruptions that share common features with cutaneous T-cell lymphoma.
  • In summary, studies of oncogenic viruses shed light on molecular mechanisms leading to tumor formation and aid in recognition of new pathways of carcinogenesis.
  • [MeSH-major] Herpesvirus 8, Human. Human T-lymphotropic virus 1. Papillomaviridae. Skin Neoplasms / virology
  • [MeSH-minor] Carcinoma, Squamous Cell / physiopathology. Carcinoma, Squamous Cell / virology. Cell Transformation, Neoplastic. Humans. Sarcoma, Kaposi / physiopathology. Sarcoma, Kaposi / virology

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  • (PMID = 17641489.001).
  • [ISSN] 1421-5721
  • [Journal-full-title] Current problems in dermatology
  • [ISO-abbreviation] Curr. Probl. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 69
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97. Nagy K, Marschalkó M, Kemény B, Horváth A: Localization of human T-cell lymphotropic virus-1 gag proviral sequences in dermato-immunological disorders with eosinophilia. Acta Microbiol Immunol Hung; 2005;52(3-4):385-96
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  • [Title] Localization of human T-cell lymphotropic virus-1 gag proviral sequences in dermato-immunological disorders with eosinophilia.
  • The mechanisms leading to the development of eosinophilia were investigated in 65 patients with immunodermatological disorders, including the role of eosinophilotactic cytokines and the possible involvement of human T-cell leukemia virus, HTLV.
  • HTLV-1 gag proviral sequences were revealed in two cases of lymphoproliferative disorders such as angiolymphoid hyperplasia with eosinophilia (ALHE) and CD4+ cutaneous lymphoma, respectively.
  • The possible indirect role of human retroviruses through induction of eosinophilic chemotactic cytokines is hypothesized.
  • [MeSH-major] Eosinophilia / virology. Gene Products, gag / chemistry. Human T-lymphotropic virus 1 / isolation & purification. Lymphoproliferative Disorders / virology. Proviruses / isolation & purification. Skin Diseases / virology. Skin Diseases, Vesiculobullous / virology
  • [MeSH-minor] Base Sequence. Chemokine CCL11. Chemokines, CC / blood. DNA, Viral / chemistry. Female. Genes, gag. Granulocyte-Macrophage Colony-Stimulating Factor / blood. HTLV-I Infections / complications. HTLV-I Infections / virology. Humans. Interleukin-5 / blood. Male. Sequence Analysis, DNA

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  • (PMID = 16400878.001).
  • [ISSN] 1217-8950
  • [Journal-full-title] Acta microbiologica et immunologica Hungarica
  • [ISO-abbreviation] Acta Microbiol Immunol Hung
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Chemokines, CC; 0 / DNA, Viral; 0 / Gene Products, gag; 0 / Interleukin-5; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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98. Sato H, Oka T, Shinnou Y, Kondo T, Washio K, Takano M, Takata K, Morito T, Huang X, Tamura M, Kitamura Y, Ohara N, Ouchida M, Ohshima K, Shimizu K, Tanimoto M, Takahashi K, Matsuoka M, Utsunomiya A, Yoshino T: Multi-step aberrant CpG island hyper-methylation is associated with the progression of adult T-cell leukemia/lymphoma. Am J Pathol; 2010 Jan;176(1):402-15
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  • [Title] Multi-step aberrant CpG island hyper-methylation is associated with the progression of adult T-cell leukemia/lymphoma.
  • However, little is known about the association of epigenetic abnormalities with multistep tumorigenic events in adult T cell leukemia/lymphoma (ATLL).
  • To determine whether epigenetic abnormalities induce the progression of ATLL, we analyzed the methylation profiles of the SHP1, p15, p16, p73, HCAD, DAPK, hMLH-1, and MGMT genes by methylation specific PCR assay in 65 cases with ATLL patients.
  • The number of CpG island methylated genes increased with disease progression and aberrant hypermethylation in specific genes was detected even in HTLV-1 carriers and correlated with progression to ATLL.
  • The CpG island methylator phenotype (CIMP) was observed most frequently in lymphoma type ATLL and was also closely associated with the progression and crisis of ATLL.
  • The present findings strongly suggest that the multistep accumulation of aberrant CpG methylation in specific target genes and the presence of CIMP are deeply involved in the crisis, progression, and prognosis of ATLL, as well as indicate the value of CpG methylation and CIMP for new diagnostic and prognostic biomarkers.
  • [MeSH-major] CpG Islands / genetics. DNA Methylation / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Base Sequence. Disease Progression. Gene Silencing. Genes, Neoplasm / genetics. Humans. Kaplan-Meier Estimate. Middle Aged. Models, Genetic. Molecular Sequence Data. Neoplasm Proteins / metabolism. Polymerase Chain Reaction