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

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

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  • (PMID = 17986383.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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3. Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K: Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines. Cancer Lett; 2007 Nov 18;257(2):206-15
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  • [Title] Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.
  • The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing HTLV-I-infected cells.
  • In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient ATL cell lines caused rapid death, whereas DHMEQ-treated mice survived.
  • Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted ATL cells.
  • These results demonstrate that DHMEQ has therapeutic efficacy on ATL cells, regardless of Tax expression.
  • [MeSH-major] Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency. Leukemia, T-Cell / prevention & control. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cell Line, Tumor. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism

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  • (PMID = 17764832.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin
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4. Saito M, Mori A, Irie T, Tanaka M, Morioka M, Uchiyama Y, Taukamoto E: [Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ]. Rinsho Ketsueki; 2009 Dec;50(12):1669-70
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  • [Title] [Picture in clinical hematology no. 41: PET/ CT findings in case of ATLL ].
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / radiography. Leukemia-Lymphoma, Adult T-Cell / radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed

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  • (PMID = 20068272.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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5. 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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6. 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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7. 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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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells.
  • Regulatory T (Treg) cells, which represent 5% to 10% of peripheral T cells, regulate the activities of T-cell subsets by performing immunosuppressive functions and thus preventing the development of autoimmune responses.
  • Recently, it has been demonstrated that the tumor cells in adult T-cell leukemia lymphomas can function as Treg, raising the question of whether any variant of primary cutaneous T-cell lymphoma may also express a regulatory phenotype.
  • We describe an extraordinary case of primary cutaneous T-cell lymphoma clinically characterized by protean cutaneous manifestations and histologically showing a pattern consistent with epidermotropic pleomorphic medium-/large-cell primary cutaneous T-cell lymphoma.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Forkhead Transcription Factors / immunology. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Regulatory / immunology


9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. Iwanaga M, Watanabe T, Utsunomiya A, Okayama A, Uchimaru K, Koh KR, Ogata M, Kikuchi H, Sagara Y, Uozumi K, Mochizuki M, Tsukasaki K, Saburi Y, Yamamura M, Tanaka J, Moriuchi Y, Hino S, Kamihira S, Yamaguchi K, Joint Study on Predisposing Factors of ATL Development investigators: Human T-cell leukemia virus type I (HTLV-1) proviral load and disease progression in asymptomatic HTLV-1 carriers: a nationwide prospective study in Japan. Blood; 2010 Aug 26;116(8):1211-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia virus type I (HTLV-1) proviral load and disease progression in asymptomatic HTLV-1 carriers: a nationwide prospective study in Japan.
  • Definitive risk factors for the development of adult T-cell leukemia (ATL) among asymptomatic human T-cell leukemia virus type I (HTLV-1) carriers remain unclear.
  • Recently, HTLV-1 proviral loads have been evaluated as important predictors of ATL, but a few small prospective studies have been conducted.
  • We prospectively evaluated 1218 asymptomatic HTLV-1 carriers (426 males and 792 females) who were enrolled during 2002 to 2008.
  • The proviral load at enrollment was significantly higher in males than females (median, 2.10 vs 1.39 copies/100 peripheral blood mononuclear cells [PBMCs]; P < .001), in those 40 to 49 and 50 to 59 years of age than that of those 40 years of age and younger (P = .02 and .007, respectively), and in those with a family history of ATL than those without the history (median, 2.32 vs 1.33 copies/100 PBMCs; P = .005).
  • During follow-up, 14 participants progressed to overt ATL.
  • None developed ATL among those with a baseline proviral load lower than approximately 4 copies.
  • Multivariate Cox analyses indicated that not only a higher proviral load, advanced age, family history of ATL, and first opportunity for HTLV-1 testing during treatment for other diseases were independent risk factors for progression of ATL.
  • [MeSH-major] HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. Viral Load / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers / analysis. Blotting, Southern. Carrier State. Child. DNA, Viral / genetics. Disease Progression. Female. Follow-Up Studies. Humans. Japan / epidemiology. Male. Middle Aged. Prognosis. Prospective Studies. Young Adult

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  • (PMID = 20448111.001).
  • [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 / Biomarkers; 0 / DNA, Viral
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12. Takatsuki K: Discovery of adult T-cell leukemia. Retrovirology; 2005;2:16
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  • [Title] Discovery of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) was first reported as a distinct clinical entity in 1977 in Japan.
  • The ATL cells are of mature T-helper phenotype and have a characteristic appearance with indented nuclei.
  • Central to the identification of the disease is a striking geographic clustering in southwestern Japan and the isolation of human T-cell lymphotropic virus type-1 (HTLV-1) from the cell lines of patients.
  • Several diseases were found to be related to HTLV-1 infection.
  • Moreover, it was noted that an immunodeficiency state may be induced by HTLV-1 infection.
  • In Japan, HTLV-1 carriers have been estimated to be 1.2 million, and more than 700 cases of ATL have been diagnosed each year.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / history
  • [MeSH-minor] Adult. History, 20th Century. Humans. Japan / epidemiology

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  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [CommentIn] Retrovirology. 2005;2:15 [15743525.001]
  • (PMID = 15743528.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC555581
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13. 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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14. Nakase K, Hara M, Kozuka T, Tanimoto K, Nawa Y: Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma. Bone Marrow Transplant; 2006 Jan;37(1):41-4
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  • [Title] Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a highly aggressive haematological malignancy.
  • More than 40 cases of ATLL treated by allogeneic bone marrow transplantation (BMT) from sibling donors have been reported, while there have been only a few cases of unrelated BMT for treatment of this disease.
  • We began performing allogeneic BMT from unrelated donors in 1999 to improve the outcome of ATLL patients with no suitable sibling donors.
  • Eight ATLL patients underwent unrelated BMT; five received the conventional conditioning regimen consisting of cyclophosphamide and total body irradiation, while three received a reduced-intensity preparative regimen.
  • Two patients died due to encephalopathy of unknown aetiology on days 10 and 35, and one patient died due to progression of ATLL 25 months after BMT.
  • Five patients are currently alive and disease-free at a median of 20 months after BMT.
  • Proviral human T-lymphotropic virus type-I (HTLV-I) DNA load in peripheral blood mononuclear cells (PBMCs) was assessed in four cases before and after BMT.
  • HTLV-I proviral DNA load was reduced significantly after transplantation.
  • Unrelated BMT is feasible for treatment of ATLL.
  • Further studies in a larger number of cases are required to determine the optimal conditioning regimen and stem cell source.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy. Living Donors. Transplantation Conditioning
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Histocompatibility Testing. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Retrospective Studies. Transplantation, Homologous. Whole-Body Irradiation / methods


15. 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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16. 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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17. 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
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  • [Other-IDs] NLM/ PMC1950877
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18. 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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19. Nicot C, Harrod RL, Ciminale V, Franchini G: Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions. Oncogene; 2005 Sep 5;24(39):6026-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.
  • The human T-cell leukemia/lymphoma virus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.
  • To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).
  • [MeSH-major] Human T-lymphotropic virus 1 / genetics. Viral Nonstructural Proteins / genetics

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  • (PMID = 16155609.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI058944; United States / NCI NIH HHS / CA / R01 CA106258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viral Nonstructural Proteins
  • [Number-of-references] 54
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20. Beltrán B, Palomino E, Quiñones P, Morales D, Cotrina E: [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature]. Rev Gastroenterol Peru; 2010 Apr-Jun;30(2):153-7
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  • [Title] [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature].
  • [Transliterated title] Leucemia/linfoma T del adulto gástrico: reporte de cuatro casos y revisión de la literatura.
  • Adult T-cell leukemia/lymphoma (ATLL) is an aggressive disease associated with human T-cell lymphotropic virus type-I (HTLV-I) with heterogeneous clinical presentation and outcomes.
  • We describe clinical and endoscopic findings of cases and review literature.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Stomach Neoplasms
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Prednisone / administration & dosage. Prevalence. Stomach Ulcer / etiology. Vincristine / administration & dosage

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  • (PMID = 20644608.001).
  • [ISSN] 1609-722X
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Peru
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VB0R961HZT / Prednisone; CHOEP protocol; CHOP protocol
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21. 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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22. Agbottah E, Yeh WI, Berro R, Klase Z, Pedati C, Kehn-Hall K, Wu W, Kashanchi F: Two specific drugs, BMS-345541 and purvalanol A induce apoptosis of HTLV-1 infected cells through inhibition of the NF-kappaB and cell cycle pathways. AIDS Res Ther; 2008 Jun 10;5:12
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  • [Title] Two specific drugs, BMS-345541 and purvalanol A induce apoptosis of HTLV-1 infected cells through inhibition of the NF-kappaB and cell cycle pathways.
  • Human T-cell leukemia virus type-1 (HTLV-1) induces adult T-cell leukemia/lymphoma (ATL/L), a fatal lymphoproliferative disorder, and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic progressive disease of the central nervous system after a long period of latent infection.
  • Although the mechanism of transformation and leukemogenesis is not fully elucidated, there is evidence to suggest that the viral oncoprotein Tax plays a crucial role in these processes through the regulation of several pathways including NF-kappaB and the cell cycle pathways.
  • The observation that NF-kappaB, which is strongly induced by Tax, is indispensable for the maintenance of the malignant phenotype of HTLV-1 by regulating the expression of various genes involved in cell cycle regulation and inhibition of apoptosis provides a possible molecular target for these infected cells.
  • To develop potential new therapeutic strategies for HTLV-1 infected cells, in this present study, we initially screened a battery of NF-kappaB and CDK inhibitors (total of 35 compounds) to examine their effects on the growth and survival of infected T-cell lines.
  • Two drugs namely BMS-345541 and Purvalanol A exhibited higher levels of growth inhibition and apoptosis in infected cell as compared to uninfected cells.
  • BMS-345541 inhibited IKKbeta kinase activity from HTLV-1 infected cells with an IC50 (the 50% of inhibitory concentration) value of 50 nM compared to 500 nM from control cells as measured by in vitro kinase assays.
  • The effects of Purvalanol A were associated with suppression of CDK2/cyclin E complex activity as previously shown by us.
  • Combination of both BMS-345541 and Purvalanol A showed a reduced level of HTLV-1 p19 Gag production in cell culture.
  • The apparent apoptosis in these infected cells were associated with increased caspase-3 activity and PARP cleavage.

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  • (PMID = 18544167.001).
  • [ISSN] 1742-6405
  • [Journal-full-title] AIDS research and therapy
  • [ISO-abbreviation] AIDS Res Ther
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI043894; United States / NIAID NIH HHS / AI / R21 AI065236
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2483717
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23. Tsukasaki K, Hermine O, Bazarbachi A, Ratner L, Ramos JC, Harrington W Jr, O'Mahony D, Janik JE, Bittencourt AL, Taylor GP, Yamaguchi K, Utsunomiya A, Tobinai K, Watanabe T: Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting. J Clin Oncol; 2009 Jan 20;27(3):453-9
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  • [Title] Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting.
  • Adult T-cell leukemia-lymphoma (ATL) is a distinct peripheral T-lymphocytic malignancy associated with a retrovirus designated human T-cell lymphotropic virus type I (HTLV-1).
  • The diversity in clinical features and prognosis of patients with this disease has led to its subclassification into the following four categories: acute, lymphoma, chronic, and smoldering types.
  • The chronic and smoldering subtypes are considered indolent and are usually managed with watchful waiting until disease progression, analogous to the management of some patients with chronic lymphoid leukemia (CLL) or other indolent histology lymphomas.
  • Patients with aggressive ATL generally have a poor prognosis because of multidrug resistance of malignant cells, a large tumor burden with multiorgan failure, hypercalcemia, and/or frequent infectious complications as a result of a profound T-cell immunodeficiency.
  • Under the sponsorship of the 13th International Conference on Human Retrovirology: HTLV, a group of ATL researchers joined to form a consensus statement based on established data to define prognostic factors, clinical subclassifications, and treatment strategies.
  • A set of response criteria specific for ATL reflecting a combination of those for lymphoma and CLL was proposed.
  • Clinical subclassification is useful but is limited because of the diverse prognosis among each subtype.
  • A treatment strategy based on the clinical subclassification and prognostic factors is suggested, including watchful waiting approach, chemotherapy, antiviral therapy, allogeneic hematopoietic stem-cell transplantation (alloHSCT), and targeted therapies.

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  • (PMID = 19064971.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Number-of-references] 61
  • [Other-IDs] NLM/ PMC2737379
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24. Ohkura S, Yamashita M, Ishida T, Babu PG, Koyanagi Y, Yamamoto N, Miura T, Hayami M: Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A. AIDS Res Hum Retroviruses; 2005 Apr;21(4):325-30
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  • [Title] Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A.
  • Seven isolates of human T cell leukemia virus type 1 (HTLV-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of HTLV-1 in the subcontinent.
  • The new Indian HTLV-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.
  • These results demonstrate that Indian HTLV-1s are genetically heterogeneous and include the most divergent strain of subgroup A.
  • On the basis of these results, we speculate that subgroup A HTLV- 1s may have been present for thousands of years in India.
  • [MeSH-major] HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Child. DNA, Viral / chemistry. Female. Humans. India. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics

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  • (PMID = 15943577.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY607576/ AY607577/ AY607578/ AY607579/ AY607580/ AY607581/ AY607582
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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25. Fujita A, Tomita N, Fujita H, Motohashi K, Hyo R, Yamazaki E, Hattori M, Fujisawa S, Kanamori H, Ogawa K, Motomura S, Kodama F, Ishigatsubo Y: Features of primary extranodal lymphoma in Kanagawa, a human T-cell leukemia virus type 1 nonendemic area in Japan. Med Oncol; 2009;26(1):49-54
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  • [Title] Features of primary extranodal lymphoma in Kanagawa, a human T-cell leukemia virus type 1 nonendemic area in Japan.
  • We sought to determine the frequency of primary extranodal lymphoma (ENL) and its characteristics in Kanagawa, a human T-cell leukemia virus type 1 (HTLV-1) nonendemic area in Japan.
  • Subjects were 847 newly diagnosed patients with malignant lymphoma at the Yokohama City University Hospital and 8 affiliated hospitals mainly located in Kanagawa prefecture from 1999 to 2005.
  • We compared the clinicopathological characteristics of primary ENL with primary nodal lymphoma (NL).
  • Among the 395 cases of primary ENL, diffuse large B-cell lymphoma (61.2%) was most frequently diagnosed, followed by extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (13.3%) and follicular lymphoma (5.6%).
  • The frequency of primary ENL is approximately 50% of the total lymphoma cases in Kanagawa, an HTLV-1 nonendemic area in Japan.
  • [MeSH-major] HTLV-I Infections / epidemiology. Human T-lymphotropic virus 1. Lymphoma / epidemiology. Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Female. Gastrointestinal Neoplasms / epidemiology. Gastrointestinal Neoplasms / pathology. Gastrointestinal Neoplasms / virology. Humans. Japan. Lymphoma, Large B-Cell, Diffuse / epidemiology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / virology. Male. Middle Aged. Neoplasm Staging. Prevalence. Survival Rate. Tonsillar Neoplasms / epidemiology. Tonsillar Neoplasms / pathology. Tonsillar Neoplasms / virology

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26. Miyazaki M, Yasunaga J, Taniguchi Y, Tamiya S, Nakahata T, Matsuoka M: Preferential selection of human T-cell leukemia virus type 1 provirus lacking the 5' long terminal repeat during oncogenesis. J Virol; 2007 Jun;81(11):5714-23
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  • [Title] Preferential selection of human T-cell leukemia virus type 1 provirus lacking the 5' long terminal repeat during oncogenesis.
  • In adult T-cell leukemia (ATL) cells, a defective human T-cell leukemia virus type 1 (HTLV-1) provirus lacking the 5' long terminal repeat (LTR), designated type 2 defective provirus, is frequently observed.
  • To investigate the mechanism underlying the generation of the defective provirus, we sequenced HTLV-1 provirus integration sites from cases of ATL.
  • In HTLV-1 proviruses retaining both LTRs, 6-bp repeat sequences were adjacent to the 5' and 3' LTRs.
  • Quantification indicated frequencies of type 2 defective provirus of less than 3.9% for two carriers, which are much lower than those seen for ATL cases (27.8%).
  • The HTLV-1 bZIP factor gene, located on the minus strand, is expressed in ATL cells with this defective provirus, and its coding sequences are intact, suggesting its significance in oncogenesis.
  • [MeSH-major] Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. Terminal Repeat Sequences
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Basic-Leucine Zipper Transcription Factors / chemistry. Basic-Leucine Zipper Transcription Factors / genetics. Basic-Leucine Zipper Transcription Factors / metabolism. Cell Line, Tumor. Humans. Molecular Sequence Data. Viral Proteins / chemistry. Viral Proteins / genetics. Viral Proteins / metabolism. Virus Integration / genetics

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  • (PMID = 17344291.001).
  • [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 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC1900290
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27. 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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28. 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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29. 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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30. 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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31. Ratner L: Pathogenesis and treatment of human T-cell leukemia virus infection. Immunol Res; 2005;32(1-3):217-23
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  • [Title] Pathogenesis and treatment of human T-cell leukemia virus infection.
  • The pathogenesis of human T-cell leukemia virus (HTLV)-induced adult T-cell leukemia-lymphoma (ATLL) was explored using an infectious molecular viral clone and a transgenic mouse model.
  • Activation of nuclear factor-kappaB by the HTLV transcriptional transactivator protein Tax was found to be important for lymphocyte immortalization and tumorigenesis.
  • Translational clinical studies of chemotherapy, interferon-alpha, and nucleoside reverse transcriptase inhibitors have also assisted in identifying the pathogenic features of ATLL.

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  • (PMID = 16106073.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA093062-02; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCI NIH HHS / CA / CA063417-05; United States / NCI NIH HHS / CA / R21 CA093062; United States / NCI NIH HHS / CA / P01 CA100730-02; United States / NCI NIH HHS / CA / CA093062-02; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / R01 CA063417-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Retroviral Agents; 0 / Antineoplastic Agents; 0 / Gene Products, tax; 0 / NF-kappa B
  • [Number-of-references] 36
  • [Other-IDs] NLM/ NIHMS94163; NLM/ PMC2652731
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32. Farre L, de Oliveira Mde F, Primo J, Vandamme AM, Van Weyenbergh J, Bittencourt AL: Early sequential development of infective dermatitis, human T cell lymphotropic virus type 1-associated myelopathy, and adult T cell leukemia/lymphoma. Clin Infect Dis; 2008 Feb 1;46(3):440-2
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  • [Title] Early sequential development of infective dermatitis, human T cell lymphotropic virus type 1-associated myelopathy, and adult T cell leukemia/lymphoma.
  • We describe a patient with human T cell lymphotropic virus type 1 (HTLV-1)-associated infective dermatitis who developed HTLV-1-associated myelopathy/tropical spastic paraparesis and adult T cell leukemia/lymphoma at 16 years of age.
  • [MeSH-major] Dermatitis / virology. Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / virology. Paraparesis, Tropical Spastic / virology
  • [MeSH-minor] Child. Female. HTLV-I Antibodies / cerebrospinal fluid. Humans. Polymerase Chain Reaction

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  • (PMID = 18173359.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
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33. Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R: Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut. CMAJ; 2006 Sep 12;175(6):579
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  • [Title] Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / ethnology
  • [MeSH-minor] Adult. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic

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  • [Cites] Tissue Antigens. 1998 Nov;52(5):444-51 [9864034.001]
  • [Cites] CMAJ. 2006 Jan 17;174(2):150-1 [16415454.001]
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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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34. Sawada S, Ishikawa C, Tanji H, Nakachi S, Senba M, Okudaira T, Uchihara JN, Taira N, Ohshiro K, Yamada Y, Tanaka Y, Uezato H, Ohshima K, Sasai K, Burgering BM, Duc Dodon M, Fujii M, Sunakawa H, Mori N: Overexpression of caveolin-1 in adult T-cell leukemia. Blood; 2010 Mar 18;115(11):2220-30
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  • [Title] Overexpression of caveolin-1 in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a T-cell malignancy causatively associated with human T-cell leukemia virus type 1 (HTLV-1).
  • To determine the role of caveolin-1 in leukemogenesis, we examined caveolin-1 expression levels in HTLV-1-infected T-cell lines and ATL cells.
  • These cells expressed high levels of caveolin-1 compared with uninfected T-cell lines and normal peripheral blood mononuclear cells (PBMCs).
  • Caveolin-1-positive ATL cells were detected in ATL lymph nodes and skin lesions, and caveolin-1 was also detected in the plasma of patients with ATL.
  • Infection of a human T-cell line, an epithelial cell line, and normal PBMCs with HTLV-1 induced caveolin-1 expression.
  • HTLV-1-infected T-cell lines, and ATL cells are known to be resistant to transforming growth factor beta (TGF-beta)-induced growth inhibition.
  • Caveolin-1 was colocalized with TGF-beta type I receptor in HTLV-1-infected T-cell lines and suppressed TGF-beta signaling.
  • Caveolin-1 knockdown in an HTLV-1-infected T-cell line exhibited susceptibility to TGF-beta.
  • Thus, we describe a new function for Tax, repression of TGF-beta signaling through caveolin-1 expression, which may play a critical role in ATL leukemogenesis.
  • [MeSH-major] Caveolin 1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism
  • [MeSH-minor] Adult. Cell Line. Cell Membrane / metabolism. Cell Proliferation. Cyclic AMP Response Element-Binding Protein / metabolism. Gene Expression Regulation, Leukemic. Humans. NF-kappa B / metabolism. Promoter Regions, Genetic / genetics. Protein-Serine-Threonine Kinases / metabolism. Receptors, Transforming Growth Factor beta / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. T-Lymphocytes / virology. Transcriptional Activation / genetics. Transforming Growth Factor beta / metabolism

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  • [RetractionIn] Blood. 2010 Aug 26;116(8):1386 [20574044.001]
  • (PMID = 20061557.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caveolin 1; 0 / Cyclic AMP Response Element-Binding Protein; 0 / NF-kappa B; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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35. 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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36. 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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37. Harhaj EW, Harhaj NS: Mechanisms of persistent NF-kappaB activation by HTLV-I tax. IUBMB Life; 2005 Feb;57(2):83-91
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  • [Title] Mechanisms of persistent NF-kappaB activation by HTLV-I tax.
  • Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL).
  • The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease.
  • Tax activation of NF-kappaB is critical for the immortalization and survival of HTLV-I-infected T cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Models, Biological. NF-kappa B / metabolism. Signal Transduction / physiology

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  • (PMID = 16036567.001).
  • [ISSN] 1521-6543
  • [Journal-full-title] IUBMB life
  • [ISO-abbreviation] IUBMB Life
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA99926
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B
  • [Number-of-references] 55
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38. Kawaguchi A, Orba Y, Kimura T, Iha H, Ogata M, Tsuji T, Ainai A, Sata T, Okamoto T, Hall WW, Sawa H, Hasegawa H: Inhibition of the SDF-1alpha-CXCR4 axis by the CXCR4 antagonist AMD3100 suppresses the migration of cultured cells from ATL patients and murine lymphoblastoid cells from HTLV-I Tax transgenic mice. Blood; 2009 Oct 1;114(14):2961-8
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  • [Title] Inhibition of the SDF-1alpha-CXCR4 axis by the CXCR4 antagonist AMD3100 suppresses the migration of cultured cells from ATL patients and murine lymphoblastoid cells from HTLV-I Tax transgenic mice.
  • Adult T-cell leukemia (ATL) is a T-cell malignancy caused by human T lymphotropic virus type I, and presents as an aggressive leukemia with characteristic widespread leukemic cell infiltration into visceral organs and skin.
  • The molecular mechanisms associated with leukemic cell infiltration are poorly understood.
  • We have used mouse models of ATL to investigate the role of chemokines in this process.
  • Transfer of splenic lymphomatous cells from transgenic to SCID mice reproduces a leukemia and lymphoma that is histologically identical to human disease.
  • It could be shown that lymphomatous cells exhibit specific chemotactic activity in response to stromal cell-derived factor-1alpha (SDF-1alpha).
  • Investigation of cultured cells from human ATL patients revealed identical findings.
  • These results demonstrate the involvement of the SDF-1alpha/CXCR4 interaction as one mechanism of leukemic cell migration and this may provide a novel target as part of combination therapy for ATL.
  • [MeSH-major] Anti-HIV Agents / pharmacology. Cell Movement / drug effects. Chemokine CXCL12 / antagonists & inhibitors. Heterocyclic Compounds / pharmacology. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Receptors, CXCR4 / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Animals. Cells, Cultured. Female. Gene Products, tax / genetics. Humans. Immunoblotting. Immunoenzyme Techniques. Lymphocytes. Male. Mice. Mice, Inbred C57BL. Mice, SCID. Mice, Transgenic. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction


39. 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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40. 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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41. 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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42. 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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43. Kawakami H, Tomita M, Okudaira T, Ishikawa C, Matsuda T, Tanaka Y, Nakazato T, Taira N, Ohshiro K, Mori N: Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells. Int J Cancer; 2007 Apr 15;120(8):1811-20
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  • [Title] Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells.
  • The geldanamycin derivative 17-AAG is currently tested in clinical trials and known to inhibit the function of Hsp90 and promote the proteasomal degradation of its misfolded client proteins.
  • ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.
  • Since Hsp90 is overexpressed in HTLV-I-infected T-cell lines and primary ATL cells, we analyzed the effects of 17-AAG on cell survival, apoptosis and expression of signal transduction proteins.
  • HTLV-I-infected T-cell lines and primary ATL cells were significantly more sensitive to 17-AAG in cell survival assays than normal PBMCs.
  • 17-AAG induced the inhibition of cell cycle and apoptosis.
  • These effects could be mediated by inactivation of NF-kappaB, AP-1 and PI3K/Akt pathways, as well as reduction of expression of proteins involved in the G1-S cell cycle transition and apoptosis.
  • Collectively, our results indicate that 17-AAG suppresses ATL cell survival through, at least in part, destabilization of several client proteins and suggest that 17-AAG is a potentially useful chemotherapeutic agent for ATL.
  • [MeSH-major] Apoptosis / drug effects. Benzoquinones / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Human T-lymphotropic virus 1 / drug effects. Lactams, Macrocyclic / therapeutic use. Leukemia, T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. T-Lymphocytes / virology
  • [MeSH-minor] Adult. Cell Cycle / drug effects. Humans. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [RetractionIn] Int J Cancer. 2011 Dec 1;129(11):2762-3 [21960263.001]
  • (PMID = 17230513.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 4GY0AVT3L4 / tanespimycin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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44. 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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45. 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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46. Michael B, Nair AM, Datta A, Hiraragi H, Ratner L, Lairmore MD: Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity. Virology; 2006 Oct 25;354(2):225-39
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  • [Title] Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity.
  • Human T-lymphotropic virus type-1 (HTLV-1) is a deltaretrovirus that causes adult T cell leukemia/lymphoma, and is implicated in a variety of lymphocyte-mediated inflammatory disorders.
  • HTLV-1 provirus has regulatory and accessory genes in four pX open reading frames.
  • HTLV-1 pX ORF-II encodes two proteins, p13II and p30II, which are incompletely defined in virus replication or pathogenesis.
  • We have demonstrated that pX ORF-II mutations block virus replication in vivo and that ORF-II encoded p30II, a nuclear-localizing protein that binds with CREB-binding protein (CBP)/p300, represses CREB and Tax responsive element (TRE)-mediated transcription.
  • Herein, we have identified p30II motifs important for p300 binding and in regulating TRE-mediated transcription in the absence and presence of HTLV-1 provirus.
  • Collectively, our data indicate that HTLV-1 p30II modulates viral gene expression in a cooperative manner with p300-mediated acetylation.

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  • (PMID = 16890266.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-70529; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCI NIH HHS / CA / CA92009; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / R01 CA092009; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Retroviridae Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Viral Proteins; 0 / tof protein, Human T-lymphotropic virus 1; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors; EC 2.3.1.48 / p300-CBP-associated factor
  • [Other-IDs] NLM/ NIHMS183540; NLM/ PMC3044896
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47. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
  • Extranodal adult T-cell leukemia/lymphoma (ATLL) of the head and neck is a rare disease.
  • We studied the clinicopathological features of nine patients with ATLL involving extranodal head and neck sites and conducted a literature review.
  • Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large cell-type.
  • Five patients with localised disease showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
  • Patients with localised disease documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
  • ATLL should be included in the differential diagnosis of extranodal head and neck lymphoma.
  • Localised extranodal ATLL of the head and neck may exhibit indolent clinical behaviours.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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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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48. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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49. Sakai C, Murotani N: [Adult T-cell leukemia/lymphoma in a patient on hemodialysis-resistance to CHOP, but unexpected effect and remission achieved by sobuzoxane alone]. Gan To Kagaku Ryoho; 2010 Feb;37(2):347-50
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  • [Title] [Adult T-cell leukemia/lymphoma in a patient on hemodialysis-resistance to CHOP, but unexpected effect and remission achieved by sobuzoxane alone].
  • The serum soluble IL-2 receptor was 47,500 U/mL, and HTLV-1 antibody was positive.
  • The pathological diagnosis was peripheral T-cell lymphoma, CD4(+).
  • He was clinically diagnosed as having an adult T-cell leukemia/lymphoma, lymphoma type, and clinical stage II.
  • At the time of reporting, May 2009, the patient was well without recurrence of ATLL, and the remission has lasted 26 months or more.
  • The reason why CHOP-resistant ATLL responded dramatically to SBZ alone is not clear, but the plasma concentration of the metabolite of SBZ was possibly very high because of renal failure.
  • Another possibility is that hemodialysis removed the growth factor(s) or anti-apoptotic factor(s) derived from ATLL cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm. Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Piperazines / therapeutic use. Renal Dialysis. Renal Insufficiency / complications

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  • (PMID = 20154500.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Piperazines; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; R1308VH37P / sobuzoxane; VB0R961HZT / Prednisone; CHOP protocol
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50. Ching YP, Chan SF, Jeang KT, Jin DY: The retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplication. Nat Cell Biol; 2006 Jul;8(7):717-24
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  • Human T-cell leukaemia virus type I (HTLV-I) is etiologically associated with adult T-cell leukaemia (ATL).
  • ATL cells are aneuploid, but the causes of aneuploidy are incompletely understood.
  • Here, we show that centrosome amplification is frequent in HTLV-I-transformed cells and that this phenotype is caused by the viral Tax oncoprotein.
  • Our findings suggest that the HTLV-I Tax oncoprotein targets TAX1BP2 causing genomic instability and aneuploidy.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Centrosome / metabolism. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism

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  • (PMID = 16767081.001).
  • [ISSN] 1465-7392
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ139275
  • [Grant] United States / FIC NIH HHS / TW / R01 TW06186-01; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / VAC14 protein, human
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51. 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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52. 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
  •  go-up   go-down


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

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

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  • (PMID = 19273122.001).
  • [ISSN] 1093-4715
  • [Journal-full-title] Frontiers in bioscience (Landmark edition)
  • [ISO-abbreviation] Front Biosci (Landmark Ed)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA054559; United States / NCI NIH HHS / CA / CA054559-14; United States / NCI NIH HHS / CA / R01 CA054559-14; United States / NCI NIH HHS / CA / 2R1 CA054559; United States / NCI NIH HHS / CA / CA054559-15; United States / NCI NIH HHS / CA / CA054559-13A1; United States / NCI NIH HHS / CA / CA054559; United States / NIAID NIH HHS / AI / AI077414-01A2; United States / NIAID NIH HHS / AI / R01 AI077414; United States / NIAID NIH HHS / AI / R01 AI077414-01A2; United States / NCI NIH HHS / CA / R01 CA054559-13A1; United States / NCI NIH HHS / CA / R01 CA054559-15
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 181
  • [Other-IDs] NLM/ NIHMS126265; NLM/ PMC2739244
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56. Doi K, Wu X, Taniguchi Y, Yasunaga J, Satou Y, Okayama A, Nosaka K, Matsuoka M: Preferential selection of human T-cell leukemia virus type I provirus integration sites in leukemic versus carrier states. Blood; 2005 Aug 1;106(3):1048-53
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  • [Title] Preferential selection of human T-cell leukemia virus type I provirus integration sites in leukemic versus carrier states.
  • Human T-cell leukemia virus type I (HTLV-I) is a causative agent of neoplastic disease, adult T-cell leukemia (ATL).
  • Although the encoding viral proteins play an important role in oncogenesis, the role of the HTLV-I proviral integration site remains unsolved.
  • We determined the integration sites of HTLV-I proviruses in ATL cells and HTLV-I-infected cells in asymptomatic carriers.
  • In carrier and ATL cells, HTLV-I provirus was integrated into the transcriptional unit at frequencies of 26.8% (15/56) and 33.9% (20/59), respectively, which were equivalent to the frequency calculated based on random integration (33.2%).
  • In addition, HTLV-I provirus was prone to integration near the transcriptional start sites in leukemic cells (P = .006), and the transcriptional direction of the provirus was in accordance with that of integrated cellular genes in 70% of cases.
  • Taken together, during natural course from carrier to onset of ATL, HTLV-I-infected cells with integration sites favorable for viral gene transcription are susceptible to malignant transformation due to increased viral gene expression.
  • [MeSH-major] Carrier State / virology. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / virology. Virus Integration
  • [MeSH-minor] Base Sequence. Chromosome Mapping. Chromosomes, Human. Humans. Polymerase Chain Reaction. RNA, Messenger. Repetitive Sequences, Nucleic Acid. Transcription Initiation Site. Transcription, Genetic

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  • (PMID = 15840694.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger
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57. Pezeshkpoor F, Yazdanpanah MJ, Shirdel A: Specific cutaneous manifestations in adult T-cell leukemia/lymphoma. Int J Dermatol; 2008 Apr;47(4):359-62
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  • [Title] Specific cutaneous manifestations in adult T-cell leukemia/lymphoma.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is an aggressive malignancy which may occur in individuals infected with human T-cell lymphotropic virus type-I (HTLV-I).
  • HTLV-I is endemic in Khorasan, with a frequency of 2.3% in the general population.
  • As specific cutaneous manifestations of lymphoma may occur in a significant number of patients, we studied these manifestations in ATLL patients admitted to the Hematology and Dermatology Departments of Ghaem Hospital, Mashhad, Iran, during 1995-2004.
  • METHODS: In this descriptive study, demographic and clinical information was obtained from 23 patients suffering from ATLL with specific cutaneous lesions (atypical lymphocytes on histopathology of cutaneous lesions), and was analyzed statistically.
  • CONCLUSION: The most common type of specific skin lesion in ATLL was maculopapular eruption, especially with a generalized distribution.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Skin / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Iran. Male. Middle Aged

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  • (PMID = 18377598.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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58. Mone A, Puhalla S, Whitman S, Baiocchi RA, Cruz J, Vukosavljevic T, Banks A, Eisenbeis CF, Byrd JC, Caligiuri MA, Porcu P: Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia. Blood; 2005 Nov 15;106(10):3380-2
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  • [Title] Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due to the human T-cell lymphotropic virus-1 (HTLV-1).
  • More effective agents and new approaches to detect and treat minimal residual disease are needed.
  • ATL cells express CD52, the target of the antibody alemtuzumab, which is active in a preclinical model of ATL and is cytotoxic for p53-deficient cells.
  • A patient with refractory chronic ATL in transformation achieved longer than a 1-year complete hematologic response following 12 weeks of outpatient subcutaneous alemtuzumab.
  • Persistent suppression of HTLV-1 viral load, even at recovery of T cells, after alemtuzumab and efficient in vitro complement-mediated cytotoxicity of primary ATL cells with mutated TP53 were observed.
  • The unprecedented response and the profound suppression of HTLV-1 viral load observed in this patient suggest that further clinical investigation of alemtuzumab in ATL is warranted.

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  • (PMID = 16076875.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA10215-02; United States / NCI NIH HHS / CA / P01 CA95426; United States / NCI NIH HHS / CA / T32 CA009338
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Interferon-alpha; 0 / Tumor Suppressor Protein p53; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine
  • [Other-IDs] NLM/ PMC1895052
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59. Tsuji Y, Hatanaka M, Maeda T, Seya T, Takenaka H, Shimizu A: Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in human T cell leukemia cell lines. Int J Mol Med; 2005 Nov;16(5):889-93
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  • [Title] Differential-expression and tyrosine-phosphorylation profiles of caveolin isoforms in human T cell leukemia cell lines.
  • Caveolin-1 and -2 are expressed in most cell types, but are not expressed in normal blood cells and cell lines.
  • We previously demonstrated that caveolin-1 is expressed in a panel of human leukemia cell lines that show an activated T cell phenotype.
  • Using this method we detected caveolin-1beta, -2alpha and -2beta, but not caveolin-3 in the leukemia cell lines.
  • This modification is likely to cause the lack of reactivity of caveolin-1alpha to the mAb, and suggests a possible close relationship to cell activation.
  • [MeSH-major] Leukemia, T-Cell / metabolism. Tyrosine / metabolism
  • [MeSH-minor] Antibodies / immunology. Antibodies, Monoclonal / immunology. Cell Line, Tumor. Humans. Phosphorylation. Protein Isoforms / analysis. Protein Isoforms / immunology. Protein Isoforms / metabolism

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  • (PMID = 16211260.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Protein Isoforms; 42HK56048U / Tyrosine
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60. Shtalrid M, Shvidel L, Korenfeld R, Duek A, Landau Z, Berrebi A: HTLV-1 associated adult T-cell leukemia/lymphoma in Israel: report of two patients of Romanian origin. Haematologica; 2005 Mar;90(3):ECR13
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  • [Title] HTLV-1 associated adult T-cell leukemia/lymphoma in Israel: report of two patients of Romanian origin.
  • Human T-lymphotropic virus type 1 (HTLV-1) was the first human oncovirus isolated by Gallo et al. in 1980 and established as an etiological agent for adult T-cell leukemia/ lymphoma (ATL).
  • Although more than 15 million individuals are infected by HTLV-1 through the world, the spread of the virus is highly endemic.
  • The HTLV-1 infection is prevailing in southwestern Japan, inter-tropical Africa, Central and South America.
  • In Kyushu district, Japan, the seroprevalence reaches >30% in the adult population.
  • In the US, Europe and the Middle East the HTLV-1 infection is very rare, and cases of ATL have been reported sporadically.
  • We describe here acute ATL in two patients of Jewish- Romanian origin.
  • The epidemiological anamnesis and screening indicate that both patients acquired the HTLV-1 from their mothers leaving in Romania.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / transmission
  • [MeSH-minor] Family Health. Humans. Infectious Disease Transmission, Vertical. Israel / epidemiology. Jews. Romania / ethnology

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  • (PMID = 15753054.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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61. Nair A, Michael B, Hiraragi H, Fernandez S, Feuer G, Boris-Lawrie K, Lairmore M: Human T lymphotropic virus type 1 accessory protein p12I modulates calcium-mediated cellular gene expression and enhances p300 expression in T lymphocytes. AIDS Res Hum Retroviruses; 2005 Apr;21(4):273-84
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  • [Title] Human T lymphotropic virus type 1 accessory protein p12I modulates calcium-mediated cellular gene expression and enhances p300 expression in T lymphocytes.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T cell leukemia/lymphoma (ATLL), an aggressive CD4+ T lymphocyte malignancy.
  • Activation of T lymphocytes is required for effective retroviral integration into the host cell genome and subsequent viral replication, but the molecular mechanisms involved in HTLV-1-mediated T cell activation remain unclear.
  • HTLV-1 encodes various accessory proteins such as p12I, which has been demonstrated to be critical for HTLV-1 infectivity in vivo in rabbits and in vitro in quiescent primary human T lymphocytes.
  • This hydrophobic protein localizes in the endoplasmic reticulum, increases intracellular calcium, and activates nuclear factor of activated T cell-mediated transcription.
  • Our data indicate that p12I altered the expression of genes associated with a network of interrelated pathways including T cell signaling, cell proliferation, and apoptosis.
  • This is the first report of a viral protein influencing the transcription of p300, a rate-limiting coadapter critical in HTLV-1-mediated T cell activation.
  • Collectively, our data strongly indicate that HTLV-1 p12I modulates cellular gene expression patterns to hasten the activation of T lymphocytes and thereby promote efficient viral infection.

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  • (PMID = 15943569.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-70529; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730-04; United States / NCI NIH HHS / CA / CA100730; United States / NCRR NIH HHS / RR / RR14324; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCRR NIH HHS / RR / R01 RR014324; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / CA100730-04; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Viral; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Viral Regulatory and Accessory Proteins; 0 / p12I protein, Human T-lymphotropic virus 1
  • [Other-IDs] NLM/ NIHMS94122; NLM/ PMC2668121
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62. Jin Q, Alkhatib B, Cornetta K, Alkhatib G: Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1. Virology; 2010 Jan 20;396(2):203-12
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  • [Title] Alternate receptor usage of neuropilin-1 and glucose transporter protein 1 by the human T cell leukemia virus type 1.
  • Recent studies have demonstrated that neuropilin 1 (NP-1) is involved in HTLV-1 entry; however, the role NP-1 plays in this process is not understood.
  • We demonstrated that ectopic expression of human NP-1 but not NP-2 cDNA increased susceptibility to HTLV-1.
  • SiRNA-mediated inhibition of NP-1 expression correlated with significant reduction of HTLV-1 Env-mediated fusion.
  • The vascular endothelial growth factor (VEGF(165)) caused downmodulation of surface NP-1 and inhibited HTLV-1 infection of U87 cells.
  • HTLV-1 Env forms complexes with both NP-1 and GLUT-1 in primary human astrocytes.
  • The alternate usage of these two cellular receptors may have important implications regarding HTLV-1 neuro-tropism.

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  • (PMID = 19913864.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA098095-01; United States / NCI NIH HHS / CA / CA098095-01; United States / NCI NIH HHS / CA / R21 CA098095-02; United States / NCI NIH HHS / CA / 1R21CA98095-01; United States / NCI NIH HHS / CA / CA098095-02; United States / NCI NIH HHS / CA / R21 CA098095
  • [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 / Glucose Transporter Type 1; 0 / Vascular Endothelial Growth Factor A; 0 / Viral Envelope Proteins; 144713-63-3 / Neuropilin-1
  • [Other-IDs] NLM/ NIHMS154887; NLM/ PMC2789895
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63. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • We also analyzed the expression of NOTCH1 target genes (HES1, CCND1, and MYC), all of which were expressed in the sample of the PTCL-u patient with the NOTCH1 mutation, but found only MYC to be expressed in the sample from the ATL patient.
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Adult. DNA Mutational Analysis. Humans

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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64. Takeuchi H, Takahashi M, Norose Y, Takeshita T, Fukunaga Y, Takahashi H: Transformation of breast milk macrophages by HTLV-I: implications for HTLV-I transmission via breastfeeding. Biomed Res; 2010 Feb;31(1):53-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transformation of breast milk macrophages by HTLV-I: implications for HTLV-I transmission via breastfeeding.
  • Human T cell leukemia virus type I (HTLV-I), a causative agent of adult T-cell leukemia (ATL), is transmitted from mother to child predominantly by breastfeeding.
  • The source of HTLV-I-infected cells in breast milk has been thought to be T cells, however, the majority of cells in breast milk are CD14(+) macrophages but not CD3(+) T lymphocytes, and no data are available regarding HTLV-I transmission through breast milk macrophages (BrMMpsi).
  • To explore the potential of BrMMpsi as a possible source of infection in mother to child transmission (MTCT) of HTLV-I, an immortalized cell line (HTLV-BrMMpsi) has been established from BrMMpsi by infection with HTLV-I.
  • HTLV-BrMMpsi retained macrophage characteristics and did not express a complete dendritic cell (DC) phenotype; nevertheless, HTLV-BrMMpsi efficiently promoted T cell proliferation in primary allogeneic mixed lymphocyte reaction (MLR) like DC.
  • Moreover, HTLV-I infection could be transmitted from HTLV-BrMMpsi to activated T cells in the peripheral blood.
  • These findings suggested that BrMMpsi might be an appropriate HTLV-I reservoir involved in MTCT transmission via breastfeeding.
  • [MeSH-major] Breast Feeding. Cell Transformation, Viral. Colostrum / virology. HTLV-I Infections / transmission. Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / virology. Macrophages / virology. Milk, Human / virology
  • [MeSH-minor] Adult. Cell Line, Transformed. Cell Proliferation. Coculture Techniques. Female. Humans. Infant, Newborn. Pregnancy. T-Lymphocytes / metabolism

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  • (PMID = 20203420.001).
  • [ISSN] 1880-313X
  • [Journal-full-title] Biomedical research (Tokyo, Japan)
  • [ISO-abbreviation] Biomed. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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65. Sibon D, Gabet AS, Zandecki M, Pinatel C, Thête J, Delfau-Larue MH, Rabaaoui S, Gessain A, Gout O, Jacobson S, Mortreux F, Wattel E: HTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death. J Clin Invest; 2006 Apr;116(4):974-83
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  • [Title] HTLV-1 propels untransformed CD4 lymphocytes into the cell cycle while protecting CD8 cells from death.
  • Human T cell leukemia virus type 1 (HTLV-1) infects both CD4+ and CD8+ lymphocytes, yet it induces adult T cell leukemia/lymphoma (ATLL) that is regularly of the CD4+ phenotype.
  • In fact, the clonal expansion of HTLV-1-positive CD8+ and CD4+ lymphocytes relied on 2 distinct mechanisms--infection prevented cell death in the former while recruiting the latter into the cell cycle.
  • Cell cycling, but not apoptosis, depended on the level of viral-encoded tax expression.
  • Therefore, HTLV-1 infection establishes a preleukemic phenotype that is restricted to CD4+ infected clones.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. CD8-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / pathogenicity
  • [MeSH-minor] Adult. Apoptosis. Carrier State / virology. Cell Cycle. Cell Proliferation. Cells, Cultured. Female. Humans. Male. Middle Aged. Preleukemia / metabolism. Preleukemia / virology. Time Factors

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  • (PMID = 16585963.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1421359
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66. Zámecníkova A, Al Bahar S, Elshinnawy SE: Genomic instability and rapid clinical course in adult T-cell lymphoma/leukemia patient. Leuk Res; 2010 Dec;34(12):1617-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic instability and rapid clinical course in adult T-cell lymphoma/leukemia patient.
  • Adult T-cell leukemia/lymphoma is a distinct clinical entity characterized by a clonal proliferation of malignant T-lymphocytes.
  • The etiologic agent of the disease is a Human T-cell lymphotropic virus type I.
  • It occurs almost exclusively in areas where the virus is endemic; however the disease develops only in the minority of patients who are virus carriers.
  • Karyotyping findings and their correlation with clinical features are still limited in T-cell malignancies, complicated by clinical heterogeneity and a plethora of secondary abnormalities.
  • This study describes detailed chromosomal and fluorescence in situ hybridization results observed in a patient with adult T-cell leukemia/lymphoma and correlates them with clinical characteristics.
  • [MeSH-major] Genomic Instability. HTLV-I Infections / genetics. Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes
  • [MeSH-minor] Adult. Female. Humans. Karyotyping

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