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66. 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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67. 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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68. 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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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. Sjölund J, Manetopoulos C, Stockhausen MT, Axelson H: The Notch pathway in cancer: differentiation gone awry. Eur J Cancer; 2005 Nov;41(17):2620-9
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  • Its association to human cancer is firmly established in T-cell leukaemia where point mutations or chromosomal translocations lead to constitutive signalling.
  • Accumulating data indicate that deregulated Notch activity is involved also in the genesis of other human cancers, such as pancreatic cancer, medulloblastoma and mucoepidermoid carcinoma.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Receptors, Notch
  • [MeSH-minor] Animals. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Carcinoma, Mucoepidermoid / genetics. Carcinoma, Mucoepidermoid / pathology. Epstein-Barr Virus Infections / genetics. Epstein-Barr Virus Infections / pathology. Humans. Medulloblastoma / genetics. Medulloblastoma / pathology. Mice

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  • (PMID = 16239105.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Notch
  • [Number-of-references] 90
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71. Senba-Nakata K, Hatano Y, Ishikawa K, Ishikawa T, Otani Y, Takeuchi Y, Katagiri K, Okamoto O, Fujiwara S: Etretinate combined with low-dose prednisolone for an aged patient with adult T-cell leukaemia/lymphoma. Clin Exp Dermatol; 2010 Jun;35(4):e153-4
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  • [Title] Etretinate combined with low-dose prednisolone for an aged patient with adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy

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  • (PMID = 19925487.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 65M2UDR9AG / Etretinate; 9PHQ9Y1OLM / Prednisolone
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72. 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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73. 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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  • [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

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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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7
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4. Shanmugam H, Eow GI, Nadarajan VS: A case report of adult T-cell leukaemia/lymphoma. Malays J Pathol; 2009 Jun;31(1):63-6
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  • [Title] A case report of adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a rare T lymphoproliferative disorder which is aetiologically linked with human T-cell lymphotropic virus type-1 (HTLV-1).
  • HTLV-1 is endemic in Japan, Caribbean and Africa.
  • The highest incidence of ATLL is in Japan although sporadic cases have been reported elsewhere in the world.
  • We describe a case of ATLL with an unusual presentation which we believe is the first reported case of ATLL in Malaysia based on our literature search.
  • A 51-year-old Indian lady was referred to University Malaya Medical Centre for an incidental finding of lymphocytosis while being investigated for pallor and giddiness.
  • Clinical examination revealed bilateral shotty cervical lymph nodes with no hepato-splenomegaly or skin lesions.
  • Immunophenotyping of the bone marrow mononuclear cells showed CD3+, CD4+, CD5+, CD7- and CD25+ which is characteristic of ATLL phenotype.
  • HTLV-1 infection was confirmed by the presence of HTLV-1 proviral DNA in the tumor cells using conventional Polymerase Chain Reaction (PCR) and real-time PCR.
  • Here, we discuss the pathogenesis and characteristics of ATLL as well as the detection of HTLV-1 by real time PCR.
  • [MeSH-major] Leukemia, T-Cell / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Antigens, CD / metabolism. Bone Marrow Cells / pathology. Bone Marrow Cells / virology. DNA, Viral / analysis. Female. Flow Cytometry. HTLV-I Infections / complications. HTLV-I Infections / pathology. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunophenotyping. L-Lactate Dehydrogenase / blood. Leukocytosis / etiology. Leukocytosis / pathology. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymph Nodes / virology. Middle Aged. Monocytes / pathology. Polymerase Chain Reaction

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  • (PMID = 19694316.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / DNA, Viral; EC 1.1.1.27 / L-Lactate Dehydrogenase
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75. Kohno T, Yamada Y, Akamatsu N, Kamihira S, Imaizumi Y, Tomonaga M, Matsuyama T: Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells. Cancer Sci; 2005 Aug;96(8):527-33
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  • [Title] Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells.
  • Adult T-cell leukemia/lymphoma (ATLL) is a lymphoproliferative disorder caused by human T lymphotropic virus type 1 (HTLV-I).
  • Although ATLL cells display an activated helper/inducer T-cell phenotype, CD4+ and CD25+, they are known to exhibit strong immunosuppressive activity.
  • As regulatory T cells (Treg cells) express CD4+ and CD25+ molecules and possess potent immune response suppressive activity, we investigated a possible link between ATLL cells and Treg cells.
  • In primary ATLL cells, the expression levels of the Treg cell marker molecules Foxp3 and glucocorticoid-induced tumor necrosis factor receptor family related protein (GITR) were significantly higher than in those from healthy adults.
  • Furthermore, ATLL cells are unresponsive in vitro to concanavalin A stimulation and suppress the proliferation of normal T cells.
  • GITR mRNA expression was induced by the HTLV-I transactivator Tax, and GITR promoter analyses revealed that this induction depends on the kappaB site from -431 bp to -444 bp upstream of the putative transcription site.
  • Taken together, ATLL cells may originate from HTLV-I-infected Treg cells, and GITR seems to be involved in the progression to ATLL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Cell Division. Cell Line, Tumor. Concanavalin A. DNA-Binding Proteins / genetics. Forkhead Transcription Factors. Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Glucocorticoid-Induced TNFR-Related Protein. Humans. Lymphocyte Activation. Receptors, Nerve Growth Factor / genetics. Receptors, Tumor Necrosis Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16108835.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Gene Products, tax; 0 / Glucocorticoid-Induced TNFR-Related Protein; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF18 protein, human; 11028-71-0 / Concanavalin A
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76. Ramos JC, Ruiz P Jr, Ratner L, Reis IM, Brites C, Pedroso C, Byrne GE Jr, Toomey NL, Andela V, Harhaj EW, Lossos IS, Harrington WJ Jr: IRF-4 and c-Rel expression in antiviral-resistant adult T-cell leukemia/lymphoma. Blood; 2007 Apr 1;109(7):3060-8
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  • [Title] IRF-4 and c-Rel expression in antiviral-resistant adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) is a generally fatal malignancy.
  • Most ATLL patients fare poorly with conventional chemotherapy; however, antiviral therapy with zidovudine (AZT) and interferon alpha (IFN-alpha) has produced long-term clinical remissions.
  • We studied primary ATLL tumors and identified molecular features linked to sensitivity and resistance to antiviral therapy.
  • This finding was independent of the disease form.
  • Elevated expression of the putative c-Rel target, interferon regulatory factor-4 (IRF-4), was observed in 10 (91%) of 11 nonresponders and in all tested patients with c-Rel+ tumors and occurred in the absence of the HTLV-1 oncoprotein Tax.
  • Gene rearrangement studies demonstrated the persistence of circulating T-cell clones in long-term survivors maintained on antiviral therapy.
  • The expression of nuclear c-Rel and IRF-4 occurs in the absence of Tax in primary ATLL and is associated with antiviral resistance.
  • AZT and IFN-alpha is a suppressive rather than a curative regimen, and patients in clinical remission should remain on maintenance therapy indefinitely.

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  • (PMID = 17138822.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA070058; United States / NCI NIH HHS / CA / CA-10521; United States / NCI NIH HHS / CA / R01 CA082274; United States / NCI NIH HHS / CA / CA-082274; United States / NCI NIH HHS / CA / U01-CA-070058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / DNA-Binding Proteins; 0 / HIVEN86A protein, human; 0 / Interferon Regulatory Factors; 0 / Interferon Type I; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / Recombinant Proteins; 0 / interferon regulatory factor-4; 4B9XT59T7S / Zidovudine
  • [Other-IDs] NLM/ PMC1852214
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77. Mitterlechner T, Fiegl M, Mühlböck H, Oberaigner W, Dirnhofer S, Tzankov A: Epidemiology of non-Hodgkin lymphomas in Tyrol/Austria from 1991 to 2000. J Clin Pathol; 2006 Jan;59(1):48-55
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  • [Title] Epidemiology of non-Hodgkin lymphomas in Tyrol/Austria from 1991 to 2000.
  • AIMS: To analyse the entity specific incidence and disease specific survival (DSS) of non-Hodgkin lymphomas (NHLs) in Tyrol/Austria, 1991-2000.
  • METHODS: Data from 1307 NHLs (excluding primary cutaneous lymphomas and monoclonal gammopathies of undetermined significance) were obtained.
  • Except for 29 cases of small lymphocytic (CLL/SLL), lymphoblastic leukaemia (ALL), and myeloma (MM), which were diagnosed cytologically, diagnoses were reclassified on paraffin wax embedded archival material according to new World Health Organisation criteria.
  • There was a significant increase in diffuse large B cell lymphoma (DLBCL) and decrease in CLL/SLL in men, and a decrease in MM in women.
  • Age, T-NHL, lambda light chain restriction in MM, and male sex in CLL/SLL were associated with poor prognosis.
  • In B-NHL, DSS decreased in the following order: hairy cell leukaemia, marginal zone lymphoma, follicular lymphoma, Burkitt lymphoma, ALL, DLBCL, CLL, MM, and mantle cell lymphoma.
  • [MeSH-major] Lymphoma, Non-Hodgkin / epidemiology
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Austria / epidemiology. Child. Child, Preschool. Epidemiologic Methods. Female. Humans. Infant. Infant, Newborn. Male. Middle Aged. Sex Distribution

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  • (PMID = 16394280.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860250
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78. Ishikawa C, Tafuku S, Kadekaru T, Sawada S, Tomita M, Okudaira T, Nakazato T, Toda T, Uchihara JN, Taira N, Ohshiro K, Yasumoto T, Ohta T, Mori N: Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer; 2008 Dec 1;123(11):2702-12
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  • [Title] Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol.
  • Adult T-cell leukemia (ATL) is a fatal malignancy of T lymphocytes caused by human T-cell leukemia virus type 1 (HTLV-1) infection and remains incurable.
  • We evaluated the anti-ATL effects of fucoxanthin and its metabolite, fucoxanthinol.
  • Both carotenoids inhibited cell viability of HTLV-1-infected T-cell lines and ATL cells, and fucoxanthinol was approximately twice more potent than fucoxanthin.
  • In contrast, other carotenoids, beta-carotene and astaxanthin, had mild inhibitory effects on HTLV-1-infected T-cell lines.
  • Importantly, uninfected cell lines and normal peripheral blood mononuclear cells were resistant to fucoxanthin and fucoxanthinol.
  • Both carotenoids induced cell cycle arrest during G(1) phase by reducing the expression of cyclin D1, cyclin D2, CDK4 and CDK6, and inducing the expression of GADD45alpha, and induced apoptosis by reducing the expression of Bcl-2, XIAP, cIAP2 and survivin.
  • The induced apoptosis was associated with activation of caspase-3, -8 and -9.
  • Mice with severe combined immunodeficiency harboring tumors induced by inoculation of HTLV-1-infected T cells responded to treatment with fucoxanthinol with suppression of tumor growth, showed extensive tissue distribution of fucoxanthinol, and the presence of therapeutically effective serum concentrations of fucoxanthinol.
  • Our preclinical data suggest that fucoxanthin and fucoxanthinol could be potentially useful therapeutic agents for patients with ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Phaeophyta / chemistry. Xanthophylls / therapeutic use. beta Carotene / analogs & derivatives
  • [MeSH-minor] Acetylation. Animals. Caspases / metabolism. Cell Survival / drug effects. Female. Human T-lymphotropic virus 1 / drug effects. Humans. Mice. NF-kappa B / metabolism. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


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

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


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

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  • (PMID = 16146533.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
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82. Robert MP, Faure C, Reman O, Miocque S: Leopard spot retinopathy: an early clinical marker of leukaemia recurrence? Ann Hematol; 2008 Nov;87(11):927-9
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  • [Title] Leopard spot retinopathy: an early clinical marker of leukaemia recurrence?
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasm Recurrence, Local / complications. Retinal Diseases / complications. Retinal Diseases / pathology
  • [MeSH-minor] Adult. Biomarkers. Humans. Male

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  • (PMID = 18542961.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers
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83. Bhatti FA, Hussain I, Ali MZ: Adult B lymphoblastic leukaemia/lymphoma with hypodiploidy (-9) and a novel chromosomal translocation t(7;12)(q22;p13) presenting with severe eosinophilia - case report and review of literature. J Hematol Oncol; 2009;2:26
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  • [Title] Adult B lymphoblastic leukaemia/lymphoma with hypodiploidy (-9) and a novel chromosomal translocation t(7;12)(q22;p13) presenting with severe eosinophilia - case report and review of literature.
  • Patients suffering from adult acute lymphoblastic leukemia are acutely ill and present most commonly with fever, pallor, bleeding, lymphadenopathy, hepatosplenomegaly and presence of lymphoblasts in the peripheral blood and bone marrow.
  • We describe a rare presentation of acute lymphoblastic leukemia, in a young adult male who had vague and minimal symptoms with mild splenomegaly.
  • The blasts were positive for common precursor B cell markers on flow cytometry.
  • The patient had a unique cytogenetic abnormality t(7;12)(q22;p13),-9, not previously described in acute lymphoblastic leukemia.
  • [MeSH-major] Eosinophilia / complications. Eosinophilia / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. Diploidy. Humans. Male. Translocation, Genetic

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  • (PMID = 19545391.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 26
  • [Other-IDs] NLM/ PMC2706857
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84. Younis I, Green PL: The human T-cell leukemia virus Rex protein. Front Biosci; 2005 Jan 1;10:431-45
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  • [Title] The human T-cell leukemia virus Rex protein.
  • A critical step in the life cycle of complex retroviruses, including HTLV-1 and HTLV-2 is the ability of these viruses to adopt a mechanism by which the genome-length unspliced mRNA as well as the partially spliced mRNAs are exported from the nucleus instead of being subjected to splicing or degradation.
  • In HTLV, this is accomplished through the expression of the viral Rex, which recognizes a specific response element on the incompletely spliced mRNAs, stabilizes them, inhibits their splicing, and utilizes the CRM1-dependent cellular pathway for transporting them from the nucleus to the cytoplasm.
  • Rex itself is regulated by phosphorylation, which implies that proper activation of the protein in response to certain cellular cues is an important tool for the virus to ensure that specific viral gene expression is allowed only when the host cell can provide the best conditions for virion production.
  • Having such a critical role in HTLV life cycle, Rex is indispensable for efficient viral replication, infection and spread.
  • Indeed, Rex is considered to regulate the switch between the latent and productive phases of the HTLV life cycle.
  • Without a functional Rex, the virus would still produce regulatory and some accessory gene products; however, structural and enzymatic post-transcriptional gene expression would be severely repressed, essentially leading to non-productive viral replication.
  • More detailed understanding of the exact molecular mechanism of action of Rex will thus allow for better design of therapeutic drugs against Rex function and ultimately HTLV replication.
  • Herein we summarize the progress made towards understanding Rex function and its role in the HTLV life cycle.

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  • (PMID = 15574380.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA77556; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCI NIH HHS / CA / CA92009; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / R01 CA077556; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / R01 CA092009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, rex
  • [Number-of-references] 167
  • [Other-IDs] NLM/ NIHMS94141; NLM/ PMC2659543
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85. Mitani S, Kamata H, Fujiwara M, Aoki N, Okada S, Watanabe M, Tango T, Mori S: Missense mutation with/without nonsense mutation of the p53 gene is associated with large cell morphology in human malignant lymphoma. Pathol Int; 2007 Jul;57(7):430-6
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  • [Title] Missense mutation with/without nonsense mutation of the p53 gene is associated with large cell morphology in human malignant lymphoma.
  • Mutations in p53 gene exons 5-9 were studied in 44 non-Hodgkin's lymphomas (NHL) consisting of 35 B-NHL and 9 T-NHL.
  • Missense mutations were found in two diffuse large B-cell lymphomas (DLBL) and one peripheral T-cell lymphoma (unspecified).
  • Double transversion missense and nonsense mutations were detected in one DLBL and one adult T-cell leukemia/lymphoma.
  • Cytomorphometric analysis was therefore conducted by measuring the gross area of 100 lymphoma cell nuclei in 44 cases and the results were compared between lymphomas harboring p53 missense mutation with/without nonsense mutation and lymphomas harboring p53 silent mutation or lacking mutation.
  • It was found that the lymphomas harboring p53 missense mutation with/without nonsense mutation had a highly significantly larger nuclear gross area than lymphomas with silent p53 mutation or lacking mutation (two-sample t-test, P < 0.00001; Exact Wilcoxon rank-sum test, P < 0.00001).
  • This result suggests that p53 mutation might induce enlargement of neoplastic cell nuclei by some molecular mechanism.
  • [MeSH-major] Codon, Nonsense. Genes, p53 / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Mutation, Missense
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / pathology. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Humans. Male. Middle Aged

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  • (PMID = 17587242.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / DNA, Neoplasm
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86. González Pérez P, Serrano-Pozo A, Franco-Macías E, Montes-Latorre E, Gómez-Aranda F, Campos T: Vincristine-induced acute neurotoxicity versus Guillain-Barré syndrome: a diagnostic dilemma. Eur J Neurol; 2007 Jul;14(7):826-8
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  • [Title] Vincristine-induced acute neurotoxicity versus Guillain-Barré syndrome: a diagnostic dilemma.
  • We report the case of a patient with acute lymphoblastic leukaemia who, after the initiation of treatment with vincristine (VCR), developed a fulminant motor polyradiculoneuropathy resembling an axonal variant of Guillain-Barré syndrome (GBS).
  • This report shows that differentiating between axonal GBS and VCR-induced acute neurotoxicity may be a challenge for clinicians.
  • [MeSH-major] Guillain-Barre Syndrome / diagnosis. Polyradiculoneuropathy / chemically induced. Vincristine / adverse effects
  • [MeSH-minor] Action Potentials. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Erectile Dysfunction / chemically induced. Fatal Outcome. Humans. Hydrocortisone / administration & dosage. Male. Methotrexate / administration & dosage. Paraparesis / chemically induced. Paresthesia / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisone / administration & dosage. Remission Induction. Urination Disorders / chemically induced

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  • Hazardous Substances Data Bank. CYTARABINE .
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  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
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  • (PMID = 17594344.001).
  • [ISSN] 1468-1331
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; VB0R961HZT / Prednisone; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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87. Ejima Y: [An autopsied case of adult T-cell leukemia/lymphoma (ATLL) presenting with specific MRI findings in the cerebral cortex]. Brain Nerve; 2007 Nov;59(11):1305-13
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  • [Title] [An autopsied case of adult T-cell leukemia/lymphoma (ATLL) presenting with specific MRI findings in the cerebral cortex].
  • [MeSH-major] Cerebral Cortex. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Magnetic Resonance Imaging
  • [MeSH-minor] Aged. Cerebral Infarction / pathology. Diagnosis, Differential. Humans. Hypoxia, Brain / diagnosis. Male

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

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  • (PMID = 16061970.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-02
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS183536; NLM/ PMC3060566
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89. 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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90. Hardell L, Eriksson M, Carlberg M, Sundström C, Mild KH: Use of cellular or cordless telephones and the risk for non-Hodgkin's lymphoma. Int Arch Occup Environ Health; 2005 Sep;78(8):625-32
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  • [Title] Use of cellular or cordless telephones and the risk for non-Hodgkin's lymphoma.
  • OBJECTIVES: To evaluate the use of cellular and cordless telephones as the risk factor for non-Hodgkin's lymphoma (NHL).
  • NHL of the B-cell type was not associated with the use of cellular or cordless telephones.
  • Regarding T-cell NHL and >5 year latency period, the use of analogue cellular phones yielded: odds ratio (OR) = 1.46, 95%; confidence interval (CI) = 0.58-3.70, digital: OR=1.92, 95%; CI=0.77-4.80 and cordless phones: OR=2.47; CI=1.09-5.60.
  • The corresponding results for certain, e.g. cutaneous and leukaemia, T-cell lymphoma for analogue phones were: OR=3.41, 95%; CI=0.78-15.0, digital: OR=6.12, 95%; CI=1.26-29.7 and cordless phones: OR=5.48, 95%; CI=1.26-23.9.
  • CONCLUSIONS: The results indicate an association between T-cell NHL and the use of cellular and cordless telephones, however based on low numbers and must be interpreted with caution.
  • Regarding B-cell NHL no association was found.
  • [MeSH-major] Cell Phones / statistics & numerical data. Lymphoma, Non-Hodgkin / etiology
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Microwaves / adverse effects. Middle Aged. Risk Factors

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  • (PMID = 16001209.001).
  • [ISSN] 0340-0131
  • [Journal-full-title] International archives of occupational and environmental health
  • [ISO-abbreviation] Int Arch Occup Environ Health
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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91. Atsumi E, Yara S, Higa F, Hirata T, Haranaga S, Tateyama M, Fujita J: Influence of human T lymphotropic virus type I infection on the etiology of community-acquired pneumonia. Intern Med; 2009;48(12):959-65
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  • [Title] Influence of human T lymphotropic virus type I infection on the etiology of community-acquired pneumonia.
  • BACKGROUND: Human T lymphotropic virus type I (HTLV-I), the cause of human T cell leukemia, is associated with a high incidence of several other infectious diseases.
  • However, the relationship between pulmonary infections and HTLV-I infection is still unclear.
  • OBJECTIVE: A large-scale retrospective study was conducted on hospital inpatients to evaluate the relationship between community-acquired pneumonia (CAP) and HTLV-I infection.
  • The presence of serum HTLV-I antibody was determined in all patients on admission.
  • Prevalence of HTLV-I infection was analyzed between CAP patients and all inpatients.
  • We also compared HTLV-I-positive CAP patients and HTLV-I-negative CAP patients for severity and manifestation of pneumonia.
  • RESULTS: The prevalence of HTLV-I was higher in CAP patients than in all inpatients (18.9%: 13.7%, p=0.011).
  • The rates of renal diseases and collagen vascular disorders were higher in the HTLV-I-positive CAP patients than in the HTLV-I-negative CAP patients.
  • Multivariate analysis revealed that HTLV-I infection, gender, COPD and collagen vascular disorders were all independent risk factors for CAP.
  • The severity indices of CAP, the PORT score and the CURB-65 score, were higher in the HTLV-I-positive patients than in the HTLV-I-negative patients.
  • CONCLUSION: This study demonstrates that HTLV-I infection might be an independent risk factor for CAP and that HTLV-I-infected patients tend to demonstrate a relatively severe form of pneumonia.
  • [MeSH-major] Community-Acquired Infections / etiology. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Pneumonia / etiology
  • [MeSH-minor] Adult. Aged. Female. HTLV-I Antibodies / blood. Humans. Male. Middle Aged. Multivariate Analysis. Prevalence. Retrospective Studies. Risk Factors. Severity of Illness Index

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  • (PMID = 19525581.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
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92. Feng X, Ratner L: Human T-cell leukemia virus type 1 blunts signaling by interferon alpha. Virology; 2008 Apr 25;374(1):210-6
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  • [Title] Human T-cell leukemia virus type 1 blunts signaling by interferon alpha.
  • Although many animal viruses block the interferon (IFN) signaling pathway, this issue has not been previously investigated in retrovirus-infected cells.
  • For this purpose, an infectious molecular clone of human T-cell leukemia virus type 1 (HTLV-1) was transfected into 293T or HeLa cells and was found to reduce interferon-stimulated response element (ISRE) reporter activity.
  • HTLV-1 reduced the phosphorylation of tyrosine kinase 2 (TYK2) and signal transducer and transcriptional activator 2 (STAT2), suggesting a specific effect of HTLV-1 on the ability of an adaptor tyrosine kinase to transfer an IFN signal to the STAT-transcriptional activator complex.

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  • (PMID = 18234266.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100730-010005; United States / NCI NIH HHS / CA / P50 CA094056; United States / NCI NIH HHS / CA / R21 CA109678-02; United States / NCI NIH HHS / CA / CA094056-070003; United States / NCI NIH HHS / CA / R21 CA109678; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA105218-03; United States / NCI NIH HHS / CA / P50 CA094056-070003; United States / NCI NIH HHS / CA / CA109678-02; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / P01 CA100730-010005; United States / NCI NIH HHS / CA / CA063417-09; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / CA109678; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / R01 CA105218-03; United States / NCI NIH HHS / CA / R01 CA105218; United States / NCI NIH HHS / CA / P01 CA100730; United States / NCI NIH HHS / CA / R01 CA063417-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / STAT2 Transcription Factor; 0 / STAT2 protein, human; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human
  • [Other-IDs] NLM/ NIHMS47609; NLM/ PMC2373983
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93. Richard V, Nadella MV, Green PL, Lairmore MD, Feuer G, Foley JG, Rosol TJ: Transcriptional regulation of parathyroid hormone-related protein promoter P3 by ETS-1 in adult T-cell leukemia/lymphoma. Leukemia; 2005 Jul;19(7):1175-83
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  • [Title] Transcriptional regulation of parathyroid hormone-related protein promoter P3 by ETS-1 in adult T-cell leukemia/lymphoma.
  • Parathyroid hormone-related protein (PTHrP) plays a primary role in the development of humoral hypercalcemia of malignancy seen in the majority of adult T-cell leukemia/lymphoma (ATLL) patients with human T-cell lymphotropic virus type-1 (HTLV-1) infection.
  • HTLV-1 Tax has been shown to complex with ETS-1 and SP1 to transactivate the PTHrP P3 promoter.
  • Previously, we established a SCID/bg mouse model of human ATL with RV-ATL cells and showed that PTHrP expression was independent of Tax.
  • In this study, we report an inverse correlation of PTHrP with tax/rex mRNA in multiple HTLV-1-positive cell lines and RV-ATL cells.
  • Stimulation of Jurkat T cells with PMA/ionomycin upregulated the PTHrP P3 promoter by a previously characterized Ets binding site and also induced protein/DNA complex formation identical to that observed in RV-ATL cells.
  • Further, we provide evidence that cotransfection with Ets-1 and constitutively active Mek-1 in HTLV-1-negative transformed T cells with stimulation by PMA/ionomycin not only resulted in a robust induction of PTHrP P3 but also formed a complex with ETS-1/P3 EBS similar to that in ATLL cells.
  • Our data demonstrate that transcriptional regulation of PTHrP in ATLL cells can be controlled by T-cell receptor signaling and the ETS and MAPK ERK pathway in a Tax-independent manner.

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  • (PMID = 15889157.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077911; United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCRR NIH HHS / RR / RR00168; United States / NCI NIH HHS / CA / CA100730; United States / NCRR NIH HHS / RR / P51 RR000168; United States / NCRR NIH HHS / RR / K26 RR000168; United States / NCI NIH HHS / CA / CA77911; United States / NCI NIH HHS / CA / P01 CA100730-03; None / None / / P01 CA100730-01; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / P01 CA100730-01; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS1 protein, human; 0 / Ets1 protein, mouse; 0 / Gene Products, rex; 0 / Gene Products, tax; 0 / Parathyroid Hormone-Related Protein; 0 / Proto-Oncogene Protein c-ets-1; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell; 0 / Transcription Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS94146; NLM/ PMC2661941
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94. Cooper CM, James K, Wilks RJ: HTLV-1 related knowledge, attitude and behaviour patterns among mothers who participated in the Jamaica Breastfeeding Intervention Study (1996-2000). West Indian Med J; 2010 Jan;59(1):35-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1 related knowledge, attitude and behaviour patterns among mothers who participated in the Jamaica Breastfeeding Intervention Study (1996-2000).
  • Human T-cell Lymphotropic Virus type-1 (HTLV-1), the first human retrovirus associated with a malignant disease, is endemic in Jamaica.
  • Women are at greater risk of contracting the virus as it is more efficiently transmitted from male to female than in the reverse.
  • The study aims to document the knowledge, attitude and behaviour pattern (KABP) of a group of women five years after they had participated in a mother-to-child transmission of HTLV-1 risk reduction study.
  • There were large deficiencies in the knowledge and practice of women at risk of being infected with HTLV-1.
  • Only 58% knew that HTLV-1 is sexually transmitted.
  • A minority was aware of HTLV-1 associated diseases: Adult T-cell lymphoma/leukaemia (ATL) -30.7%; Tropical Spastic Paraparesis (TSP) -42%; Infective dermatitis -42%).
  • Ten (11.4%) believed that HTLV-1 infection can cause HIV/AIDS and only 33% knew that there was no cure for the virus.
  • Controlling HTLV-1 spread must be based on interrupting transmission.
  • In Jamaica, donated blood is screened for HTLV-1 and sharing of infected needle is an insignificant mode of transmission.
  • However although safe practices in breastfeeding and sexual intercourse are proven ways to reduce HTLV-1 transmission, these data show that knowledge and safe practices among those at risk may not be retained and health education will need to be sustained.
  • [MeSH-major] Breast Feeding. HTLV-I Infections / transmission. Health Knowledge, Attitudes, Practice. Human T-lymphotropic virus 1. Mothers
  • [MeSH-minor] Adult. Chi-Square Distribution. Cross-Sectional Studies. Demography. Female. Focus Groups. Health Education. Humans. Infectious Disease Transmission, Vertical. Jamaica / epidemiology. Male. Middle Aged. Regression Analysis. Surveys and Questionnaires

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  • (PMID = 20931911.001).
  • [ISSN] 0043-3144
  • [Journal-full-title] The West Indian medical journal
  • [ISO-abbreviation] West Indian Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Jamaica
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95. Ishikawa C, Matsuda T, Okudaira T, Tomita M, Kawakami H, Tanaka Y, Masuda M, Ohshiro K, Ohta T, Mori N: Bisphosphonate incadronate inhibits growth of human T-cell leukaemia virus type I-infected T-cell lines and primary adult T-cell leukaemia cells by interfering with the mevalonate pathway. Br J Haematol; 2007 Feb;136(3):424-32
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  • [Title] Bisphosphonate incadronate inhibits growth of human T-cell leukaemia virus type I-infected T-cell lines and primary adult T-cell leukaemia cells by interfering with the mevalonate pathway.
  • Anti-resorptive bisphosphonates are used for the treatment of hypercalcaemia and bone complications associated with malignancies and osteoporosis, but also have been shown to have anti-tumour effects in various cancers.
  • Adult T-cell leukaemia (ATL) is a fatal T-cell malignancy caused by infection with human T-cell leukaemia virus type I (HTLV-I), and remains incurable.
  • ATL is associated with osteolytic bone lesions and hypercalcaemia, both of which are major factors in the morbidity of ATL.
  • Thus, the search for anti-ATL agents that have both anti-tumour and anti-resorptive activity is warranted.
  • The bisphosphonate agent, incadronate, prevented cell growth of HTLV-I-infected T-cell lines and primary ATL cells, but not of non-infected T-cell lines or normal peripheral blood mononuclear cells.
  • Incadronate induced S-phase cell cycle arrest and apoptosis in HTLV-I-infected T-cell lines, and treatment of these cells with substrates of the mevalonate pathway blocked the incadronate-mediated growth suppression.
  • Importantly, treatment with incadronate reduced tumour formation from an HTLV-I-infected T-cell line when these cells were inoculated subcutaneously into severe combined immunodeficient mice.
  • These findings suggest that incadronate could be potentially useful for the treatment of ATL.
  • [MeSH-major] Antimetabolites / therapeutic use. Diphosphonates / therapeutic use. Human T-lymphotropic virus 1. Leukemia, T-Cell / drug therapy. Mevalonic Acid / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Aged. Animals. Apoptosis / drug effects. Biomarkers / analysis. Blotting, Western / methods. Caspases / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Inhibitor of Apoptosis Proteins. Jurkat Cells. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / metabolism. Male. Mice. Mice, SCID. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins / analysis. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Signal Transduction / drug effects

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  • (PMID = 17233845.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / BIRC5 protein, human; 0 / Biomarkers; 0 / Diphosphonates; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 138330-18-4 / cimadronate; EC 3.4.22.- / Caspases; S5UOB36OCZ / Mevalonic Acid
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96. Toulza F, Nosaka K, Takiguchi M, Pagliuca T, Mitsuya H, Tanaka Y, Taylor GP, Bangham CR: FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia. Int J Cancer; 2009 Nov 15;125(10):2375-82
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  • [Title] FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL).
  • It has been postulated that ATLL cells might act as regulatory T cells (T(regs)) which, in common with ATLL cells, express both CD25 and FoxP3, and so contribute to the severe immune suppression typical of ATLL.
  • We report here that the frequency of CD25(+) cells varied independently of the frequency of FoxP3(+) cells in both a cross-sectional study and in a longitudinal study of 2 patients with chronic ATLL.
  • Furthermore, the capacity of ATLL cells to suppress proliferation of heterologous CD4(+)CD25(-) cells correlated with the frequency of CD4(+) FoxP3(+) cells but was independent of CD25 expression.
  • Finally, the frequency of CD4(+)FoxP3(+) cells was inversely correlated with the lytic activity of HTLV-1-specific CTLs in patients with ATLL.
  • We conclude that ATLL is not a tumor of FoxP3(+) regulatory T cells, and that a population of FoxP3(+) cells distinct from ATLL cells has regulatory functions and may impair the cell-mediated immune response to HTLV-1 in patients with ATLL.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Proliferation. Chronic Disease. Female. Flow Cytometry. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate

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

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  • (PMID = 18840303.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Epitopes, T-Lymphocyte; 0 / Gene Products, tax; 0 / Recombinant Fusion Proteins; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Other-IDs] NLM/ PMC2579301
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98. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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99. Suga M, Yamaguchi M, Ichimiya M, Yoshikawa Y, Hamamoto Y, Muto M: A rare case of the cutaneous form of adult T-cell leukaemia/lymphoma: assessment of remission by PCR for clonal T-cell receptor gamma gene rearrangements in an electron beam-irradiated cutaneous lesion. Clin Exp Dermatol; 2005 Jan;30(1):40-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare case of the cutaneous form of adult T-cell leukaemia/lymphoma: assessment of remission by PCR for clonal T-cell receptor gamma gene rearrangements in an electron beam-irradiated cutaneous lesion.
  • Adult T-cell leukaemia/lymphoma is a lymphoproliferative disorder aetiologically associated with human T-cell lymphotropic virus type I infection.
  • A cutaneous lesion often develops in the disease, and in rare cases, is even the only manifestation.
  • Here we report a rare case of 'cutaneous' adult T-cell leukaemia/lymphoma with neither atypical cells in the peripheral blood nor lymph node involvement.
  • To evaluate whether or not there were residual lymphoma cells in the skin, we performed PCR to detect clonal T cell receptor gamma gene rearrangements.
  • The findings suggest that this procedure is useful for the evaluation of therapeutic effects and the early detection of lymphoma recurrence.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Cutaneous / genetics

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  • (PMID = 15663501.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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100. Bremer E, Samplonius DF, Peipp M, van Genne L, Kroesen BJ, Fey GH, Gramatzki M, de Leij LF, Helfrich W: Target cell-restricted apoptosis induction of acute leukemic T cells by a recombinant tumor necrosis factor-related apoptosis-inducing ligand fusion protein with specificity for human CD7. Cancer Res; 2005 Apr 15;65(8):3380-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Target cell-restricted apoptosis induction of acute leukemic T cells by a recombinant tumor necrosis factor-related apoptosis-inducing ligand fusion protein with specificity for human CD7.
  • Current treatment of human T-cell leukemia and lymphoma is predominantly limited to conventional cytotoxic therapy and is associated with limited therapeutic response and significant morbidity.
  • Therefore, more potent and leukemia-specific therapies with favorable toxicity profiles are urgently needed.
  • Here, we report on the construction of a novel therapeutic fusion protein, scFvCD7:sTRAIL, designed to induce target antigen-restricted apoptosis in human T-cell tumors.
  • ScFvCD7:sTRAIL consists of the death-inducing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genetically linked to an scFv antibody fragment specific for the T-cell surface antigen CD7.
  • Treatment with scFvCD7:sTRAIL induced potent CD7-restricted apoptosis in a series of malignant T-cell lines, whereas normal resting leukocytes, activated T cells, and vascular endothelial cells (human umbilical vein endothelial cells) showed no detectable apoptosis.
  • In mixed culture experiments with CD7-positive and CD7-negative tumor cells, scFvCD7:sTRAIL induced very potent bystander apoptosis of CD7-negative tumor cells.
  • In vitro treatment of blood cells freshly derived from T-acute lymphoblastic leukemia patients resulted in marked apoptosis of the malignant T cells that was strongly augmented by vincristin.
  • In conclusion, scFvCD7:sTRAIL is a novel recombinant protein causing restricted apoptosis in human leukemic T cells with low toxicity for normal human blood and endothelial cells.
  • [MeSH-major] Antigens, CD7 / immunology. Apoptosis / drug effects. Immunotoxins / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Membrane Glycoproteins / pharmacology. Recombinant Fusion Proteins / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Apoptosis Regulatory Proteins. CHO Cells. Cell Line, Tumor. Cricetinae. Drug Synergism. Epitopes. Humans. Immunoglobulin Fragments / genetics. Immunoglobulin Fragments / immunology. Immunoglobulin Fragments / pharmacology. Jurkat Cells / cytology. Jurkat Cells / drug effects. T-Lymphocytes / drug effects. T-Lymphocytes / immunology. T-Lymphocytes / pathology. TNF-Related Apoptosis-Inducing Ligand. Vincristine / pharmacology

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  • (PMID = 15833872.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD7; 0 / Apoptosis Regulatory Proteins; 0 / Epitopes; 0 / Immunoglobulin Fragments; 0 / Immunotoxins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine
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