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

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

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  • (PMID = 15761473.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 100730; United States / FIC NIH HHS / TW / TW005705-03; United States / FIC NIH HHS / TW / TW 05705; United States / FIC NIH HHS / TW / R03 TW005705; United States / FIC NIH HHS / TW / R03 TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-02; United States / FIC NIH HHS / TW / R03 TW005705-03; United States / FIC NIH HHS / TW / R03 TW005705-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; SY7Q814VUP / Calcium
  • [Number-of-references] 84
  • [Other-IDs] NLM/ NIHMS183534; NLM/ PMC3057663
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23. Lyell V, Khatamzas E, Allain T: Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report. J Med Case Rep; 2007;1:56
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  • [Title] Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
  • Human T cell lymphotrophic virus type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.
  • Although there is a long latency, carriers have a 1-5% chance of developing adult T cell leukaemia/lymphoma, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.
  • We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have lymphoma and was positive for HTLV-1.

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  • (PMID = 17651486.001).
  • [ISSN] 1752-1947
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  • [ISO-abbreviation] J Med Case Rep
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  • [Other-IDs] NLM/ PMC1950877
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2
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4. 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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25. Miyamura F, Kako S, Yamagami H, Sato K, Sato M, Terasako K, Kimura S, Nakasone H, Aoki S, Okuda S, Yamazaki R, Oshima K, Yoshinaga K, Higuchi T, Nishida J, Demitsu T, Kakehashi A, Kanda Y: Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Oct;90(3):397-401
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  • [Title] Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation.
  • Only some carriers of human T cell lymphotropic virus type I (HTLV-1) develop adult T cell leukemia/lymphoma (ATLL) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset ATLL.
  • A 25-year-old female developed ATLL and underwent allogeneic hematopoietic stem cell transplantation (HSCT) in non-remission.
  • She had chronic refractory eczema and corneal injury at the onset of ATLL.
  • Remission of ATLL was achieved, and the HTLV-1 proviral load decreased after HSCT.
  • More than a year has passed since the transplantation was performed, and she has had no recurrence of either ATLL or lesions in the skin and eye.
  • Her clinical course suggests a possible association between skin and eye lesions and HTLV-1 infection.
  • Special attention is needed when HTLV-1 carriers develop eye or skin lesions.
  • [MeSH-major] Corneal Diseases / therapy. Eczema / therapy. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Chronic Disease. Female. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Humans. Transplantation, Homologous. Treatment Outcome. Viral Load


76. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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77. 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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78. Ohashi T, Nagai M, Okada H, Takayanagi R, Shida H: Activation and detection of HTLV-I Tax-specific CTLs by epitope expressing single-chain trimers of MHC class I in a rat model. Retrovirology; 2008;5:90
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  • [Title] Activation and detection of HTLV-I Tax-specific CTLs by epitope expressing single-chain trimers of MHC class I in a rat model.
  • BACKGROUND: Human T cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) in infected individuals after a long incubation period.
  • Immunological studies have suggested that insufficient host T cell response to HTLV-I is a potential risk factor for ATL.
  • To understand the relationship between host T cell response and HTLV-I pathogenesis in a rat model system, we have developed an activation and detection system of HTLV-I Tax-specific cytotoxic T lymphocytes (CTLs) by Epitope expressing Single-Chain Trimers (SCTs) of MHC class I.
  • Human cell lines transfected with the established expression vectors were able to induce IFN-gamma and TNF-alpha production by a Tax180-188-specific CTL line, 4O1/C8.
  • CONCLUSION: We have generated a SCT of rat MHC-I linked to Tax epitope peptide, which can be applicable for the induction of Tax-specific CTLs in rat model systems of HTLV-I infection.
  • These systems will be useful tools in understanding the role of HTLV-I specific CTLs in HTLV-I pathogenesis.
  • [MeSH-major] Epitopes, T-Lymphocyte / genetics. Gene Expression. Gene Products, tax / genetics. Genes, MHC Class I. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / genetics. T-Lymphocytes, Cytotoxic / immunology. Transcriptional Activation
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line. Cells, Cultured. Cytokines / genetics. Cytokines / immunology. Disease Models, Animal. Female. Genetic Vectors / genetics. Humans. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / virology. Molecular Sequence Data. Rats. Rats, Inbred F344. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / immunology

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

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

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  • (PMID = 15833872.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD7; 0 / Apoptosis Regulatory Proteins; 0 / Epitopes; 0 / Immunoglobulin Fragments; 0 / Immunotoxins; 0 / Membrane Glycoproteins; 0 / Recombinant Fusion Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 5J49Q6B70F / Vincristine
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81. Hayase H, Ishizu A, Ikeda H, Miyatake Y, Baba T, Higuchi M, Abe A, Tomaru U, Yoshiki T: Aberrant gene expression by CD25+CD4+ immunoregulatory T cells in autoimmune-prone rats carrying the human T cell leukemia virus type-I gene. Int Immunol; 2005 Jun;17(6):677-84
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  • [Title] Aberrant gene expression by CD25+CD4+ immunoregulatory T cells in autoimmune-prone rats carrying the human T cell leukemia virus type-I gene.
  • Transgenic rats expressing the env-pX gene of human T cell leukemia virus type-I under the control of the viral long terminal repeat promoter (env-pX rats) developed systemic autoimmune diseases.
  • Prior to disease manifestation, the immunosuppressive function of CD25(+)CD4(+) T (T-reg) cells was impaired in these rats.
  • Since T cell differentiation appeared to be disordered in env-pX rats, we assumed that the impairment of T-reg cells might be caused by an abortive differentiation in the thymus.
  • However, reciprocal bone marrow transfers between env-pX and wild-type rats revealed that direct effects of the transgene unrelated to the thymus framework induced the abnormality of T-reg cells.
  • Expression of the Foxp3 gene and cell-surface markers supported a naive phenotype for env-pX T-reg cells.
  • Array analyses of gene expression showed some interesting profiles, e.g. up-regulation of genes associated with the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways in env-pX T-reg cells.
  • We suggest that investigation of the pathology of T-reg cells in our autoimmune-prone rat model may aid in understanding the roles of T-reg cells in human autoimmune diseases.
  • [MeSH-major] Autoimmune Diseases / immunology. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antigens, CD / analysis. Antigens, CD4 / genetics. Bone Marrow Transplantation. Disease Models, Animal. Forkhead Transcription Factors / biosynthesis. Forkhead Transcription Factors / genetics. Forkhead Transcription Factors / immunology. Gene Expression Regulation / immunology. Immediate-Early Proteins / immunology. Immediate-Early Proteins / metabolism. Janus Kinase 1. Male. Protein-Tyrosine Kinases / biosynthesis. Protein-Tyrosine Kinases / immunology. Rats. Receptors, Interleukin-2 / genetics. Spleen / cytology. Spleen / immunology. Suppressor of Cytokine Signaling Proteins / biosynthesis. Suppressor of Cytokine Signaling Proteins / immunology

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

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

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

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  • (PMID = 15994832.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Crebbp protein, mouse; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.1.- / Chuk protein, mouse; EC 2.7.1.- / IKBKE protein, human; EC 2.7.1.- / Ikbke protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; EC 2.7.11.10 / Ikbkb protein, mouse
  • [Other-IDs] NLM/ PMC1168794
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85. Armstrong F, Brunet de la Grange P, Gerby B, Rouyez MC, Calvo J, Fontenay M, Boissel N, Dombret H, Baruchel A, Landman-Parker J, Roméo PH, Ballerini P, Pflumio F: NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity. Blood; 2009 Feb 19;113(8):1730-40
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  • [Title] NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity.
  • Understanding the pathways that regulate the human T-cell acute lymphoblastic leukemia (T-ALL) initiating cells (T-LiC) activity has been hampered by the lack of biologic assays in which this human disease can be studied.
  • Here we show that coculture of primary human T-ALL with a mouse stromal cell line expressing the NOTCH ligand delta-like-1 (DL1) reproducibly allowed maintenance of T-LiC and long-term growth of blast cells.
  • Human T-ALL mutated or not on the NOTCH receptor required sustained activation of the NOTCH pathway via receptor/ligand interaction for growth and T-LiC activity.
  • On the reverse, inhibition of the NOTCH pathway during primary cultures abolished in vitro cell growth and in vivo T-LiC activity.
  • Altogether, these results demonstrate the major role of the NOTCH pathway activation in human T-ALL development and in the maintenance of leukemia-initiating cells.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Receptor, Notch1 / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Cell Communication / physiology. Cell Culture Techniques / methods. Coculture Techniques. Genes, T-Cell Receptor gamma / genetics. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Oligopeptides / pharmacology. Stromal Cells / cytology. Stromal Cells / physiology. Tumor Cells, Cultured

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  • (PMID = 18984862.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / Oligopeptides; 0 / Receptor, Notch1; 0 / benzyloxycarbonyl-leucyl-leucyl-norleucinal; EC 3.4.- / Amyloid Precursor Protein Secretases
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86. Tong X, Zhang L, Zhang L, Hu M, Leng J, Yu B, Zhou B, Hu Y, Zhang Q: The mechanism of chemokine receptor 9 internalization triggered by interleukin 2 and interleukin 4. Cell Mol Immunol; 2009 Jun;6(3):181-9
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  • In previous study, we found that the chemokine receptor 9 (CCR9) was highly expressed on CD4+ T cells from patients with T-cell lineage acute lymphocytic leukemia (T-ALL) and mediated leukemia cell infiltration and metastasis.
  • Combined use of interleukin 2 (IL-2) and IL-4 promoted the internalization of CCR9 and therefore attenuated leukemia cell infiltration and metastasis.
  • In this study, we preliminarily investigated the mechanism of internalization of CCR9 on MOLT4 cell model (a human leukemia T-cell line, naturally expresses CCR9) and found that IL-2 upregulated the cell surface expression of IL-4Ralpha (CD124) greatly, whereas IL-4 had no significant influence on alpha (CD25) and beta subunits (CD122) of IL-2R.
  • Furthermore, GRK2 was upregulated and translocated to cell membrane in IL-2 and IL-4 treated cells which indicated that PKC could be a prerequisite for GRK2 activity.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / metabolism. Flow Cytometry. G-Protein-Coupled Receptor Kinase 2 / genetics. G-Protein-Coupled Receptor Kinase 2 / metabolism. G-Protein-Coupled Receptor Kinase 3 / genetics. G-Protein-Coupled Receptor Kinase 3 / metabolism. G-Protein-Coupled Receptor Kinase 5 / genetics. G-Protein-Coupled Receptor Kinase 5 / metabolism. G-Protein-Coupled Receptor Kinases / genetics. G-Protein-Coupled Receptor Kinases / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Interleukin-2 Receptor alpha Subunit / metabolism. Interleukin-2 Receptor beta Subunit / metabolism. Isoquinolines / pharmacology. Leukemia, T-Cell / genetics. Leukemia, T-Cell / metabolism. Leukemia, T-Cell / pathology. Protein Kinase Inhibitors / pharmacology. RNA Interference. Receptors, Interleukin-2 / metabolism. Receptors, Interleukin-4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sulfonamides / pharmacology

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

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

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  • (PMID = 16840318.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1563733
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89. Komuro T, Okamoto S: Pure intracerebral mass lesion of adult T-cell leukemia/lymphoma--case report. Neurol Med Chir (Tokyo); 2010;50(6):492-4
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  • [Title] Pure intracerebral mass lesion of adult T-cell leukemia/lymphoma--case report.
  • A 48-year-old female presented with a rare case of adult T-cell leukemia/lymphoma (ATL) occurring as only intracerebral mass lesion manifesting as progressively worsening headaches, transient mild weakness of the left lower extremity, bilateral papilledema, and left homonymous hemianopsia.
  • The patient underwent gross total removal, and the histological diagnosis was intracerebral ATL.
  • Intracerebral ATL should be considered in the differential diagnosis of intracerebral mass without leukemia or systemic lymphoma.
  • [MeSH-major] Brain Neoplasms / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Occipital Lobe / pathology

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

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  • (PMID = 15793300.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / C19orf10 protein, human; 0 / IL27 protein, human; 0 / Interleukins; 0 / NF-kappa B
  • [Other-IDs] NLM/ PMC1602381
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91. Barnes JA, Abramson JS: Adult T-cell leukemia/lymphoma: complexities in diagnosis and novel treatment strategies. Oncology (Williston Park); 2009 Dec;23(14):1267, 1270
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  • [Title] Adult T-cell leukemia/lymphoma: complexities in diagnosis and novel treatment strategies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Deltaretrovirus Antibodies / blood. Diagnosis, Differential. Emigrants and Immigrants. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Transplantation, Homologous. United States

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  • [CommentOn] Oncology (Williston Park). 2009 Dec;23(14):1250-6 [20120837.001]
  • (PMID = 20120839.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Deltaretrovirus Antibodies
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92. Yang Y, Takeuchi S, Tsukasaki K, Yamada Y, Hata T, Mori N, Fukushima A, Seo H, Koeffler HP, Taguchi H: Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma. Leuk Res; 2005 Jan;29(1):47-51
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  • [Title] Methylation analysis of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma.
  • We investigated methylation status of the adenomatous polyposis coli (APC) gene in adult T-cell leukemia/lymphoma (ATL).
  • APC methylation was found in 15 of 31 (48%) primary samples, and 2 of 4 (50%) ATL cell lines.
  • Methylation of the APC gene occurred more frequently in acute ATL (12/21) (57%) than chronic ATL (1/8) (13%) (P = 0.03).
  • APC was not expressed in the APC-methylated ATL cell line ST1.
  • Demethylation with 5-azacytidine treatment restored APC expression in the ST1 cell line.
  • Our data show that hypermethylation of the APC gene is involved in the pathogenesis of ATL.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. DNA Methylation. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Azacitidine / pharmacology. Cell Line, Tumor. CpG Islands / genetics. Disease Progression. Humans. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Leuk Res. 2005 May;29(5):475-6 [15755498.001]
  • (PMID = 15541474.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; M801H13NRU / Azacitidine
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93. Morozov VA, Syrtsev AV, Ellerbrok H, Nikolaeva EV, Bavykin AS, Pauli G: Mycosis fungoides in European Russia: no antibodies to human T cell leukemia virus type I structural proteins, but virus-like sequences in blood and saliva. Intervirology; 2005;48(6):362-71
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  • [Title] Mycosis fungoides in European Russia: no antibodies to human T cell leukemia virus type I structural proteins, but virus-like sequences in blood and saliva.
  • OBJECTIVE: Mycosis fungoides (MF) is the most frequent form of cutaneous T cell lymphoma (CTCL).
  • Human T cell leukemia virus type 1 (HTLV-1) involvement in MF progression is a matter of debate.
  • The goal of the investigation was to search for HTLV-1 markers in a group of MF patients from a nonendemic area to HTLV-1.
  • MATERIALS AND METHODS: Fifty MF patients and 60 healthy donors from Moscow and the Moscow region were examined for HTLV-1 markers by Western blot, PCR, nested PCR, PCR/Southern hybridization, TaqMan real-time PCR and sequencing.
  • RESULTS: Plasma samples from MF patients were repeatedly negative for antibodies to HTLV-1 structural proteins.
  • HTLV-1 tax-related sequences (corresponding to the second exon) were found in blood from 20 of 50 MF patients and in 3 of 5 saliva specimens.
  • Three of 8 sequenced tax-like amplimers were identical and 5 of 8 contained 1-2 substitutions. tax transcripts and antibodies to p40(tax) were detected in some 'PCR-tax'-positive MF patients.
  • Defective HTLV-1 genomes were demonstrated in 2 of 50 MF patients.
  • Phylogenetic analysis of the defective genome 5'-LTR sequence revealed a relationship with HTLV-1a sequences from the transcontinental subgroup of HTLV-1.
  • CONCLUSIONS: HTLV-1 tax-like sequences were revealed in blood and for the first time in saliva from MF patients living in an HTLV-1 nonendemic region.
  • [MeSH-major] Blood / virology. Genes, pX. HTLV-I Antibodies / blood. Human T-lymphotropic virus 1 / genetics. Mycosis Fungoides / virology. Saliva / virology. Skin Neoplasms / virology
  • [MeSH-minor] Adult. Amino Acid Substitution. Blotting, Southern. Blotting, Western. DNA, Viral / chemistry. DNA, Viral / genetics. Defective Viruses. Female. Genome, Viral. Humans. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Russia. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16024940.001).
  • [ISSN] 0300-5526
  • [Journal-full-title] Intervirology
  • [ISO-abbreviation] Intervirology
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF515451
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / HTLV-I Antibodies
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94. Yamamoto K, Utsunomiya A, Tobinai K, Tsukasaki K, Uike N, Uozumi K, Yamaguchi K, Yamada Y, Hanada S, Tamura K, Nakamura S, Inagaki H, Ohshima K, Kiyoi H, Ishida T, Matsushima K, Akinaga S, Ogura M, Tomonaga M, Ueda R: Phase I study of KW-0761, a defucosylated humanized anti-CCR4 antibody, in relapsed patients with adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma. J Clin Oncol; 2010 Mar 20;28(9):1591-8
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  • [Title] Phase I study of KW-0761, a defucosylated humanized anti-CCR4 antibody, in relapsed patients with adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma.
  • This phase I study assessed the safety, pharmacokinetics, recommended phase II dose and efficacy of KW-0761 in patients with relapsed CCR4-positive adult T-cell leukemia-lymphoma (ATL) or peripheral T-cell lymphoma (PTCL).
  • Other treatment-related grade 3 to 4 toxicities were lymphopenia (n = 10), neutropenia (n = 3), leukopenia (n = 2), herpes zoster (n = 1), and acute infusion reaction/cytokine release syndrome (n = 1).
  • CONCLUSION: KW-0761 was tolerated at all the dose levels tested, demonstrating potential efficacy against relapsed CCR4-positive ATL or PTCL.
  • [MeSH-major] Antibodies, Anti-Idiotypic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell, Peripheral / drug therapy. Receptors, CCR4 / antagonists & inhibitors

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

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

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

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

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

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  • (PMID = 20019193.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2797900
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100. Kawakami H, Tomita M, Matsuda T, Ohta T, Tanaka Y, Fujii M, Hatano M, Tokuhisa T, Mori N: Transcriptional activation of survivin through the NF-kappaB pathway by human T-cell leukemia virus type I tax. Int J Cancer; 2005 Jul 20;115(6):967-74
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  • [Title] Transcriptional activation of survivin through the NF-kappaB pathway by human T-cell leukemia virus type I tax.
  • We previously reported the survivin expression profile in ATL, a CD4-positive T-cell malignancy caused by HTLV-I.
  • HTLV-I Tax is thought to play an important role in immortalization of T cells.
  • We have shown also that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by deprivation of IL-2 and converted its growth from being IL-2 dependent to being IL-2 independent through the NF-kappaB pathway.
  • In our study, we demonstrate that constitutive expression of survivin was associated with resistance to apoptosis after IL-2 deprivation in Tax-expressing CTLL-2 cells.
  • Our findings suggest that activated NF-kappaB signaling contributes directly to malignant progression of ATL by preventing apoptosis, acting through the prosurvival protein survivin.
  • [MeSH-major] Gene Products, tax / pharmacology. Leukemia-Lymphoma, Adult T-Cell / metabolism. Microtubule-Associated Proteins / metabolism. NF-kappa B / metabolism
  • [MeSH-minor] Animals. Apoptosis. Base Sequence. Gene Expression Regulation, Leukemic. Human T-lymphotropic virus 1. Humans. Inhibitor of Apoptosis Proteins. Interleukin-2 / metabolism. Jurkat Cells. Mice. Neoplasm Proteins. Promoter Regions, Genetic. Signal Transduction. Transcriptional Activation. Transfection. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15729715.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Gene Products, tax; 0 / Inhibitor of Apoptosis Proteins; 0 / Interleukin-2; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins
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