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1. Osborne GE, Pagliuca A, Ho A, du Vivier AW: Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody). Br J Dermatol; 2006 Sep;155(3):617-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody).
  • We describe a patient with erythrodermic adult T-cell leukaemia/lymphoma resistant to multiple systemic therapies who, on the commencement of daclizumab, a humanized anti-interleukin-2 receptor antibody, developed a rapid and sustained complete response with resolution of previously debilitating erythroderma, suggesting significant activity of this agent in this disease process.

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  • (PMID = 16911291.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; CUJ2MVI71Y / daclizumab
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2. Saito K, Saito M, Taniura N, Okuwa T, Ohara Y: Activation of the PI3K-Akt pathway by human T cell leukemia virus type 1 (HTLV-1) oncoprotein Tax increases Bcl3 expression, which is associated with enhanced growth of HTLV-1-infected T cells. Virology; 2010 Aug 1;403(2):173-80
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  • [Title] Activation of the PI3K-Akt pathway by human T cell leukemia virus type 1 (HTLV-1) oncoprotein Tax increases Bcl3 expression, which is associated with enhanced growth of HTLV-1-infected T cells.
  • Bcl3 is a member of the IkappaB family that regulates genes involved in cell proliferation and apoptosis.
  • Recent reports indicated that Bcl3 is overexpressed in HTLV-1-infected T cells via Tax-mediated transactivation, and acts as a negative regulator of viral transcription.
  • However, the role of Bcl3 in cellular signal transduction and the growth of HTLV-1-infected T cells have not been reported.
  • In this study, we showed that the knockdown of Bcl3 by short hairpin RNA inhibited the growth of HTLV-1-infected T cells.
  • Although phosphatidylinositol-3 kinase (PI3K) inhibitor reduced Bcl3 expression, inactivation of glycogen synthase kinase 3 (GSK3), an effector kinase of the PI3K/Akt signaling pathway, restored Bcl3 expression in Tax-negative but not in Tax-positive T cells.
  • Our results indicate that the overexpression of Bcl3 in HTLV-1-infected T cells is regulated not only by transcriptional but also by post-transcriptional mechanisms, and is involved in overgrowth of HTLV-1-infected T cells.
  • [MeSH-major] Gene Products, tax / physiology. Human T-lymphotropic virus 1 / pathogenicity. Oncogene Protein v-akt / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins / biosynthesis. T-Lymphocytes / virology. Transcription Factors / biosynthesis. Virulence Factors / physiology
  • [MeSH-minor] Cell Line. Cell Proliferation. Gene Knockdown Techniques. Humans. RNA, Small Interfering / genetics

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  • (PMID = 20471052.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [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 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / Virulence Factors; 0 / proto-oncogene protein bcl-3; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Oncogene Protein v-akt
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3. 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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4. 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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5. Heidecker G, Lloyd PA, Soheilian F, Nagashima K, Derse D: The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1. J Virol; 2007 Sep;81(18):9769-77
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  • [Title] The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1.
  • The PPPY motif in the matrix (MA) domain of human T-cell leukemia virus type 1 (HTLV-1) Gag associates with WWP1, a member of the HECT domain containing family of E3 ubiquitin ligases.
  • Virus-like particles produced by the K74R mutant did not contain ubiquitinated MA and showed a fourfold reduction in the release of infectious particles.
  • This finding indicates that the interaction between Gag and WWP1 is required for functions other than Gag ubiquitination.

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  • (PMID = 17609263.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / PHS HHS / / N01 C0 12400; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, gag; 0 / Ubiquitin; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / WWP1 protein, human
  • [Other-IDs] NLM/ PMC2045422
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6. Nakase K, Hara M, Kozuka T, Tanimoto K, Nawa Y: Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma. Bone Marrow Transplant; 2006 Jan;37(1):41-4
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  • [Title] Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a highly aggressive haematological malignancy.
  • More than 40 cases of ATLL treated by allogeneic bone marrow transplantation (BMT) from sibling donors have been reported, while there have been only a few cases of unrelated BMT for treatment of this disease.
  • We began performing allogeneic BMT from unrelated donors in 1999 to improve the outcome of ATLL patients with no suitable sibling donors.
  • Eight ATLL patients underwent unrelated BMT; five received the conventional conditioning regimen consisting of cyclophosphamide and total body irradiation, while three received a reduced-intensity preparative regimen.
  • Two patients died due to encephalopathy of unknown aetiology on days 10 and 35, and one patient died due to progression of ATLL 25 months after BMT.
  • Five patients are currently alive and disease-free at a median of 20 months after BMT.
  • Proviral human T-lymphotropic virus type-I (HTLV-I) DNA load in peripheral blood mononuclear cells (PBMCs) was assessed in four cases before and after BMT.
  • HTLV-I proviral DNA load was reduced significantly after transplantation.
  • Unrelated BMT is feasible for treatment of ATLL.
  • Further studies in a larger number of cases are required to determine the optimal conditioning regimen and stem cell source.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy. Living Donors. Transplantation Conditioning
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Histocompatibility Testing. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Retrospective Studies. Transplantation, Homologous. Whole-Body Irradiation / methods


7. Kashima K, Daa T, Yokoyama S: Detection of HTLV-1 gene on cytologic smear slides. Methods Mol Biol; 2005;304:183-9
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  • [Title] Detection of HTLV-1 gene on cytologic smear slides.
  • In this chapter we describe a method for the detection of human T-cell leukemia virus type 1 (HTLV-1) genes in cytologic smears by polymerase chain reaction (PCR).
  • We use two sets of primers for detection of HTLV-1 genes, and the products of amplification by PCR that correspond to the pX and tax regions are expected to be 127 and 159 base pairs long, respectively.
  • Although this method does not provide proof of the monoclonal integration of HTLV-1 genes, it can be applied when adult T-cell leukemia/lymphoma is suspected cytologically but fresh samples for Southern blotting are unavailable.
  • [MeSH-major] Cytodiagnosis / methods. Genes, Viral. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Polymerase Chain Reaction / methods

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  • (PMID = 16061975.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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8. Yasunami T, Wang YH, Tsuji K, Takanashi M, Yamada Y, Motoji T: Multidrug resistance protein expression of adult T-cell leukemia/lymphoma. Leuk Res; 2007 Apr;31(4):465-70
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  • [Title] Multidrug resistance protein expression of adult T-cell leukemia/lymphoma.
  • In adult T-cell leukemia/lymphoma (ATL), it is difficult to achieve remission and the reason for the resistance to chemotherapeutic agents may be linked to the presence of multidrug resistance (MDR) proteins.
  • Lung resistance-related protein (LRP), multidrug resistance-associated protein and P-glycoprotein are three MDR proteins which we examined in ATL cells using multiparametric flow cytometry and real-time RT-PCR.
  • This indicates LRP may be contributing to drug resistance in ATL patients, and the suppression of LRP function could be a new strategy for ATL treatment.
  • [MeSH-major] Drug Resistance, Multiple. Gene Expression Regulation, Leukemic. Gene Expression Regulation, Neoplastic. Leukemia-Lymphoma, Adult T-Cell / metabolism. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / metabolism
  • [MeSH-minor] Adult. Aged. Antibiotics, Antineoplastic / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17134750.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 80168379AG / Doxorubicin
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9. Coskun AK, Sutton RE: Expression of glucose transporter 1 confers susceptibility to human T-cell leukemia virus envelope-mediated fusion. J Virol; 2005 Apr;79(7):4150-8
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  • [Title] Expression of glucose transporter 1 confers susceptibility to human T-cell leukemia virus envelope-mediated fusion.
  • Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus identified and causes both adult T-cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy, among other disorders.
  • In vitro, HTLV-1 has an extremely broad host cell tropism in that it is capable of infecting most mammalian cell types, although at the same time viral titers remain relatively low.
  • Although glut-1 was shown to bind specifically to the ectodomain of HTLV-1 and HTLV-2 envelope glycoproteins, which was reversible with small interfering RNA directed against glut-1, cellular susceptibility to HTLV upon expression of glut-1 was not established.
  • Here we show that expression of glut-1 in relatively resistant MDBK cells conferred increased susceptibility to both HTLV-1- and HTLV-2-pseudotyped particles. glut-1 also markedly increased syncytium formation in MDBK cells after exposure to HTLV-1.
  • Another assay also demonstrated HTLV-1 envelope-cell fusion in the presence of glut-1.
  • Taken together, these results provide additional evidence that glut-1 is a receptor for HTLV.
  • [MeSH-major] Cell Fusion. Giant Cells / physiology. Human T-lymphotropic virus 1 / physiology. Human T-lymphotropic virus 2 / physiology. Monosaccharide Transport Proteins / biosynthesis. Receptors, Virus / biosynthesis
  • [MeSH-minor] Animals. Cattle. Cell Line. Cells, Cultured. Flow Cytometry. Glucose Transporter Type 1. Microscopy, Fluorescence. Staining and Labeling

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  • (PMID = 15767416.001).
  • [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 / Glucose Transporter Type 1; 0 / Monosaccharide Transport Proteins; 0 / Receptors, Virus
  • [Other-IDs] NLM/ PMC1061550
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10. Taniguchi Y, Nosaka K, Yasunaga J, Maeda M, Mueller N, Okayama A, Matsuoka M: Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms. Retrovirology; 2005;2:64
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  • [Title] Silencing of human T-cell leukemia virus type I gene transcription by epigenetic mechanisms.
  • BACKGROUND: Human T-cell leukemia virus type I (HTLV-I) causes adult T-cell leukemia (ATL) after a long latent period.
  • Among accessory genes encoded by HTLV-I, the tax gene is thought to play a central role in oncogenesis.
  • To clarify the role of epigenetic changes, we analyzed DNA methylation and histone modification in the whole HTLV-I provirus genome.
  • RESULTS: The gag, pol and env genes of HTLV-I provirus were more methylated than pX region, whereas methylation of 5'-LTR was variable and 3'-LTR was not methylated at all.
  • In ATL cell lines, complete DNA methylation of 5'-LTR was associated with transcriptional silencing of viral genes.
  • HTLV-I provirus was more methylated in primary ATL cells than in carrier state, indicating the association with disease progression.
  • Analysis of histone modification in the HTLV-I provirus showed that the methylated provirus was associated with hypoacetylation.
  • However, the tax gene transcript could not be detected in fresh ATL cells regardless of hyperacetylated histone H3 in 5'-LTR.
  • The transcription rapidly recovered after in vitro culture in such ATL cells.
  • CONCLUSION: These results showed that epigenetic changes of provirus facilitated ATL cells to evade host immune system by suppressing viral gene transcription.
  • [MeSH-major] Epigenesis, Genetic. Gene Silencing. Human T-lymphotropic virus 1 / genetics. Transcription, Genetic
  • [MeSH-minor] Carrier State / virology. Cell Line. DNA Methylation. Histones / metabolism. Humans. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. Terminal Repeat Sequences

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  • (PMID = 16242045.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histones
  • [Other-IDs] NLM/ PMC1289293
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11. Higuchi M, Tsubata C, Kondo R, Yoshida S, Takahashi M, Oie M, Tanaka Y, Mahieux R, Matsuoka M, Fujii M: Cooperation of NF-kappaB2/p100 activation and the PDZ domain binding motif signal in human T-cell leukemia virus type 1 (HTLV-1) Tax1 but not HTLV-2 Tax2 is crucial for interleukin-2-independent growth transformation of a T-cell line. J Virol; 2007 Nov;81(21):11900-7
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  • [Title] Cooperation of NF-kappaB2/p100 activation and the PDZ domain binding motif signal in human T-cell leukemia virus type 1 (HTLV-1) Tax1 but not HTLV-2 Tax2 is crucial for interleukin-2-independent growth transformation of a T-cell line.
  • Human T-cell leukemia virus type 1 (HTLV-1) but not HTLV-2 is associated with adult T-cell leukemia, and the distinct pathogenicity of these two closely related viruses is thought to stem from the distinct biological functions of the respective transforming proteins, HTLV-1 Tax1 and HTLV-2 Tax2.
  • Using RNA interference methods, we further show that NF-kappaB2/p100 is required for the transformation induced by Tax1, as determined by the ability to convert a T-cell line (CTLL-2) from interleukin-2 (IL-2)-dependent to -independent growth.
  • These results reveal that the activation of NF-kappaB2/p100 plays a crucial role in the Tax1-mediated transformation of T cells and that NF-kappaB2/p100 activation and PBM function are both responsible for the augmented transforming activity of Tax1 relative to Tax2, thus suggesting that these Tax1-specific functions play crucial roles in HTLV-1 leukemogenesis.
  • [MeSH-major] Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / metabolism. Human T-lymphotropic virus 2 / metabolism. Interleukin-2 / metabolism. Leukemia / pathology. NF-kappa B p52 Subunit / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Amino Acid Motifs. Animals. Cell Line, Transformed. Cell Line, Tumor. Cell Transformation, Viral. Humans. Mice. Protein Structure, Tertiary


12. Wielgosz MM, Rauch DA, Jones KS, Ruscetti FW, Ratner L: Cholesterol dependence of HTLV-I infection. AIDS Res Hum Retroviruses; 2005 Jan;21(1):43-50
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  • [Title] Cholesterol dependence of HTLV-I infection.
  • Cholesterol-rich plasma membrane microdomains are important for entry of many viruses, including retroviruses.
  • Depletion of cholesterol with 2-hydroxypropyl-beta-cyclodextrin inhibits entry of human T cell leukemia virus type I (HTLV-1) and HTLV-I envelope pseudotyped lentivirus particles.
  • Using a soluble fusion protein of the HTLV-I surface envelope protein with the immunoglobulin Fc domain, the HTLV-I receptor was found to colocalize with a raft-associated marker and to cluster in specific plasma membrane microdomains.
  • Depletion of cholesterol did not alter receptor binding activity, suggesting a requirement for cholesterol in a postbinding virus entry step.

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  • (PMID = 15665643.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA093062-02; United States / NCI NIH HHS / CA / R21 CA093062; United States / NCI NIH HHS / CA / P01 CA100730-02; United States / NCI NIH HHS / CA / CA093062-02; United States / NCI NIH HHS / CA / CA063417-09; None / None / / P01 CA100730-01; United States / NCI NIH HHS / CA / P01 CA100730-01; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / R01 CA063417-09
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HTLV-I receptor; 0 / Receptors, Virus; 0 / Viral Envelope Proteins; 0 / beta-Cyclodextrins; 94035-02-6 / 2-hydroxypropyl-beta-cyclodextrin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ NIHMS94161; NLM/ PMC2671014
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13. Foucar K: Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome. Am J Clin Pathol; 2007 Apr;127(4):496-510
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  • [Title] Mature T-cell leukemias including T-prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The 2005 Society for Hematopathology/European Association for Haematopathology Workshop Session 1 was devoted to case presentations with discussions of 3 types of mature T-cell leukemias--T-cell prolymphocytic leukemia, adult T-cell leukemia/lymphoma, and Sézary syndrome.
  • The application of clinical, morphologic, immunophenotypic, and genetic studies to the assessment and characterization of these 3 disorders is presented, along with specific diagnostic recommendations and differential diagnostic considerations.
  • [MeSH-major] Leukemia, Prolymphocytic / diagnosis. Leukemia, T-Cell / diagnosis. Sezary Syndrome / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antigens, CD / metabolism. Chromosome Aberrations. Diagnosis, Differential. Humans. Immunophenotyping

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  • (PMID = 17369126.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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14. Wang SS, Carreon JD, Hanchard B, Chanock S, Hisada M: Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica. Int J Cancer; 2009 Sep 15;125(6):1479-82
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  • [Title] Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica.
  • We evaluated whether risk of non-Hodgkin lymphoma (NHL), particularly adult T-cell leukemia/lymphoma (ATL) related to human T-lymphotropic virus (HTLV) infection was associated with 63 single nucleotide polymorphisms (SNPs) from 38 candidate genes.
  • The 395 NHL cases registered in Jamaica were matched by age, sex, calendar-year and HTLV serostatus to 309 controls from the same population.
  • Interleukin 13 (IL13) Ex4+98A>G SNP (rs20541) was associated with decreased NHL risk (OR(AG/AA) = 0.62,95% CI = 0.44-0.87, p = 0.006), as was vascular cell adhesion molecule-1, VCAM1 Ex9+149G>A SNP (rs1041163) (OR(CT) = 0.77, 95% CI = 0.54-1.10, OR(CC) = 0.35, 95% CI = 0.16-0.76, p-trend = 0.007).
  • Both results were stronger in analyses restricted to ATL cases and HTLV-positive controls, suggesting a role for these genes in ATL etiology (IL13 OR(AG/AA) = 0.54, 95% CI = 0.36-0.84, p = 0.005; VCAM1 OR(CT) = 0.65, 95% CI = 0.42-1.01, OR(CC) = 0.20, 95% CI = 0.08-0.54, p-trend = 0.001).
  • [MeSH-major] HTLV-I Infections / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Polymorphism, Single Nucleotide / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Genetic Predisposition to Disease. Human T-lymphotropic virus 1 / immunology. Humans. Interleukin-13 / genetics. Interleukin-5 / genetics. Jamaica / epidemiology. Male. Middle Aged. Vascular Cell Adhesion Molecule-1 / genetics. Young Adult

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  • [Copyright] 2009 UICC
  • (PMID = 19533685.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL5 protein, human; 0 / Interleukin-13; 0 / Interleukin-5; 0 / Vascular Cell Adhesion Molecule-1
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15. Machijima Y, Ishikawa C, Sawada S, Okudaira T, Uchihara JN, Tanaka Y, Taira N, Mori N: Anti-adult T-cell leukemia/lymphoma effects of indole-3-carbinol. Retrovirology; 2009;6:7
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  • [Title] Anti-adult T-cell leukemia/lymphoma effects of indole-3-carbinol.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is a malignancy derived from T cells infected with human T-cell leukemia virus type 1 (HTLV-1), and it is known to be resistant to standard anticancer therapies.
  • The aim of this study was to determine the potential anti-ATLL effects of I3C both in vitro and in vivo.
  • RESULTS: In the in vitro study, I3C inhibited cell viability of HTLV-1-infected T-cell lines and ATLL cells in a dose-dependent manner.
  • Importantly, I3C did not exert any inhibitory effect on uninfected T-cell lines and normal peripheral blood mononuclear cells.
  • The induced apoptosis was associated with activation of caspase-3, -8 and -9, and poly(ADP-ribose) polymerase cleavage.
  • Inoculation of HTLV-1-infected T cells in mice with severe combined immunodeficiency resulted in tumor growth.
  • CONCLUSION: Our preclinical data suggest that I3C could be potentially a useful chemotherapeutic agent for patients with ATLL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Survival / drug effects. Human T-lymphotropic virus 1 / drug effects. Indoles / pharmacology. Indoles / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. T-Lymphocytes
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle Proteins / drug effects. Cell Line, Transformed. Cell Line, Tumor. G1 Phase / drug effects. Humans. Mice. Mice, SCID. Treatment Outcome


16. Zimmerman EI, Huang M, Leisewitz AV, Wang Y, Yang J, Graves LM: Identification of a novel point mutation in ENT1 that confers resistance to Ara-C in human T cell leukemia CCRF-CEM cells. FEBS Lett; 2009 Jan 22;583(2):425-9
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  • [Title] Identification of a novel point mutation in ENT1 that confers resistance to Ara-C in human T cell leukemia CCRF-CEM cells.
  • The genetic basis for the Ara-C resistance of CCRF-CEM Ara-C/8C leukemia cells was investigated.

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  • (PMID = 19116148.001).
  • [ISSN] 1873-3468
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM069976-04; United States / NIGMS NIH HHS / GM / R01 GM069976; United States / NIGMS NIH HHS / GM / R01-GM069976; United States / NIGMS NIH HHS / GM / GM069976-01A1; United States / NIGMS NIH HHS / GM / R01 GM069976-01A1; United States / NIGMS NIH HHS / GM / GM069976-03; United States / NIGMS NIH HHS / GM / R01 GM069976-02; United States / NIGMS NIH HHS / GM / GM069976-02; United States / NIGMS NIH HHS / GM / R01 GM069976-03; United States / NIGMS NIH HHS / GM / R01 GM069976-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine; 38048-32-7 / 4-nitrobenzylthioinosine; 46S541971T / Thioinosine; TE7660XO1C / Glycine
  • [Other-IDs] NLM/ NIHMS92165; NLM/ PMC2647365
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17. Takeuchi S, Hofmann WK, Tsukasaki K, Takeuchi N, Ikezoe T, Matsushita M, Uehara Y, Phillip Koeffler H: Loss of H19 imprinting in adult T-cell leukaemia/lymphoma. Br J Haematol; 2007 May;137(4):380-1
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  • [Title] Loss of H19 imprinting in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Genes, Tumor Suppressor. Leukemia-Lymphoma, Adult T-Cell / genetics. RNA, Untranslated
  • [MeSH-minor] Adult. Gene Deletion. Genomic Imprinting. Humans. RNA, Long Noncoding

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  • (PMID = 17408396.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / H19 long non-coding RNA; 0 / RNA, Long Noncoding; 0 / RNA, Untranslated
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18. Zane L, Sibon D, Mortreux F, Wattel E: Clonal expansion of HTLV-1 infected cells depends on the CD4 versus CD8 phenotype. Front Biosci (Landmark Ed); 2009;14:3935-41
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  • [Title] Clonal expansion of HTLV-1 infected cells depends on the CD4 versus CD8 phenotype.
  • As other deltaretroviruses HTLV-1 replication in vivo includes a first short step of reverse transcription that is followed by the persistent clonal expansion of infected cells.
  • In vivo these cells include the CD4+ and CD8+ lymphocytes yet the virus induces adult T cell leukemia/lymphoma (ATLL) that is regularly of the CD4+ phenotype.
  • In fact, the clonal expansion of HTLV-1 positive CD8+ and CD4+ lymphocytes relies on two distinct mechanisms: infection prevented cell death in the former whereas recruiting the latter into the cell cycle.
  • Therefore, HTLV-1 infection establishes a preleukemic phenotype that is restricted to CD4+ infected clones.
  • Investigating the mechanisms underlying apoptosis, cell cycling and DNA repair in cloned cells from naturally infected individuals will permit to deciphering the molecular pathogenesis of HTLV-1 infection.
  • [MeSH-major] CD4-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / cytology. Human T-lymphotropic virus 1 / physiology
  • [MeSH-minor] Genetic Variation. Humans. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / virology. Paraparesis, Tropical Spastic / blood. Paraparesis, Tropical Spastic / virology. Virus Replication

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  • (PMID = 19273324.001).
  • [ISSN] 1093-4715
  • [Journal-full-title] Frontiers in bioscience (Landmark edition)
  • [ISO-abbreviation] Front Biosci (Landmark Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 61
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19. Nyborg JK, Egan D, Sharma N: The HTLV-1 Tax protein: revealing mechanisms of transcriptional activation through histone acetylation and nucleosome disassembly. Biochim Biophys Acta; 2010 Mar-Apr;1799(3-4):266-74
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  • [Title] The HTLV-1 Tax protein: revealing mechanisms of transcriptional activation through histone acetylation and nucleosome disassembly.
  • The human T-cell leukemia virus, type-1 (HTLV-1)-encoded Tax protein is required for high-level transcription of the virus.
  • Tax expression in vivo recruits p300 to the HTLV-1 promoter and correlates with depletion of nucleosomes from the integrated provirus.
  • We recently developed a novel in vitro, chromatin-based experimental system that recapitulates the eviction of nucleosomes from the HTLV-1 promoter observed in vivo.
  • In this review, we will discuss HTLV-1, Tax transactivation, and our recent findings that uncover the critical role of Tax in promoting chromatin transitions that accompany activation of viral transcription.

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  • [Copyright] 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19782779.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA055035-16; United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA055035; United States / NCI NIH HHS / CA / R01 CA055035-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Histones; 0 / Nucleosomes
  • [Number-of-references] 116
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20. Akimoto M, Kozako T, Sawada T, Matsushita K, Ozaki A, Hamada H, Kawada H, Yoshimitsu M, Tokunaga M, Haraguchi K, Uozumi K, Arima N, Tei C: Anti-HTLV-1 tax antibody and tax-specific cytotoxic T lymphocyte are associated with a reduction in HTLV-1 proviral load in asymptomatic carriers. J Med Virol; 2007 Jul;79(7):977-86
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  • [Title] Anti-HTLV-1 tax antibody and tax-specific cytotoxic T lymphocyte are associated with a reduction in HTLV-1 proviral load in asymptomatic carriers.
  • Previous studies have suggested that higher anti-human T-lymphotropic virus 1 (HTLV-1) antibody titer and lower anti-HTLV-1 Tax antibody reactivity are risk factors for adult T-cell leukemia/lymphoma.
  • Forty-five carriers were examined for anti-HTLV-1 and anti-Tax antibody by ELISA.
  • In addition, 43 of the 45 carriers with HLA-A*0201 and/or A*2402 were examined for frequency of Tax-specific cytotoxic T lymphocytes (CTLs) using HTLV-1/HLA tetramers, and 44 were examined for proviral load by real-time PCR.
  • The frequencies of Tax11-19 and Tax301-309-specific CTLs were significantly higher in the anti-Tax antibody-positive group as compared with the antibody-negative group (P = 0.002 and 0.033, respectively).
  • Anti-HTLV-1 antibody titer had a positive correlation with proviral load (P = 0.019), whereas anti-Tax antibody did not show a significant correlation.
  • Synergistic interactions of humoral and cellular immunity against Tax protein were demonstrated in HTLV-1 carriers.
  • Tax-specific CTL may reduce HTLV-1 proviral load to prevent asymptomatic carriers from developing adult T-cell leukemia/lymphoma.
  • [MeSH-major] Carrier State / immunology. Carrier State / virology. Gene Products, tax / immunology. HTLV-I Antibodies / blood. HTLV-I Infections / immunology. HTLV-I Infections / virology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Sequence. Female. Human T-lymphotropic virus 1 / immunology. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Peptide Fragments / genetics. Peptide Fragments / immunology. Proviruses / immunology. Proviruses / isolation & purification. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 17516523.001).
  • [ISSN] 0146-6615
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [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 / HTLV-I Antibodies; 0 / Peptide Fragments
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21. Appert A, Nam CH, Lobato N, Priego E, Miguel RN, Blundell T, Drynan L, Sewell H, Tanaka T, Rabbitts T: Targeting LMO2 with a peptide aptamer establishes a necessary function in overt T-cell neoplasia. Cancer Res; 2009 Jun 01;69(11):4784-90
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  • [Title] Targeting LMO2 with a peptide aptamer establishes a necessary function in overt T-cell neoplasia.
  • LMO2 is a transcription regulator involved in human T-cell leukemia, including some occurring in X-SCID gene therapy trials, and in B-cell lymphomas and prostate cancer.
  • LMO2 functions in transcription complexes via protein-protein interactions involving two LIM domains and causes a preleukemic T-cell development blockade followed by clonal tumors.
  • The peptide inhibits Lmo2 function in a mouse T-cell tumor transplantation assay by preventing Lmo2-dependent T-cell neoplasia.
  • Lmo2 is, therefore, required for sustained T-cell tumor growth, in addition to its preleukemic effect.
  • [MeSH-major] Aptamers, Peptide / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. DNA-Binding Proteins / physiology. Drug Delivery Systems / methods. Metalloproteins / antagonists & inhibitors. Metalloproteins / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19487290.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0600914; United Kingdom / Medical Research Council / / MC/ U105178807; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Aptamers, Peptide; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins
  • [Other-IDs] NLM/ PMC2690635; NLM/ UKMS4469
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22. Kohno T, Yamada Y, Tawara M, Takasaki Y, Kamihira S, Tomonaga M, Matsuyama T: Inactivation of p14ARF as a key event for the progression of adult T cell leukemia/lymphoma. Leuk Res; 2007 Dec;31(12):1625-32
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  • [Title] Inactivation of p14ARF as a key event for the progression of adult T cell leukemia/lymphoma.
  • These results indicate that the inactivation of p14ARF plays a key role in the progression of ATLL.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Leukemia-Lymphoma, Adult T-Cell / etiology. Tumor Suppressor Protein p14ARF / metabolism
  • [MeSH-minor] Acute Disease. Adult. Chronic Disease. Disease Progression. Genes, p53 / genetics. Humans. Mutation. Polymerase Chain Reaction. Prognosis. RNA, Messenger / analysis. Survival Rate

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  • (PMID = 18246599.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF
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23. Shimizu S, Yasui C, Koizumi K, Ikeda H, Tsuchiya K: Cutaneous-type adult T-cell leukemia/lymphoma presenting as a solitary large skin nodule: a review of the literature. J Am Acad Dermatol; 2007 Nov;57(5 Suppl):S115-7
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  • [Title] Cutaneous-type adult T-cell leukemia/lymphoma presenting as a solitary large skin nodule: a review of the literature.
  • Adult T-cell leukemia/lymphoma (ATLL) often involves the skin.
  • While the clinical manifestations of the cutaneous-type ATLL are variable, including multiple papules, nodules, plaques, or erythroderma, a solitary skin nodule alone is rare, and only 2 cases have been reported in the literature.
  • We present a 58-year-old Japanese patient with cutaneous-type ATLL that presented as a large, solitary skin nodule as the sole clinical feature.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Skin Neoplasms / pathology

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  • (PMID = 17938020.001).
  • [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; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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24. McGirr KM, Buehuring GC: Tax & rex: overlapping genes of the Deltaretrovirus group. Virus Genes; 2006 Jun;32(3):229-39
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  • Bovine leukemia virus and human T-cell leukemia viruses I and II, members of the Deltaretrovirus group, have two regulatory genes, tax and rex, that are coded in overlapping reading frames.
  • We found that sequence variations in the rex gene of each virus result in amino acid differences significantly more often than variations in the tax gene.
  • For all three viruses the highest ratio of non-synonymous to synonymous changes was found in the rex gene.
  • Nucleotide C was present in all genes of the three viruses at the highest frequency and this bias was most pronounced in the rex gene.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cattle. Codon. Computational Biology. Consensus Sequence. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 2 / genetics. Humans. Leukemia Virus, Bovine / genetics. Sequence Alignment. Software

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  • (PMID = 16732475.001).
  • [ISSN] 0920-8569
  • [Journal-full-title] Virus genes
  • [ISO-abbreviation] Virus Genes
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32GM07127
  • [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 / Codon
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25. Kondo R, Higuchi M, Takahashi M, Oie M, Tanaka Y, Gejyo F, Fujii M: Human T-cell leukemia virus type 2 Tax protein induces interleukin 2-independent growth in a T-cell line. Retrovirology; 2006;3:88
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  • [Title] Human T-cell leukemia virus type 2 Tax protein induces interleukin 2-independent growth in a T-cell line.
  • BACKGROUND: While human T-cell leukemia virus type 1 (HTLV-1) is a causative agent of adult T-cell leukemia, HTLV type 2 (HTLV-2) is not associated with this malignancy.
  • Accumulating evidence suggests that Tax, a transforming protein of HTLV-1 or HTLV-2, plays a crucial role in the distinctive pathogenesis of these two infections.
  • We herein examined whether Tax2 by itself has a growth promoting activity in a mouse T-cell line CTLL-2, and compared the activity with that of Tax1.
  • RESULTS: We found that Tax2 converts the cell growth of CTLL-2 from an interleukin(IL)-2-dependent growth into an independent one.
  • While the HTLV-2-transformed human T-cell lines produce a significant amount of IL-2, Tax2-transformed CTLL-2 cells only produced a minimal amount of IL-2.
  • These results thus suggest that NFAT-inducible gene(s) other than IL-2 play a role in the cell growth of Tax2-transformed CTLL-2 cells.
  • CONCLUSION: These results show that HTLV-2 Tax2 by itself has a growth promoting activity toward a T-cell line CTLL-2, and the CTLL-2 assay used in this study may therefore be a useful tool for comparing the activity of Tax2 with that of Tax1 in T-cells, thereby elucidating the mechanism of HTLV-1 specific leukemogenesis.
  • [MeSH-major] Cell Transformation, Viral. Gene Products, tax / physiology. Human T-lymphotropic virus 2 / physiology. Interleukin-2 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / virology
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Proliferation. Humans. Mice

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  • (PMID = 17140451.001).
  • [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 / Gene Products, tax; 0 / Interleukin-2
  • [Other-IDs] NLM/ PMC1697825
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26. Yokote T, Akioka T, Hara S, Oka S, Miyamoto H, Yamano T, Sugino M, Tsuji M, Hanafusa T: Patients with malignancy requiring urgent therapy: CASE 2. Bilateral renal swelling induced by adult T-cell leukemia/lymphoma. J Clin Oncol; 2005 Sep 20;23(27):6793-4
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  • [Title] Patients with malignancy requiring urgent therapy: CASE 2. Bilateral renal swelling induced by adult T-cell leukemia/lymphoma.
  • [MeSH-major] Acute Kidney Injury / etiology. Bone Marrow / pathology. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Biopsy, Needle. Disease Progression. Fatal Outcome. Humans. Immunohistochemistry. Male. Middle Aged. Rare Diseases. Risk Assessment. Severity of Illness Index

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  • (PMID = 16170187.001).
  • [ISSN] 0732-183X
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
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27. Michael B, Nair AM, Datta A, Hiraragi H, Ratner L, Lairmore MD: Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity. Virology; 2006 Oct 25;354(2):225-39
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  • [Title] Histone acetyltransferase (HAT) activity of p300 modulates human T lymphotropic virus type 1 p30II-mediated repression of LTR transcriptional activity.
  • Human T-lymphotropic virus type-1 (HTLV-1) is a deltaretrovirus that causes adult T cell leukemia/lymphoma, and is implicated in a variety of lymphocyte-mediated inflammatory disorders.
  • HTLV-1 provirus has regulatory and accessory genes in four pX open reading frames.
  • HTLV-1 pX ORF-II encodes two proteins, p13II and p30II, which are incompletely defined in virus replication or pathogenesis.
  • We have demonstrated that pX ORF-II mutations block virus replication in vivo and that ORF-II encoded p30II, a nuclear-localizing protein that binds with CREB-binding protein (CBP)/p300, represses CREB and Tax responsive element (TRE)-mediated transcription.
  • Herein, we have identified p30II motifs important for p300 binding and in regulating TRE-mediated transcription in the absence and presence of HTLV-1 provirus.
  • Collectively, our data indicate that HTLV-1 p30II modulates viral gene expression in a cooperative manner with p300-mediated acetylation.

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  • (PMID = 16890266.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-70529; United States / NCI NIH HHS / CA / CA100730; United States / NCI NIH HHS / CA / P01 CA100730-03; United States / NCI NIH HHS / CA / CA92009; United States / NCI NIH HHS / CA / CA100730-03; United States / NCI NIH HHS / CA / R01 CA092009; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Retroviridae Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Viral Proteins; 0 / tof protein, Human T-lymphotropic virus 1; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors; EC 2.3.1.48 / p300-CBP-associated factor
  • [Other-IDs] NLM/ NIHMS183540; NLM/ PMC3044896
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28. Li K, Zhang S, Kronqvist M, Wallin M, Ekström M, Derse D, Garoff H: Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. J Virol; 2008 Jul;82(14):7135-43
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  • [Title] Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env.
  • Human T-cell leukemia virus (HTLV-1) Env carries a typical disulfide isomerization motif, C(225)XXC, in the C-terminal domain SU.
  • The importance of the CXXC-mediated disulfide isomerization for infection was studied using murine leukemia virus vectors pseudotyped with wild-type or C225A HTLV-1 Env.
  • We conclude that the fusion activity of HTLV-1 Env is controlled by an SU CXXC-mediated isomerization of the intersubunit disulfide.
  • [MeSH-major] Disulfides / metabolism. Gene Products, env / metabolism. Human T-lymphotropic virus 1 / physiology. Virus Internalization
  • [MeSH-minor] Amino Acid Substitution / genetics. Animals. Cell Line. Cricetinae. Dithiothreitol / pharmacology. Humans. Mutation, Missense. Rats. Reducing Agents / pharmacology

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  • (PMID = 18480461.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Disulfides; 0 / Gene Products, env; 0 / Reducing Agents; T8ID5YZU6Y / Dithiothreitol
  • [Other-IDs] NLM/ PMC2446982
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29. Silic-Benussi M, Cavallari I, Vajente N, Vidali S, Chieco-Bianchi L, Di Lisa F, Saggioro D, D'Agostino DM, Ciminale V: Redox regulation of T-cell turnover by the p13 protein of human T-cell leukemia virus type 1: distinct effects in primary versus transformed cells. Blood; 2010 Jul 8;116(1):54-62
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  • [Title] Redox regulation of T-cell turnover by the p13 protein of human T-cell leukemia virus type 1: distinct effects in primary versus transformed cells.
  • The present study investigated the function of p13, a mitochondrial protein of human T-cell leukemia virus type 1 (HTLV-1).
  • In transformed cells (Jurkat, HeLa), p13 did not affect ROS unless the cells were subjected to glucose deprivation, which led to a p13-dependent increase in ROS and cell death.
  • Using RNA interference we confirmed that expression of p13 also influences glucose starvation-induced cell death in the context of HTLV-1-infected cells.
  • These findings suggest that p13 may have a distinct impact on cell turnover depending on the inherent ROS levels; in the context of the HTLV-1 propagation strategy, p13 could increase the pool of "normal" infected cells while culling cells acquiring a transformed phenotype, thus favoring lifelong persistence of the virus in the host.
  • [MeSH-major] Human T-lymphotropic virus 1 / metabolism. Reactive Oxygen Species / metabolism. Retroviridae Proteins / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Cell Line. Cells, Cultured. Gene Expression Regulation, Viral. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HeLa Cells. Host-Pathogen Interactions. Humans. Jurkat Cells. Lentivirus / genetics. Microscopy, Confocal. Mitochondria / metabolism. Oxidation-Reduction. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transduction, Genetic

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  • (PMID = 20395415.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 147336-22-9 / Green Fluorescent Proteins
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30. Yamada Y: [Progress of the ATLL study: an overview]. Rinsho Ketsueki; 2005 May;46(5):339-49
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  • [Title] [Progress of the ATLL study: an overview].
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Apoptosis / genetics. Carboplatin / administration & dosage. Cyclin-Dependent Kinase Inhibitor p16. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Genes, p16. Genes, p53 / genetics. Hematopoietic Stem Cell Transplantation. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / pathogenicity. Humans. Leukemic Infiltration. Mutation. Nitrosourea Compounds / administration & dosage. Prednisolone / administration & dosage. Receptors, Cytokine. Vincristine / administration & dosage. Vindesine / administration & dosage

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINDESINE .
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  • (PMID = 16444967.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nitrosourea Compounds; 0 / Receptors, Cytokine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; BG3F62OND5 / Carboplatin; RSA8KO39WH / Vindesine; LSG15 regimen
  • [Number-of-references] 107
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31. Kim YM, Ramírez JA, Mick JE, Giebler HA, Yan JP, Nyborg JK: Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation. J Biol Chem; 2007 Jun 29;282(26):18750-7
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  • [Title] Molecular characterization of the Tax-containing HTLV-1 enhancer complex reveals a prominent role for CREB phosphorylation in Tax transactivation.
  • Transcriptional activation of human T-cell leukemia virus type 1 (HTLV-1) is mediated by the viral oncoprotein Tax, which utilizes cellular transcriptional machinery to perform this function.
  • The coactivator CREB-binding protein (CBP)/p300 binds to this promoter-bound ternary complex, which promotes the initiation of HTLV-1 transcription.
  • Consonant with a fundamental role for CREB phosphorylation in Tax recruitment to the complex, we found that CREB is highly phosphorylated in a panel of HTLV-1-infected human T-cell lines.
  • Because pCREB has been implicated in leukemogenesis, enhancement of CREB phosphorylation by the virus may play a role in the etiology of adult T-cell leukemia.

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  • (PMID = 17449469.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA055035; United States / NCI NIH HHS / CA / CA55035; United States / NCI NIH HHS / CA / CA055035-14S1; United States / NCI NIH HHS / CA / CA055035-14; United States / NCI NIH HHS / CA / R01 CA055035-14S1; United States / NCI NIH HHS / CA / CA55035-S1; United States / NCI NIH HHS / CA / R01 CA055035-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein
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32. Norris PJ, Hirschkorn DF, DeVita DA, Lee TH, Murphy EL: Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells. Virulence; 2010 Jan-Feb;1(1):19-28
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  • [Title] Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells.
  • Most human T cell leukemia virus type 1 (HTLV-1) infected subjects remain asymptomatic throughout their lives, with a few individuals developing HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) or adult T cell leukemia.
  • Lymphocytes from about half of HTLV-1 infected subjects spontaneously proliferate in vitro, and how this phenomenon relates to symptomatic disease outcome and viral burden is poorly understood.
  • Spontaneous proliferation was measured in lymphocyte subsets, and these findings were correlated with HTLV-1 proviral load and Tax expression in PBMCs.
  • We found that in addition to previously described vigorous CD8+ T cell spontaneous proliferation, natural killer (NK) cells spontaneously proliferated to a similar high level, resulting in expansion of CD56-expressing NK cells.
  • Spontaneous NK cell proliferation positively correlated with HTLV-1 proviral load but not with Tax expression or the presence of HAM/TSP.
  • The strongest correlate with clinical outcome in this cohort was the ability of cells to express Tax, while HTLV-1 proviral load was more closely related to spontaneous NK cell proliferation.
  • These results demonstrate that spontaneous proliferation, Tax expression, and proviral load are inter-related but not equivalent, and that spontaneous lymphocyte proliferation is not restricted to T cells, the targets of HTLV-1 infection.

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  • (PMID = 20640055.001).
  • [ISSN] 2150-5608
  • [Journal-full-title] Virulence
  • [ISO-abbreviation] Virulence
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL062235-04; United States / NHLBI NIH HHS / HL / R01 HL062235; United States / NHLBI NIH HHS / HL / HL-062235; United States / NHLBI NIH HHS / HL / R01 HL062235-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Gene Products, tax; 0 / NCAM1 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Keywords] NOTNLM ; HAM/TSP / HTLV / NK cell / T cell / Tax
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33. Hasegawa H, Yamada Y, Harasawa H, Tsuji T, Murata K, Sugahara K, Tsuruda K, Ikeda S, Imaizumi Y, Tomonaga M, Masuda M, Takasu N, Kamihira S: Sensitivity of adult T-cell leukaemia lymphoma cells to tumour necrosis factor-related apoptosis-inducing ligand. Br J Haematol; 2005 Jan;128(2):253-65
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  • [Title] Sensitivity of adult T-cell leukaemia lymphoma cells to tumour necrosis factor-related apoptosis-inducing ligand.
  • Adult T-cell leukaemia lymphoma (ATLL) is a neoplasm of T-lymphocyte origin aetiologically associated with human T-lymphotropic virus type 1 (HTLV-I), and is resistant to standard anti-cancer therapy.
  • We thus characterized the sensitivity of ATLL cells to TRAIL in this study.
  • Although most primary ATLL cells and cell lines expressed TRAIL death receptors on their surface, they showed only restricted sensitivity to TRAIL.
  • Among the 10 ATLL cell lines examined, one was sensitive, but two had insufficient death-receptor expression, two had an unknown resistant mechanism with abrogation of the death signal upstream of caspase-8, and the remaining five showed attenuation of the signal in both extrinsic and intrinsic pathways by X-linked inhibitor of apoptosis and Bcl-2/Bcl-xL respectively.
  • Furthermore, the level of HTLV-I tax expression was significantly correlated to TRAIL resistance.
  • Interestingly, ATLL cells themselves expressed TRAIL on the cell surface.
  • Constitutive production of TRAIL may offer resistance, thus allowing the development of TRAIL-resistant ATLL cells.
  • Consequently, the resistant mechanism in ATLL cells against TRAIL was assigned to multiple factors and was not explained by a definitive single agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Membrane Glycoproteins / therapeutic use. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 15638862.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
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34. Morris JC, Waldmann TA: Antibody-based therapy of leukaemia. Expert Rev Mol Med; 2009;11:e29
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  • [Title] Antibody-based therapy of leukaemia.
  • Over the past decade, monoclonal antibodies have dramatically impacted the treatment of haematological malignancies, as evidenced by the effect of rituximab on the response rate and survival of patients with follicular and diffuse large B cell non-Hodgkin's lymphoma.
  • Currently, only two monoclonal antibodies - the anti-CD33 immunotoxin gemtuzumab ozogamicin and the CD52-directed antibody alemtuzumab - are approved for treatment of relapsed acute myeloid leukaemia in older patients and B cell chronic lymphocytic leukaemia, respectively.
  • Although not approved for such treatment, alemtuzumab is also active against T cell prolymphocytic leukaemia, cutaneous T cell lymphoma and Sézary syndrome, and adult T cell leukaemia and lymphoma.
  • In addition, rituximab has demonstrated activity against B cell chronic lymphocytic and hairy cell leukaemia.
  • Monoclonal antibodies targeting CD4, CD19, CD20, CD22, CD23, CD25, CD45, CD66 and CD122 are now being studied in the clinic for the treatment of leukaemia.
  • Improved interactions with Fc receptors on immune effector cells can enhance destruction of target cells through antibody-dependent cellular cytotoxicity and complement-mediated cell lysis.
  • The antibodies can also be armed with cellular toxins or radionuclides to enhance the destruction of leukaemia cells.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Hematologic Neoplasms / therapy. Immunologic Factors / therapeutic use. Immunotoxins / therapeutic use. Leukemia / therapy
  • [MeSH-minor] Adult. Antigens, CD / immunology. Clinical Trials as Topic. Humans

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  • (PMID = 19788782.001).
  • [ISSN] 1462-3994
  • [Journal-full-title] Expert reviews in molecular medicine
  • [ISO-abbreviation] Expert Rev Mol Med
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Immunologic Factors; 0 / Immunotoxins
  • [Number-of-references] 193
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35. Laugel B, Boulter JM, Lissin N, Vuidepot A, Li Y, Gostick E, Crotty LE, Douek DC, Hemelaar J, Price DA, Jakobsen BK, Sewell AK: Design of soluble recombinant T cell receptors for antigen targeting and T cell inhibition. J Biol Chem; 2005 Jan 21;280(3):1882-92
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  • [Title] Design of soluble recombinant T cell receptors for antigen targeting and T cell inhibition.
  • The use of recombinant T cell receptors (TCRs) to target therapeutic interventions has been hindered by the naturally low affinity of TCR interactions with peptide major histocompatibility complex ligands.
  • Here, we use multimeric forms of soluble heterodimeric alphabeta TCRs for specific detection of target cells pulsed with cognate peptide, discrimination of quantitative changes in antigen display at the cell surface, identification of virus-infected cells, inhibition of antigen-specific cytotoxic T lymphocyte activation, and identification of cross-reactive peptides.
  • Notably, the A6 TCR specific for the immunodominant HLA A2-restricted human T cell leukemia virus type 1 Tax(11-19) epitope bound to HLA A2-HuD(87-95) (K(D) 120 microm by surface plasmon resonance), an epitope implicated as a causal antigen in the paraneoplastic neurological degenerative disorder anti-Hu syndrome.
  • [MeSH-major] Antigens / immunology. Receptors, Antigen, T-Cell / immunology. T-Lymphocytes / immunology

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  • (PMID = 15531581.001).
  • [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 / Antigens; 0 / Receptors, Antigen, T-Cell; 0 / Recombinant Proteins
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36. Kawakami H, Tomita M, Okudaira T, Ishikawa C, Matsuda T, Tanaka Y, Nakazato T, Taira N, Ohshiro K, Mori N: Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells. Int J Cancer; 2007 Apr 15;120(8):1811-20
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  • [Title] Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells.
  • The geldanamycin derivative 17-AAG is currently tested in clinical trials and known to inhibit the function of Hsp90 and promote the proteasomal degradation of its misfolded client proteins.
  • ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable.
  • Since Hsp90 is overexpressed in HTLV-I-infected T-cell lines and primary ATL cells, we analyzed the effects of 17-AAG on cell survival, apoptosis and expression of signal transduction proteins.
  • HTLV-I-infected T-cell lines and primary ATL cells were significantly more sensitive to 17-AAG in cell survival assays than normal PBMCs.
  • 17-AAG induced the inhibition of cell cycle and apoptosis.
  • These effects could be mediated by inactivation of NF-kappaB, AP-1 and PI3K/Akt pathways, as well as reduction of expression of proteins involved in the G1-S cell cycle transition and apoptosis.
  • Collectively, our results indicate that 17-AAG suppresses ATL cell survival through, at least in part, destabilization of several client proteins and suggest that 17-AAG is a potentially useful chemotherapeutic agent for ATL.
  • [MeSH-major] Apoptosis / drug effects. Benzoquinones / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Human T-lymphotropic virus 1 / drug effects. Lactams, Macrocyclic / therapeutic use. Leukemia, T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. T-Lymphocytes / virology
  • [MeSH-minor] Adult. Cell Cycle / drug effects. Humans. NF-kappa B / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [RetractionIn] Int J Cancer. 2011 Dec 1;129(11):2762-3 [21960263.001]
  • (PMID = 17230513.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / NF-kappa B; 0 / Transcription Factor AP-1; 4GY0AVT3L4 / tanespimycin; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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37. Bench BJ, Suarez VH, Watanabe CM: An efficient one-pot synthesis of tethered cyclohexadiene enaminonitriles from methyl-ketones: an effective route to quinazolines. Bioorg Med Chem Lett; 2008 May 15;18(10):3126-30
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  • The substituted enaminonitrile intermediates also exhibited weak anti-microbial activity and cytotoxicity against human T-cell leukemia.

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  • (PMID = 17967539.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM008523
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Cyclohexenes; 0 / Ketones; 0 / Nitriles; 0 / Quinazolines; 0F8Z5909QZ / 1,4-cyclohexadiene
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38. Rauch D, Gross S, Harding J, Niewiesk S, Lairmore M, Piwnica-Worms D, Ratner L: Imaging spontaneous tumorigenesis: inflammation precedes development of peripheral NK tumors. Blood; 2009 Feb 12;113(7):1493-500
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  • We developed a mouse model of spontaneous lymphoma in which malignant transformation is coupled with light emission that can be detected noninvasively using bioluminescent imaging.
  • The human T-cell leukemia virus (HTLV) type 1 transcriptional transactivator Tax is an oncogene sufficient to produce lymphoma in transgenic animal models.
  • Using the granzyme B promoter to restrict Tax expression to the mature natural killer (NK)/T-cell compartment, we have reproduced many elements of HTLV-associated adult T-cell leukemia/lymphoma.
  • Tax activates signaling cascades associated with transformation, inflammation, and tumorigenesis.
  • Based on these findings, we propose that Tax expression in activated lymphocytes initiates a cascade of events that leads to NK/T cell recruitment, activation, and transformation.

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  • (PMID = 18971418.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA094056; United States / NCI NIH HHS / CA / CA100730-06; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / P01 CA100730-06; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / CA94056; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / tax protein, Human T-lymphotrophic virus 1; EC 1.13.12.- / Luciferases; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse
  • [Other-IDs] NLM/ PMC2644076
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39. Nitta T, Kanai M, Sugihara E, Tanaka M, Sun B, Nagasawa T, Sonoda S, Saya H, Miwa M: Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells. Cancer Sci; 2006 Sep;97(9):836-41
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  • [Title] Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells.
  • Centrosomes play pivotal roles in cell polarity, regulation of the cell cycle and chromosomal segregation.
  • Centrosome amplification was recently described as a possible cause of aneuploidy in certain solid tumors and leukemias.
  • ATL is a T-cell malignancy caused by HTLV-1.
  • Although the precise mechanism of cell transformation is unclear, the HTLV-1-encoded protein, Tax, is thought to play a crucial role in leukemogenesis.
  • Here we demonstrate that lymphocytes isolated from patients with ATL show centrosome amplification and that a human T cell line shows centrosome amplification after induction of Tax, which was suppressed by CDK inhibitors.
  • Micronuclei formation was also observed after centrosome amplification in Tax-induced human T cells.
  • These findings suggest that Tax deregulates CDK activity and induces centrosome amplification, which might be associated with cellular transformation by HTLV-1 and chromosomal instability in HTLV-1-infected human T cells.
  • [MeSH-major] Cell Transformation, Viral / genetics. Centrosome / physiology. Gene Products, tax / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. T-Lymphocytes / virology

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  • (PMID = 16805820.001).
  • [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 / Gene Products, tax
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40. Jones KS, Petrow-Sadowski C, Bertolette DC, Huang Y, Ruscetti FW: Heparan sulfate proteoglycans mediate attachment and entry of human T-cell leukemia virus type 1 virions into CD4+ T cells. J Virol; 2005 Oct;79(20):12692-702
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  • [Title] Heparan sulfate proteoglycans mediate attachment and entry of human T-cell leukemia virus type 1 virions into CD4+ T cells.
  • Heparan sulfate proteoglycans (HSPGs) are used by a number of viruses to facilitate entry into host cells.
  • For the retrovirus human T-cell leukemia virus type 1 (HTLV-1), it has recently been reported that HSPGs are critical for efficient binding of soluble HTLV-1 SU and the entry of HTLV pseudotyped viruses into non-T cells.
  • However, the primary in vivo targets of HTLV-1, CD4(+) T cells, have been reported to express low or undetectable levels of HSPGs.
  • For this study, we reexamined the expression of HSPGs in CD4(+) T cells and examined their role in HTLV-1 attachment and entry.
  • Enzymatic modification of HSPGs on the surfaces of either established CD4(+) T-cell lines or primary CD4(+) T cells dramatically reduced the binding of both soluble HTLV-1 SU and HTLV-1 virions.
  • HSPGs also affected the efficiency of HTLV-1 entry, since blocking the interaction with HSPGs markedly reduced both the internalization of HTLV-1 virions and the titer of HTLV-1 pseudotyped viral infection in CD4(+) T cells.
  • Thus, HSPGs play a critical role in the binding and entry of HTLV-1 into CD4(+) T cells.

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  • (PMID = 16188972.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / CO-12400
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heparan Sulfate Proteoglycans
  • [Other-IDs] NLM/ PMC1235841
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41. Kuhlmann AS, Villaudy J, Gazzolo L, Castellazzi M, Mesnard JM, Duc Dodon M: HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT). Retrovirology; 2007;4:92
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  • [Title] HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT).
  • Thus, in patients with adult-T cell leukaemia (ATL), an HTLV-1 (Human T cell Leukaemia virus type 1)-associated disease, leukemic cells display a high telomerase activity, mainly through transcriptional up-regulation of the human telomerase catalytic subunit (hTERT).
  • The HBZ (HTLV-1 bZIP) protein coded by the minus strand of HTLV-1 genome and expressed in ATL cells has been shown to increase the transcriptional activity of JunD, an AP-1 protein.
  • CONCLUSION: These observations establish for the first time that HBZ by intervening in the re-activation of telomerase, may contribute to the development and maintenance of the leukemic process.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / metabolism. Human T-lymphotropic virus 1 / physiology. Proto-Oncogene Proteins c-jun / metabolism. Telomerase / biosynthesis. Transcription, Genetic. Up-Regulation. Viral Proteins / metabolism

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 18078517.001).
  • [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 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Messenger; 0 / Sp1 Transcription Factor; 0 / Viral Proteins; 9007-49-2 / DNA; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2235888
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42. Kobayashi H, Ngato T, Sato K, Aoki N, Kimura S, Tanaka Y, Aizawa H, Tateno M, Celis E: In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes. Clin Cancer Res; 2006 Jun 15;12(12):3814-22
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  • [Title] In vitro peptide immunization of target tax protein human T-cell leukemia virus type 1-specific CD4+ helper T lymphocytes.
  • PURPOSE: Adult T-cell leukemia/lymphoma induced by human T-cell leukemia virus type 1 (HTLV-1) is usually a fatal lymphoproliferative malignant disease.
  • HTLV-1 Tax protein plays a critical role in HTLV-1-associated leukemogenesis and is an attractive target for vaccine development.
  • Although HTLV-1 Tax is the most dominant antigen for HTLV-1-specific CD8(+) CTLs in HTLV-1-infected individuals, few epitopes recognized by CD4(+) helper T lymphocytes in HTLV-1 Tax protein have been described.
  • The aim of the present study was to study T-helper-cell responses to HTLV-1 Tax and to identify naturally processed MHC class II-restricted epitopes that could be used for vaccine development.
  • EXPERIMENTAL DESIGN: An MHC class II binding peptide algorithm was used to predict potential T-helper cell epitope peptides from HTLV-1 Tax.
  • We assessed the ability of the corresponding peptides to elicit helper T-cell responses by in vitro vaccination of purified CD4(+) T lymphocytes.
  • RESULTS: Peptides Tax(191-205) and Tax(305-319) were effective in inducing T-helper-cell responses.
  • Both these epitopes were found to be naturally processed by HTLV-1(+) T-cell lymphoma cells and by autologous antigen-presenting cells that were pulsed with HTLV-1 Tax(+) tumor lysates.
  • Notably, the two newly identified helper T-cell epitopes are found to lie proximal to known CTL epitopes, which will facilitate the development of prophylactic peptide-based vaccine capable of inducing simultaneous CTL and T-helper responses.
  • CONCLUSION: Our data suggest that HTLV-1 Tax protein could serve as tumor-associated antigen for CD4(+) helper T cells and that the present epitopes might be used for T-cell-based immunotherapy against tumors expressing HTLV-1.

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  • (PMID = 16778109.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA103921; United States / NCI NIH HHS / CA / R01CA80782; United States / NCI NIH HHS / CA / R01CA103921; United States / NCI NIH HHS / CA / R01 CA080782; United States / NCI NIH HHS / CA / P50CA91956; United States / NCI NIH HHS / CA / P50 CA091956
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / HLA-D Antigens; 0 / Peptides
  • [Other-IDs] NLM/ NIHMS14245; NLM/ PMC1986724
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43. Kchour G, Tarhini M, Sharifi N, Farid R, Khooei AR, Shirdel A, Afshari JT, Sadeghian A, Otrock Z, Hermine O, El-Sabban M, Bazarbachi A: Increased microvessel density in involved organs from patients with HTLV-I associated adult T cell leukemia lymphoma. Leuk Lymphoma; 2008 Feb;49(2):265-70
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  • [Title] Increased microvessel density in involved organs from patients with HTLV-I associated adult T cell leukemia lymphoma.
  • Adult T-cell leukemia-lymphoma (ATLL) is a rapidly progressive lymphoproliferative disorder secondary to infection with the human T cell lymphotropic virus type I (HTLV-I).
  • We have previously shown that ATLL derived cells secrete high levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (b-FGF), induce endothelial tube formation in vitro and establish functional gap junction-mediated communication with endothelial cells.
  • We also demonstrated that plasma from ATLL and tropical spastic paraparesis/HTLV-I associated myelopathy patients exhibit very high levels of VEGF and b-FGF.
  • Recently, we showed that treatment with the combination of zidovudine and interferon alpha reduced both HTLV-I proviral load and importantly VEGF plasma levels suggesting a potential anti-angiogenic effect of this therapy.
  • In this report, we evaluated microvessel density (MVD) in involved organs from 20 patients with ATLL, as compared to normal organs from matched controls.
  • We show evidence of significantly increased MVD in all tested involved organs from ATLL patients, suggesting that angiogenesis plays an important role in the development or organ invasion of ATLL, and could represent a potentially interesting target for anti-angiogenic therapy of ATLL.
  • [MeSH-major] Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / etiology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neovascularization, Pathologic
  • [MeSH-minor] Adult. Aged. Bone Marrow / blood supply. Capillaries. Case-Control Studies. Female. Humans. Immunohistochemistry. Lymph Nodes / blood supply. Male. Middle Aged. Skin / blood supply. Testis / blood supply

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  • (PMID = 18231912.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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44. Pancewicz J, Taylor JM, Datta A, Baydoun HH, Waldmann TA, Hermine O, Nicot C: Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia. Proc Natl Acad Sci U S A; 2010 Sep 21;107(38):16619-24
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  • [Title] Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia.
  • Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemia (ATL).
  • The disease has a dismal prognosis and is invariably fatal.
  • In this study, we report a high frequency of constitutively activated Notch in ATL patients.
  • We found activating mutations in Notch in more than 30% of ATL patients.
  • These activating mutations are phenotypically different from those previously reported in T-ALL leukemias and may represent polymorphisms for activated Notch in human cancers.
  • Compared with the exclusive activating frameshift mutations in the proline, glutamic acid, serine, and threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in this domain leading to reduced CDC4/Fbw7-mediated degradation and stabilization of the intracellular cleaved form of Notch1 (ICN1).
  • Finally, we demonstrated that inhibition of Notch signaling by γ-secretase inhibitors reduced tumor cell proliferation and tumor formation in ATL-engrafted mice.
  • These data suggest that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for therapeutic intervention in ATL patients.


46. Siu YT, Chin KT, Siu KL, Yee Wai Choy E, Jeang KT, Jin DY: TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats. J Virol; 2006 Jul;80(14):7052-9
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  • [Title] TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats.
  • Human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription from the long terminal repeats (LTR).
  • Thus, both TORC and p300 families of coactivators are essential for optimal activation of HTLV-1 transcription by Tax.
  • [MeSH-major] Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / physiology. Phosphoproteins / metabolism. Terminal Repeat Sequences / physiology. Transcription Factors / metabolism. Virus Activation / physiology

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  • (PMID = 16809310.001).
  • [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 / ATF4 protein, human; 0 / CREB1 protein, human; 0 / CRTC1 protein, human; 0 / CRTC2 protein, human; 0 / CRTC3 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / Phosphoproteins; 0 / Trans-Activators; 0 / Transcription Factors; 145891-90-3 / Activating Transcription Factor 4; EC 2.3.1.48 / p300-CBP Transcription Factors
  • [Other-IDs] NLM/ PMC1489057
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47. Tholouli E, Liu Yin JA: Successful treatment of HTLV-1-associated acute adult T-cell leukemia lymphoma by allogeneic bone marrow transplantation: a 12 year follow-up. Leuk Lymphoma; 2006 Aug;47(8):1691-2
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  • [Title] Successful treatment of HTLV-1-associated acute adult T-cell leukemia lymphoma by allogeneic bone marrow transplantation: a 12 year follow-up.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Remission Induction. Transplantation, Homologous

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  • (PMID = 16966289.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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48. Hattori N, Nakamaki T, Ariizumi H, Homma M, Yamochi-Onizuka T, Ota H, Tomoyasu S: Over-expression of CCL3 MIP-1alpha in a blastoid mantle cell lymphoma with hypercalcemia. Eur J Haematol; 2010 May;84(5):448-52
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  • [Title] Over-expression of CCL3 MIP-1alpha in a blastoid mantle cell lymphoma with hypercalcemia.
  • We analyzed a case with the blastoid variant of mantle cell lymphoma (MCL-BV), a rare subtype of B-cell lymphoma, presenting with marked hypercalcemia at diagnosis.
  • Enzyme-linked immunosorbent assay (ELISA) showed elevated serum levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1alpha (MIP-1alpha), and type I collagen telopeptide, but not parathyroid hormone, calcitriol or parathyroid hormone-related peptide at diagnosis, suggesting local osteoclastic hypercalcemia in this case.
  • By reverse transcription polymerase chain reaction (RT-PCR) analysis, we found predominant expression of mRNA for MIP-1alpha in addition to those for receptor-activator of nuclear-factor kappa B ligand (RANKL), TNF-alpha, and IL-6 in lymphoma cells obtained from the patient.
  • In the present case, MIP-1alpha, an osteoclast-activating factor produced by mantle lymphoma cells, may contribute to the development of hypercalcemia.
  • It likely acts through RANKL expression in tumor cells and/or stroma cells, as indicated in multiple myeloma (MM) and adult T-cell leukemia/lymphoma (ATLL).
  • Furthermore, MIP-1alpha is also involved in the development of an aggressive phenotype on MCL by stimulating proliferation of these lymphoma cells.
  • In summary, the present study demonstrated that MIP-1alpha is an important factor in the development of both hypercalcemia and an aggressive phenotype in some types of B-cell lymphoma.
  • [MeSH-major] Chemokine CCL3 / blood. Hypercalcemia / metabolism. Lymphoma, Mantle-Cell / metabolism
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20050882.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokine CCL3
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49. 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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50. Yano H, Ishida T, Imada K, Sakai T, Ishii T, Inagaki A, Iida S, Uchiyama T, Ueda R: Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF. Br J Haematol; 2008 Mar;140(5):586-9
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  • [Title] Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / therapy. Receptors, CCR4 / immunology
  • [MeSH-minor] Adult. Animals. Antineoplastic Agents / therapeutic use. Disease Models, Animal. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Mice. Mice, SCID

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  • (PMID = 18205860.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 134088-74-7 / nartograstim; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2268953
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51. Yoshie O: Expression of CCR4 in adult T-cell leukemia. Leuk Lymphoma; 2005 Feb;46(2):185-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of CCR4 in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a malignancy of mature T cells that is etiologically associated with human T-cell leukemia virus type 1 (HTLV-1).
  • The frequent manifestation of ATL is infiltration of leukemic cells into various organs.
  • Besides certain cell adhesion molecules and matrix metalloproteineses, chemokine receptors may play important roles in tissue infiltration of ATL.
  • Identification of a unique set of chemokine receptors expressed by ATL would thus provide valuable information about the molecular mechanism of tissue infiltration of ATL.
  • This may also reveal that ATL frequently develops from a certain subset of T cells that express a particular set of chemokine receptors.
  • Since HTLV-1 encodes a potent viral transcriptional activator Tax, which is known to induce various cellular genes, expression of some chemokine receptors may be affected by Tax.
  • This, however, may relate more to HTLV-1-infected T cells, since ATL cells usually do not express Tax.
  • Finally, identification of a unique set of chemokine receptors expressed by ATL may also provide a new therapeutic target.
  • These considerations prompted us to examine the chemokine receptor expression in ATL.
  • We found that in the majority of ATL cases, leukemic cells consistently express CCR4.
  • Since CCR4 is known to be involved in T cell migration into skin, this may in part explain the frequent skin infiltration in ATL.
  • Thus, the majority of ATL may predominantly originate from either Th2 or regulatory T cells.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Chemokine / analysis

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  • (PMID = 15621800.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
  • [Number-of-references] 44
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52. Kchour G, Makhoul NJ, Mahmoudi M, Kooshyar MM, Shirdel A, Rastin M, Rafatpanah H, Tarhini M, Zalloua PA, Hermine O, Farid R, Bazarbachi A: Zidovudine and interferon-alpha treatment induces a high response rate and reduces HTLV-1 proviral load and VEGF plasma levels in patients with adult T-cell leukemia from North East Iran. Leuk Lymphoma; 2007 Feb;48(2):330-6
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  • [Title] Zidovudine and interferon-alpha treatment induces a high response rate and reduces HTLV-1 proviral load and VEGF plasma levels in patients with adult T-cell leukemia from North East Iran.
  • Human T-cell lymphotropic virus type I (HTLV-I) associated adult T-cell leukemia/lymphoma (ATLL) is endemic in southern Japan, the Caribbean, intertropical Africa, and Brazil.
  • ATLL is an aggressive T-cell lymphoproliferative disorder.
  • Patients with ATLL have high plasma levels of VEGF that induce angiogenesis.
  • Prognosis of ATLL remains poor because of immunosuppression and intrinsic resistance to chemotherapy.
  • Important advances in the treatment of ATLL were reported with the combination of zidovudine (AZT) and interferon-alpha.
  • We investigated the effect of AZT/IFN treatment on vascular endothelium growth factor (VEGF) plasma levels and HTLV-I proviral load in ATLL patients from the region of Mashhad.
  • We also confirmed that VEGF plasma levels and HTLV-I proviral load are higher in ATLL patients than in asymptomatic carriers.
  • We finally showed that AZT/IFN treatment reduced both HTLV-I proviral load and importantly VEGF plasma levels, suggesting a potential antiangiogenic effect of this therapy.
  • These results provide further evidence for the efficacy and the mechanism of action of AZT/IFN therapy for ATLL in a developing country.
  • [MeSH-major] Antiviral Agents / therapeutic use. HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1 / drug effects. Interferon-alpha / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Proviruses / isolation & purification. Vascular Endothelial Growth Factor A / blood. Zidovudine / therapeutic use
  • [MeSH-minor] Adult. Drug Therapy, Combination. Female. Humans. Iran / epidemiology. Male. Middle Aged. Treatment Outcome. Viral Load

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  • (PMID = 17325893.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 4B9XT59T7S / Zidovudine
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53. Tanosaki R, Tobinai K: Adult T-cell leukemia-lymphoma: current treatment strategies and novel immunological approaches. Expert Rev Hematol; 2010 Dec;3(6):743-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia-lymphoma: current treatment strategies and novel immunological approaches.
  • Adult T-cell leukemia-lymphoma (ATL) is a peripheral T-cell malignancy, closely associated with human T-cell lymphotropic virus type I infection.
  • Clinically, ATL is classified into four subtypes: acute, lymphoma, chronic and smoldering type.
  • Although the prognosis of chronic and smoldering-type ATL is relatively good, that of patients with acute- or lymphoma-type ATL still remains extremely poor.
  • Allogeneic stem cell transplantation is promising and approximately 40% of aggressive ATL patients are expected to survive long-term, although transplantation-related mortality is as high as 40-50%.
  • Stem cell transplantation using reduced-intensity conditioning is also effective and safer, with graft-versus-ATL and graft-versus-human T-cell lymphotropic virus type I effects observed after transplantation.
  • Novel approaches including new agents such as purine nucleoside phosphorylase inhibitors and histone deacetylase inhibitors, or targeted immunotherapy using antichemokine receptor-4 antibody or dendritic cell/peptide vaccine are also warranted.
  • [MeSH-major] Immunotherapy. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Humans. Interferon-alpha / therapeutic use. Kaplan-Meier Estimate. Stem Cell Transplantation. Transplantation, Homologous

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  • (PMID = 21091150.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Interferon-alpha
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54. Jeang KT: Human T cell leukemia virus type 1 (HTLV-1) and oncogene or oncomiR addiction? Oncotarget; 2010 Oct;1(6):453-6
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  • [Title] Human T cell leukemia virus type 1 (HTLV-1) and oncogene or oncomiR addiction?
  • The mechanism of HTLV-1 transformation of cells to Adult T cell leukemia (ATL) remains not fully understood.
  • Emerging evidence suggests that Tax is not needed to maintain the transformed ATL phenotype.
  • Recent studies have shown that HTLV-1 transformed cells show deregulated expression of cellular microRNAs (miRNAs).
  • Here we discuss the possibility that early ATL cells are Tax-oncogene-addicted while late ATL cells are oncogenic microRNA (oncomiR) - addicted.
  • [MeSH-major] Gene Expression Regulation. Gene Products, tax. Human T-lymphotropic virus 1 / genetics. MicroRNAs / genetics. Oncogenes / genetics
  • [MeSH-minor] Adult. HTLV-I Infections / genetics. HTLV-I Infections / virology. Humans

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  • (PMID = 21311101.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AI001023-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS242806; NLM/ PMC3058865
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55. Chaadaeva AV, Tenkeeva II, Moiseeva EV, Svirshchevskaia EV, Demushkin VP: [Antitumor activity of the plant remedy peptide extract PE-PM in a new mouse T-lymphoma/eukemia model]. Biomed Khim; 2009 Jan-Feb;55(1):81-8
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  • [Title] [Antitumor activity of the plant remedy peptide extract PE-PM in a new mouse T-lymphoma/eukemia model].
  • A new mouse ASF-LL model of adult T-lymphoma/leukemia (ATLL) in humans was characterized by cytological, histopathological, and flow cytometry analyses.
  • Encouraging similarities of morphological, pathological, and clinical signs were found.
  • These included characteristic flower appearance of leukemic cells, lymphadenopathy and hepatosplenomegaly, multiple growths in the skin, urogenital tissues, lungs and pituitary gland, CD4+CD25+ phenotype of the majority of tumor cells that were selectin-L positive, a rapid clinical course, and poor response to standard chemotherapy.
  • We have tested antitumor activity of a peptide extract PE-PM obtained from a mixture of Chelidonium majus L., Inula helenium L., Equisetum arvense L. and Inonotus obliquus in new mouse T-lymphoma/leukemia model ASF-LL.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Complex Mixtures / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Neoplasms, Experimental / drug therapy. Peptides / pharmacology. Plant Proteins / pharmacology. Plants, Medicinal / chemistry

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  • (PMID = 19351037.001).
  • [ISSN] 2310-6972
  • [Journal-full-title] Biomedit︠s︡inskai︠a︡ khimii︠a︡
  • [ISO-abbreviation] Biomed Khim
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Complex Mixtures; 0 / Peptides; 0 / Plant Proteins
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56. Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K: Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines. Cancer Lett; 2007 Nov 18;257(2):206-15
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  • [Title] Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.
  • The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing HTLV-I-infected cells.
  • In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient ATL cell lines caused rapid death, whereas DHMEQ-treated mice survived.
  • Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted ATL cells.
  • These results demonstrate that DHMEQ has therapeutic efficacy on ATL cells, regardless of Tax expression.
  • [MeSH-major] Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency. Leukemia, T-Cell / prevention & control. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cell Line, Tumor. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism

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  • (PMID = 17764832.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin
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57. Hsi ED: T-cell lymphoma in the head and neck? Think about adult T-cell leukemia/lymphoma. Leuk Lymphoma; 2009 Feb;50(2):150-1
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  • [Title] T-cell lymphoma in the head and neck? Think about adult T-cell leukemia/lymphoma.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Adult. HTLV-I Infections / complications. HTLV-I Infections / pathology. Human T-lymphotropic virus 1 / physiology. Humans

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  • [CommentOn] Leuk Lymphoma. 2009 Feb;50(2):187-95 [19197730.001]
  • (PMID = 19235010.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
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58. Saito M: Immunogenetics and the Pathological Mechanisms of Human T-Cell Leukemia VirusType 1- (HTLV-1-)Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). Interdiscip Perspect Infect Dis; 2010;2010:478461
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  • [Title] Immunogenetics and the Pathological Mechanisms of Human T-Cell Leukemia VirusType 1- (HTLV-1-)Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP).
  • Human T-cell leukemia virus type 1 (HTLV-1) is a replication-competent human retrovirus associated with two distinct types of disease only in a minority of infected individuals: the malignancy known as adult T-cell leukemia (ATL) and a chronic inflammatory central nervous system disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
  • Although the factors that cause these different manifestations of HTLV-1 infection are not fully understood, accumulating evidence suggests that complex virus-host interactions play an important role in determining the risk of HAM/TSP.
  • This review focuses on the role of the immune response in controlling or limiting viral persistence in HAM/TSP patients, and the reason why some HTLV-1-infected people develop HAM/TSP whereas the majority remains asymptomatic carriers of the virus.

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  • (PMID = 20169122.001).
  • [ISSN] 1687-7098
  • [Journal-full-title] Interdisciplinary perspectives on infectious diseases
  • [ISO-abbreviation] Interdiscip Perspect Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2821641
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59. Javier RT: Cell polarity proteins: common targets for tumorigenic human viruses. Oncogene; 2008 Nov 24;27(55):7031-46
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  • [Title] Cell polarity proteins: common targets for tumorigenic human viruses.
  • Loss of polarity and disruption of cell junctions are common features of epithelial-derived cancer cells, and mounting evidence indicates that such defects have a direct function in the pathology of cancer.
  • Supporting this idea, results with several different human tumor viruses indicate that their oncogenic potential depends in part on a common ability to inactivate key cell polarity proteins.
  • For example, adenovirus (Ad) type 9 is unique among human Ads by causing exclusively estrogen-dependent mammary tumors in experimental animals and in having E4 region-encoded open reading frame 1 (E4-ORF1) as its primary oncogenic determinant.
  • Most notably, the E4-ORF1 PBM mediates interactions with a selected group of cellular PDZ proteins, three of which include the cell polarity proteins Dlg1, PATJ and ZO-2.
  • Data further indicate that these interactions promote disruption of cell junctions and a loss of cell polarity.
  • In addition, one or more of the E4-ORF1-interacting cell polarity proteins, as well as the cell polarity protein Scribble, are common targets for the high-risk human papillomavirus (HPV) E6 or human T-cell leukemia virus type 1 (HTLV-1) Tax oncoproteins.
  • Underscoring the significance of these observations, in humans, high-risk HPV and HTLV-1 are causative agents for cervical cancer and adult T-cell leukemia, respectively.
  • Consequently, human tumor viruses should serve as powerful tools for deciphering mechanisms whereby disruption of cell junctions and loss of cell polarity contribute to the development of many human cancers.
  • This review article discusses evidence supporting this hypothesis, with an emphasis on the human Ad E4-ORF1 oncoprotein.
  • [MeSH-major] Cell Polarity. Membrane Proteins / physiology. Neoplasms / etiology. Virus Attachment. Virus Diseases / complications
  • [MeSH-minor] Adenovirus Infections, Human / virology. Adenoviruses, Human / physiology. Animals. Cell Transformation, Viral / physiology. Gene Products, tax / physiology. Human T-lymphotropic virus 1 / metabolism. Human T-lymphotropic virus 1 / physiology. Human papillomavirus 6 / metabolism. Human papillomavirus 6 / physiology. Humans. Models, Biological. Oncogene Proteins, Viral / metabolism. Oncogene Proteins, Viral / physiology. Protein Binding

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  • (PMID = 19029943.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA058541
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E4 protein, Adenovirus 9; 0 / Gene Products, tax; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Number-of-references] 233
  • [Other-IDs] NLM/ NIHMS411909; NLM/ PMC3501650
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60. Zhang X, Hakata Y, Tanaka Y, Shida H: CRM1, an RNA transporter, is a major species-specific restriction factor of human T cell leukemia virus type 1 (HTLV-1) in rat cells. Microbes Infect; 2006 Mar;8(3):851-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CRM1, an RNA transporter, is a major species-specific restriction factor of human T cell leukemia virus type 1 (HTLV-1) in rat cells.
  • Rat ortholog of human CRM1 has been found to be responsible for the poor activity of viral Rex protein, which is essential for RNA export of human T cell leukemia virus type 1 (HTLV-1).
  • Here, we examined the species-specific barrier of HTLV-1 by establishing rat cell lines, including both adherent and CD4(+) T cells, which express human CRM1 at physiological levels.
  • We demonstrated that expression of human CRM1 in rat cells is not harmful to cell growth and is sufficient to restore the synthesis of the viral structural proteins, Gag and Env, at levels similar to those in human cells.
  • An HTLV-1 pseudovirus infection system suggested that the released virus particles are fully infectious.
  • Our newly developed reporter cell system revealed that Env proteins produced in rat cells are fully fusogenic, which is the basis for cell-cell HTLV-1 infection.
  • These results, in conjunction with reports describing efficient entry of HTLV-1 into rat cells, may indicate that HTLV-1 is unique in that its major species-specific barrier is determined by CRM1 at a viral RNA export step.
  • These observations will enable us to construct a transgenic rat model expressing human CRM1 that is sensitive to HTLV-1 infection.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
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  • (PMID = 16504563.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Karyopherins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Viral Proteins; 0 / exportin 1 protein
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61. Chuang SS, Ichinohasama R, Chu JS, Ohshima K: Differential diagnosis of angioimmunoblastic T-cell lymphoma with seropositivity for anti-HTLV antibody from adult T-cell leukemia/lymphoma. Int J Hematol; 2010 May;91(4):687-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential diagnosis of angioimmunoblastic T-cell lymphoma with seropositivity for anti-HTLV antibody from adult T-cell leukemia/lymphoma.
  • Angioimmunoblastic lymphoma (AITL) is a nodal peripheral T-cell lymphoma characterized by a proliferation of arborizing vessels and hyperplastic follicular dendritic cells as well as a polymorphous lymphoid infiltrate including neoplastic cells with clear cytoplasm.
  • Adult T-cell leukemia/lymphoma (ATLL) is caused by the retrovirus human T-cell leukemia virus type I (HTLV-I), and the neoplastic cells are usually large and pleomorphic.
  • Recently, a rare morphologic variant of ATLL with AITL-like features has been reported.
  • Here, we presented a case of peripheral T-cell lymphoma with morphological features of AITL in Taiwan, a country non-endemic for HTLV, and the patient was seropositive for anti-HTLV antibody, which raised the possibility of ATLL with AITL-like features.
  • Furthermore, Southern blot analysis using DNA extracted from the nodal tissue was negative for HTLV-I proviral integration.
  • Our investigations indicated that in an HTLV-I non-endemic area, a peripheral T-cell lymphoma with typical morphologic and immunophenotypic features of AITL could be confidently diagnosed as AITL even if the patient was seropositive for anti-HTLV antibody.
  • [MeSH-major] HTLV-I Antibodies / blood. HTLV-I Infections / complications. HTLV-I Infections / immunology. Immunoblastic Lymphadenopathy. Lymphoma, T-Cell
  • [MeSH-minor] Aged, 80 and over. Biopsy. Diagnosis, Differential. Female. Humans. Lymph Nodes / pathology

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  • (PMID = 20198459.001).
  • [ISSN] 1865-3774
  • [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 / HTLV-I Antibodies
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62. Ueda M, Imada K, Imura A, Koga H, Hishizawa M, Uchiyama T: Expression of functional interleukin-21 receptor on adult T-cell leukaemia cells. Br J Haematol; 2005 Jan;128(2):169-76
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  • [Title] Expression of functional interleukin-21 receptor on adult T-cell leukaemia cells.
  • Adult T-cell leukaemia (ATL) is caused by human T-cell leukaemia virus type I (HTLV-I).
  • It has been suggested that cytokines play a role in the development and in the neoplastic cell growth of ATL.
  • In this study, we examined the expression of IL-21R and the effect of IL-21 on ATL cells.
  • Real-time reverse transcription polymerase chain reaction showed that HTLV-I-infected cell lines and primary ATL cells expressed IL-21R mRNA.
  • Cell surface expression of IL-21R on these cells was confirmed by flow cytometric analysis using a newly developed monoclonal antibody against human IL-21R.
  • Notably, IL-21 induced the proliferation of ATL-43T and ED-40515(+) cells, both of which were derived from leukaemic cell clones of ATL.
  • Taken together, these findings provide the first evidence that ATL cells express functional IL-21R, suggesting that it may contribute to the pathophysiology of ATL.
  • In addition, the IL-21/IL-21R system may represent a new target for the treatment of ATL.
  • [MeSH-major] Leukemia, T-Cell / immunology. RNA, Messenger / analysis. Receptors, Interleukin / genetics. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Blotting, Western / methods. Cell Line, Transformed. Cell Line, Tumor. Cell Proliferation. DNA-Binding Proteins / metabolism. Flow Cytometry. Human T-lymphotropic virus 1. Humans. Interleukin-21 Receptor alpha Subunit. Milk Proteins / metabolism. Phosphorylation. Receptors, Interleukin-21. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor. STAT5 Transcription Factor. Signal Transduction. Trans-Activators / metabolism


63. Shembade N, Harhaj NS, Yamamoto M, Akira S, Harhaj EW: The human T-cell leukemia virus type 1 Tax oncoprotein requires the ubiquitin-conjugating enzyme Ubc13 for NF-kappaB activation. J Virol; 2007 Dec;81(24):13735-42
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  • [Title] The human T-cell leukemia virus type 1 Tax oncoprotein requires the ubiquitin-conjugating enzyme Ubc13 for NF-kappaB activation.
  • Ubiquitination of the human T-cell leukemia virus 1 Tax oncoprotein provides an important regulatory mechanism that promotes the Tax-mediated activation of NF-kappaB.

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  • (PMID = 17942533.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA099926; United States / NCI NIH HHS / CA / R01 CA99926
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / IKBKG protein, human; 0 / NF-kappa B; 0 / Ubiquitin; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.10 / I-kappa B Kinase; EC 6.3.2.19 / Ubc13 protein, mouse; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
  • [Other-IDs] NLM/ PMC2168884
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64. Sargent JT, Smith OP: Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders. Br J Haematol; 2010 May;149(4):465-77
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  • Hypercalcaemia is a common metabolic complication of malignant disease often requiring emergency intervention.
  • Although it is more frequently associated with solid tumours, malignancy-associated hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.
  • Its association with myeloma and adult T-cell leukaemia/lymphoma is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.
  • Haematologists need to be familiar with the clinical manifestations of, the differential diagnosis to be considered and the most effective management strategies that are currently available for MAH.
  • [MeSH-minor] Adult. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans

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  • (PMID = 20377591.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 96
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65. Marzano AV, Vezzoli P, Fanoni D, Venegoni L, Berti E: Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells. J Am Acad Dermatol; 2009 Aug;61(2):348-55
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  • [Title] Primary cutaneous T-cell lymphoma expressing FOXP3: a case report supporting the existence of malignancies of regulatory T cells.
  • Regulatory T (Treg) cells, which represent 5% to 10% of peripheral T cells, regulate the activities of T-cell subsets by performing immunosuppressive functions and thus preventing the development of autoimmune responses.
  • Recently, it has been demonstrated that the tumor cells in adult T-cell leukemia lymphomas can function as Treg, raising the question of whether any variant of primary cutaneous T-cell lymphoma may also express a regulatory phenotype.
  • We describe an extraordinary case of primary cutaneous T-cell lymphoma clinically characterized by protean cutaneous manifestations and histologically showing a pattern consistent with epidermotropic pleomorphic medium-/large-cell primary cutaneous T-cell lymphoma.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Forkhead Transcription Factors / immunology. Lymphoma, T-Cell, Cutaneous / pathology. Skin Neoplasms / pathology. T-Lymphocytes, Regulatory / immunology


66. Hishiki T, Ohshima T, Ego T, Shimotohno K: BCL3 acts as a negative regulator of transcription from the human T-cell leukemia virus type 1 long terminal repeat through interactions with TORC3. J Biol Chem; 2007 Sep 28;282(39):28335-43
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  • [Title] BCL3 acts as a negative regulator of transcription from the human T-cell leukemia virus type 1 long terminal repeat through interactions with TORC3.
  • By associating with cyclic AMP-responsive element-binding protein (CREB), the human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates transcription from the HTLV-1 long terminal repeat (LTR), which contains multiple cyclic AMP-responsive elements.
  • In this study, we performed a yeast two-hybrid screen using the N-terminal region of TORC3 as bait and identified B-cell chronic lymphatic leukemia protein 3 (BCL3) as a protein interacting with TORC3.
  • By using a luciferase assay, we determined that BCL3 inhibited transcription from the HTLV-1 LTR in a manner dependent on TORC3.
  • These results suggest that BCL3 functions as a repressor of HTLV-1 LTR-mediated transcription through interactions with TORC3.
  • In addition to stimulating transcription from the HTLV-1 LTR, Tax also enhances BCL3 expression; thus, transcription from the LTR is regulated by both positive and negative feedback mechanisms.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism. Terminal Repeat Sequences / physiology. Transcription Factors / metabolism. Transcription, Genetic / physiology

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  • (PMID = 17644518.001).
  • [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 / CREB1 protein, human; 0 / CRTC3 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Enzyme Inhibitors; 0 / Gene Products, tax; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3; 3X2S926L3Z / trichostatin A
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67. Liu M, Yang L, Zhang L, Liu B, Merling R, Xia Z, Giam CZ: Human T-cell leukemia virus type 1 infection leads to arrest in the G1 phase of the cell cycle. J Virol; 2008 Sep;82(17):8442-55
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  • [Title] Human T-cell leukemia virus type 1 infection leads to arrest in the G1 phase of the cell cycle.
  • Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma.
  • Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission.
  • Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene.
  • HTLV-1-infected HeLa cells, like their tax-transduced counterparts, expressed high levels of p21(CIP1/WAF1) and p27(KIP1), developed mitotic abnormalities, and became arrested in G(1) in senescence.
  • In contrast, cells of a human osteosarcoma lineage (HOS) continued to divide after HTLV-1 infection or Tax expression, albeit at a reduced growth rate and with mitotic aberrations.
  • Unique to HOS cells is the dramatic reduction of p21(CIP1/WAF1) and p27(KIP1) expression, which is in part associated with the constitutive activation of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway.
  • The loss of p21(CIP1/WAF1) and p27(KIP1) in HOS cells apparently allows HTLV-1- and Tax-induced G(1) arrest to be bypassed.
  • Finally, HTLV-1 infection and Tax expression also cause human SupT1 T cells to arrest in the G(1) phase of the cell cycle.
  • These results suggest that productive HTLV-1 infection ordinarily leads to Tax-mediated G(1) arrest.
  • However, T cells containing somatic mutations that inactivate p21(CIP1/WAF1) and p27(KIP1) may continue to proliferate after HTLV-1 infection and Tax expression.