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6. Bellon M, Lepelletier Y, Hermine O, Nicot C: Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia. Blood; 2009 May 14;113(20):4914-7
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  • [Title] Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia.
  • Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease.
  • MicroRNAs (miRNAs) are differentially expressed during hematopoiesis and lineage commitment of hematopoietic stem cell progenitors (HSCPs).
  • Here, we report aberrant expression of hematopoietic-specific miR-223, miR-181a, miR-150, miR-142.3p, and miR-155 in HTLV-I-infected cells in vitro and uncultured ex vivo ATL cells.
  • Our results suggest that HTLV-I-infected cells have an unbalanced expression of miRNA that favors T-cell differentiation.
  • Strikingly, our data also revealed significant differences between ex vivo ATL tumor cells and in vitro HTLV-I cell lines.
  • Specifically, miR-150 and miR-223 were up-regulated in ATL patients but consistently down-regulated in HTLV-I cell lines, suggesting that ATL cells and in vitro-established cells are derived from distinct cellular populations.

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  • [Cites] J Virol. 2005 Nov;79(22):14069-78 [16254341.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12481-6 [16885212.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1931-6 [16990772.001]
  • [Cites] Genes Dev. 2007 Mar 1;21(5):578-89 [17344418.001]
  • [Cites] Cell. 2007 Apr 6;129(1):147-61 [17382377.001]
  • [Cites] Science. 2007 Apr 27;316(5824):608-11 [17463290.001]
  • [Cites] Cell. 2007 Oct 5;131(1):146-59 [17923094.001]
  • [Cites] Nat Med. 2008 Apr;14(4):429-36 [18376405.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Dev Cell. 2008 Jun;14(6):815-6 [18539110.001]
  • [Cites] Nat Immunol. 2008 Aug;9(8):839-45 [18645592.001]
  • [Cites] J Exp Med. 2008 Sep 1;205(9):1983-91 [18725525.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Oncogene. 1989 Jun;4(6):671-6 [2660069.001]
  • [Cites] Haematologia (Budap). 1994;26(1):1-9 [7959369.001]
  • [Cites] J Virol. 1996 Jun;70(6):4038-44 [8648741.001]
  • [Cites] Semin Immunol. 2005 Apr;17(2):155-65 [15737576.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):311-21 [15803157.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1361-8 [15864353.001]
  • [Cites] Cell. 2005 Dec 2;123(5):819-31 [16325577.001]
  • (PMID = 19246560.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / R01CA106258; United States / NCI NIH HHS / CA / R01CA115398
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2686141
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7. Hidaka T, Nakahata S, Hatakeyama K, Hamasaki M, Yamashita K, Kohno T, Arai Y, Taki T, Nishida K, Okayama A, Asada Y, Yamaguchi R, Tsubouchi H, Yokota J, Taniwaki M, Higashi Y, Morishita K: Down-regulation of TCF8 is involved in the leukemogenesis of adult T-cell leukemia/lymphoma. Blood; 2008 Jul 15;112(2):383-93
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  • [Title] Down-regulation of TCF8 is involved in the leukemogenesis of adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) is caused by latent human T-lymphotropic virus-1 (HTLV-1) infection.
  • To clarify the molecular mechanism underlying leukemogenesis after viral infection, we precisely mapped 605 chromosomal breakpoints in 61 ATLL cases by spectral karyotyping and identified frequent chromosomal breakpoints in 10p11, 14q11, and 14q32.
  • Single nucleotide polymorphism (SNP) array-comparative genomic hybridization (CGH), genetic, and expression analyses of the genes mapped within a common breakpoint cluster region in 10p11.2 revealed that in ATLL cells, transcription factor 8 (TCF8) was frequently disrupted by several mechanisms, including mainly epigenetic dysregulation.
  • TCF8 mutant mice frequently developed invasive CD4(+) T-cell lymphomas in the thymus or in ascitic fluid in vivo.
  • Down-regulation of TCF8 expression in ATLL cells in vitro was associated with resistance to transforming growth factor beta1 (TGF-beta1), a well-known characteristic of ATLL cells, suggesting that escape from TGF-beta1-mediated growth inhibition is important in the pathogenesis of ATLL.
  • These findings indicate that TCF8 has a tumor suppressor role in ATLL.
  • [MeSH-major] Homeodomain Proteins / physiology. Leukemia-Lymphoma, Adult T-Cell / etiology. Transcription Factors / physiology. Transforming Growth Factor beta1 / physiology
  • [MeSH-minor] Animals. Chromosome Breakage. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 14. Down-Regulation / genetics. Humans. Karyotyping. Mice. Tumor Cells, Cultured

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  • (PMID = 18467597.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / ZEB1 protein, human
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8. Tawara M, Hogerzeil SJ, Yamada Y, Takasaki Y, Soda H, Hasegawa H, Murata K, Ikeda S, Imaizumi Y, Sugahara K, Tsuruda K, Tsukasaki K, Tomonaga M, Hirakata Y, Kamihira S: Impact of p53 aberration on the progression of Adult T-cell Leukemia/Lymphoma. Cancer Lett; 2006 Mar 28;234(2):249-55
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  • [Title] Impact of p53 aberration on the progression of Adult T-cell Leukemia/Lymphoma.
  • Based on statistical analysis of its age-dependent occurrence, a multi-step carcinogenesis model has been proposed for Adult T-cell Leukemia/Lymphoma (ATLL).
  • We have previously reported that the deletion of the p16 gene is a key event in ATLL progression.
  • In the current study, we report for the first time that the aberrations of p16 and p53 are mutually exclusive in ATLL and either of the two events is sufficient for the ATLL progression.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Aberrations. Genes, p16. Genes, p53. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Male. Polymorphism, Single-Stranded Conformational. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15896902.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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9. Faris M: Potential for molecular targeted therapy for adult T-cell leukemia/lymphoma. Int Rev Immunol; 2008 Jan-Apr;27(1-2):71-8
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  • [Title] Potential for molecular targeted therapy for adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma is an aggressive lymphoproliferative disorder of CD4+ T lymphocytes associated with human T-cell leukemia virus type 1 (HTLV-I) infection.
  • Approximately 5% of infected people will develop an aggressive form of ATL, characterized by high circulating cell count, skin and organ infiltration and expression of cytokine, chemokine and survival genes.
  • The available therapies for ATL have minimal efficacy, with few responders and poor survival.
  • Recent advances have led to the identification of key molecules and cellular pathways involved in HTLV-1 mediated cellular transformation and tumor progression.
  • We describe within a few key elements that contribute to neoplastic development of ATL, in addition to interesting molecular drug targets that may lead to more effective therapeutic strategies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Basic-Leucine Zipper Transcription Factors / metabolism. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / virology. Cytokines / immunology. Cytokines / metabolism. Gene Products, tax / metabolism. HTLV-I Infections / drug therapy. HTLV-I Infections / immunology. HTLV-I Infections / virology. Human T-lymphotropic virus 1 / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. Viral Proteins / metabolism

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  • (PMID = 18300056.001).
  • [ISSN] 0883-0185
  • [Journal-full-title] International reviews of immunology
  • [ISO-abbreviation] Int. Rev. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Basic-Leucine Zipper Transcription Factors; 0 / Cytokines; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Viral Proteins
  • [Number-of-references] 28
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10. 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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11. Braun C, Duffau P, Mahon FX, Rosier E, Leguay T, Etienne G, Michaud M: [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia]. Rev Med Interne; 2007 Feb;28(2):116-9
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  • [Title] [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia].
  • [Transliterated title] Une pancréatite aiguë révélant une leucémie/lymphome T de l'adulte.
  • INTRODUCTION: Hypercalcemia frequently occurs in the course of Adult T-cell leukemia/lymphoma (ATLL).
  • We report the first case of acute pancreatitis revealing ATLL.
  • EXEGESIS: A 41-year-old woman, without medical history, presented with acute pancreatitis.
  • Biochemical tests showed severe hypercalcemia and the peripheral white blood cell count revealed an atypical lymphocytosis.
  • ATLL was diagnosed by immunophenotypic and morphological analysis of circulating lymphocytes, bone marrow and lymphatic node biopsy.
  • CONCLUSION: In spite of the high prevalence of hypercalcemia in ATLL, acute pancreatitis revealing this pathology is an exceptional condition.

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  • (PMID = 17157965.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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12. Oyama K, Kanekura T, Yoshii N, Yonekura K, Mera K, Hirayama Y, Umekita Y, Yoshida H, Umemura Y, Kanzaki T: Case of adult T-cell leukemia with pulmonary involvement presenting as nodular shadows. J Dermatol; 2008 Apr;35(4):225-8
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  • [Title] Case of adult T-cell leukemia with pulmonary involvement presenting as nodular shadows.
  • A 60-year-old man with a diagnosis of smoldering adult T-cell leukemia (ATL) had been treated successfully for 4 years with psoralen and ultraviolet A therapy, gamma-interferon, oral etoposide and sobuzoxane.
  • Upon autopsy, numerous nodules were found in the bilateral lower lobes; microscopically, the nodules were diffusely infiltrated by ATL cells.
  • Our review of the published work found only two previously reported cases of ATL with pulmonary involvement manifested as nodular shadows.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / radiography. Lung Neoplasms / radiography. Skin Neoplasms / pathology

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  • (PMID = 18419680.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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13. Utsunomiya A, Ishida T, Inagaki A, Ishii T, Yano H, Komatsu H, Iida S, Yonekura K, Takeuchi S, Takatsuka Y, Ueda R: Clinical significance of a blood eosinophilia in adult T-cell leukemia/lymphoma: a blood eosinophilia is a significant unfavorable prognostic factor. Leuk Res; 2007 Jul;31(7):915-20
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  • [Title] Clinical significance of a blood eosinophilia in adult T-cell leukemia/lymphoma: a blood eosinophilia is a significant unfavorable prognostic factor.
  • We investigated the clinical significance of a blood eosinophilia in a cohort of 158 consecutive patients with adult T-cell leukemia/lymphoma (ATLL), and multivariate analysis revealed that a blood eosinophilia was an independent and a significant unfavorable prognostic factor.
  • The present study shows that measurement of the blood eosinophil count is useful for predicting the prognosis and for determining a suitable treatment strategy for ATLL patients.
  • [MeSH-major] Eosinophilia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers / blood. Cohort Studies. Eosinophils / pathology. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 17123603.001).
  • [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 / Biomarkers; EC 1.1.1.27 / L-Lactate Dehydrogenase
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4. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • We also analyzed the expression of NOTCH1 target genes (HES1, CCND1, and MYC), all of which were expressed in the sample of the PTCL-u patient with the NOTCH1 mutation, but found only MYC to be expressed in the sample from the ATL patient.
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics
  • [MeSH-minor] Adult. DNA Mutational Analysis. Humans

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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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15. Townsend AR, Millward M, Price T, Mainwaring P, Spencer A, Longenecker A, Palladino MA, Lloyd GK, Spear MA, Padrik P: Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm). J Clin Oncol; 2009 May 20;27(15_suppl):3582

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  • [Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).
  • Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.
  • METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).
  • Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.
  • Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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  • (PMID = 27961753.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Hishizawa M, Imada K, Sakai T, Nishikori M, Arima N, Tsudo M, Ishikawa T, Uchiyama T: Antibody responses associated with the graft-versus-leukemia effect in adult T-cell leukemia. Int J Hematol; 2006 May;83(4):351-5

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  • [Title] Antibody responses associated with the graft-versus-leukemia effect in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a peripheral T-cell neoplasm caused by human T-cell leukemia virus type 1 (HTLV-1).
  • The prognosis of ATL, especially the acute and lymphoma subtypes, is poor with conventional and high-dose chemotherapy.
  • The effectiveness of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for ATL has been reported, suggesting the presence of a graft-versus-leukemia (GVL) effect against this malignancy.
  • To identify the target antigens associated with tumor rejection, we used SEREX (serological identification of antigens by recombinant cDNA expression cloning) to screen ATL complementary DNA expression libraries with sera from an ATL patient who had a GVL response after allo-HSCT.
  • Furthermore, aberrant AMFR expression was found in at least some ATL patients.
  • Taken together, these findings suggest that AMFR may be one of the GVL antigens that provoke effective antitumor immunity against ATL in allogeneic settings.
  • [MeSH-major] Antibody Formation / immunology. Antigens, Neoplasm / immunology. Graft vs Leukemia Effect / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Cytokine / immunology
  • [MeSH-minor] Cloning, Molecular. Female. Gene Expression Regulation. Gene Library. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Organ Specificity. Receptors, Autocrine Motility Factor. Transplantation, Homologous. Ubiquitin-Protein Ligases

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  • (PMID = 16757438.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Receptors, Cytokine; EC 6.3.2.19 / AMFR protein, human; EC 6.3.2.19 / Receptors, Autocrine Motility Factor; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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17. Merle H, Donnio A, Gonin C, Jean-Charles A, Panelatti G, Plumelle Y: Retinal vasculitis caused by adult T-cell leukemia/lymphoma. Jpn J Ophthalmol; 2005 Jan-Feb;49(1):41-5
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  • [Title] Retinal vasculitis caused by adult T-cell leukemia/lymphoma.
  • BACKGROUND: To report a case of lymphomatous infiltration and bilateral retinal vasculitis observed among 83 cases of adult T-cell leukemia (ATL) treated in the University Hospital Center in Fort-de-France (Martinique, French West Indies) between 1984 and 2003.
  • CASE: A complete clinical ophthalmologic examination was performed in this patient along with fluorescein angiography.
  • OBSERVATIONS: After being checked for diffuse adenopathies, myodesopsias, and phosphenes, the 35-year-old patient was diagnosed with ATL.
  • The ocular impairment, present since the onset of ATL as peripheral subretinal infiltrates, spread progressively and afferently to the rest of the retina in the form of an essentially venous vasculitis.
  • Impairment of the vitreous was noted only in the end stages of disease progression.
  • CONCLUSION: Among the more than 300 seropositive for human T-cell lymphotropic virus type 1 (HTLV-1) or patients with HTLV-1-associated myelopathy/tropical spastic paraparesis treated at our hospital in the last 20 years, and among the 83 cases of ATL, only this single case of retinal vasculitis associated with HTLV-1 was observed (1/83, 1.2%) in Martinique, confirming the geographic variability of the clinical phenotype of HTLV-1 infection.
  • The incidence of retinal vasculitis in ATL patients may signify an even worse prognosis than initially indicated.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / complications. Retinal Vasculitis / etiology
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Blotting, Western. Drug Therapy, Combination. Enzyme-Linked Immunosorbent Assay. Fatal Outcome. Female. Fluorescein Angiography. HTLV-I Antibodies / blood. Humans. Leukemic Infiltration. Retina / pathology

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  • (PMID = 15692773.001).
  • [ISSN] 0021-5155
  • [Journal-full-title] Japanese journal of ophthalmology
  • [ISO-abbreviation] Jpn. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / HTLV-I Antibodies
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18. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • Both cases were thought to represent therapy-related AML because the patients had previously received combination chemotherapy including epipodophyllotoxin, anthracycline, and alkylating agents for the ATL.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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19. Yamada Y, Kamihira S: Inactivation of tumor suppressor genes and the progression of adult T-cell leukemia-lymphoma. Leuk Lymphoma; 2005 Nov;46(11):1553-9
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  • [Title] Inactivation of tumor suppressor genes and the progression of adult T-cell leukemia-lymphoma.
  • Almost three decades have passed since adult T-cell leukemia-lymphoma (ATLL) was proposed as a new disease entity.
  • During this period, its causative agent, human T-cell leukemia virus type-1 (HTLV-1), was found and a crucial role of the viral product Tax in the development of ATLL was disclosed.
  • However, the long latent period after infection with HTLV-1 indicates the need for additional factors for full-blown ATLL, most of which are supposed to be provided by somatic mutations of cellular genes.
  • Recent progress in cell-cycle research has revealed that the uncontrolled and superior proliferative activity of malignant cells is mainly caused by the breakdown of cell-cycle regulation and that most malignancies carry aberrations in p16-pRB and/or p53 pathways.
  • ATLL is not an exception, despite the consistent association of HTLV-1 in primary leukemia cells, and accumulating evidence indicates that the breakdown of these pathways is indeed involved in the leukemogenesis of ATLL, especially in its later steps, which serve as the key events for promotion of indolent ATLL to aggressive ATLL.
  • [MeSH-major] Gene Silencing. Genes, Tumor Suppressor. Leukemia-Lymphoma, Adult T-Cell / etiology
  • [MeSH-minor] Disease Progression. Genes, cdc. Humans

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  • (PMID = 16236609.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 47
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20. Ishitsuka K, Tamura K: Treatment of adult T-cell leukemia/lymphoma: past, present, and future. Eur J Haematol; 2008 Mar;80(3):185-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of adult T-cell leukemia/lymphoma: past, present, and future.
  • Adult T-cell leukemia/lymphoma (ATLL) is a peripheral T-cell malignancy caused by human T-cell lymphotrophic virus type I.
  • Clinical manifestations of ATLL range from smoldering to chronic, lymphoma and acute.
  • Patients with acute and lymphoma type ATLL require therapeutic intervention.
  • Conventional chemotherapeutic regimens used against other malignant lymphoma have been administered to ATLL patients, but the therapeutic outcomes of acute and lymphoma type ATLL remain very poor.
  • Promising results of allogeneic stem cell transplantation (SCT) for ATLL patients have recently been reported and the treatment outcome might be improved for some ATLL patients.
  • Besides conventional chemotherapy and SCT, interferon, zidovudine, arsenic trioxide, targeted therapy against surface molecule on ATLL cells, retinoid derivatives, and bortezomib have been administered to ATLL patients in pilot or phase I/II studies.
  • Further studies are required to confirm the clinical benefits of these novel therapeutics.
  • This article reviews the current status and future directions of ATLL treatment.
  • [MeSH-major] Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Clinical Trials as Topic / trends. Forecasting. France / epidemiology. Humans. Japan / epidemiology. Prospective Studies. Stem Cell Transplantation / trends

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  • (PMID = 18081707.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 157
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21. Yokote T, Akioka T, Oka S, Hara S, Kobayashi K, Nakajima H, Yamano T, Ikemoto T, Shimizu A, Tsuji M, Hanafusa T: Flow cytometric immunophenotyping of adult T-cell leukemia/lymphoma using CD3 gating. Am J Clin Pathol; 2005 Aug;124(2):199-204

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flow cytometric immunophenotyping of adult T-cell leukemia/lymphoma using CD3 gating.
  • Adult T-cell leukemia/lymphoma (ATLL) is a lymphoproliferative neoplasm of helper T lymphocytes caused by human T-cell leukemia virus type-1 (HTLV-1).
  • The disease was first described in Kyushu, in southwestern Japan, and most frequently occurs in endemic areas, such as Japan, the Caribbean basin, West Africa, Brazil, and northern Iran.
  • ATLL is essentially a disease of adults, characterized clinically by generalized lymphadenopathy, hepatosplenomegaly, skin lesions, and hypercalcemia.
  • In the present study, flow cytometric immunophenotyping with CD3 gating was performed on 30 samples from 26 patients who had been given a diagnosis of ATLL.
  • In 14 of the 30 samples, an abnormal CD3(low) T-cell population was distinguishable from the normal T-cell populations by flow cytometric analysis.
  • Herein we report a novel strategy for flow cytometric immunophenotyping of ATLL facilitated by CD3(low) gating.
  • [MeSH-major] Antigens, CD3 / metabolism. Biomarkers, Tumor / analysis. Flow Cytometry. Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Antigens, CD4 / metabolism. Antigens, CD7 / metabolism. Antigens, CD8 / metabolism. Humans. Immunohistochemistry. Immunophenotyping. Middle Aged. Retrospective Studies. Sensitivity and Specificity

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  • (PMID = 16040289.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD7; 0 / Antigens, CD8; 0 / Biomarkers, Tumor
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22. Yano H, Ishida T, Inagaki A, Ishii T, Kusumoto S, Komatsu H, Iida S, Utsunomiya A, Ueda R: Regulatory T-cell function of adult T-cell leukemia/lymphoma cells. Int J Cancer; 2007 May 1;120(9):2052-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulatory T-cell function of adult T-cell leukemia/lymphoma cells.
  • Adult T-cell leukemia/lymphoma (ATLL) patients are highly immunocompromised, but the underlying mechanism responsible for this state remains obscure.
  • Recent studies demonstrated that FOXP3, which is a master control gene of naturally occurring regulatory T (Treg) cells, is expressed in the tumor cells from a subset of patients with ATLL.
  • Since most ATLL cells express both CD4 and CD25, these tumors might originate from CD4(+)CD25(+)FOXP3(+) Treg cells, based on their phenotypic characteristics.
  • However, whether ATLL cells actually function as Treg cells has not yet been clearly demonstrated.
  • Here, we show that ATLL cells from a subset of patients are not only hypo-responsive to T-cell receptor-mediated activation, but also suppress the proliferation of autologous CD4(+) non-ATLL cells.
  • Furthermore, ATLL cells from this subset of patients secrete only small amounts of IFN-gamma, and suppress IFN-gamma production by autologous CD4(+) non-ATLL cells.
  • These are the first data showing that ATLL cells from a subset of patients function as Treg cells in an autologous setting.
  • The present study provides novel insights into understanding the immunopathogenesis of ATLL, i.e., how HTLV-1-infected cells can survive in the face of host immune responses.
  • It also adds to our understanding of ATLL patients' severely immunocompromised state.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / physiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17278106.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00355472
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / RNA, Messenger; 0 / Receptors, CCR4; 0 / Receptors, Chemokine; 82115-62-6 / Interferon-gamma
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23. Koga Y, Iwanaga M, Soda M, Inokuchi N, Sasaki D, Hasegawa H, Yanagihara K, Yamaguchi K, Kamihira S, Yamada Y: Trends in HTLV-1 prevalence and incidence of adult T-cell leukemia/lymphoma in Nagasaki, Japan. J Med Virol; 2010 Apr;82(4):668-74

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trends in HTLV-1 prevalence and incidence of adult T-cell leukemia/lymphoma in Nagasaki, Japan.
  • Most previous studies aimed at estimating the number of human T-cell leukemia virus type-1 (HTLV-1) carriers in endemic areas have been based on seroprevalence rates in blood donors; however, this may result in underestimation because of the healthy donor effect.
  • In the present study, the number of HTLV-1 carriers in Nagasaki City was estimated based on the seroprevalence rates in a hospital-based population from Nagasaki University Hospital.
  • In accordance with previous reports, seroprevalence of HTLV-1 was higher in females, and year of birth-specific seroprevalence showed a significant annual decline in both genders (P for trend: <0.0001).
  • The estimated number of HTLV-1 carriers in Nagasaki City was 36,983.
  • The incidence of adult T-cell leukemia/lymphoma (ATLL) among HTLV-1 carriers was estimated using data from the Nagasaki Prefectural Cancer Registry.
  • The estimated annual incidence of ATLL was 61 per 100,000 HTLV-1 carriers, and the crude lifetime risk of the development was 7.29% for males and 3.78% for females.
  • There is a large pool of HTLV-1 carriers aged over 70 years, and a continuing development of cases of ATLL among the elderly is therefore expected.
  • [MeSH-major] HTLV-I Infections / complications. HTLV-I Infections / epidemiology. Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Carrier State / epidemiology. Child. Child, Preschool. Female. Hospitals. Humans. Incidence. Infant. Infant, Newborn. Japan. Male. Middle Aged. Seroepidemiologic Studies. Young Adult

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20166187.001).
  • [ISSN] 1096-9071
  • [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
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24. Satou Y, Matsuoka M: Implication of the HTLV-I bZIP factor gene in the leukemogenesis of adult T-cell leukemia. Int J Hematol; 2007 Aug;86(2):107-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implication of the HTLV-I bZIP factor gene in the leukemogenesis of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a leukemia derived from CD4+ mature T-cells and induced by human T-cell leukemia virus type I (HTLV-I) infection.
  • Although previous studies have revealed many aspects of its leukemogenesis, enigmas remain about how HTLV-I transforms mature T-cells in infected individuals.
  • Furthermore, an effective therapy for ATL has not yet been established.
  • The critical role of a nonstructural regulatory viral protein, Tax, in transformation has been established through many molecular studies, in vitro cell culture experiments, and transgenic mouse model systems.
  • In addition, other accessory viral proteins have been implicated in ATL pathogenesis.
  • Recent studies of a minus strand viral gene, HTLV-I bZIP factor (HBZ), suggest it plays a role in ATL leukemogenesis.
  • In this review, we summarize the molecular and cellular mechanisms involved in the leukemogenesis induced by HTLV-I; we consider both viral and host cellular factors and focus particularly on the viral gene HBZ.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / physiology. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / etiology. Viral Proteins / physiology
  • [MeSH-minor] Cell Transformation, Viral. Humans

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  • (PMID = 17875522.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Viral Proteins
  • [Number-of-references] 68
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25. Okada J, Imafuku S, Tsujita J, Moroi Y, Urabe K, Furue M: Case of adult T-cell leukemia/lymphoma manifesting marked purpura. J Dermatol; 2007 Nov;34(11):782-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case of adult T-cell leukemia/lymphoma manifesting marked purpura.
  • Antibody to human T-lymphotropic virus type 1 (HTLV-1) was present in the serum and samples from skin lesions revealed HTLV-1 proviral DNA integration, as well as a clonal T-cell receptor Cbeta1 gene rearrangement.
  • We therefore diagnosed this case as adult T-cell leukemia/lymphoma (ATL), and the purpuric lesions as ATL-specific.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pigmentation Disorders / etiology. Purpura / etiology
  • [MeSH-minor] Blotting, Southern. Female. Gene Rearrangement, beta-Chain T-Cell Antigen Receptor. Humans. Lymphocytes / immunology. Middle Aged. Skin / pathology. Skin / virology

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  • (PMID = 17973821.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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26. Shimakage M, Inoue N, Ohshima K, Kawahara K, Oka T, Yasui K, Matsumoto K, Inoue H, Watari A, Higashiyama S, Yutsudo M: Down-regulation of ASY/Nogo transcription associated with progression of adult T-cell leukemia/lymphoma. Int J Cancer; 2006 Oct 1;119(7):1648-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of ASY/Nogo transcription associated with progression of adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) is an aggressive form of human leukemia/lymphoma.
  • Although this disease is initiated by infection with human T-lymphotropic virus type 1 (HTLV-1), many HTLV-1 carriers survive for a long period without aggressive illness, suggesting that other factors may play roles in the progression of ATLL to an aggressive state.
  • Previously, we have reported that ASY/Nogo mRNA was markedly down-regulated in human small-cell lung carcinomas, whereas it was expressed in normal tissues and other lung carcinomas, such as adenocarcinoma and squamous cell carcinoma.
  • To understand whether or not ASY/Nogo gene is involved in the progression of ATLL, we examined the expression of ASY/Nogo mRNA in smoldering, chronic and aggressive ATLL, and found that the expression level of ASY/Nogo mRNA was markedly reduced in clinically aggressive ATLL.
  • HTLV-1 Tax expression was not affected by the down-regulation of ASY/Nogo mRNA.
  • These results indicate that the ASY/Nogo gene may act as a suppressor against ATLL progression, independent of Tax expression.
  • [MeSH-major] Down-Regulation / genetics. Gene Expression Regulation, Neoplastic / genetics. Intracellular Signaling Peptides and Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Membrane Proteins / genetics. Myelin Proteins / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Products, tax / genetics. Humans. Male. Middle Aged. RNA, Messenger / genetics

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16646068.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Myelin Proteins; 0 / Nogo protein; 0 / RNA, Messenger
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27. Ratner L, Grant C, Zimmerman B, Fritz J, Weil G, Denes A, Suresh R, Campbell N, Jacobson S, Lairmore M: Effect of treatment of Strongyloides infection on HTLV-1 expression in a patient with adult T-cell leukemia. Am J Hematol; 2007 Oct;82(10):929-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of treatment of Strongyloides infection on HTLV-1 expression in a patient with adult T-cell leukemia.
  • Human T-cell leukemia virus type 1 (HTLV-1) is associated with adult T-cell leukemia-lymphoma (ATLL) in about 5% of infected individuals.
  • Coinfection by Strongyloides stercoralis has been suggested to be a cofactor for development of ATLL.
  • We describe a patient who presented with HTLV-1-associated chronic ATLL and Strongyloides infection.
  • Studies of this patient's viral RNA levels demonstrated stimulation of HTLV-1 replication by Strongyloides, which resolved with anti-helminthic therapy.
  • This case provides support for the hypothesis that Strongyloides is a cofactor for ATLL via T-cell stimulation.

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  • [Cites] Int J Hematol. 2003 Feb;77(2):164-70 [12627852.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2466-75 [11971181.001]
  • [Cites] Blood. 2002 Jan 1;99(1):88-94 [11756157.001]
  • [Cites] Am J Trop Med Hyg. 2006 Feb;74(2):246-9 [16474078.001]
  • [Cites] J Infect Dis. 2001 Jan 15;183(2):197-205 [11120926.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Mem Inst Oswaldo Cruz. 2000 Sep-Oct;95(5):711-2 [10998221.001]
  • [Cites] Adv Cancer Res. 2003;89:69-132 [14587871.001]
  • [Cites] Clin Microbiol Rev. 2004 Jan;17(1):208-17 [14726461.001]
  • [Cites] Oncogene. 2004 Jun 24;23(29):4966-74 [15107832.001]
  • [Cites] Adv Cancer Res. 1989;53:33-72 [2552758.001]
  • [Cites] Clin Exp Immunol. 1990 Aug;81(2):207-11 [2143707.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Am J Med. 1992 Feb;92(2):202-8 [1543206.001]
  • [Cites] Br J Cancer. 1994 Oct;70(4):771-4 [7917938.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] Parasite Immunol. 2004 Nov-Dec;26(11-12):487-97 [15771684.001]
  • [Cites] J Infect Dis. 2005 Feb 15;191(4):612-8 [15655786.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Apr 1;20(4):394-402 [10096585.001]
  • [Cites] Am J Clin Pathol. 1997 Jan;107(1):81-7 [8980372.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Jun 1;12(2):182-6 [8680890.001]
  • [Cites] J Infect Chemother. 2004 Dec;10(6):348-51 [15614460.001]
  • (PMID = 17617788.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA100730-069003; United States / NCI NIH HHS / CA / CA100730-05; United States / NCI NIH HHS / CA / CA63417; United States / NCI NIH HHS / CA / CA10073; United States / NCI NIH HHS / CA / R01 CA063417; United States / NCI NIH HHS / CA / P01 CA100730-05; United States / NCI NIH HHS / CA / R01 CA105218; United States / NCI NIH HHS / CA / CA100730-069003; United States / NCI NIH HHS / CA / CA105218
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthelmintics; 0 / DNA, Viral; 0 / RNA, Viral; 70288-86-7 / Ivermectin
  • [Other-IDs] NLM/ NIHMS94116; NLM/ PMC2652703
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28. Fett NM, Siddiqui J, Creswell CH, Zhang D, Lloyd R, Wood GS: Adult T-cell leukemia/lymphoma in a patient from Romania: a case report and review of the literature. J Cutan Pathol; 2008 Oct;35 Suppl 1:32-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma in a patient from Romania: a case report and review of the literature.
  • Adult T-cell leukemia/lymphoma (ATLL) is a rare malignancy caused by human T-cell leukemia virus-1.
  • ATLL is endemic to Japan, and to date, there are only four case reports of patients from Romania who have developed ATLL.
  • Here, we describe a woman living in Madison, Wisconsin, originally from Romania, who presented with an atypical papulosquamous eruption and was ultimately diagnosed with smoldering ATLL.
  • Narrow-band ultraviolet-B (UV-B) therapy and mid-potency topical steroids resulted in skin clearing for approximately 5 months after diagnosis; however, she subsequently relapsed with disease refractory to both narrow band UV-B and psoralen plus ultraviolet A (PUV-A), progressed to acute ATLL and expired secondary to complications.
  • [MeSH-major] HTLV-I Infections / complications. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Ultraviolet Therapy
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Female. Flow Cytometry. Humans. Immunohistochemistry. Polymerase Chain Reaction. Respiratory Tract Infections / pathology. Romania. Vitiligo / pathology

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  • [Copyright] Copyright Blackwell Munksgaard 2008.
  • (PMID = 18544058.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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29. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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30. Kawakami T, Kawanabe T, Soma Y: Granuloma annulare-like skin lesions as an initial manifestation in a Japanese patient with adult T-cell leukemia/lymphoma. J Am Acad Dermatol; 2009 May;60(5):848-52
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  • [Title] Granuloma annulare-like skin lesions as an initial manifestation in a Japanese patient with adult T-cell leukemia/lymphoma.
  • Histologic examination revealed epithelioid cell granulomas associated with dense atypical lymphocytes in the dermis.
  • Immunohistochemical staining of skin specimens showed a prominent infiltration of CD3+, CD4+, CD5+, and CD25+ cells.
  • Human T-cell leukemia virus type I proviral DNA was detected in the blood and cerebrospinal fluid by Southern blot analysis and polymerase chain reaction assay.
  • The patient was given the diagnosis of adult T-cell leukemia/lymphoma based on the initial cutaneous manifestations.
  • The granuloma annulare-like skin lesions in our patient could be considered as a peculiar immunologic hypersensitivity reaction of the host against the tumor cells or persistent human T-cell leukemia virus type I viral antigens.
  • Dermatologists should be aware that this skin condition may be an initial manifestation of adult T-cell leukemia/lymphoma.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Skin / pathology
  • [MeSH-minor] Aged. Antigens, CD3 / analysis. Antigens, CD4 / analysis. Antigens, CD5 / analysis. Blotting, Southern. DNA, Viral / analysis. Human T-lymphotropic virus 1 / genetics. Humans. Immunohistochemistry. Interleukin-2 Receptor alpha Subunit / analysis. Male. Polymerase Chain Reaction. Proviruses / genetics

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  • (PMID = 19389526.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD5; 0 / DNA, Viral; 0 / Interleukin-2 Receptor alpha Subunit
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31. Idutsu K, Abe Y, Otonari J, Tachikawa Y, Ohtsuka R, Choi I, Muta K, Takayanagi R: [Human herpesvirus 6 encephalitis in a patient with adult T-cell leukemia/lymphoma]. Rinsho Ketsueki; 2007 Aug;48(8):664-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Human herpesvirus 6 encephalitis in a patient with adult T-cell leukemia/lymphoma].
  • Human herpesvirus 6 (HHV-6) reactivates in immunocompromised patients, and HHV-6 encephalitis has often been reported as a complication of transplantation.
  • We describe a 37-year-old woman with the acute type of adult T-cell leukemia/lymphoma who developed HHV-6 encephalitis before chemotherapy.
  • HHV-6 encephalitis should be listed as a differential diagnosis of encephalopathy developing in immunocompromised patients.
  • [MeSH-major] Encephalitis, Herpes Simplex / complications. Herpesvirus 6, Human. Leukemia-Lymphoma, Adult T-Cell / complications. Opportunistic Infections / complications. Roseolovirus Infections / complications
  • [MeSH-minor] Adult. Female. Humans

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  • (PMID = 17867305.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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32. Yamaguchi T, Maeda Y, Ueda S, Hijikata Y, Morita Y, Miyatake JI, Matsuda M, Kanamaru A: Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia. Leukemia; 2005 Jun;19(6):1010-7
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia.
  • We previously reported that all-trans retinoic acid (ATRA) inhibits growth in human T-cell leukemia virus type 1 (HTLV-1)-positive T-cell lines and fresh cells from patients with adult T-cell leukemia.
  • In the present study, we observed that NF-kappaB transcriptional activity as well as cell growth decreased significantly in HTLV-1-positive T-cell lines in the presence of ATRA.
  • Furthermore, we observed that ATRA reduced HTLV-1 proviral DNA, HTLV-1 genes (gag, tax, or pol mRNA) using the real-time quantitative polymerase chain reaction.
  • SIL-2R was reduced by ATRA in both protein level (culture supernantant) and mRNA level in HTLV-1-positive T-cell lines.
  • Interestingly, ATRA significantly inhibited RT activity similar to azidothimidine (AZT) in HTLV-1-positive T-cell lines.
  • Moreover, AZT inhibited proviral DNA but not NF-kappaB transcriptional activity, and sIL-2R on HTLV-1; however, ATRA inhibited of NF-kappaB, proviral DNA and sIL-2R on HTLV-1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / metabolism. Signal Transduction / drug effects. Tretinoin / pharmacology
  • [MeSH-minor] Adult. Cell Division / drug effects. Deltaretrovirus Infections / drug therapy. Deltaretrovirus Infections / metabolism. Deltaretrovirus Infections / physiopathology. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Viral / drug effects. Gene Products, gag / genetics. Gene Products, pol / genetics. Genes, pX / genetics. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / growth & development. Humans. In Vitro Techniques. Jurkat Cells. NF-kappa B / metabolism. Proviruses / genetics. Receptors, Interleukin-2 / metabolism. Solubility. Transcriptional Activation / drug effects. Viral Load

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  • (PMID = 15843825.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gene Products, gag; 0 / Gene Products, pol; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; 5688UTC01R / Tretinoin
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33. Morimoto H, Tsukada J, Kominato Y, Tanaka Y: Reduced expression of human mismatch repair genes in adult T-cell leukemia. Am J Hematol; 2005 Feb;78(2):100-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced expression of human mismatch repair genes in adult T-cell leukemia.
  • In this study, we investigated the expression of six human DNA mismatch repair (MMR) genes, human MutS homologues 2 (hMSH2), 3 (hMSH3), and 6 (hMSH6), human MutL homologue 1 (hMLH1), human post-meiotic segregations 1 (hPMS1) and 2 (hPMS2), in primary leukemic cells obtained from 11 patients with acute-type adult T-cell leukemia (ATL) by using reverse transcription-polymerase chain reaction (RT-PCR).
  • In contrast to normal peripheral lymphocytes, all primary ATL samples had reduced or loss of expression of two or more MMR genes, and the expression of several MMR genes was simultaneously suppressed in each ATL patient.
  • Interestingly, methylation-specific PCR indicated methylation of hPMS1 promoter in all of four ATL cases examined. hPMS1 expression, but not hMSH2 expression, was restored by treatment with a DNA demethylation agent, 5-aza-2'-deoxycytidine, suggesting that methylation plays a crucial role in inhibition of the hPMS1 gene expression in ATL.
  • Our results demonstrate that defect of both human MutS and human MutL systems in primary ATL cells.
  • [MeSH-major] Adenosine Triphosphatases / genetics. Base Pair Mismatch / genetics. DNA Repair Enzymes / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15682421.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / G-T mismatch-binding protein; 0 / MLH1 protein, human; 0 / MSH3 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / PMS1 protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein; EC 6.5.1.- / DNA Repair Enzymes
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34. Matsubar Y, Hori T, Morita R, Sakaguchi S, Uchiyama T: Delineation of immunoregulatory properties of adult T-cell leukemia cells. Int J Hematol; 2006 Jul;84(1):63-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Delineation of immunoregulatory properties of adult T-cell leukemia cells.
  • We characterized leukemic cells from 20 adult T-cell leukemia (ATL) cases and 7 ATL-derived cell lines in terms of Foxp3 messenger RNA (mRNA) expression, cytokine production, cell surface markers associated with regulatory T-cells (Treg), and in vitro immunoregulatory activity and compared the results with those of cells from 3 T-cell-type chronic lymphocytic leukemia (T-CLL) patients and normal CD4+ T-cells.
  • Real-time polymerase chain reaction analysis showed that cells from 10 ATL cases, 1 T-CLL case, and 1 ATL cell line had higher Foxp3 mRNA levels than CD4+ T-cells.
  • In 5 ATL cases, Foxp3 levels were comparable to those of CD4+CD25+ T-cells.
  • Flow cytometric analysis revealed that CTLA-4 expression correlated with Foxp3 mRNA level in ATL cells.
  • The cells of all ATL cases examined produced no interleukin 2 or interferon gamma after iono-mycin and phorbolmyristate acetate stimulation.
  • An in vitro inhibition assay showed that the proliferation of normal CD4+CD25- T-cells stimulated with anti-CD3 monoclonal antibody and autologous dendritic cells was significantly suppressed by coculture with Foxp3-high ATL cells.
  • These results indicate that Foxp3 expression is variable in ATL cases and that Foxp3-high ATL cells, which resemble Treg phenotypically as well as functionally, may be involved in immune suppression in ATL.
  • [MeSH-major] Gene Expression Regulation, Leukemic / immunology. Immune Tolerance. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Aged. Cell Line, Tumor. Coculture Techniques. Female. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 16867905.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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35. Bitar N, Hajj HE, Houmani Z, Sabbah A, Otrock ZK, Mahfouz R, Zaatari G, Bazarbachi A: Adult T-cell leukemia/lymphoma in the Middle East: first report of two cases from Lebanon. Transfusion; 2009 Sep;49(9):1859-64
Hazardous Substances Data Bank. ZIDOVUDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma in the Middle East: first report of two cases from Lebanon.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATL) is an aggressive lymphoproliferative disorder caused by human T-cell leukemia virus type I (HTLV-I).
  • HTLV-I is endemic in southern Japan, the Caribbean, Central and South America, certain areas of Africa, and the southeastern United States.
  • CASE REPORTS: In this report, the first two cases of ATL diagnosed in Lebanon are described.
  • The first patient of Lebanese origin presented with acute ATL.
  • The second patient of Romanian origin developed acute ATL in early relapse after autologous transplantation for ATL.
  • Both patients had lymphocytosis, severe hypercalcemia, and CD25+ T-cell immunophenotype on peripheral blood.
  • In both patients, HTLV-I serology was positive by enzyme-linked immunosorbent assay and confirmed by Western blot and HTLV-I oncoprotein Tax expression was documented in the leukemic cells.
  • Upon screening, seven direct family members of the first patient were HTLV-I positive; four of them were regular blood donors.
  • CONCLUSIONS: Screening blood donors for HTLV-I seropositivity is not currently performed in Lebanon.
  • A large screening study in Lebanon is needed to confirm whether South Lebanon is a new endemic region for HTLV-I infection and to recommend mandatory screening of blood donors for HTLV-I infection.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Bone Density Conservation Agents / therapeutic use. Diphosphonates / therapeutic use. Fatal Outcome. Female. Gene Products, tax / blood. Humans. Imidazoles / therapeutic use. Interferon-alpha / therapeutic use. Lebanon. Middle Aged. Zidovudine / therapeutic use

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  • (PMID = 19453978.001).
  • [ISSN] 1537-2995
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Gene Products, tax; 0 / Imidazoles; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine; 6XC1PAD3KF / zoledronic acid
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36. 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
Hazardous Substances Data Bank. ZIDOVUDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Blood. 1994 Sep 15;84(6):1942-9 [8080997.001]
  • [Cites] Oncogene. 1994 Nov;9(11):3289-97 [7936653.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] Genes Dev. 1995 Aug 15;9(16):1965-77 [7649478.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4063-75 [7492762.001]
  • [Cites] Mol Cell Biol. 1996 Apr;16(4):1283-94 [8657101.001]
  • [Cites] Intervirology. 1995;38(3-4):238-46 [8682622.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Jun 1;12(2):182-6 [8680890.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6005-15 [16155607.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15989-94 [16236719.001]
  • [Cites] Bone Marrow Transplant. 2006 Jan;37(1):41-4 [16247419.001]
  • [Cites] J Pathol. 2006 Apr;208(5):714-23 [16400625.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Blood. 1998 Jan 15;91(2):570-6 [9427711.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3557-61 [9808547.001]
  • [Cites] Genes Dev. 1999 Feb 15;13(4):382-7 [10049353.001]
  • [Cites] Int J Cancer. 2000 Mar 1;85(5):720-5 [10699955.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] J Exp Med. 2000 Apr 17;191(8):1281-92 [10770796.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 May 23;97(11):6055-60 [10811897.001]
  • [Cites] Blood. 2000 Oct 1;96(7):2537-42 [11001908.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1613-22 [11080800.001]
  • [Cites] Cancer Lett. 2000 Nov 10;160(1):89-97 [11098089.001]
  • [Cites] Blood. 2001 Feb 1;97(3):744-51 [11157493.001]
  • [Cites] Oncologist. 2001;6(1):34-55 [11161227.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Br J Haematol. 2001 Jun;113(3):779-84 [11380470.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3640-50 [8670867.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S179-85 [8797721.001]
  • [Cites] Science. 1997 Jan 24;275(5299):540-3 [8999800.001]
  • [Cites] Nat Genet. 1997 Oct;17(2):226-30 [9326949.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Br J Haematol. 1999 Jun;105(3):743-51 [10354140.001]
  • [Cites] Exp Hematol. 1999 Jul;27(7):1168-75 [10390192.001]
  • [Cites] J Immunol. 1999 Sep 1;163(5):2713-22 [10453013.001]
  • [Cites] Mol Diagn. 1999 Jun;4(2):101-17 [10462626.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Br J Haematol. 2005 Jan;128(2):253-65 [15638862.001]
  • [Cites] J Cutan Pathol. 2005 Mar;32(3):227-34 [15701085.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):297-309 [15803156.001]
  • [Cites] Blood. 2005 Jul 1;106(1):235-40 [15790788.001]
  • [Cites] Carcinogenesis. 2005 Aug;26(8):1382-8 [15831528.001]
  • [Cites] Br J Haematol. 2001 Jul;114(1):63-9 [11472346.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6369-86 [11533227.001]
  • [Cites] Oncogene. 2001 Oct 25;20(48):7098-103 [11704834.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Jpn J Cancer Res. 2001 Dec;92(12):1284-92 [11749693.001]
  • [Cites] J Interferon Cytokine Res. 2002 Jan;22(1):111-20 [11846982.001]
  • [Cites] Oncogene. 2002 Feb 14;21(8):1251-62 [11850845.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1069-85 [12040438.001]
  • [Cites] Jpn J Cancer Res. 2002 Jun;93(6):685-94 [12079517.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] J Immunol. 2002 Sep 15;169(6):3120-30 [12218129.001]
  • [Cites] Oncogene. 2002 Oct 3;21(44):6751-65 [12360402.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Leuk Lymphoma. 2002 Dec;43(12):2249-55 [12613509.001]
  • [Cites] J Virol. 2003 May;77(9):5286-94 [12692230.001]
  • [Cites] Blood. 2003 May 1;101(9):3681-6 [12511414.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] Leuk Lymphoma. 2003;44 Suppl 3:S21-6 [15202521.001]
  • [Cites] Leuk Lymphoma. 2003;44 Suppl 3:S41-7 [15202524.001]
  • [Cites] J Exp Med. 2004 Jul 19;200(2):247-53 [15249594.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1357-63 [15190257.001]
  • [Cites] Haematol Blood Transfus. 1981;26:502-14 [6274766.001]
  • [Cites] J Exp Med. 1985 Dec 1;162(6):2169-74 [2866223.001]
  • [Cites] Blood. 1987 Nov;70(5):1407-11 [2889484.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • (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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37. Ueda S, Maeda Y, Yamaguchi T, Hanamoto H, Hijikata Y, Tanaka M, Takai S, Hirase C, Morita Y, Kanamaru A: Influence of Epstein-Barr virus infection in adult T-cell leukemia. Hematology; 2008 Jun;13(3):154-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of Epstein-Barr virus infection in adult T-cell leukemia.
  • The involvement of adult T-cell leukemia (ATL) cells in organs such as the skin and lymph nodes is observed in about 50% of cases of ATL.
  • Epstein-Barr virus (EBV) infection has often been observed in the clinical course of ATL.
  • In this study, we established two B-cell lines from peripheral blood of patients with ATL.
  • EBV DNA, proviral DNA for HTLV-1 and Tax mRNA were detected in both lines.
  • As part of the characterization of these cells, an enhanced expression of intercellular adhesion molecule-1 (ICAM-1) (CD54) or ICAM-3 (ICAM-3) (CD50), lymphocyte function-1 (LFA-1) (CD11a/CD18), and Mac-1 (CD11b/CD18) was observed.
  • To investigate the role of the interaction of these viruses, we transfected EBV and/or HTLV-1 into a healthy donor's lymphocytes, an EBV-infected B cell line, Raji, and a HTLV-1 negative T-cell line, Jurkat.
  • Enhanced expression of adhesion molecules was also observed in double transfectants (EBV and HTLV-1).
  • In the clinical course of ATL, LMP-1, EBNA-2, CD50 and CD54 were detected in lymph nodes and skin specimens by immunohistochemical staining.
  • Furthermore, high levels of interleukin-4 (IL-4) were detected in these cell lines and transfectants.
  • The results indicated that coinfection with HTLV-1 and EBV may induce aggressive organ involvement through the enhanced expression of adhesion molecules via IL-4 signaling.
  • A new mechanism of ATL involvement is discussed.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Leukemia-Lymphoma, Adult T-Cell / complications
  • [MeSH-minor] Adult. Antigens, CD / genetics. B-Lymphocytes / pathology. B-Lymphocytes / virology. Cell Adhesion Molecules / genetics. Cell Line. Cell Line, Tumor. Gene Products, tax / genetics. Herpesvirus 4, Human / genetics. Human T-lymphotropic virus 1 / genetics. Humans. Intercellular Adhesion Molecule-1 / genetics. Macrophage-1 Antigen / genetics. Proviruses / genetics

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  • (PMID = 18702873.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cell Adhesion Molecules; 0 / Gene Products, tax; 0 / ICAM3 protein, human; 0 / Macrophage-1 Antigen; 0 / tax protein, Human T-lymphotrophic virus 1; 126547-89-5 / Intercellular Adhesion Molecule-1
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38. Shu ST, Martin CK, Thudi NK, Dirksen WP, Rosol TJ: Osteolytic bone resorption in adult T-cell leukemia/lymphoma. Leuk Lymphoma; 2010 Apr;51(4):702-14
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  • [Title] Osteolytic bone resorption in adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATLL) is caused by human T lymphotropic virus type 1 (HTLV-1).
  • Patients with ATLL frequently develop humoral hypercalcemia of malignancy (HHM) resulting from increased osteoclastic bone resorption.
  • Our goal was to investigate the mechanisms of ATLL-induced osteoclastic bone resorption.
  • Murine calvaria co-cultured with HTLV-1-infected cells directly or conditioned media from cell cultures had increased osteoclast activity that was dependent on RANKL, indicating that factors secreted from ATLL cells had a stimulatory effect on bone resorption.
  • Factors released from resorbing bone stimulated proliferation of HTLV-1-infected T-cells.
  • Parathyroid hormone-related protein (PTHrP) and macrophage inflammatory protein-1alpha (MIP-1alpha), both osteoclast stimulators, were expressed in HTLV-1-infected T-cell lines.
  • Interestingly, when HTLV-1-infected T-cells were co-cultured with pre-osteoblasts, the expression of osteoprotegerin (OPG), an osteoclast inhibitory factor, was significantly down-regulated in the pre-osteoblasts.
  • When OPG was added into the ex vivo osteoclastogenesis assay induced by HTLV-1-infected T-cells, osteoclastogenesis was strongly inhibited.
  • In addition, HTLV-1-infected T-cells inhibited expression of early osteoblast genes and induced late genes.
  • These regulators will serve as future therapeutic targets for the treatments of HHM in ATLL.

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  • [Cites] J Immunol. 2000 Mar 1;164(5):2718-27 [10679113.001]
  • [Cites] Endocrine. 2009 Feb;35(1):47-56 [18987998.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3349-53 [11369623.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36241-50 [11451955.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36703-10 [11481336.001]
  • [Cites] Rev Endocr Metab Disord. 2000 Nov;1(4):253-63 [11706739.001]
  • [Cites] J Cell Biochem. 2001;84(1):1-11 [11746511.001]
  • [Cites] J Clin Invest. 2001 Dec;108(12):1833-41 [11748267.001]
  • [Cites] Blood. 2002 Jan 15;99(2):634-40 [11781248.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1341-9 [11830485.001]
  • [Cites] Cancer Detect Prev. 2002;26(3):222-8 [12269770.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4129-38 [12393612.001]
  • [Cites] Mol Cell Endocrinol. 2003 Jan 31;199(1-2):165-77 [12581888.001]
  • [Cites] J Virol. 2003 May;77(9):5286-94 [12692230.001]
  • [Cites] Ann N Y Acad Sci. 2003 May;995:109-16 [12814943.001]
  • [Cites] Blood. 2003 Jul 1;102(1):311-9 [12649140.001]
  • [Cites] Clin Chem. 2003 Aug;49(8):1398-402 [12881458.001]
  • [Cites] Oncogene. 2004 Jan 22;23(3):845-51 [14647437.001]
  • [Cites] Neuropathology. 2004 Jun;24(2):131-5 [15139590.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 May;50(2):87-100 [15157658.001]
  • [Cites] J Bone Miner Res. 2004 Jul;19(7):1105-11 [15176993.001]
  • [Cites] Blood. 2004 Aug 1;104(3):802-9 [15090453.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4473-5 [1693772.001]
  • [Cites] Blood. 1993 Aug 1;82(3):722-31 [8338942.001]
  • [Cites] J Pathol. 1995 Feb;175(2):227-36 [7738719.001]
  • [Cites] Mol Cell Biol. 1995 Aug;15(8):4064-75 [7623802.001]
  • [Cites] Miner Electrolyte Metab. 1995;21(1-3):166-70 [7565442.001]
  • [Cites] Neurology. 1998 Jun;50(6):1920 [9633766.001]
  • [Cites] Endocrinology. 1999 Oct;140(10):4382-9 [10499489.001]
  • [Cites] Clin Breast Cancer. 2005 Feb;5 Suppl(2):S46-53 [15807924.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2005;15(2):115-32 [16022632.001]
  • [Cites] Calcif Tissue Int. 2005 May;76(5):326-35 [15868281.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1175-83 [15889157.001]
  • [Cites] Clin Cancer Res. 2005 Sep 1;11(17):6109-15 [16144909.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Clin Exp Immunol. 2005 Oct;142(1):12-20 [16178851.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2006 Jan;26(1):200-5 [16254204.001]
  • [Cites] Br J Haematol. 2006 May;133(3):301-4 [16643432.001]
  • [Cites] Curr Opin Rheumatol. 2006 Jul;18(4):396-404 [16763461.001]
  • [Cites] Cancer Metastasis Rev. 2006 Dec;25(4):559-71 [17165129.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1752-62 [17554373.001]
  • [Cites] Eur Urol. 2007 Sep;52(3):791-7 [17207914.001]
  • [Cites] Mol Cancer Ther. 2007 Oct;6(10):2609-17 [17938257.001]
  • [Cites] Cell Metab. 2008 Aug;8(2):132-45 [18680714.001]
  • [Cites] Blood. 2000 Jul 15;96(2):671-5 [10887133.001]
  • (PMID = 20214446.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100730; United States / NCRR NIH HHS / RR / T32 RR007073; United States / NCI NIH HHS / CA / P01 CA100730-09; United States / NCI NIH HHS / CA / F32 CA130458-01; United States / NCI NIH HHS / CA / F32 CA130458; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ NIHMS270807; NLM/ PMC3057200
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39. Takasaki Y, Iwanaga M, Imaizumi Y, Tawara M, Joh T, Kohno T, Yamada Y, Kamihira S, Ikeda S, Miyazaki Y, Tomonaga M, Tsukasaki K: Long-term study of indolent adult T-cell leukemia-lymphoma. Blood; 2010 Jun 3;115(22):4337-43
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  • [Title] Long-term study of indolent adult T-cell leukemia-lymphoma.
  • The long-term prognosis of indolent adult T-cell leukemia-lymphoma (ATL) is not clearly elucidated.
  • From 1974 to 2003, newly diagnosed indolent ATL in 90 patients (65 chronic type and 25 smoldering type) was analyzed.
  • The median survival time was 4.1 years; 12 patients remained alive for more than 10 years, 44 progressed to acute ATL, and 63 patients died.
  • The prognosis of indolent ATL in this study was poorer than expected.
  • These findings suggest that even patients with indolent ATL should be carefully observed in clinical practice.
  • Further studies are required to develop treatments for indolent ATL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / mortality

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  • (PMID = 20348391.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Ishikawa C, Tafuku S, Kadekaru T, Sawada S, Tomita M, Okudaira T, Nakazato T, Toda T, Uchihara JN, Taira N, Ohshiro K, Yasumoto T, Ohta T, Mori N: Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer; 2008 Dec 1;123(11):2702-12
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  • [Title] Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol.
  • Adult T-cell leukemia (ATL) is a fatal malignancy of T lymphocytes caused by human T-cell leukemia virus type 1 (HTLV-1) infection and remains incurable.
  • We evaluated the anti-ATL effects of fucoxanthin and its metabolite, fucoxanthinol.
  • Both carotenoids inhibited cell viability of HTLV-1-infected T-cell lines and ATL cells, and fucoxanthinol was approximately twice more potent than fucoxanthin.
  • In contrast, other carotenoids, beta-carotene and astaxanthin, had mild inhibitory effects on HTLV-1-infected T-cell lines.
  • Importantly, uninfected cell lines and normal peripheral blood mononuclear cells were resistant to fucoxanthin and fucoxanthinol.
  • Both carotenoids induced cell cycle arrest during G(1) phase by reducing the expression of cyclin D1, cyclin D2, CDK4 and CDK6, and inducing the expression of GADD45alpha, and induced apoptosis by reducing the expression of Bcl-2, XIAP, cIAP2 and survivin.
  • The induced apoptosis was associated with activation of caspase-3, -8 and -9.
  • Mice with severe combined immunodeficiency harboring tumors induced by inoculation of HTLV-1-infected T cells responded to treatment with fucoxanthinol with suppression of tumor growth, showed extensive tissue distribution of fucoxanthinol, and the presence of therapeutically effective serum concentrations of fucoxanthinol.
  • Our preclinical data suggest that fucoxanthin and fucoxanthinol could be potentially useful therapeutic agents for patients with ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Phaeophyta / chemistry. Xanthophylls / therapeutic use. beta Carotene / analogs & derivatives
  • [MeSH-minor] Acetylation. Animals. Caspases / metabolism. Cell Survival / drug effects. Female. Human T-lymphotropic virus 1 / drug effects. Humans. Mice. NF-kappa B / metabolism. Transcription Factor AP-1 / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


41. Uozumi K: Treatment of adult T-cell leukemia. J Clin Exp Hematop; 2010;50(1):9-25
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  • [Title] Treatment of adult T-cell leukemia.
  • Adult T-cell Leukemia (ATL) is an aggressive malignant disease of CD4+ T-cells associated with human T-cell leukemia virus type I (HTLV-I).
  • Prognosis of ATL patients is directly correlated to the subtype of ATL.
  • Treatment of the aggressive forms (acute and lymphoma types) of ATL remains inadequate, as most ATL patients receive conventional chemotherapy without stem cell rescue.
  • At present, LSG15 is the standard chemotherapy for the treatment of aggressive ATL, but the efficacy of LSG15 in most patients is transient.
  • Improved outcome after allogeneic stem cell transplantation (allo-SCT), despite a high incidence of graft-versus-host disease, has been reported.
  • Thus, allogeneic bone marrow transplantation and allogeneic peripheral blood SCT may have great potential for eradication of HTLV-1 and cure of ATL.
  • Recently, reduced-intensity conditioning stem cell transplantation was also reported to be effective for ATL.
  • Although several issues, including selection criteria for patients and sources of stem cells remain to be resolved, allo-SCT may be considered as a treatment option for patients with aggressive ATL.
  • To evaluate whether allo-SCT is more effective than the standard chemotherapy (LSG15) for aggressive ATL, an up front phase II clinical trial of JCOG-LSG is now being planned.
  • Novel innovative targeted strategies, such as antiretroviral therapy, arsenic trioxide, nuclear factor-kappaB inhibitors, proteasome inhibitors, histone deacetylase inhibitors, several monoclonal antibodies including anti-CC chemokine receptor 4, anti-folate, purine nucleotide phosphorylase inhibitor, mTOR (mammalian target of rapamycin) inhibitor, bendamustine, small molecule Bcl-2 inhibitors and Tax-targeted immunotherapy, should be promptly studied in order to develop curative treatments for ATL in the near future.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Graft vs Host Disease. Human T-lymphotropic virus 1. Humans. Remission Induction

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  • (PMID = 20505272.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
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42. Sanda T, Asamitsu K, Ogura H, Iida S, Utsunomiya A, Ueda R, Okamoto T: Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor. Leukemia; 2006 Apr;20(4):590-8
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  • [Title] Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor.
  • NF-kappaB is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.
  • In this study, we demonstrate that NF-kappaB is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IkappaBalpha and p65 subunit of NF-kappaB, activation of NF-kappaB DNA binding, and upregulation of various target genes including bcl-xL, bcl-2, XIAP, c-IAP1, survivin, cyclinD1, ICAM-1 and VCAM-1.
  • The effects of a novel IkappaB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.
  • We found that ACHP could inhibit the phosphorylation of IkappaBalpha and p65, as well as NF-kappaB DNA-binding, associated with downregulation of the NF-kappaB target genes and induce cell growth arrest and apoptosis in these cells.
  • When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.
  • Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.
  • These findings indicate that ACHP and its derivatives are effective in inducing ATL cell death and thus feasible candidates for the treatment of ATL.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / metabolism. Nicotinic Acids / pharmacology. Nitriles / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Binding Sites. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Gene Expression Regulation, Enzymologic / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. In Vitro Techniques. Phosphorylation. Protein Subunits / antagonists & inhibitors. Protein Subunits / genetics. Protein Subunits / metabolism. Structure-Activity Relationship. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism

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  • (PMID = 16453001.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-6-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-4-piperidin-4-yl nicotinonitrile; 0 / Enzyme Inhibitors; 0 / Nicotinic Acids; 0 / Nitriles; 0 / Protein Subunits; 0 / Transcription Factor RelA; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase
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43. Kannagi M: Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia. Int J Hematol; 2007 Aug;86(2):113-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia.
  • Host T-cell responses to human T-cell leukemia virus type I (HTLV-I) control the expansion of HTLV-I-infected cells and are determinants of the equilibrium proviral load in vivo.
  • Insufficient T-cell responses are regarded as an immunologic risk factor for adult T-cell leukemia (ATL) because they allow increased proviral loads, which represent an epidemiologic risk factor for ATL.
  • ATL cells from approximately half of ATL cases retain the ability to express HTLV-I Tax, a major target antigen of HTLV-I-specific cytotoxic T-lymphocytes (CTL), whereas Tax-specific CTL in ATL patients are inactive.
  • Tax-specific CTL responses are strongly activated after hematopoietic stem cell transplantation in some ATL patients in long-term remission, indicating that HTLV-I Tax is expressed in vivo rather than being silent, and that the donor-derived T-cell system can recognize it.
  • These findings strongly suggest that reactivation of Tax-specific CTL by vaccines may be promising for prophylaxis of ATL in the high-risk group of HTLV-I carriers and for therapy of ATL in patients whose tumor cells are capable of expressing Tax.
  • [MeSH-major] Human T-lymphotropic virus 1 / immunology. Immunity. Leukemia-Lymphoma, Adult T-Cell / immunology

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  • (PMID = 17875523.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
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44. Fukuda R, Hayashi A, Utsunomiya A, Nukada Y, Fukui R, Itoh K, Tezuka K, Ohashi K, Mizuno K, Sakamoto M, Hamanoue M, Tsuji T: Alteration of phosphatidylinositol 3-kinase cascade in the multilobulated nuclear formation of adult T cell leukemia/lymphoma (ATLL). Proc Natl Acad Sci U S A; 2005 Oct 18;102(42):15213-8
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  • [Title] Alteration of phosphatidylinositol 3-kinase cascade in the multilobulated nuclear formation of adult T cell leukemia/lymphoma (ATLL).
  • Adult T cell leukemia/lymphoma (ATLL) has been characterized as one of the most aggressive human neoplasias and its incidence is thought to be caused by both genetic and epigenetic alterations to the host cellular genes of T cells infected with human T cell leukemia virus type I (HTLV-I).
  • A multilobulated nuclear appearance is an important diagnostic marker of ATLL, and we have now identified that the molecular mechanisms underlying these formations occur through microtubule rearrangement via phosphatidylinositol 3-kinase (PI3-kinase) activation by AILIM/ICOS signaling.
  • We also show that PTEN and/or SHIP-1, which are PIP3 inositol phosphatases that inhibit the activation of downstream effectors of the PI3-kinase cascade, are disrupted in both ATLL neoplasias and in multilobulated nuclei-forming Jurkat cells.
  • This down-regulation of PTEN was found to be essential for the formation of ATLL-type nuclear lobules.
  • Furthermore, PI3-kinase and PTEN activities were observed to be closely associated with cellular proliferation.
  • Thus, our results suggest that alteration of PI3-kinase signaling cascades, as a result of the down-regulation of inositol phosphatases, induces ATLL-type multilobulated nuclear formation and is also associated with the cellular proliferation of malignant T cell leukemias/lymphomas.
  • [MeSH-major] Cell Nucleus. Leukemia-Lymphoma, Adult T-Cell. Phosphatidylinositol 3-Kinases / metabolism. Second Messenger Systems / physiology. T-Lymphocytes / cytology
  • [MeSH-minor] Adult. Antigens, CD / metabolism. Antigens, Differentiation, T-Lymphocyte / metabolism. Cell Proliferation. Enzyme Activation. Human T-lymphotropic virus 1. Humans. Inducible T-Cell Co-Stimulator Protein. Jurkat Cells. Microtubules / metabolism. PTEN Phosphohydrolase / metabolism. Phosphoric Monoester Hydrolases / metabolism

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  • [Cites] Cell Struct Funct. 2003 Feb;28(1):11-21 [12655146.001]
  • [Cites] J Immunol. 2002 Nov 15;169(10):5441-50 [12421919.001]
  • [Cites] Nat Rev Immunol. 2003 Jul;3(7):544-56 [12876557.001]
  • [Cites] Eur J Immunol. 2003 Aug;33(8):2223-32 [12884297.001]
  • [Cites] Cell. 2003 Jul 25;114(2):201-14 [12887922.001]
  • [Cites] Hum Mol Genet. 2003 Oct 15;12 Spec No 2:R239-48 [12928488.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Oct 24;310(3):691-702 [14550257.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):312-20 [14686488.001]
  • [Cites] Int Immunol. 2004 Oct;16(10):1515-22 [15339883.001]
  • [Cites] Leukemia. 2004 Nov;18(11):1839-49 [15457186.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Jpn J Clin Oncol. 1983;13 Suppl 2:165-87 [6603526.001]
  • [Cites] Jpn J Clin Oncol. 1983;13 Suppl 2:245-56 [6603533.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4524-8 [3012571.001]
  • [Cites] Jpn J Cancer Res. 1989 Mar;80(3):191-5 [2498254.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):237-43 [2303290.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 2;91(16):7415-9 [8052599.001]
  • [Cites] Nature. 1999 Jan 21;397(6716):263-6 [9930702.001]
  • [Cites] Curr Opin Cell Biol. 1999 Apr;11(2):203-10 [10209159.001]
  • [Cites] Genes Dev. 2000 Mar 1;14(5):505-20 [10716940.001]
  • [Cites] FASEB J. 2000 May;14(7):895-903 [10783143.001]
  • [Cites] N Engl J Med. 2000 Oct 5;343(14):1020-34 [11018170.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Sep 16;276(1):335-45 [11006126.001]
  • [Cites] Trends Cell Biol. 2000 Nov;10(11):466-73 [11050418.001]
  • [Cites] Immunity. 2001 May;14(5):523-34 [11371355.001]
  • [Cites] Mol Cell. 2001 May;7(5):937-47 [11389841.001]
  • [Cites] Am J Hum Genet. 2002 Apr;70(4):829-44 [11875759.001]
  • [Cites] Curr Opin Immunol. 2002 Jun;14(3):384-90 [11973139.001]
  • [Cites] Cell Growth Differ. 2002 Jul;13(7):285-96 [12133897.001]
  • [Cites] Nat Immunol. 2003 Apr;4(4):313-9 [12660731.001]
  • (PMID = 16217039.001).
  • [ISSN] 0027-8424
  • [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 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / ICOS protein, human; 0 / Inducible T-Cell Co-Stimulator Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.56 / inositol-polyphosphate 5-phosphatase; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC1257720
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45. Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J: HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia. J Gen Intern Med; 2007 Mar;22(3):420-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
  • BACKGROUND: Since the initial description of human T cell lymphotropic virus (HTLV-1), clusters of this infection have been detected globally.
  • Unlike HIV infection, most patients infected with HTLV-1 remain asymptomatic throughout their lifetime.
  • CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with HTLV-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.
  • HTLV-1-associated adult T cell leukemia lymphoma (ATLL) was diagnosed in this patient by bone marrow and lymph node biopsy.
  • This is believed to be the first description of this type of reaction to pneumocystis jiroveci in a HTLV-1-infected ATLL patient.
  • [MeSH-major] HTLV-I Infections / diagnosis. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pneumocystis jirovecii. Pneumonia, Pneumocystis / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

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  • [Cites] Leuk Lymphoma. 1994 Aug;14(5-6):395-400 [7812198.001]
  • [Cites] Leuk Lymphoma. 1994 Feb;12(5-6):471-6 [8180610.001]
  • [Cites] Clin Infect Dis. 1996 Jun;22(6):1111-2 [8783726.001]
  • [Cites] J Clin Invest. 1996 Oct 1;98(7):1544-9 [8833902.001]
  • [Cites] Leukemia. 1997 Mar;11(3):453-4 [9067590.001]
  • [Cites] Int J Hematol. 1997 Oct;66(3):257-78 [9401272.001]
  • [Cites] Aust N Z J Med. 1999 Feb;29(1):102-3 [10200829.001]
  • [Cites] Intern Med. 1999 Feb;38(2):83-5 [10225661.001]
  • [Cites] Semin Neurol. 2005 Sep;25(3):315-27 [16170744.001]
  • [Cites] Eur Respir J. 2000 Jan;15(1):213-6 [10678649.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):435-8 [11378559.001]
  • [Cites] Am J Kidney Dis. 2002 Feb;39(2):E8 [11840399.001]
  • [Cites] Thorax. 2002 May;57(5):435-7 [11978921.001]
  • [Cites] J R Soc Med. 2003 Mar;96(3):126-7 [12612113.001]
  • [Cites] Am J Clin Pathol. 1975 Mar;63(3):384-90 [1090147.001]
  • [Cites] J Clin Invest. 1986 Aug;78(2):592-6 [3016032.001]
  • [Cites] Cancer Res. 1989 Jul 15;49(14):3849-52 [2544261.001]
  • [Cites] Semin Diagn Pathol. 1989 Aug;6(3):273-86 [2678337.001]
  • [Cites] Arch Pathol Lab Med. 1989 Nov;113(11):1281-4 [2684091.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Br J Cancer. 1991 Oct;64(4):745-8 [1911223.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] J La State Med Soc. 1992 Jan;144(1):35-8 [1538186.001]
  • [Cites] J Biol Chem. 1993 Jan 15;268(2):1174-9 [8380405.001]
  • [Cites] Blood. 1993 Feb 15;81(4):1017-24 [8427983.001]
  • [Cites] Endocrinology. 1993 Jun;132(6):2551-6 [8099324.001]
  • [Cites] J Biol Chem. 1993 Aug 5;268(22):16730-6 [8393873.001]
  • [Cites] Clin Infect Dis. 1995 Oct;21(4):1014-6 [8645790.001]
  • (PMID = 17356979.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1824742
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46. Miyamura F, Kako S, Yamagami H, Sato K, Sato M, Terasako K, Kimura S, Nakasone H, Aoki S, Okuda S, Yamazaki R, Oshima K, Yoshinaga K, Higuchi T, Nishida J, Demitsu T, Kakehashi A, Kanda Y: Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Oct;90(3):397-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of young-onset adult T cell leukemia/lymphoma and preceding chronic refractory eczema and corneal injury by allogeneic hematopoietic stem cell transplantation.
  • Only some carriers of human T cell lymphotropic virus type I (HTLV-1) develop adult T cell leukemia/lymphoma (ATLL) after a long latency period, and an association has been reported between chronic refractory eczema, known as infective dermatitis, and young-onset ATLL.
  • A 25-year-old female developed ATLL and underwent allogeneic hematopoietic stem cell transplantation (HSCT) in non-remission.
  • She had chronic refractory eczema and corneal injury at the onset of ATLL.
  • Remission of ATLL was achieved, and the HTLV-1 proviral load decreased after HSCT.
  • More than a year has passed since the transplantation was performed, and she has had no recurrence of either ATLL or lesions in the skin and eye.
  • Her clinical course suggests a possible association between skin and eye lesions and HTLV-1 infection.
  • Special attention is needed when HTLV-1 carriers develop eye or skin lesions.
  • [MeSH-major] Corneal Diseases / therapy. Eczema / therapy. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Chronic Disease. Female. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Humans. Transplantation, Homologous. Treatment Outcome. Viral Load


47. Umehara F, Hagiwara T, Yoshimura M, Higashi K, Arimura K: Enlarged, multifocal upper limb neuropathy with HTLV-I associated myelopathy in a patient with chronic adult T-cell leukemia. J Neurol Sci; 2008 Mar 15;266(1-2):167-70
Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enlarged, multifocal upper limb neuropathy with HTLV-I associated myelopathy in a patient with chronic adult T-cell leukemia.
  • The authors herein describe a case of multifocal peripheral neuropathy with HTLV-I-associated myelopathy (HAM) in a patient with chronic adult T-cell leukemia (ATL).
  • The clinical features included subacute progressive sensory-motor neuropathy in the bilateral upper limbs, and bilateral pyramidal tract involvement with bladder dysfunction.
  • Anti-HTLV-I antibody was positive in both the serum and CSF.
  • The HTLV-I proviral load in the peripheral blood mononuclear cells was high.
  • Chemotherapy for ATL resulted in marked improvement of motor functions in the upper limbs.
  • This is the first case of multifocal upper limb neuropathy with HAM in a patient with chronic ATL.
  • [MeSH-major] Leukemia, Prolymphocytic, T-Cell / complications. Paraparesis, Tropical Spastic / complications. Peripheral Nervous System Diseases / etiology. Peripheral Nervous System Diseases / pathology. Upper Extremity / pathology
  • [MeSH-minor] Blood Cell Count. Contrast Media. Female. Fluorodeoxyglucose F18. Gadolinium. Humans. Magnetic Resonance Imaging. Middle Aged. Neural Conduction / physiology. Neurologic Examination. Peripheral Nerves / pathology. Peripheral Nerves / physiopathology. Positron-Emission Tomography

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  • (PMID = 18096188.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Contrast Media; 0Z5B2CJX4D / Fluorodeoxyglucose F18; AU0V1LM3JT / Gadolinium
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48. O'Mahony D, Debnath I, Janik J, Aisner D, Jaffe E, Waldmann T, Morris J: Cardiac involvement with human T-cell lymphotrophic virus type-1-associated adult T-cell leukemia/lymphoma: The NIH experience. Leuk Lymphoma; 2008 Mar;49(3):439-46
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  • [Title] Cardiac involvement with human T-cell lymphotrophic virus type-1-associated adult T-cell leukemia/lymphoma: The NIH experience.
  • Malignant cardiac involvement is rare in patients with human T cell lymphotrophic virus type-1-associated adult T cell leukemia/lymphoma (ATLL).
  • We report a single institution experience of eight patients with pathologically documented cardiac involvement with ATLL.
  • Cardiac involvement with ATLL was most often identified post-mortem; however, three cases were diagnosed clinically.
  • All but one of the patients had the acute or lymphomatous subtypes of ATLL and had progressed through at least one prior systemic therapy.
  • Patients with ATLL-related cardiac disease were also found to have pulmonary involvement suggesting that this may be a sign of increased risk of cardiac involvement.
  • One patient with the chronic form of ATLL remains alive 10 years after undergoing cardiac valve replacement.
  • [MeSH-major] Heart Neoplasms. Leukemia-Lymphoma, Adult T-Cell / complications
  • [MeSH-minor] Adult. Female. Human T-lymphotropic virus 1. Humans. Leukemic Infiltration. Male. Middle Aged. National Institutes of Health (U.S.). Retrospective Studies. Survival Rate. United States

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  • (PMID = 18297519.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
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49. Suzuki S, Uozumi K, Maeda M, Yamasuji Y, Hashimoto S, Komorizono Y, Owatari S, Tokunaga M, Haraguchi K, Arima N: Adult T-cell leukemia in a liver transplant recipient that did not progress after onset of graft rejection. Int J Hematol; 2006 Jun;83(5):429-32
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  • [Title] Adult T-cell leukemia in a liver transplant recipient that did not progress after onset of graft rejection.
  • A liver allograft recipient developed acute-type adult T-cell leukemia (ATL) during tacrolimus treatment, 2 years after undergoing transplantation for subacute fulminant hepatitis.
  • Both donor and recipient were asymptomatic carriers of human T-cell lymphotropic virus type I (HTLV-I), but the ATL cells originated from the recipient.
  • Liver biopsies showed CD4+ ATL cell infiltration at the onset of ATL but not at the terminal stage.
  • Moreover, Southern blotting revealed clonal integration of HTLV-I into the host genome of lymphoma cells at onset but not at the terminal stage.
  • ATL after liver transplantation has not been previously described.
  • The clinical course of the posttransplantational ATL was atypical, because it did not progress after the onset of rejection.
  • [MeSH-major] Hepatitis / complications. Leukemia-Lymphoma, Adult T-Cell / etiology. Liver Failure, Acute / complications. Liver Transplantation. Living Donors


50. Nakamura M, Hamasaki T, Tokitou M, Baba M, Hashimoto Y, Aoyama H: Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis. Bioorg Med Chem; 2009 Jul 1;17(13):4740-6
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  • [Title] Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis.
  • Adult T cell leukemia (ATL), caused by infection of human T-lymphotropic virus type 1 (HTLV-1), has a poor prognosis and curative therapy is unavailable, so it is important to find or design superior lead compounds for the drug treatment of ATL.
  • We used our micro-reversed fragment-based drug design hypothesis and multi-template hypothesis to extract the tetrahydrotetramethylnaphthalene (TMN) skeleton from tamibarotene, a useful medicament for the treatment of acute promyelocytic leukemia (APL).
  • Structural development of TMN yielded highly ATL cell-selective growth inhibitors, including 2-acetyl-3-hydroxy-5,6,7,8-tetrahydro-5,5,8,8-tetramethylnaphthalene (6).
  • Structure-activity relationship analysis suggests the existence of a specific target molecule for ATL cell-selective inhibition of proliferation through G2 arrest.
  • [MeSH-major] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tetrahydronaphthalenes / chemistry. Tetrahydronaphthalenes / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Drug Design. Human T-lymphotropic virus 1 / isolation & purification. Humans. Models, Molecular. Molecular Structure. Retinoids. Small Molecule Libraries. Structure-Activity Relationship. T-Lymphocytes / cytology. T-Lymphocytes / virology

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  • (PMID = 19443225.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Retinoids; 0 / Small Molecule Libraries; 0 / Tetrahydronaphthalenes
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51. Kohno T, Yamada Y, Akamatsu N, Kamihira S, Imaizumi Y, Tomonaga M, Matsuyama T: Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells. Cancer Sci; 2005 Aug;96(8):527-33
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  • [Title] Possible origin of adult T-cell leukemia/lymphoma cells from human T lymphotropic virus type-1-infected regulatory T cells.
  • Adult T-cell leukemia/lymphoma (ATLL) is a lymphoproliferative disorder caused by human T lymphotropic virus type 1 (HTLV-I).
  • Although ATLL cells display an activated helper/inducer T-cell phenotype, CD4+ and CD25+, they are known to exhibit strong immunosuppressive activity.
  • As regulatory T cells (Treg cells) express CD4+ and CD25+ molecules and possess potent immune response suppressive activity, we investigated a possible link between ATLL cells and Treg cells.
  • In primary ATLL cells, the expression levels of the Treg cell marker molecules Foxp3 and glucocorticoid-induced tumor necrosis factor receptor family related protein (GITR) were significantly higher than in those from healthy adults.
  • Furthermore, ATLL cells are unresponsive in vitro to concanavalin A stimulation and suppress the proliferation of normal T cells.
  • GITR mRNA expression was induced by the HTLV-I transactivator Tax, and GITR promoter analyses revealed that this induction depends on the kappaB site from -431 bp to -444 bp upstream of the putative transcription site.
  • Taken together, ATLL cells may originate from HTLV-I-infected Treg cells, and GITR seems to be involved in the progression to ATLL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Cell Division. Cell Line, Tumor. Concanavalin A. DNA-Binding Proteins / genetics. Forkhead Transcription Factors. Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Glucocorticoid-Induced TNFR-Related Protein. Humans. Lymphocyte Activation. Receptors, Nerve Growth Factor / genetics. Receptors, Tumor Necrosis Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16108835.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Gene Products, tax; 0 / Glucocorticoid-Induced TNFR-Related Protein; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF18 protein, human; 11028-71-0 / Concanavalin A
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52. Zimmerman B, Niewiesk S, Lairmore MD: Mouse models of human T lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma. Vet Pathol; 2010 Jul;47(4):677-89
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  • [Title] Mouse models of human T lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma.
  • Human T-lymphotropic virus type-1 (HTLV-1), the first human retrovirus discovered, is the causative agent of adult T-cell leukemia/lymphoma (ATL) and a number of lymphocyte-mediated inflammatory conditions including HTLV-1-associated myelopathy/tropical spastic paraparesis.
  • Development of animal models to study the pathogenesis of HTLV-1-associated diseases has been problematic.
  • Mechanisms of early infection and cell-to-cell transmission can be studied in rabbits and nonhuman primates, but lesion development and reagents are limited in these species.
  • The mouse provides a cost-effective, highly reproducible model in which to study factors related to lymphoma development and the preclinical efficacy of potential therapies against ATL.
  • Expansion of various strains of immunodeficient mice has accelerated the testing of drugs and targeted therapy against ATL.
  • This review compares various mouse models to illustrate recent advances in the understanding of HTLV-1-associated ATL development and how improvements in these models are critical to the future development of targeted therapies against this aggressive T-cell lymphoma.

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  • [Cites] Blood. 2005 Feb 1;105(3):1231-6 [15383455.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Carcinogenesis. 2005 Aug;26(8):1382-8 [15831528.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1384-90 [15959532.001]
  • [Cites] Immunol Res. 2005;32(1-3):217-23 [16106073.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6005-15 [16155607.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2462-71 [15956280.001]
  • [Cites] Nutr Cancer. 2005;52(2):189-201 [16201850.001]
  • [Cites] J Biol Chem. 2005 Oct 21;280(42):35713-22 [16105841.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3380-2 [16076875.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4294-302 [16118323.001]
  • [Cites] Int J Cancer. 2006 Feb 1;118(3):765-72 [16106398.001]
  • [Cites] Blood. 2006 Jan 15;107(2):716-24 [16174765.001]
  • [Cites] J Virol. 2006 Apr;80(7):3469-76 [16537614.001]
  • [Cites] Mol Cancer Ther. 2006 Mar;5(3):704-12 [16546985.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] J Virol. 2006 Nov;80(21):10683-91 [16943297.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] Br J Haematol. 2007 Feb;136(3):424-32 [17233845.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1071-5 [2300570.001]
  • [Cites] Ann Neurol. 1990 Jul;28(1):50-6 [2375633.001]
  • [Cites] Blood. 1990 Oct 15;76(8):1657-61 [1976391.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2350-7 [7662981.001]
  • [Cites] Blood. 1996 Feb 1;87(3):956-67 [8562967.001]
  • [Cites] Intern Med. 1995 Oct;34(10):947-52 [8563094.001]
  • [Cites] Intervirology. 1995;38(3-4):229-37 [8682621.001]
  • [Cites] Jpn J Cancer Res. 1996 Sep;87(9):887-92 [8878449.001]
  • [Cites] J Clin Immunol. 1996 Nov;16(6):305-14 [8946274.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1971-4 [8946939.001]
  • [Cites] Virology. 1996 Dec 15;226(2):167-75 [8955035.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6977-84 [11156399.001]
  • [Cites] Cancer Treat Res. 2001;104:75-88 [11191136.001]
  • [Cites] Leuk Res. 2001 Apr;25(4):323-31 [11248329.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):2219-28 [11395400.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1200-8 [11493471.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1083-6 [11861386.001]
  • [Cites] Nat Med. 2002 May;8(5):509-13 [11984596.001]
  • [Cites] Leuk Res. 2002 Jun;26(6):561-7 [12007504.001]
  • [Cites] Blood. 2002 Jul 1;100(1):208-16 [12070029.001]
  • [Cites] Microbiol Mol Biol Rev. 2002 Sep;66(3):396-406, table of contents [12208996.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3175-82 [12384415.001]
  • [Cites] J Infect Dis. 2002 Nov 15;186(10):1514-7 [12404172.001]
  • [Cites] Leukemia. 2003 Jan;17(1):26-38 [12529656.001]
  • [Cites] Int J Cancer. 2007 May 15;120(10):2251-61 [17278100.001]
  • [Cites] Cancer Sci. 2007 Jun;98(6):772-8 [17388788.001]
  • [Cites] Rev Med Virol. 2007 Sep-Oct;17(5):301-11 [17621367.001]
  • [Cites] Am J Hematol. 2007 Oct;82(10):929-31 [17617788.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714.001]
  • [Cites] Cancer Lett. 2007 Nov 18;257(2):206-15 [17764832.001]
  • [Cites] Gene Ther. 2007 Dec;14(23):1662-7 [17898798.001]
  • [Cites] Cancer Res. 2007 Dec 15;67(24):11859-66 [18089816.001]
  • [Cites] Eur J Haematol. 2008 Mar;80(3):185-96 [18081707.001]
  • [Cites] Int J Cancer. 2008 Dec 1;123(11):2702-12 [18798263.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3788-97 [18689544.001]
  • [Cites] J Virol. 2008 Dec;82(23):11958-63 [18922876.001]
  • [Cites] Cancer Sci. 2008 Nov;99(11):2286-94 [18771528.001]
  • [Cites] Blood. 2009 Feb 5;113(6):1287-93 [18948574.001]
  • [Cites] Blood. 2009 Feb 12;113(7):1493-500 [18971418.001]
  • [Cites] Front Biosci (Landmark Ed). 2009;14:1479-89 [19273141.001]
  • [Cites] Retrovirology. 2009;6:19 [19228429.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Science. 1991 Aug 30;253(5023):1026-8 [1887217.001]
  • [Cites] Int J Cancer. 1991 Nov 11;49(5):764-9 [1682281.001]
  • [Cites] J Infect Dis. 1991 Dec;164(6):1193-6 [1955718.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Int J Cancer. 1992 Jan 2;50(1):124-30 [1345820.001]
  • [Cites] Leukemia. 1992;6 Suppl 1:24-6 [1347800.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] Jpn J Cancer Res. 1992 Apr;83(4):320-3 [1506264.001]
  • [Cites] J Exp Med. 1992 Oct 1;176(4):981-9 [1402668.001]
  • [Cites] Oncogene. 1992 Dec;7(12):2399-405 [1461648.001]
  • [Cites] J Virol. 1993 Mar;67(3):1211-7 [8437212.001]
  • [Cites] Blood. 1993 Aug 1;82(3):722-31 [8338942.001]
  • [Cites] J Neuropathol Exp Neurol. 1993 Jul;52(4):424-30 [8355031.001]
  • [Cites] Virology. 1993 Sep;196(1):309-18 [8356801.001]
  • [Cites] Blood. 1993 Oct 15;82(8):2501-9 [8400297.001]
  • [Cites] Jpn J Cancer Res. 1993 Aug;84(8):831-3 [8407544.001]
  • [Cites] Virology. 1993 Nov;197(1):196-204 [8212554.001]
  • [Cites] Lancet. 1994 Jan 22;343(8891):213-6 [7904671.001]
  • [Cites] Int J Cancer. 1994 Aug 1;58(3):446-51 [8050826.001]
  • [Cites] J Virol. 1994 Oct;68(10):6323-31 [8083972.001]
  • [Cites] J Virol. 1995 Feb;69(2):1328-33 [7815516.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] Retrovirology. 2009;6:71 [19650892.001]
  • [Cites] Vet Pathol. 2009 Sep;46(5):1003-14 [19429977.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3208-15 [19666871.001]
  • [Cites] J Virol. 2003 May;77(9):5286-94 [12692230.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4576-82 [12560223.001]
  • [Cites] Blood. 2003 Jul 1;102(1):284-8 [12649132.001]
  • [Cites] J Long Term Eff Med Implants. 2003;13(2):127-40 [14510286.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6453-7 [14559836.001]
  • [Cites] J Virol. 2004 May;78(9):4582-90 [15078940.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1357-63 [15190257.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2556-76 [15358581.001]
  • [Cites] Acta Pathol Microbiol Scand. 1969;77(4):758-60 [5383844.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Nature. 1983 Feb 10;301(5900):527-30 [6823332.001]
  • [Cites] Med Microbiol Immunol. 1984;173(1):57-64 [6088962.001]
  • [Cites] Jpn J Cancer Res. 1985 Feb;76(2):86-94 [2984072.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Princess Takamatsu Symp. 1984;15:121-7 [6152756.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Lancet. 1986 Jul 12;2(8498):104-5 [2873363.001]
  • [Cites] Int J Cancer. 1986 Dec 15;38(6):867-75 [2878891.001]
  • [Cites] Int J Cancer. 1987 Sep 15;40(3):403-7 [2887518.001]
  • [Cites] Science. 1987 Sep 11;237(4820):1324-9 [2888190.001]
  • [Cites] Science. 1987 Sep 11;237(4820):1340-3 [2888191.001]
  • [Cites] Curr Top Microbiol Immunol. 1988;137:197-202 [3416632.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [Cites] J Virol. 1989 Jul;63(7):3185-9 [2724422.001]
  • [Cites] Int J Cancer. 1989 Aug 15;44(2):332-6 [2759739.001]
  • [Cites] Nature. 1989 Sep 7;341(6237):72-4 [2788824.001]
  • [Cites] Am J Pathol. 1989 Dec;135(6):1025-33 [2688429.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):413-7 [2403646.001]
  • [Cites] N Engl J Med. 1990 Feb 8;322(6):383-8 [2300089.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:260-2 [9209359.001]
  • [Cites] J Virol. 1998 May;72(5):3952-7 [9557681.001]
  • [Cites] Blood. 1998 Jun 15;91(12):4747-51 [9616173.001]
  • [Cites] Virology. 1998 Sep 1;248(2):332-41 [9721242.001]
  • [Cites] J Pathol. 1998 Oct;186(2):209-14 [9924438.001]
  • [Cites] J Immunol. 1999 Mar 1;162(5):2956-63 [10072546.001]
  • [Cites] J Virol. 1999 Jul;73(7):6031-40 [10364355.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3305-11 [15292059.001]
  • (PMID = 20442421.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / RR023965-03; United States / NCRR NIH HHS / RR / K01 RR023965; United States / NCRR NIH HHS / RR / K01 RR023965-03; United States / NCI NIH HHS / CA / P01 CA100730-08; United States / NCI NIH HHS / CA / CA100730-08; United States / NCI NIH HHS / CA / P01CA100730; United States / NCRR NIH HHS / RR / K01 RR 023965; United States / NCI NIH HHS / CA / P01 CA100730
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS278394; NLM/ PMC3147149
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53. Mone A, Puhalla S, Whitman S, Baiocchi RA, Cruz J, Vukosavljevic T, Banks A, Eisenbeis CF, Byrd JC, Caligiuri MA, Porcu P: Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia. Blood; 2005 Nov 15;106(10):3380-2
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  • [Title] Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due to the human T-cell lymphotropic virus-1 (HTLV-1).
  • More effective agents and new approaches to detect and treat minimal residual disease are needed.
  • ATL cells express CD52, the target of the antibody alemtuzumab, which is active in a preclinical model of ATL and is cytotoxic for p53-deficient cells.
  • A patient with refractory chronic ATL in transformation achieved longer than a 1-year complete hematologic response following 12 weeks of outpatient subcutaneous alemtuzumab.
  • Persistent suppression of HTLV-1 viral load, even at recovery of T cells, after alemtuzumab and efficient in vitro complement-mediated cytotoxicity of primary ATL cells with mutated TP53 were observed.
  • The unprecedented response and the profound suppression of HTLV-1 viral load observed in this patient suggest that further clinical investigation of alemtuzumab in ATL is warranted.

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  • [Cites] Oncogene. 1999 Nov 22;18(49):6948-58 [10602469.001]
  • [Cites] Int J Hematol. 2000 Apr;71(3):290-3 [10846838.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1721-6 [11535503.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1069-85 [12040438.001]
  • [Cites] Blood. 2002 Aug 1;100(3):768-73 [12130484.001]
  • [Cites] Int J Hematol. 2002 Jul;76(1):91-3 [12138903.001]
  • [Cites] N Engl J Med. 2002 Aug 8;347(6):452-3 [12167696.001]
  • [Cites] Cytotherapy. 2001;3(3):137-43 [12171721.001]
  • [Cites] Med Oncol. 2002;19 Suppl:S27-32 [12180489.001]
  • [Cites] Leukemia. 2003 Jan;17(1):26-38 [12529656.001]
  • [Cites] Clin Lab Haematol. 2003 Apr;25(2):111-7 [12641615.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4267-72 [12543862.001]
  • [Cites] Leuk Lymphoma. 2003 Apr;44(4):611-8 [12769337.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6453-7 [14559836.001]
  • [Cites] Leukemia. 2004 Jan;18(1):167-9 [14603340.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1846-54 [14630799.001]
  • [Cites] Blood. 2004 May 1;103(9):3278-81 [14726385.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2852-9 [15353320.001]
  • [Cites] Cancer Biother Radiopharm. 2004 Aug;19(4):391-8 [15453953.001]
  • [Cites] J Immunol. 1985 May;134(5):3056-61 [3980990.001]
  • [Cites] Blood. 2005 Jan 1;105(1):289-91 [15217834.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 May 1;16(7):665-75 [10791877.001]
  • (PMID = 16076875.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA10215-02; United States / NCI NIH HHS / CA / P01 CA95426; United States / NCI NIH HHS / CA / T32 CA009338
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Interferon-alpha; 0 / Tumor Suppressor Protein p53; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine
  • [Other-IDs] NLM/ PMC1895052
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54. Ishida Y, Yamashita K, Sasaki H, Takajou I, Kubuki Y, Morishita K, Tsubouchi H, Okayama A: Activation of complement system in adult T-cell leukemia (ATL) occurs mainly through lectin pathway: a serum proteomic approach using mass spectrometry. Cancer Lett; 2008 Nov 18;271(1):167-77
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  • [Title] Activation of complement system in adult T-cell leukemia (ATL) occurs mainly through lectin pathway: a serum proteomic approach using mass spectrometry.
  • Adult T-cell leukemia (ATL) is a fatal malignancy caused by infection with human T lymphotropic virus type-1 (HTLV-1).
  • To search for a new biomarker of ATL, we analyzed sera from ATL patients using ProteinChip arrays.
  • The spectral comparison of ATL patients with HTLV-1 carriers and healthy volunteers showed that the intensities of five peaks (1779, 1866, 2022, 4467, and 8930 m/z) were significantly increased in ATL, while those of four peaks (4067, 4151, 8130, and 8597 m/z) were decreased.
  • From these differentially expressed peaks, we chose peaks of 1779, 1866, and 2022 m/z as biomarker candidates of ATL.
  • MS/MS ion search using tandem mass spectrometry and immunoprecipitation assay using anti-C3 antibody showed that factors derived from these candidate peaks were identified as C3f, which is a component of the complement system and a fragment of complement C3.
  • These results indicate that the complement system was activated in ATL.
  • Further analysis of markers specific to the activation pathways (classical, alternative, and lectin pathways) in the complement system showed that the serum concentration of the marker of the lectin pathway was significantly higher in ATL patients.
  • These results suggest that activation of the complement system in ATL occurs mainly through the lectin pathway.
  • [MeSH-major] Complement Activation. Lectins / metabolism. Leukemia, T-Cell / metabolism. Proteomics. Tandem Mass Spectrometry / methods
  • [MeSH-minor] Adult. Case-Control Studies. Gene Expression Profiling. Humans. Immunoprecipitation. Neoplasm Proteins / blood. Neoplasm Proteins / genetics

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  • (PMID = 18691810.001).
  • [ISSN] 1872-7980
  • [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 / Lectins; 0 / Neoplasm Proteins
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55. Kchour G, Tarhini M, Kooshyar MM, El Hajj H, Wattel E, Mahmoudi M, Hatoum H, Rahimi H, Maleki M, Rafatpanah H, Rezaee SA, Yazdi MT, Shirdel A, de Thé H, Hermine O, Farid R, Bazarbachi A: Phase 2 study of the efficacy and safety of the combination of arsenic trioxide, interferon alpha, and zidovudine in newly diagnosed chronic adult T-cell leukemia/lymphoma (ATL). Blood; 2009 Jun 25;113(26):6528-32
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  • [Title] Phase 2 study of the efficacy and safety of the combination of arsenic trioxide, interferon alpha, and zidovudine in newly diagnosed chronic adult T-cell leukemia/lymphoma (ATL).
  • Adult T-cell leukemia/lymphoma (ATL) is resistant to chemotherapy and carries a dismal prognosis particularly for the acute and lymphoma subtypes.
  • Chronic ATL has a relatively better outcome, but poor long-term survival is noted when patients are managed with a watchful-waiting policy or with chemotherapy.
  • In ATL cell lines, arsenic trioxide shuts off constitutive NF-kappaB activation and potentiates interferon-alpha apoptotic effects through proteasomal degradation of Tax.
  • Clinically, arsenic/interferon therapy exhibits some efficacy in refractory aggressive ATL patients.
  • These results prompted us to investigate the efficacy and safety of the combination of arsenic, interferon-alpha, and zidovudine in 10 newly diagnosed chronic ATL patients.
  • In conclusion, treatment of chronic ATL with arsenic, interferon-alpha, and zidovudine is feasible and exhibits an impressive response rate with moderate toxicity.
  • Long-term follow up will clarify whether this will translate to disease cure.
  • Overall, these clinical results strengthen the concept of oncogene-targeted cancer therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Arsenicals / administration & dosage. Arsenicals / adverse effects. Drug Eruptions / etiology. Drug Synergism. Drug-Induced Liver Injury / etiology. Female. Gastrointestinal Diseases / chemically induced. Hematologic Diseases / chemically induced. Human T-lymphotropic virus 1 / isolation & purification. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Oxides / administration & dosage. Oxides / adverse effects. Proviruses / isolation & purification. Remission Induction. Viral Load. Zidovudine / administration & dosage. Zidovudine / adverse effects

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  • (PMID = 19411628.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Interferon-alpha; 0 / Oxides; 4B9XT59T7S / Zidovudine; S7V92P67HO / arsenic trioxide
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56. Okamura J, Utsunomiya A, Tanosaki R, Uike N, Sonoda S, Kannagi M, Tomonaga M, Harada M, Kimura N, Masuda M, Kawano F, Yufu Y, Hattori H, Kikuchi H, Saburi Y: Allogeneic stem-cell transplantation with reduced conditioning intensity as a novel immunotherapy and antiviral therapy for adult T-cell leukemia/lymphoma. Blood; 2005 May 15;105(10):4143-5
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  • [Title] Allogeneic stem-cell transplantation with reduced conditioning intensity as a novel immunotherapy and antiviral therapy for adult T-cell leukemia/lymphoma.
  • Sixteen patients with adult T-cell leukemia/lymphoma (ATL) who were all over 50 years of age underwent allogeneic stem cell transplantation with reduced-conditioning intensity (RIST) from HLA-matched sibling donors after a conditioning regimen consisting of fludarabine (180 mg/m2), busulfan (8 mg/kg), and rabbit antithymocyte globulin (5 mg/kg).
  • Disease relapse was the main cause of treatment failure.
  • After RIST, the human T-cell leukemia virus type 1 (HTLV-1) proviral load became undetectable in 8 patients.
  • RIST is thus considered to be a feasible treatment for ATL.
  • Our data also suggest the presence of a possible graft-versus-ATL effect; an anti-HTLV-1 activity was also found to be associated with this procedure.
  • [MeSH-major] Immunotherapy. Leukemia-Lymphoma, Adult T-Cell / therapy. Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Aged. Female. Human T-lymphotropic virus 1 / physiology. Humans. Kinetics. Male. Middle Aged. Transplantation, Homologous

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  • (PMID = 15665110.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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57. Saitoh Y, Yamamoto N, Dewan MZ, Sugimoto H, Martinez Bruyn VJ, Iwasaki Y, Matsubara K, Qi X, Saitoh T, Imoto I, Inazawa J, Utsunomiya A, Watanabe T, Masuda T, Yamamoto N, Yamaoka S: Overexpressed NF-kappaB-inducing kinase contributes to the tumorigenesis of adult T-cell leukemia and Hodgkin Reed-Sternberg cells. Blood; 2008 May 15;111(10):5118-29
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  • [Title] Overexpressed NF-kappaB-inducing kinase contributes to the tumorigenesis of adult T-cell leukemia and Hodgkin Reed-Sternberg cells.
  • The nuclear factor-kappaB (NF-kappaB) transcription factors play important roles in cancer development by preventing apoptosis and facilitating the tumor cell growth.
  • However, the precise mechanisms by which NF-kappaB is constitutively activated in specific cancer cells remain largely unknown.
  • In our current study, we now report that NF-kappaB-inducing kinase (NIK) is overexpressed at the pretranslational level in adult T-cell leukemia (ATL) and Hodgkin Reed-Sternberg cells (H-RS) that do not express viral regulatory proteins.
  • The overexpression of NIK causes cell transformation in rat fibroblasts, which is abolished by a super-repressor form of IkappaBalpha.
  • Notably, depletion of NIK in ATL cells by RNA interference reduces the DNA-binding activity of NF-kappaB and NF-kappaB-dependent transcriptional activity, and efficiently suppresses tumor growth in NOD/SCID/gammac(null) mice.
  • These results indicate that the deregulated expression of NIK plays a critical role in constitutive NF-kappaB activation in ATL and H-RS cells, and suggest also that NIK is an attractive molecular target for cancer therapy.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Hodgkin Disease / etiology. Leukemia-Lymphoma, Adult T-Cell / etiology. NF-kappa B / antagonists & inhibitors. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / physiology
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Mice. RNA, Small Interfering / pharmacology. Rats. Reed-Sternberg Cells / enzymology. Reed-Sternberg Cells / pathology

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  • (PMID = 18305221.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / RNA, Small Interfering; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.25 / NF-kappa B kinase
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58. Kayo H, Yamazaki H, Nishida H, Dang NH, Morimoto C: Stem cell properties and the side population cells as a target for interferon-alpha in adult T-cell leukemia/lymphoma. Biochem Biophys Res Commun; 2007 Dec 28;364(4):808-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stem cell properties and the side population cells as a target for interferon-alpha in adult T-cell leukemia/lymphoma.
  • The cancer stem cell theory suggests that chemoresistance and recurrence of tumors are often due to the similarity of stem cell properties between normal and cancer cells.
  • Adult T-cell leukemia/lymphoma (ATLL) has poor prognosis, suggesting that ATLL cells possess common stem cell properties.
  • We analyzed side population (SP), a characteristic stem cell phenotype, and CD markers in ATLL cell lines.
  • We found that several lines contained SP with expressions of some hematopoietic stem cell markers.
  • On the other hand, treatment with interferon (IFN)-alpha is sometimes effective in ATLL, particularly combined with other drugs.
  • We examined its effect on ATLL cells and found that IFN-alpha significantly reduced the SP proportion.
  • Moreover, CD25-positive cells and phosphorylation of STAT1/5 and ERK were upregulated during this process.
  • These data suggest that their stem cell properties render ATLL cells therapy-resistant, and IFN-alpha exerts its clinical effect through a reduction of the SP cell population.
  • [MeSH-major] Drug Delivery Systems / methods. Interferon-alpha / administration & dosage. Leukemia, T-Cell / metabolism. Leukemia, T-Cell / pathology. Neoplasm Proteins / metabolism. Stem Cells / metabolism. Stem Cells / pathology
  • [MeSH-minor] Cell Line, Tumor. Humans

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  • (PMID = 17977513.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Neoplasm Proteins
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59. Nagasaki A, Miyagi T, Taira T, Shinhama A, Kojya S, Suzuki M, Aonahata M, Yoshimi N, Takasu N: Adult T-cell leukemia/lymphoma with multiple integration of HTLV-1 provirus presenting as an isolated paranasal sinus tumor: a case report. Head Neck; 2008 Jun;30(6):815-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma with multiple integration of HTLV-1 provirus presenting as an isolated paranasal sinus tumor: a case report.
  • BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is a highly aggressive T-cell lymphoma and etiologically associated with human T-lymphotropic virus type 1 (HTLV-1).
  • Patients with ATLL commonly present with leukemic changes, systemic lymphadenopathy, and/or extranodal lesion and have very poor prognosis.
  • METHODS AND RESULTS: We describe a rare case of ATLL presenting as an isolated paranasal mass.
  • Southern blot analysis of the biopsied specimens demonstrated multiple integration bands of HTLV-1 provirus of different intensities.
  • Thereafter, the patient showed an indolent clinical course with leukemic changes and pulmonary and cutaneous ATLL lesions and remains alive more than 5 years from diagnosis.
  • CONCLUSION: ATLL should be included in the differential diagnosis of sinonasal lymphoma, although the event is rare.
  • Multiple HTLV-1 provirus integrations of different intensities may be indicative of good prognosis for ATLL.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Paranasal Sinus Neoplasms / diagnosis. Proviruses / physiology
  • [MeSH-minor] Adult. Humans. Male. Virus Integration

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  • (PMID = 18023035.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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60. Yang J, Ikezoe T, Nishioka C, Furihata M, Yokoyama A: AZ960, a novel Jak2 inhibitor, induces growth arrest and apoptosis in adult T-cell leukemia cells. Mol Cancer Ther; 2010 Dec;9(12):3386-95
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  • [Title] AZ960, a novel Jak2 inhibitor, induces growth arrest and apoptosis in adult T-cell leukemia cells.
  • Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive disease in which the Jak2/Stat5 pathway is constitutively activated.
  • This study found that AZ960, a novel inhibitor of Jak2 kinase, effectively induced growth arrest and apoptosis of human T-cell lymphotropic virus type 1, HTLV-1-infected T cells (MT-1 and MT-2) in parallel with downregulation of the phosphorylated forms of Jak2 and Bcl-2 family proteins including Bcl-2 and Mcl-1.
  • Interestingly, AZ960 increased levels of Bcl-xL in MT-1 and MT-2 cells in association with accumulation of cAMP response element-binding protein bound to the Bcl-xL promoter as measured by chromatin immunoprecipitation assay.
  • Importantly, genetic inhibition of Bcl-xL by a small interfering RNA potentiated antiproliferative effects of AZ960 in MT-1 cells.
  • Taken together, Jak2 is an attractive molecular target for treatment of ATL.
  • Concomitant blockade of Jak2 and Bcl-xL may be a promising treatment strategy for this lethal disease.
  • [MeSH-major] Aminopyridines / pharmacology. Apoptosis / drug effects. Janus Kinase 2 / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / enzymology. Leukemia-Lymphoma, Adult T-Cell / pathology. Protein Kinase Inhibitors / pharmacology. Pyrazoles / pharmacology
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Cyclic AMP Response Element-Binding Protein / metabolism. Down-Regulation / drug effects. Human T-lymphotropic virus 1 / drug effects. Humans. Phosphatidylinositol 3-Kinases / metabolism. Phosphotyrosine / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism. Signal Transduction / drug effects. T-Lymphocytes / drug effects. T-Lymphocytes / enzymology. T-Lymphocytes / virology. bcl-X Protein / metabolism

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  • [Copyright] ©2010 AACR.
  • (PMID = 21159615.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-fluoro-2-(1-(4-fluorophenyl)ethylamino)-6-(5-methyl-1H-pyrazol-3-ylamino)nicotinonitrile; 0 / Aminopyridines; 0 / Apoptosis Regulatory Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / bcl-X Protein; 21820-51-9 / Phosphotyrosine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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61. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

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  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Cell Cycle. 2005 Oct;4(10):1356-9 [16131838.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2220-9 [18039953.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Oncogene. 2008 Sep 1;27(38):5148-67 [18758484.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):453-9 [19064971.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Nat Genet. 2000 Dec;26(4):484-9 [11101851.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34371-8 [11425854.001]
  • [Cites] Cancer Biol Ther. 2002 Jul-Aug;1(4):337-41 [12432242.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1696-702 [15187027.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] J Exp Med. 1985 Dec 1;162(6):2169-74 [2866223.001]
  • [Cites] Science. 1995 Jul 7;269(5220):79-81 [7604283.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6333-44 [15940249.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • (PMID = 20823234.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / CA106258; United States / NCI NIH HHS / CA / CA115398
  • [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 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2944748
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62. Miyagi T, Nagasaki A, Taira T, Shinhama A, Suzuki M, Ohshima K, Takasu N: Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature. Leuk Lymphoma; 2009 Feb;50(2):187-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extranodal adult T-cell leukemia/lymphoma of the head and neck: a clinicopathological study of nine cases and a review of the literature.
  • Extranodal adult T-cell leukemia/lymphoma (ATLL) of the head and neck is a rare disease.
  • We studied the clinicopathological features of nine patients with ATLL involving extranodal head and neck sites and conducted a literature review.
  • Histopathology included diffuse pleomorphic-type (with angiocentric features), Hodgkin-like and anaplastic large cell-type.
  • Five patients with localised disease showed prolonged survival regardless of unfavourable histology and/or aberrant provirus status, including integration of multiple copies or defective provirus.
  • Patients with localised disease documented in the literature, including our study series, had a reduced frequency of elevated lactate dehydrogenase, no hypercalcemia and longer survival.
  • ATLL should be included in the differential diagnosis of extranodal head and neck lymphoma.
  • Localised extranodal ATLL of the head and neck may exhibit indolent clinical behaviours.
  • [MeSH-major] Head and Neck Neoplasms / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Tomography, X-Ray Computed

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  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):148-9 [19235009.001]
  • [CommentIn] Leuk Lymphoma. 2009 Feb;50(2):150-1 [19235010.001]
  • (PMID = 19197730.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
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63. Ohyashiki JH, Hamamura R, Kobayashi C, Zhang Y, Ohyashiki K: A network biology approach evaluating the anticancer effects of bortezomib identifies SPARC as a therapeutic target in adult T-cell leukemia cells. Adv Appl Bioinform Chem; 2008;1:85-98
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A network biology approach evaluating the anticancer effects of bortezomib identifies SPARC as a therapeutic target in adult T-cell leukemia cells.
  • There is a need to identify the regulatory gene interaction of anticancer drugs on target cancer cells.
  • A proteasome inhibitor, bortezomib, could be a potential therapeutic agent in treating adult T-cell leukemia (ATL) patients, however, the underlying mechanism by which bortezomib induces cell death in ATL cells via gene regulatory network has not been fully elucidated.
  • Here we show that a Bayesian statistical framework by VoyaGene(®) identified a secreted protein acidic and rich in cysteine (SPARC) gene, a tumor-invasiveness related gene, as a possible modulator of bortezomib-induced cell death in ATL cells.
  • Functional analysis using RNAi experiments revealed that inhibition of the expression SPARC by siRNA enhanced the apoptotic effect of bortezomib on ATL cells in accordance with an increase of cleaved caspase 3.
  • Targeting SPARC may help to treat ATL patients in combination with bortezomib.

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  • [Cites] Matrix Biol. 2001 Jan;19(8):816-27 [11223341.001]
  • [Cites] Leuk Lymphoma. 1997 Jul;26(3-4):327-35 [9322895.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14374-9 [12391322.001]
  • [Cites] Br J Haematol. 2003 Sep;122(5):728-44 [12930383.001]
  • [Cites] J Dermatol. 2003 Sep;30(9):641-3 [14578552.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2039-46 [15026341.001]
  • [Cites] Nat Biotechnol. 2005 Feb;23(2):238-43 [15654329.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):630-9 [15659509.001]
  • [Cites] Nat Genet. 2005 Mar;37(3):243-53 [15711544.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):4051-8 [15899794.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4467-70 [15930259.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):310-6 [16052522.001]
  • [Cites] Br J Cancer. 2006 Feb 27;94(4):599-608 [16449999.001]
  • [Cites] Br J Cancer. 2007 Oct 22;97(8):1099-105 [17895889.001]
  • [Cites] Leukemia. 1998 Jun;12(6):1001 [9639435.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1357-63 [15190257.001]
  • [Cites] J Bioinform Comput Biol. 2004 Sep;2(3):533-50 [15359425.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Int J Mol Med. 2005 Aug;16(2):263-8 [16012759.001]
  • [Cites] Bioinformatics. 2006 Apr 1;22(7):815-22 [16418235.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1341-52 [16810203.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):319-25 [17235047.001]
  • [Cites] Oncogene. 2007 Dec 13;26(57):7859-71 [17603561.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3448-52 [8159767.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 21;287(2):422-6 [11554745.001]
  • (PMID = 21918608.001).
  • [ISSN] 1178-6949
  • [Journal-full-title] Advances and applications in bioinformatics and chemistry : AABC
  • [ISO-abbreviation] Adv Appl Bioinform Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3169936
  • [Keywords] NOTNLM ; SPARC / adult T cell leukemia / bortezomib / network biology
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64. Liu MM, Furusato E, Cao X, Shen D, Chan CC: Ocular manifestations and pathology of adult T-cell leukemia/lymphoma associated with human T-lymphotropic virus type 1. Rare Tumors; 2010;2(4):e63

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ocular manifestations and pathology of adult T-cell leukemia/lymphoma associated with human T-lymphotropic virus type 1.
  • The human T-cell lymphotropic virus type 1 (HTLV-1), endemic in defined geographical areas around the world, is recognized as the etiologic agent of adult T-cell leukemia/lymphoma (ATL), or HTLV-1.
  • ATL is a rare adult onset T-cell malignancy that is characterized by the presence of ATL flower cells with T-cell markers, HTLV-1 antibodies in the serum, and monoclonal integration of HTLV-1 provirus in affected cells.
  • Ocular manifestations associated with HTLV-1 virus infection have been reported and include HTLV-1 uveitis and keratoconjunctivitis sicca, but reports of ocular involvement in ATL are exceedingly rare.
  • This article describes the ocular manifestations and pathology of ATL.
  • We also report for the first time a case of a 34-year-old male with systemic ATL and prominent atypical lymphoid cell infiltration in the choroid.
  • To our knowledge, this is the first report defining prominent choroidal involvement as a distinct ocular manifestation of ATL.
  • ATL may masquerade as a variety of other conditions, and molecular techniques involving microdissection and PCR have proven to be critical diagnostic tools.
  • International collaboration will be needed to better understand the presentation and diagnosis of this rare malignancy.

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  • [Cites] Am J Ophthalmol. 2001 Mar;131(3):309-13 [11239862.001]
  • [Cites] Am J Ophthalmol. 2001 Mar;131(3):381-3 [11239876.001]
  • [Cites] Ophthalmology. 2002 Sep;109(9):1717-22 [12208722.001]
  • [Cites] Am J Ophthalmol. 2002 Oct;134(4):616-8 [12383828.001]
  • [Cites] Jpn J Ophthalmol. 2003 Nov-Dec;47(6):599-602 [14636852.001]
  • [Cites] Am J Ophthalmol. 1992 Aug 15;114(2):123-9 [1642286.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Clin Microbiol Rev. 2010 Jul;23(3):577-89 [20610824.001]
  • [Cites] Ophthalmology. 1988 Jan;95(1):110-5 [2893999.001]
  • [Cites] Am J Surg Pathol. 1984 Apr;8(4):263-75 [6324600.001]
  • [Cites] Doc Ophthalmol. 1993;83(4):255-60 [8223094.001]
  • [Cites] Ophthalmology. 1993 Dec;100(12):1794-9 [8259276.001]
  • [Cites] Br J Ophthalmol. 1993 Nov;77(11):743-4 [8280693.001]
  • [Cites] AIDS Res Hum Retroviruses. 1993 May;9(5):381-6 [8318266.001]
  • [Cites] Jpn J Ophthalmol. 2005 Jan-Feb;49(1):41-5 [15692773.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Am J Ophthalmol. 2005 Aug;140(2):327-9 [16086963.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Microsc Res Tech. 2005 Nov;68(3-4):176-96 [16276549.001]
  • [Cites] Br J Ophthalmol. 2006 Sep;90(9):1204-6 [16929066.001]
  • [Cites] Lancet Infect Dis. 2007 Apr;7(4):266-81 [17376384.001]
  • [Cites] Cancer Control. 2007 Apr;14(2):133-40 [17387298.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):453-9 [19064971.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] J Neuroophthalmol. 1994 Jun;14(2):81-3 [7951932.001]
  • [Cites] Arch Ophthalmol. 1994 Jul;112(7):954-9 [8031276.001]
  • [Cites] J Med Virol. 2010 Apr;82(4):668-74 [20166187.001]
  • [Cites] Jpn J Ophthalmol. 1989;33(1):1-12 [2733251.001]
  • [Cites] Ann Hematol. 1997 Apr;74(4):163-8 [9174543.001]
  • (PMID = 21234255.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / T32 EY007143; United States / Intramural NIH HHS / / ZIA EY000222-25
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3019598
  • [Keywords] NOTNLM ; adult T-cell leukemia/lymphoma / eye. / human T-lymphotrophic virus type 1 / pathology
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65. Yamazaki J, Mizukami T, Takizawa K, Kuramitsu M, Momose H, Masumi A, Ami Y, Hasegawa H, Hall WW, Tsujimoto H, Hamaguchi I, Yamaguchi K: Identification of cancer stem cells in a Tax-transgenic (Tax-Tg) mouse model of adult T-cell leukemia/lymphoma. Blood; 2009 Sep 24;114(13):2709-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of cancer stem cells in a Tax-transgenic (Tax-Tg) mouse model of adult T-cell leukemia/lymphoma.
  • Adult T-cell leukemia/lymphoma (ATL) is a malignant lymphoproliferative disorder caused by HTLV-I infection.
  • In ATL, chemotherapeutic responses are generally poor, which has suggested the existence of chemotherapy-resistant cancer stem cells (CSCs).
  • To identify CSC candidates in ATL, we have focused on a Tax transgenic mouse (Tax-Tg) model, which reproduces ATL-like disease both in Tax-Tg animals and also after transfer of Tax-Tg splenic lymphomatous cells (SLCs) to nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice.
  • In agreement with this, we have successfully identified candidate CSCs in a side population (0.06%), which overlapped with a minor population of CD38(-)/CD71(-)/CD117(+) cells (0.03%).
  • Whereas lymphoma did not develop after transplantation of 10(2) SLCs, 10(2) CSCs could consistently regenerate the original lymphoma.
  • In addition, lymphoma and CSCs could also be demonstrated in the bone marrow and CD117(+) CSCs were observed in both osteoblastic and vascular niches.
  • In the CSCs, Tax, Notch1, and Bmi1 expression was down-regulated, suggesting that the CSCs were derived from Pro-T cells or early hematopoietic progenitor cells.
  • Taken together, our data demonstrate that CSCs certainly exist and have the potential to regenerate lymphoma in our mouse model.
  • [MeSH-major] Genes, pX. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Disease Models, Animal. Humans. Lymphoma / pathology. Membrane Proteins / analysis. Mice. Mice, Inbred NOD. Mice, SCID. Mice, Transgenic. Models, Biological. Splenic Neoplasms / pathology. Transplantation, Heterologous. Tumor Cells, Cultured

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  • [CommentIn] Blood. 2009 Sep 24;114(13):2568-9 [19779043.001]
  • [CommentIn] Blood. 2010 Mar 11;115(10):2117-8; author reply 2118 [20223932.001]
  • (PMID = 19584402.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins
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66. Toulza F, Nosaka K, Takiguchi M, Pagliuca T, Mitsuya H, Tanaka Y, Taylor GP, Bangham CR: FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia. Int J Cancer; 2009 Nov 15;125(10):2375-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL).
  • It has been postulated that ATLL cells might act as regulatory T cells (T(regs)) which, in common with ATLL cells, express both CD25 and FoxP3, and so contribute to the severe immune suppression typical of ATLL.
  • We report here that the frequency of CD25(+) cells varied independently of the frequency of FoxP3(+) cells in both a cross-sectional study and in a longitudinal study of 2 patients with chronic ATLL.
  • Furthermore, the capacity of ATLL cells to suppress proliferation of heterologous CD4(+)CD25(-) cells correlated with the frequency of CD4(+) FoxP3(+) cells but was independent of CD25 expression.
  • Finally, the frequency of CD4(+)FoxP3(+) cells was inversely correlated with the lytic activity of HTLV-1-specific CTLs in patients with ATLL.
  • We conclude that ATLL is not a tumor of FoxP3(+) regulatory T cells, and that a population of FoxP3(+) cells distinct from ATLL cells has regulatory functions and may impair the cell-mediated immune response to HTLV-1 in patients with ATLL.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Proliferation. Chronic Disease. Female. Flow Cytometry. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate

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  • (PMID = 19544530.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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67. Yoshikawa T, Ogata N, Takahashi K, Mori S, Uemura Y, Matsumura M: Bilateral orbital tumor as initial presenting sign in human T-cell leukemia virus-1 associated adult T-cell leukemia/lymphoma. Am J Ophthalmol; 2005 Aug;140(2):327-9
Genetic Alliance. consumer health - Orbital lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral orbital tumor as initial presenting sign in human T-cell leukemia virus-1 associated adult T-cell leukemia/lymphoma.
  • PURPOSE: To report a case of human T-cell leukemia virus type1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATLL) whose initial sign was exophthalmos.
  • RESULTS: Antibodies against HTLV-1 were extremely high but atypical lymphocytes were not present in the peripheral blood.
  • Orbital biopsy revealed an orbital mass that consisted of atypical lymphocytes originally from T cells and established the diagnosis of lymphoadenopathy type of ATLL.
  • CONCLUSION: Although ocular involvement by ATLL is extremely rare, ATLL can first present in the orbit, and only the results of a biopsy can provide definitive information for its diagnosis.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Orbital Neoplasms / diagnosis
  • [MeSH-minor] Antibodies, Viral / blood. Antigens, CD / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Choroid Diseases / diagnosis. DNA, Viral / analysis. Exophthalmos / diagnosis. Humans. Magnetic Resonance Imaging. Male. Middle Aged. T-Lymphocytes / pathology. T-Lymphocytes / virology

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  • (PMID = 16086963.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Antigens, CD; 0 / DNA, Viral
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68. Albuquerque MA, Migliari DA, Sugaya NN, Kuroishi M, Capuano AC, Sousa SO, Cavalcanti MG: Adult T-cell leukemia/lymphoma with predominant bone involvement, initially diagnosed by its oral manifestation: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2005 Sep;100(3):315-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma with predominant bone involvement, initially diagnosed by its oral manifestation: a case report.
  • Adult T-cell leukemia/lymphoma (ATL/L) is a rare malignant neoplasm linked to human T-cell lymphotropic virus type 1 (HTLV-1).
  • This virus has been identified in Japan, the Caribbean, and, more recently, Brazil.
  • We report a case of ATL/L (lymphoma-type) affecting a 30-year-old Brazilian woman.
  • Histopathological and immunohistochemical analyses of oral biopsy confirmed a T-cell non-Hodgkin's lymphoma.
  • Final diagnosis of ATL/L was made based on HTLV-1 positivity.
  • She underwent multiple cycles of chemotherapy, which produced some improvement, but she died as a consequence of pulmonary and hepatic complications 4 months after the initial diagnosis.
  • Besides the process of diagnosing and typing a malignant lymphoma, this article outlines the value of computed tomography and the necessity of performing HTVL-1 investigation in patients with a diagnosis of lymphoma of T-cell lineage.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / pathology. Palatal Neoplasms / etiology
  • [MeSH-minor] Adult. Antigens, CD45 / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brazil. Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunohistochemistry. Protein Tyrosine Phosphatase, Non-Receptor Type 1. Tomography, X-Ray Computed

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  • (PMID = 16122659.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1
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69. Miura H, Maeda M, Yamamoto N, Yamaoka S: Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells. Exp Cell Res; 2005 Aug 1;308(1):29-40
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  • [Title] Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells.
  • We have recently shown constitutive IkappaB kinase (IKK) activation and aberrant p52 expression in adult T cell leukemia (ATL) cells that do not express human T cell leukemia virus type I (HTLV-I) Tax, but the mechanism of IKK activation in these cells has remained unknown.
  • Here, we demonstrate distinct regulation of IKK activity in ATL and HTLV-I-transformed T cells in response to protein synthesis inhibition or arsenite treatment.
  • Protein synthesis inhibition for 4 h by cycloheximide (CHX) barely affects IKK activity in Tax-positive HTLV-I-transformed cells, while it diminishes IKK activity in Tax-negative ATL cells.
  • Treatment of ATL cells with a proteasome inhibitor MG132 prior to protein synthesis inhibition reverses the inhibitory effect of CHX, and MG132 alone greatly enhances IKK activity.
  • In addition, treatment of HTLV-I-transformed cells with arsenite for 1 h results in down-regulation of IKK activity without affecting Tax expression, while 8 h of arsenite treatment does not impair IKK activity in ATL cells.
  • These results indicate that a labile protein sensitive to proteasome-dependent degradation governs IKK activation in ATL cells, and suggest a molecular mechanism of IKK activation in ATL cells distinct from that in HTLV-I-transformed T cells.
  • [MeSH-major] Cell Transformation, Viral / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Arsenites / pharmacology. Cell Line, Transformed. Cell Line, Tumor. Cycloheximide / antagonists & inhibitors. Cycloheximide / pharmacology. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1 / physiology. Humans. I-kappa B Kinase. Leupeptins / pharmacology. Proteasome Endopeptidase Complex / metabolism. Protein Synthesis Inhibitors / pharmacology. T-Lymphocytes / drug effects. T-Lymphocytes / metabolism

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  • (PMID = 15878527.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / Enzyme Inhibitors; 0 / Leupeptins; 0 / Protein Synthesis Inhibitors; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 98600C0908 / Cycloheximide; EC 2.7.1.- / IKBKE protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex; N5509X556J / arsenite
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70. Wang J, Hasui K, Utsunomiya A, Jia X, Matsuyama T, Murata F: Association of high proliferation in adult T-cell leukemia cells with apoptosis, and expression of p53 protein in acute type ATL. J Clin Exp Hematop; 2008 Apr;48(1):1-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of high proliferation in adult T-cell leukemia cells with apoptosis, and expression of p53 protein in acute type ATL.
  • Proliferation, apoptosis and p53 protein expression in adult T-cell leukemia (ATL) cells were investigated.
  • Twenty peripheral blood tissue specimens (PBTS) comprising 7 cases of acute type ATL, 7 cases of chronic type ATL and 6 other leukemias were examined by means of antigen retrieval and the polymer method employing anti-Ki67 antigen (MIB-1), anti-cleaved caspase-3, anti-single stranded DNA and three kinds of anti-p53 protein antibodies including DO7.
  • Most acute and chronic cases of ATL included more than 10% MIB-1-positive proliferating leukemia cells and more than 1% cleaved caspase-3-positive apoptotic cells.
  • Some cells which were positive for both MIB-1 and anti-cleaved caspase-3 antibody were observed in acute type ATL.
  • Nuclear deposition of p53 protein labeled by DO7 was often found in acute type (p < 0.05).
  • Within the medium-sized population of ATL cell nuclei, DO7-positive ATL cells had a smaller nuclear area factor (long axis x short axis) than DO7-negative ATL cells.
  • A few proliferating ATL cells entered apoptosis, and the appearance of a subclone of ATL cells with nuclear deposition of p53 protein labeled by DO7 characterized acute type.
  • [MeSH-major] Apoptosis / physiology. Cell Proliferation. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Caspase 3 / biosynthesis. Female. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Male. Middle Aged

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  • (PMID = 18434687.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; EC 3.4.22.- / Caspase 3
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71. Zhang Z, Zhang M, Garmestani K, Talanov VS, Plascjak PS, Beck B, Goldman C, Brechbiel MW, Waldmann TA: Effective treatment of a murine model of adult T-cell leukemia using 211At-7G7/B6 and its combination with unmodified anti-Tac (daclizumab) directed toward CD25. Blood; 2006 Aug 1;108(3):1007-12
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  • [Title] Effective treatment of a murine model of adult T-cell leukemia using 211At-7G7/B6 and its combination with unmodified anti-Tac (daclizumab) directed toward CD25.
  • Adult T-cell leukemia (ATL) consists of an overabundance of T cells, which express CD25.
  • Therapeutic efficacy of astatine-211 ((211)At)-labeled murine monoclonal antibody 7G7/B6 alone and in combination with daclizumab was evaluated in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice given injections of MET-1 human T-cell leukemia cells.
  • Either a single dose of 12 microCi (0.444 MBq) (211)At-7G7/B6 per mouse given intravenously or receptor-saturating doses of daclizumab given at 100 microg weekly for 4 weeks intravenously inhibited tumor growth as monitored by serum levels of human beta-2 microglobulin (beta(2)mu) and by prolonged survival of leukemia-bearing mice compared with the control groups (P < .001).
  • These results that demonstrate a significantly improved therapeutic efficacy by combining (211)At-7G7/B6 with daclizumab support a clinical trial of this regimen in patients with ATL.

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  • [Cites] Ann Rheum Dis. 2000 Nov;59 Suppl 1:i109-14 [11053100.001]
  • [Cites] N Engl J Med. 2005 Feb 3;352(5):441-9 [15689582.001]
  • [Cites] Nucl Med Biol. 2001 Oct;28(7):845-56 [11578907.001]
  • [Cites] J Clin Microbiol. 1988 Oct;26(10):2127-31 [3053764.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1377-87 [2470706.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Lancet. 1995 Aug 5;346(8971):336-40 [7623531.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4063-75 [7492762.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2535-43 [11588052.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1083-6 [11861386.001]
  • [Cites] Blood. 2002 Jul 1;100(1):208-16 [12070029.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1891-5 [12569172.001]
  • [Cites] Blood. 2003 Jul 1;102(1):284-8 [12649132.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6453-7 [14559836.001]
  • [Cites] Nucl Med Biol. 2004 Apr;31(3):357-64 [15028248.001]
  • [Cites] J Immunol. 1981 Apr;126(4):1393-7 [6970774.001]
  • [Cites] J Clin Invest. 1984 Jun;73(6):1711-8 [6327770.001]
  • [Cites] Hybridoma. 1985 Summer;4(2):91-102 [2408992.001]
  • [Cites] J Clin Invest. 1985 Aug;76(2):446-53 [2993359.001]
  • [Cites] Int J Rad Appl Instrum A. 1986;37(8):789-98 [3021680.001]
  • [Cites] Science. 1988 May 20;240(4855):1024-6 [2897133.001]
  • [Cites] J Clin Oncol. 1996 Apr;14(4):1383-400 [8648397.001]
  • [Cites] Phys Med Biol. 1996 Oct;41(10):1915-31 [8912371.001]
  • [Cites] Nucl Med Biol. 1998 Feb;25(2):89-93 [9468021.001]
  • [Cites] Cancer Res. 1998 Jul 1;58(13):2825-31 [9661897.001]
  • [Cites] Clin Cancer Res. 1996 Mar;2(3):457-70 [9816191.001]
  • [Cites] Q J Nucl Med Mol Imaging. 2004 Dec;48(4):289-96 [15640792.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:199S-204S [15653670.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1231-6 [15383455.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6977-84 [11156399.001]
  • (PMID = 16569769.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Epitopes; 0 / Immunoglobulin G; 0 / Receptors, Interleukin-2; CUJ2MVI71Y / daclizumab; XI595HAL7H / Astatine
  • [Other-IDs] NLM/ PMC1895861
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72. Callens C, Moura IC, Lepelletier Y, Coulon S, Renand A, Dussiot M, Ghez D, Benhamou M, Monteiro RC, Bazarbachi A, Hermine O: Recent advances in adult T-cell leukemia therapy: focus on a new anti-transferrin receptor monoclonal antibody. Leukemia; 2008 Jan;22(1):42-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent advances in adult T-cell leukemia therapy: focus on a new anti-transferrin receptor monoclonal antibody.
  • HTLV-I is an endemic retrovirus responsible for the adult T-cell leukemia/lymphoma (ATLL).
  • This aggressive lymphoid proliferation is associated with a bad prognosis due to the resistance of HTLV-I-infected cells to most classical chemotherapeutic agents.
  • Here we review recent advances in ATLL immunotherapy.
  • We particularly focus on promising data from our group, characterizing a new mouse monoclonal antibody (mAb A24) against the human transferrin receptor (TfR-1).
  • Monoclonal antibodies to target cell differentiation markers on ATLL cells have already been proposed as therapeutic agents.
  • However, in clinical trials acute forms of ATLL were resistant to these immunotherapies.
  • It blocks the proliferation of malignant cells (TfR-1(high)), such as HTLV-I-infected T cells but not of resting cells.
  • In HTLV-I-infected cells, A24 targets and induces apoptosis of both chronic and acute ATLL forms, independent of antibody aggregation, antibody-dependent cellular cytotoxicity and/or complement addition.
  • We are currently developing strategies to use A24 in clinical trials.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, T-Cell / therapy. Receptors, Transferrin / immunology
  • [MeSH-minor] Adult. Humans. Immunotherapy. T-Lymphocytes / immunology

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  • (PMID = 17898788.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Receptors, Transferrin
  • [Number-of-references] 53
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73. Ojima T, Abe K, Ohyashiki JH, Shirakata M, Yamamoto K: IL-2-regulated persistent human herpesvirus-6B infection facilitates growth of adult T cell leukemia cells. J Med Dent Sci; 2005 Jun;52(2):135-41
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  • [Title] IL-2-regulated persistent human herpesvirus-6B infection facilitates growth of adult T cell leukemia cells.
  • Human herpesvirus-6B (HHV-6B), a causative agent of exanthem subitum, infects human adult T cell leukemia (ATL) cell lines.
  • We established a persistent HHV-6B infection in an ATL cell line, TaY, in the presence of 20 units/ml interleukin-2 (IL-2).
  • The HHV-6B infected culture proliferated with a constant ratio of infected (1%) to the uninfected (99%) cells.
  • When the IL-2 concentration was reduced to 5 units/ml, the number of infected cells in the culture increased transiently by 60% in 11 days, a new balance of 25% infected cells and 75% uninfected cells was established thereafter.
  • PCR analysis confirmed a 125-fold increase in the amount of viral genome in the culture, while the treatment with ganciclovir reduced the proportion of infected cells, indicating that an efficient replication of virus was induced in the culture.
  • Both of these cultures were maintained in the presence of 20 or 5 units/ml IL-2 over one year without loss of infected cells.
  • Interestingly, we found that cultures containing the infected cells grew significantly faster than the parental uninfected cells at the same concentration of IL-2.
  • Because the infection induces cell cycle arrest, these results indicate that the HHV-6B-infected ATL cells stimulate the growth of the uninfected cells during persistent infection in culture.
  • [MeSH-major] Herpesvirus 6, Human / pathogenicity. Interleukin-2 / pharmacology. T-Lymphocytes / drug effects. T-Lymphocytes / virology. Virus Replication / drug effects
  • [MeSH-minor] Adult. Antiviral Agents / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. DNA, Viral / analysis. Flow Cytometry. Fluorescent Antibody Technique, Indirect. Ganciclovir / pharmacology. Humans. Leukemia, T-Cell / virology. Recombinant Proteins / pharmacology. Viral Envelope Proteins / analysis

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  • (PMID = 16187619.001).
  • [ISSN] 1342-8810
  • [Journal-full-title] Journal of medical and dental sciences
  • [ISO-abbreviation] J. Med. Dent. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / DNA, Viral; 0 / Interleukin-2; 0 / Recombinant Proteins; 0 / Viral Envelope Proteins; P9G3CKZ4P5 / Ganciclovir
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74. Tsukasaki K, Hermine O, Bazarbachi A, Ratner L, Ramos JC, Harrington W Jr, O'Mahony D, Janik JE, Bittencourt AL, Taylor GP, Yamaguchi K, Utsunomiya A, Tobinai K, Watanabe T: Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting. J Clin Oncol; 2009 Jan 20;27(3):453-9
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  • [Title] Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting.
  • Adult T-cell leukemia-lymphoma (ATL) is a distinct peripheral T-lymphocytic malignancy associated with a retrovirus designated human T-cell lymphotropic virus type I (HTLV-1).
  • The diversity in clinical features and prognosis of patients with this disease has led to its subclassification into the following four categories: acute, lymphoma, chronic, and smoldering types.
  • The chronic and smoldering subtypes are considered indolent and are usually managed with watchful waiting until disease progression, analogous to the management of some patients with chronic lymphoid leukemia (CLL) or other indolent histology lymphomas.
  • Patients with aggressive ATL generally have a poor prognosis because of multidrug resistance of malignant cells, a large tumor burden with multiorgan failure, hypercalcemia, and/or frequent infectious complications as a result of a profound T-cell immunodeficiency.
  • Under the sponsorship of the 13th International Conference on Human Retrovirology: HTLV, a group of ATL researchers joined to form a consensus statement based on established data to define prognostic factors, clinical subclassifications, and treatment strategies.
  • A set of response criteria specific for ATL reflecting a combination of those for lymphoma and CLL was proposed.
  • Clinical subclassification is useful but is limited because of the diverse prognosis among each subtype.
  • A treatment strategy based on the clinical subclassification and prognostic factors is suggested, including watchful waiting approach, chemotherapy, antiviral therapy, allogeneic hematopoietic stem-cell transplantation (alloHSCT), and targeted therapies.

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  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5458-64 [17968021.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3612-20 [11369658.001]
  • [Cites] Br J Haematol. 2001 Jun;113(3):779-84 [11380470.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3875-81 [11389029.001]
  • [Cites] Leuk Lymphoma. 2001 Jan;40(3-4):287-94 [11426550.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1160-5 [11493465.001]
  • [Cites] Blood. 2002 May 1;99(9):3383-9 [11964307.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2466-75 [11971181.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4576-82 [12560223.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3625-34 [14506150.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1838-45 [14592824.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2474-9 [14645001.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1987 Jul 11;2(8550):94-5 [2885585.001]
  • [Cites] Cancer. 1988 Feb 15;61(4):824-8 [3257406.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Cancer. 1990 Jan 15;65(2):327-32 [2295055.001]
  • [Cites] Cancer. 1991 May 15;67(10):2605-9 [2015561.001]
  • [Cites] Leuk Res. 1991;15(2-3):81-90 [2016910.001]
  • [Cites] Leuk Res. 1991;15(2-3):99-103 [2016911.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Leuk Res. 1993 Feb;17(2):157-66 [8429692.001]
  • [Cites] Cancer. 1994 Jun 1;73(11):2753-8 [8194016.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S186-90 [8797722.001]
  • [Cites] Blood. 1997 Feb 1;89(3):948-56 [9028326.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1778-85 [9164185.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1996;67:1-424 [9190379.001]
  • [Cites] Blood. 1999 Jan 1;93(1):278-83 [9864171.001]
  • [Cites] Br J Haematol. 1999 May;105(2):369-75 [10233406.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Cancer Lett. 2006 Mar 28;234(2):249-55 [15896902.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3054-61 [16425276.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):579-86 [17242396.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3060-8 [17138822.001]
  • [Cites] Leuk Res. 2007 Jun;31(6):751-7 [17188352.001]
  • [Cites] Leuk Res. 2007 Jul;31(7):915-20 [17123603.001]
  • [Cites] Am J Clin Pathol. 2007 Nov;128(5):875-82 [17951212.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • (PMID = 19064971.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Number-of-references] 61
  • [Other-IDs] NLM/ PMC2737379
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75. Nakagawa M, Nakagawa-Oshiro A, Karnan S, Tagawa H, Utsunomiya A, Nakamura S, Takeuchi I, Ohshima K, Seto M: Array comparative genomic hybridization analysis of PTCL-U reveals a distinct subgroup with genetic alterations similar to lymphoma-type adult T-cell leukemia/lymphoma. Clin Cancer Res; 2009 Jan 1;15(1):30-8
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  • [Title] Array comparative genomic hybridization analysis of PTCL-U reveals a distinct subgroup with genetic alterations similar to lymphoma-type adult T-cell leukemia/lymphoma.
  • PURPOSE: Peripheral T-cell lymphoma, unspecified (PTCL-U) comprises histopathologically and clinically heterogeneous groups.
  • EXPERIMENTAL DESIGN: We used array comparative genomic hybridization (CGH) for high-resolution analysis of 51 PTCL-U patients and the array data for examining possible correlations of histopathologic and clinical features.
  • Moreover, we compared the genetic, histopathologic, and prognostic features of the PTCL-U cases with those of 59 cases of lymphoma-type adult T-cell leukemia/lymphoma (ATLL).
  • PTCL-U cases with genomic imbalance showed distinct histopathologic and prognostic features compared with such cases without alteration and a marked genetic, histopathologic, and prognostic resemblance to lymphoma-type ATLL.
  • A correlative analysis using the array CGH data disclosed a subgroup in PTCL-U with genomic alterations and with histopathologic and clinical relevance.
  • In addition to histopathologic similarity, the strong genetic and prognostic resemblance between PTCL-U cases with genomic imbalance detected by array CGH and lymphoma-type ATLL seems to support the notion that the former may constitute a distinct PTCL-U subgroup.
  • [MeSH-major] Chromosome Aberrations. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics
  • [MeSH-minor] Adult. Comparative Genomic Hybridization. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 19118030.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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81. Ohsugi T, Horie R, Kumasaka T, Ishida A, Ishida T, Yamaguchi K, Watanabe T, Umezawa K, Urano T: In vivo antitumor activity of the NF-kappaB inhibitor dehydroxymethylepoxyquinomicin in a mouse model of adult T-cell leukemia. Carcinogenesis; 2005 Aug;26(8):1382-8

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  • [Title] In vivo antitumor activity of the NF-kappaB inhibitor dehydroxymethylepoxyquinomicin in a mouse model of adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I).
  • The nuclear transcription factor, NF-kappaB, is induced by HTLV-I and is central to the ensuing neoplasia.
  • To examine the effect of a novel NF-kappaB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), on ATL in vivo, we developed an improved severe combined immunodeficiency (SCID) mouse model for ATL.
  • Five-week-old SCID mice in which natural killer (NK) cell activity had been eliminated were inoculated intraperitoneally with the HTLV-I-infected cell lines, TL-Om1, MT-1, MT-2 and HUT-102.
  • No engraftment of TL-Om1 cells and little tumorigenesis of MT-1 cells were detected 40 days after injection.
  • In contrast, inoculation of mice with MT-2 and HUT-102 cells elicited high mortality, 100% frequency of gross tumor formation and tumor cell infiltration of various organs, all of which were reduced by coadministration of DHMEQ during the inoculation.
  • These results suggest that DHMEQ induces apoptosis in HTLV-I-transformed cells in vivo, resulting in inhibition of tumor formation and organ infiltration, thereby enhancing survival.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Benzamides / pharmacology. Cyclohexanones / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Base Sequence. Binding Sites. Cell Division / drug effects. Cell Line, Tumor. Consensus Sequence. Disease Models, Animal. Human T-lymphotropic virus 1 / drug effects. Human T-lymphotropic virus 1 / physiology. Humans. Mice. Transplantation, Heterologous

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  • (PMID = 15831528.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Cyclohexanones; 0 / NF-kappa B; 0 / dehydroxymethylepoxyquinomicin
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82. Chen J, Zhang M, Ju W, Waldmann TA: Effective treatment of a murine model of adult T-cell leukemia using depsipeptide and its combination with unmodified daclizumab directed toward CD25. Blood; 2009 Feb 5;113(6):1287-93
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  • [Title] Effective treatment of a murine model of adult T-cell leukemia using depsipeptide and its combination with unmodified daclizumab directed toward CD25.
  • Adult T-cell leukemia (ATL) is caused by human T-cell lymphotropic virus I (HTLV-1) and is an aggressive malignancy of CD4, CD25-expressing leukemia, and lymphoma cells.
  • There is no accepted curative therapy for ATL.
  • Depsipeptide, a histone deacetylase inhibitor, has demonstrated major antitumor effects in leukemias and lymphomas.
  • In this study, we investigated the therapeutic efficacy of depsipeptide alone and in combination with daclizumab (humanized anti-Tac) in a murine model of human ATL.
  • The Met-1 ATL model was established by intraperitoneal injection of ex vivo leukemic cells into nonobese diabetic/severe combined immunodeficiency mice.
  • Either depsipeptide, given at 0.5 mg/kg every other day for 2 weeks, or daclizumab, given at 100 microg weekly for 4 weeks, inhibited tumor growth as monitored by serum levels of soluble IL-2R-alpha (sIL-2R-alpha) and soluble beta2-microglobulin (beta2mu) (P < .001), and prolonged survival of the leukemia-bearing mice (P < .001) compared with the control group.
  • Combination of depsipeptide with daclizumab enhanced the antitumor effect, as shown by both sIL-2R-alpha and beta2mu levels and survival of the leukemia-bearing mice, compared with those in the depsipeptide or daclizumab alone groups (P < .001).
  • The significantly improved therapeutic efficacy by combining depsipeptide with daclizumab supports a clinical trial of this combination in the treatment of ATL.

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  • [Cites] J Natl Cancer Inst. 2000 Aug 2;92(15):1210-6 [10922406.001]
  • [Cites] Mol Cancer Res. 2007 Oct;5(10):981-9 [17951399.001]
  • [Cites] Jpn J Cancer Res. 2000 Nov;91(11):1154-60 [11092981.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6977-84 [11156399.001]
  • [Cites] Jpn J Cancer Res. 2001 May;92(5):529-36 [11376562.001]
  • [Cites] Leuk Lymphoma. 2001 Jan;40(3-4):287-94 [11426550.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2865-8 [11675364.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1083-6 [11861386.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):718-28 [11895901.001]
  • [Cites] Blood. 2002 Jul 1;100(1):208-16 [12070029.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7241-6 [12370815.001]
  • [Cites] J Exp Ther Oncol. 2002 Nov-Dec;2(6):325-32 [12440223.001]
  • [Cites] J Thorac Cardiovasc Surg. 2003 May;125(5):1132-42 [12771887.001]
  • [Cites] J Virol. 2004 May;78(9):4582-90 [15078940.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4636-43 [14996704.001]
  • [Cites] J Virol. 2004 Jul;78(13):6735-43 [15194748.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5825-9 [15313926.001]
  • [Cites] Adv Cancer Res. 2004;91:137-68 [15327890.001]
  • [Cites] J Immunol. 1981 Apr;126(4):1393-7 [6970774.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] J Clin Invest. 1984 Jun;73(6):1711-8 [6327770.001]
  • [Cites] J Clin Invest. 1985 Aug;76(2):446-53 [2993359.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10029-33 [2513570.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1415-20 [8068938.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] J Exp Med. 1995 Nov 1;182(5):1545-56 [7595224.001]
  • [Cites] Invest New Drugs. 1997;15(3):195-206 [9387042.001]
  • [Cites] Oncogene. 1998 Sep 24;17(12):1503-8 [9794227.001]
  • [Cites] J Chromatogr B Biomed Sci Appl. 1998 Nov 20;719(1-2):169-76 [9869377.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1401-8 [10438728.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1231-6 [15383455.001]
  • [Cites] J Immunol. 2005 May 1;174(9):5187-91 [15843513.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5941-6 [16585503.001]
  • [Cites] Clin Cancer Res. 2006 Jun 15;12(12):3762-73 [16778104.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Cancer J. 2007 Mar-Apr;13(2):80-3 [17476134.001]
  • [Cites] Br J Cancer. 2000 Sep;83(6):817-25 [10952788.001]
  • (PMID = 18948574.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Depsipeptides; 0 / Histones; 0 / Il2ra protein, mouse; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Receptors, Interleukin-2; CUJ2MVI71Y / daclizumab; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ PMC2637191
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83. Haneji K, Matsuda T, Tomita M, Kawakami H, Ohshiro K, Uchihara JN, Masuda M, Takasu N, Tanaka Y, Ohta T, Mori N: Fucoidan extracted from Cladosiphon okamuranus Tokida induces apoptosis of human T-cell leukemia virus type 1-infected T-cell lines and primary adult T-cell leukemia cells. Nutr Cancer; 2005;52(2):189-201
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  • [Title] Fucoidan extracted from Cladosiphon okamuranus Tokida induces apoptosis of human T-cell leukemia virus type 1-infected T-cell lines and primary adult T-cell leukemia cells.
  • Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1) and remains incurable.
  • The highest endemic area of HTLV-1 carriers in Japan is located in Okinawa, and novel treatments are urgently needed in this area.
  • We extracted fucoidan, a sulfated polysaccharide, from the brown seaweed Cladosiphon okamuranus Tokida cultivated in Okinawa, Japan and examined its tumor-suppression activity against ATL.
  • Fucoidan significantly inhibited the growth of peripheral blood mononuclear cells of ATL patients and HTLV-1-infected T-cell lines but not that of normal peripheral blood mononuclear cells.
  • Fucoidan induced apoptosis of HTLV-1-infected T-cell lines mediated through downregulation of cellular inhibitor of apoptosis protein-2 and survivin and G1 phase accumulation through the downregulation of cyclin D2, c-myc, and hyperphosphorylated form of the retinoblastoma tumor suppressor protein.
  • Further analysis showed that fucoidan inactivated NF-kappaB and activator protein-1 and inhibited NF-kappaB-inducible chemokine, C-C chemokine ligand 5 (regulated on activation, normal T expressed and secreted) production, and homotypic cell-cell adhesion of HTLV-1-infected T-cell lines.
  • In vivo use of fucoidan resulted in partial inhibition of growth of tumors of an HTLV-1-infected T-cell line transplanted subcutaneously in severe combined immune deficient mice.
  • Our results indicate that fucoidan is a potentially useful therapeutic agent for patients with ATL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, T-Cell / drug therapy. Polysaccharides / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Transformed. Human T-lymphotropic virus 1 / drug effects. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / virology. Mice. Mice, SCID. Phaeophyta / chemistry. Tumor Cells, Cultured


84. Tanosaki R, Uike N, Utsunomiya A, Saburi Y, Masuda M, Tomonaga M, Eto T, Hidaka M, Harada M, Choi I, Yamanaka T, Kannagi M, Matsuoka M, Okamura J: Allogeneic hematopoietic stem cell transplantation using reduced-intensity conditioning for adult T cell leukemia/lymphoma: impact of antithymocyte globulin on clinical outcome. Biol Blood Marrow Transplant; 2008 Jun;14(6):702-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic stem cell transplantation using reduced-intensity conditioning for adult T cell leukemia/lymphoma: impact of antithymocyte globulin on clinical outcome.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is an effective treatment for adult T cell leukemia/lymphoma (ATLL), but shows high mortality.
  • We evaluated the feasibility of reduced-intensity transplantation using fludarabine and busulfan, with particular focus on the clinical impact of antithymocyte globulin (ATG) in the conditioning regimen.
  • Fourteen elderly patients with aggressive ATLL were enrolled in the current study without ATG, and were compared to those in 15 patients who were treated similarly, but with ATG, in our previous study.
  • Analysis of combined data from both our current and previous studies disclosed that grade I-II acute GVHD was the only factor that favorably affected OS and PFS.
  • These data suggested the presence of a graft-versus-ATLL effect and the feasibility of a transplant procedure without ATG in elderly ATLL patients, but could not demonstrate the clinical benefit of incorporating ATG.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Hematopoietic Stem Cell Transplantation. Immunosuppressive Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / surgery. Transplantation Conditioning / methods
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease-Free Survival. Feasibility Studies. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Human T-lymphotropic virus 1 / isolation & purification. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Proportional Hazards Models. Proviruses / isolation & purification. Survival Analysis. T-Lymphocytes. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 18489996.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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85. Masuda M, Maruyama T, Ohta T, Ito A, Hayashi T, Tsukasaki K, Kamihira S, Yamaoka S, Hoshino H, Yoshida T, Watanabe T, Stanbridge EJ, Murakami Y: CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells. J Biol Chem; 2010 May 14;285(20):15511-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CADM1 interacts with Tiam1 and promotes invasive phenotype of human T-cell leukemia virus type I-transformed cells and adult T-cell leukemia cells.
  • CADM1 encodes a multifunctional immunoglobulin-like cell adhesion molecule whose cytoplasmic domain contains a type II PSD95/Dlg/ZO-1 (PDZ)-binding motif (BM) for associating with other intracellular proteins.
  • Although CADM1 lacks expression in T lymphocytes of healthy individuals, it is overexpressed in adult T-cell leukemia-lymphoma (ATL) cells.
  • It has been suggested that the expression of CADM1 protein promotes infiltration of leukemic cells into various organs and tissues, which is one of the frequent clinical manifestations of ATL.
  • Amino acid sequence alignment revealed that Tiam1 (T-lymphoma invasion and metastasis 1), a Rac-specific guanine nucleotide exchange factor, has a type II PDZ domain similar to those of membrane-associated guanylate kinase homologs (MAGUKs) that are known to bind to the PDZ-BM of CADM1.
  • In this study, we demonstrated that the cytoplasmic domain of CADM1 directly interacted with the PDZ domain of Tiam1 and induced formation of lamellipodia through Rac activation in HTLV-I-transformed cell lines as well as ATL cell lines.
  • Our results indicate that Tiam1 integrates signals from CADM1 to regulate the actin cytoskeleton through Rac activation, which may lead to tissue infiltration of leukemic cells in ATL patients.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Immunoglobulins / metabolism. Leukemia, T-Cell / pathology. Membrane Proteins / metabolism. Neoplasm Invasiveness. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Adhesion Molecules. Cell Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Molecular Sequence Data. Protein Binding. RNA Interference. RNA, Small Interfering. Sequence Homology, Amino Acid

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  • [Cites] Genomics. 1999 Dec 1;62(2):139-46 [10610705.001]
  • [Cites] Retrovirology. 2006;3:71 [17042961.001]
  • [Cites] Nat Genet. 2001 Apr;27(4):427-30 [11279526.001]
  • [Cites] Annu Rev Neurosci. 2001;24:1-29 [11283303.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Mol Reprod Dev. 2001 Oct;60(2):158-64 [11553913.001]
  • [Cites] Neuroreport. 2001 Oct 29;12(15):3217-21 [11711859.001]
  • [Cites] Nature. 2002 Jun 20;417(6891):867-71 [12075356.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):31014-9 [12050160.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1525-31 [12202822.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5129-33 [12234973.001]
  • [Cites] Blood. 2003 Apr 1;101(7):2601-8 [12456501.001]
  • [Cites] Biol Reprod. 2003 May;68(5):1755-63 [12606335.001]
  • [Cites] FEBS Lett. 2003 Jul 3;546(1):11-6 [12829230.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] Lab Invest. 2003 Aug;83(8):1175-83 [12920246.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35421-7 [12826663.001]
  • [Cites] Oncogene. 2003 Sep 18;22(40):6160-5 [13679854.001]
  • [Cites] Curr Opin Cell Biol. 2003 Oct;15(5):583-9 [14519393.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7979-85 [14633730.001]
  • [Cites] J Biol Chem. 2004 Jan 2;279(1):495-508 [14530271.001]
  • [Cites] Cell. 2004 Jan 23;116(2):167-79 [14744429.001]
  • [Cites] Trends Cell Biol. 2007 Jan;17(1):36-43 [17126549.001]
  • [Cites] Hepatology. 2007 Mar;45(3):684-94 [17326163.001]
  • [Cites] J Cell Biol. 2007 Mar 12;176(6):863-75 [17353362.001]
  • [Cites] J Biol Chem. 2007 May 4;282(18):13864-74 [17339315.001]
  • [Cites] Rev Med Virol. 2007 Sep-Oct;17(5):301-11 [17621367.001]
  • [Cites] J Neurosci. 2007 Nov 14;27(46):12516-30 [18003830.001]
  • [Cites] Retrovirology. 2008;5:76 [18702816.001]
  • [Cites] J Virol. 2008 Dec;82(23):11958-63 [18922876.001]
  • [Cites] Breast Cancer Res Treat. 2004 Mar;84(1):21-32 [14999151.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Oct;80(19):6061-5 [6193528.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):237-43 [2303290.001]
  • [Cites] Cell. 1994 May 20;77(4):537-49 [7999144.001]
  • [Cites] Nature. 1995 May 25;375(6529):338-40 [7753201.001]
  • [Cites] Science. 1997 Jan 3;275(5296):73-7 [8974395.001]
  • [Cites] J Cell Biol. 1997 Apr 21;137(2):387-98 [9128250.001]
  • [Cites] Science. 1997 Nov 21;278(5342):1464-6 [9367959.001]
  • [Cites] EMBO J. 1998 Jul 15;17(14):4066-74 [9670021.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):501-11 [9927410.001]
  • [Cites] Leuk Lymphoma. 2005 Feb;46(2):185-90 [15621800.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1204-13 [15471956.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):6934-42 [15905536.001]
  • [Cites] J Biol Chem. 2005 Jun 10;280(23):21955-64 [15781451.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Blood. 2005 Aug 1;106(3):779-86 [15811952.001]
  • [Cites] Int Immunol. 2005 Sep;17(9):1227-37 [16091383.001]
  • [Cites] Cancer Sci. 2005 Sep;96(9):543-52 [16128739.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42164-71 [16223734.001]
  • [Cites] Trends Cell Biol. 2006 Oct;16(10):522-9 [16949823.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1139-46 [16952304.001]
  • [Cites] Int J Cancer. 2000 Nov 1;88(3):369-76 [11054665.001]
  • (PMID = 20215110.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Guanine Nucleotide Exchange Factors; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / RNA, Small Interfering; 0 / TIAM1 protein, human; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2865322
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86. Sakai C, Murotani N: [Adult T-cell leukemia/lymphoma in a patient on hemodialysis-resistance to CHOP, but unexpected effect and remission achieved by sobuzoxane alone]. Gan To Kagaku Ryoho; 2010 Feb;37(2):347-50
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  • [Title] [Adult T-cell leukemia/lymphoma in a patient on hemodialysis-resistance to CHOP, but unexpected effect and remission achieved by sobuzoxane alone].
  • The serum soluble IL-2 receptor was 47,500 U/mL, and HTLV-1 antibody was positive.
  • The pathological diagnosis was peripheral T-cell lymphoma, CD4(+).
  • He was clinically diagnosed as having an adult T-cell leukemia/lymphoma, lymphoma type, and clinical stage II.
  • At the time of reporting, May 2009, the patient was well without recurrence of ATLL, and the remission has lasted 26 months or more.
  • The reason why CHOP-resistant ATLL responded dramatically to SBZ alone is not clear, but the plasma concentration of the metabolite of SBZ was possibly very high because of renal failure.
  • Another possibility is that hemodialysis removed the growth factor(s) or anti-apoptotic factor(s) derived from ATLL cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm. Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Piperazines / therapeutic use. Renal Dialysis. Renal Insufficiency / complications

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  • (PMID = 20154500.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Piperazines; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; R1308VH37P / sobuzoxane; VB0R961HZT / Prednisone; CHOP protocol
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87. Dbaibo GS, Kfoury Y, Darwiche N, Panjarian S, Kozhaya L, Nasr R, Abdallah M, Hermine O, El-Sabban M, de Thé H, Bazarbachi A: Arsenic trioxide induces accumulation of cytotoxic levels of ceramide in acute promyelocytic leukemia and adult T-cell leukemia/lymphoma cells through de novo ceramide synthesis and inhibition of glucosylceramide synthase activity. Haematologica; 2007 Jun;92(6):753-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide induces accumulation of cytotoxic levels of ceramide in acute promyelocytic leukemia and adult T-cell leukemia/lymphoma cells through de novo ceramide synthesis and inhibition of glucosylceramide synthase activity.
  • BACKGROUND AND OBJECTIVES: Arsenic trioxide (ATO) is an effective treatment for acute promyelocytic leukemia (APL) and potentially for human T-cell leukemia virus type I (HTLV-I) associated adult T-cell leukemia/lymphoma (ATL).
  • We, therefore, investigated the contribution of ceramide to the mechanism of action of ATO in APL and ATL.
  • DESIGN AND METHODS: A human APL-derived cell line (NB4), various ATL-derived lines and an HTLV-I-negative malignant T-cell line were cultured and treated with ATO.
  • Measurements were made of ceramide, diacylglycerol, sphingomyelinase activity, sphingomyelin mass, glucosylceramide synthase activity and the de novo ceramide synthesis.
  • RESULTS: Treatment of APL and ATL-derived cells with a clinically achievable concentration of ATO induced accumulation of cytotoxic levels of ceramide.
  • The effects of ATO on ceramide levels in APL cells were more potent than those of all-trans retinoic acid (ATRA).
  • In contrast to the effect of ATRA, ATO-induced ceramide accumulation was not due to induction of acidic sphingomyelinase, but rather resulted from both de novo ceramide synthesis and inhibition of glucosylceramide synthase activity.
  • Interestingly, the effects of ATO on de novo ceramide synthesis were similar in APL and ATL-derived cells despite the defective pathway in ATL cells.
  • [MeSH-major] Arsenicals / pharmacology. Ceramides / biosynthesis. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Glucosyltransferases / antagonists & inhibitors. Humans. Metabolic Networks and Pathways / drug effects

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  • (PMID = 17550847.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Ceramides; 0 / Oxides; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase; S7V92P67HO / arsenic trioxide
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88. Grijsen M, van den Berk G, Hoekstra E, Terpstra W, Veldman S, Jansen J: Intestinal strongyloidiasis as a presenting symptom of HTLV-1-associated adult T-cell leukemia/lymphoma. Endoscopy; 2009;41 Suppl 2:E271-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intestinal strongyloidiasis as a presenting symptom of HTLV-1-associated adult T-cell leukemia/lymphoma.
  • [MeSH-major] Duodenum / pathology. Leukemia-Lymphoma, Adult T-Cell / complications. Strongyloidiasis / diagnosis
  • [MeSH-minor] Animals. Biopsy. Endoscopy, Gastrointestinal. Fatal Outcome. HTLV-I Antibodies / analysis. Human T-lymphotropic virus 1 / immunology. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Strongyloides / isolation & purification

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  • (PMID = 19866424.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
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89. Suzuki R: Dosing of a phase I study of KW-0761, an anti-CCR4 antibody, for adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma. J Clin Oncol; 2010 Aug 10;28(23):e404-5; author reply e406
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dosing of a phase I study of KW-0761, an anti-CCR4 antibody, for adult T-cell leukemia-lymphoma and peripheral T-cell lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Clinical Trials, Phase I as Topic. Dose-Response Relationship, Drug. Humans. Maximum Tolerated Dose. Receptors, CCR4 / immunology

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  • [CommentOn] J Clin Oncol. 2010 Mar 20;28(9):1591-8 [20177026.001]
  • (PMID = 20566994.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / mogamulizumab
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90. Richardson S, Budgin JB, Junkins-Hopkins JM, Vittorio CC, Lee J, Miller WT Jr, Rook AH, Kim EJ: Low-dose bexarotene and low-dose interferon alfa-2b for adult T-cell leukemia/lymphoma associated with human T-lymphotropic virus 1. Arch Dermatol; 2005 Mar;141(3):301-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose bexarotene and low-dose interferon alfa-2b for adult T-cell leukemia/lymphoma associated with human T-lymphotropic virus 1.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Interferon-alpha / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tetrahydronaphthalenes / therapeutic use

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  • (PMID = 15781670.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / Tetrahydronaphthalenes; 99210-65-8 / interferon alfa-2b; A61RXM4375 / bexarotene
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91. Satou Y, Yasunaga J, Yoshida M, Matsuoka M: [HTLV-1 bZIP Factor (HBZ) gene has a growth-promoting effect on adult T-cell leukemia cells]. Rinsho Ketsueki; 2008 Nov;49(11):1525-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [HTLV-1 bZIP Factor (HBZ) gene has a growth-promoting effect on adult T-cell leukemia cells].
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / physiology. Cell Division / genetics. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Humans. Virus Replication

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  • (PMID = 19047782.001).
  • [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 / Basic-Leucine Zipper Transcription Factors
  • [Number-of-references] 24
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92. Hsieh YC, Chang ST, Huang WT, Ichinohasama R, Chuang SS: Adult T-cell leukemia/lymphoma comprising non-floral leukemic cells in Taiwan, a country non-endemic for human T-cell leukemia virus type I. Leuk Lymphoma; 2009 Sep;50(9):1540-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma comprising non-floral leukemic cells in Taiwan, a country non-endemic for human T-cell leukemia virus type I.
  • [MeSH-major] HTLV-I Infections / complications. Human T-lymphotropic virus 1 / physiology. Leukemia, T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / etiology. Leukemia-Lymphoma, Adult T-Cell / pathology

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  • (PMID = 19603347.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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93. Kawamura E, Habu D, Kurooka H, Hayashi T, Oe A, Kotani J, Higashiyama S, Nakamae H, Torii K, Kawabe J, Shiomi S: Adult T-cell leukemia blast crisis in a patient with acute liver failure. Indian J Gastroenterol; 2006 Jan-Feb;25(1):49

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia blast crisis in a patient with acute liver failure.
  • [MeSH-major] Blast Crisis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Liver Failure, Acute / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Liver Function Tests. Male. Middle Aged

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  • (PMID = 16567906.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] India
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94. Matsuoka M: [Mechanism of leukemogenesis by human T-cell leukemia virus type I: from infection with HTLV-I to the onset of adult T-cell leukemia]. Rinsho Ketsueki; 2006 Dec;47(12):1493-501

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Mechanism of leukemogenesis by human T-cell leukemia virus type I: from infection with HTLV-I to the onset of adult T-cell leukemia].
  • [MeSH-major] HTLV-I Infections / virology. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology. Lymphoma, T-Cell / virology
  • [MeSH-minor] Animals. Basic-Leucine Zipper Transcription Factors / genetics. Cell Proliferation. DNA Methylation. Epigenesis, Genetic / genetics. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor. Genes, Viral / genetics. Genes, Viral / physiology. Genome. Humans. Mutation. Viral Proteins / genetics

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  • (PMID = 17233467.001).
  • [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 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Viral Proteins
  • [Number-of-references] 47
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95. Tsutsumi Y, Kanamori H, Yamato H, Ehira N, Kawamura T, Obara S, Tanaka J, Asaka M, Imamura M, Masauzi N: Lung infiltration of adult T-cell leukemia cells following the administration of arsenic trioxide. Lung infiltration of ATL by AS(2)O(3). Med Hypotheses; 2006;66(1):201-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lung infiltration of adult T-cell leukemia cells following the administration of arsenic trioxide. Lung infiltration of ATL by AS(2)O(3).
  • [MeSH-major] Arsenicals / adverse effects. Arsenicals / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration / chemically induced. Lung / pathology. Oxides / adverse effects. Oxides / therapeutic use

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  • (PMID = 16165312.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Deltaretrovirus Antibodies; 0 / Oxides; S7V92P67HO / arsenic trioxide
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96. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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97. Katsuya H, Ishitsuka K, Sasaki H, Wakamatsu S, Inoue H, Takamatsu Y, Suzumiya J, Tsuboi Y, Tamura K: [Hypersomnia as a presentation of paraneoplastic limbic encephalitis in a patient with adult T cell leukemia/lymphoma]. Nihon Naika Gakkai Zasshi; 2008 Feb 10;97(2):410-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hypersomnia as a presentation of paraneoplastic limbic encephalitis in a patient with adult T cell leukemia/lymphoma].
  • [MeSH-major] Disorders of Excessive Somnolence / etiology. Leukemia-Lymphoma, Adult T-Cell / complications. Limbic Encephalitis / etiology

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  • (PMID = 18323160.001).
  • [ISSN] 0021-5384
  • [Journal-full-title] Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine
  • [ISO-abbreviation] Nippon Naika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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98. Ohno E, Ono K, Kikuchi H, Saburi Y, Utsunomiya A, Nasu M: Prolonged remission of adult T-cell leukemia/lymphoma treated with interferon-gamma following autologous peripheral blood stem cell transplantation. Leuk Lymphoma; 2005 Dec;46(12):1843-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonged remission of adult T-cell leukemia/lymphoma treated with interferon-gamma following autologous peripheral blood stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Interferon-gamma / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / therapy. Lymphoma, T-Cell / therapy. Stem Cell Transplantation

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  • (PMID = 16263592.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
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99. Fahim S, Prokopetz R, Jackson R, Faught C, McCarthy AE, Andonov A, Coulthart M, Daw Z, Olberg B, Giulivi A, Padmore R: Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut. CMAJ; 2006 Sep 12;175(6):579
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell lymphotropic virus type 1-associated adult T-cell leukemia/lymphoma in the Inuit people of Nunavut.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / ethnology
  • [MeSH-minor] Adult. Aged. Fatal Outcome. Female. Humans. Indians, North American. Lymphocytosis / blood. Medical History Taking. Middle Aged. Physical Examination. Practice Guidelines as Topic

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  • [Cites] Tissue Antigens. 1998 Nov;52(5):444-51 [9864034.001]
  • [Cites] CMAJ. 2006 Jan 17;174(2):150-1 [16415454.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):232-9 [15726602.001]
  • (PMID = 16966657.001).
  • [ISSN] 1488-2329
  • [Journal-full-title] CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne
  • [ISO-abbreviation] CMAJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1559419
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100. Farre L, Bittencourt AL, Silva-Santos G, Almeida A, Silva AC, Decanine D, Soares GM, Alcantara LC Jr, Van Dooren S, Galvão-Castro B, Vandamme AM, Van Weyenbergh J: Fas 670 promoter polymorphism is associated to susceptibility, clinical presentation, and survival in adult T cell leukemia. J Leukoc Biol; 2008 Jan;83(1):220-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fas 670 promoter polymorphism is associated to susceptibility, clinical presentation, and survival in adult T cell leukemia.
  • Fas gene mutations, aberrant transcripts, and abundant expression of Fas have been reported in adult T cell leukemia (ATL).
  • To further elucidate the role of Fas in ATL pathogenesis, we investigated whether the -670 FAS promoter A/G polymorphism (STAT1-binding site) might contribute to susceptibility and clinical outcome in ATL.
  • Thirty-one patients with ATL, 33 healthy, human T lymphotropic virus type 1-infected individuals, and 70 healthy, uninfected controls were genotyped for the FAS -670 polymorphism by PCR-restriction fragment-length polymorphism.
  • The AA genotype was significantly over-represented in ATL patients in comparison with healthy controls (P=0.006), as well as asymptomatics (P=0.037), corresponding to an odds ratio (OR) of 3.79 [95% confidence intervals (CI; 1.28-11.41)] and 4.58 [95% CI (1.13-20.03)], respectively.
  • The AA group also comprised significantly more aggressive (acute and lymphoma) clinical subtypes [P=0.012; OR=8.40; 95% CI (1.60-44.12)].
  • In conclusion, our results demonstrate that a functional Fas promoter polymorphism is significantly associated to susceptibility, clinical manifestation, and survival in ATL.
  • [MeSH-major] Antigens, CD95 / genetics. Genetic Predisposition to Disease / genetics. Leukemia, T-Cell / genetics. Polymorphism, Single Nucleotide / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Follow-Up Studies. Genotype. HTLV-I Infections / immunology. HTLV-I Infections / virology. Humans. Interferon-gamma / pharmacology. Leukocytes, Mononuclear / drug effects. RNA, Messenger / genetics. Risk Factors. Survival Rate

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  • (PMID = 17962369.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
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