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1. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • The cell cycle was examined by flow cytometric analysis.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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2. Borge M, Nannini PR, Galletti JG, Morande PE, Avalos JS, Bezares RF, Giordano M, Gamberale R: CXCL12-induced chemotaxis is impaired in T cells from patients with ZAP-70-negative chronic lymphocytic leukemia. Haematologica; 2010 May;95(5):768-75
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  • [Title] CXCL12-induced chemotaxis is impaired in T cells from patients with ZAP-70-negative chronic lymphocytic leukemia.
  • BACKGROUND: T cells from patients with chronic lymphocytic leukemia may play an important role in contributing to the onset, sustenance, and exacerbation of the disease by providing survival and proliferative signals to the leukemic clone within lymph nodes and bone marrow.
  • DESIGN AND METHODS: By performing chemotaxis assays towards CXCL12, CCL21 and CCL19, we sought to evaluate the migratory potential of T cells from chronic lymphocytic leukemia patients.
  • We next analyzed the chemokine-induced migration of T cells, dividing the chronic lymphocytic leukemia samples according to their expression of the poor prognostic factors CD38 and ZAP-70 in leukemic cells determined by flow cytometry.
  • RESULTS: We found that T cells from patients with chronic lymphocytic leukemia are less responsive to CXCL12, CCL21 and CCL19 than T cells from healthy adults despite similar CXCR4 and CCR7 expression.
  • Following separation of the patients into two groups according to ZAP-70 expression, we found that T cells from ZAP-70-negative samples showed significantly less migration towards CXCL12 compared to T cells from ZAP-70-positive samples and that this was not due to defective CXCR4 down-regulation, F-actin polymerization or to a lesser expression of ZAP-70, CD3, CD45, CD38 or CXCR7 on these cells.
  • CONCLUSIONS: Impaired migration towards CXCL12 may reduce the access of T cells from ZAP-70-negative patients to lymphoid organs, creating a less favorable microenvironment for leukemic cell survival and proliferation.
  • [MeSH-major] Cell Migration Inhibition / physiology. Chemokine CXCL12 / physiology. Chemotaxis, Leukocyte / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. T-Lymphocytes / pathology. ZAP-70 Protein-Tyrosine Kinase / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Coculture Techniques. Female. Humans. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 20145264.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chemokine CXCL12; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  • [Other-IDs] NLM/ PMC2864383
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3. Pais-Correia AM, Sachse M, Guadagnini S, Robbiati V, Lasserre R, Gessain A, Gout O, Alcover A, Thoulouze MI: Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses. Nat Med; 2010 Jan;16(1):83-9
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  • [Title] Biofilm-like extracellular viral assemblies mediate HTLV-1 cell-to-cell transmission at virological synapses.
  • Human T cell leukemia virus type 1 (HTLV-1) is a lymphotropic retrovirus whose cell-to-cell transmission requires cell contacts.
  • HTLV-1-infected T lymphocytes form 'virological synapses', but the mechanism of HTLV-1 transmission remains poorly understood.
  • We show here that HTLV-1-infected T lymphocytes transiently store viral particles as carbohydrate-rich extracellular assemblies that are held together and attached to the cell surface by virally-induced extracellular matrix components, including collagen and agrin, and cellular linker proteins, such as tetherin and galectin-3.
  • Extracellular viral assemblies rapidly adhere to other cells upon cell contact, allowing virus spread and infection of target cells.
  • Their removal strongly reduces the ability of HTLV-1-producing cells to infect target cells.
  • Our findings unveil a novel virus transmission mechanism based on the generation of extracellular viral particle assemblies whose structure, composition and function resemble those of bacterial biofilms.
  • HTLV-1 biofilm-like structures represent a major route for virus transmission from cell to cell.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Extracellular Matrix / virology. HTLV-I Infections / transmission. Human T-lymphotropic virus 1 / physiology
  • [MeSH-minor] Biofilms. Concanavalin A. Gene Products, env / metabolism. Humans. Microscopy, Electron, Transmission. Virus Assembly / physiology. Virus Attachment. Virus Internalization

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

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  • (PMID = 17986383.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / TAB2 protein, human; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP kinase kinase kinase 7; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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5. Meleshko A, Savitski VP, Shman TV, Aleinikova OV: Immunophenotypically heterogeneous acute T-lymphoblastic leukemia has invariable immunogenotype: analysis of two cases. J Pediatr Hematol Oncol; 2006 Jan;28(1):50-2
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  • [Title] Immunophenotypically heterogeneous acute T-lymphoblastic leukemia has invariable immunogenotype: analysis of two cases.
  • Two patients with acute T-lymphoblastic leukemia showed heterogeneous expression of some immunophenotypic cell markers.
  • Cell sorting was used to separate two CD34/CD117/TCRgammadelta and CD34/CD117/TCRgammadelta cell populations.
  • The authors assume the presence of two immunophenotypically different cell subsets in different maturation stages at diagnosis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / immunology. Immunophenotyping. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Adolescent. Antigens, CD34 / genetics. Antigens, CD34 / immunology. Child, Preschool. Genotype. Humans. Polymerase Chain Reaction. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / immunology. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / immunology

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  • (PMID = 16394895.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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6. Gra OA, Glotov AS, Nikitin EA, Glotov OS, Kuznetsova VE, Chudinov AV, Sudarikov AB, Nasedkina TV: Polymorphisms in xenobiotic-metabolizing genes and the risk of chronic lymphocytic leukemia and non-Hodgkin's lymphoma in adult Russian patients. Am J Hematol; 2008 Apr;83(4):279-87
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  • [Title] Polymorphisms in xenobiotic-metabolizing genes and the risk of chronic lymphocytic leukemia and non-Hodgkin's lymphoma in adult Russian patients.
  • Using allele-specific hybridization on the biochip 76 T-cell non-Hodgkin's lymphoma (NHL) patients, 83 B-cell chronic lymphocytic leukemia (B-CLL) patients, and 177 healthy donors were tested.
  • [MeSH-major] Biotransformation / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, T-Cell / genetics. Oligonucleotide Array Sequence Analysis. Xenobiotics / pharmacokinetics
  • [MeSH-minor] Adult. Alleles. Arylamine N-Acetyltransferase / genetics. Carcinogens, Environmental / pharmacokinetics. Cytochrome P-450 Enzyme System / genetics. Female. Ferredoxin-NADP Reductase / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Humans. Male. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Nucleic Acid Hybridization. Risk Factors. Russia / epidemiology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18061941.001).
  • [ISSN] 1096-8652
  • [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 / Carcinogens, Environmental; 0 / Xenobiotics; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
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7. Morozov VA, Syrtsev AV, Ellerbrok H, Nikolaeva EV, Bavykin AS, Pauli G: Mycosis fungoides in European Russia: no antibodies to human T cell leukemia virus type I structural proteins, but virus-like sequences in blood and saliva. Intervirology; 2005;48(6):362-71
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  • [Title] Mycosis fungoides in European Russia: no antibodies to human T cell leukemia virus type I structural proteins, but virus-like sequences in blood and saliva.
  • OBJECTIVE: Mycosis fungoides (MF) is the most frequent form of cutaneous T cell lymphoma (CTCL).
  • Human T cell leukemia virus type 1 (HTLV-1) involvement in MF progression is a matter of debate.
  • The goal of the investigation was to search for HTLV-1 markers in a group of MF patients from a nonendemic area to HTLV-1.
  • MATERIALS AND METHODS: Fifty MF patients and 60 healthy donors from Moscow and the Moscow region were examined for HTLV-1 markers by Western blot, PCR, nested PCR, PCR/Southern hybridization, TaqMan real-time PCR and sequencing.
  • RESULTS: Plasma samples from MF patients were repeatedly negative for antibodies to HTLV-1 structural proteins.
  • HTLV-1 tax-related sequences (corresponding to the second exon) were found in blood from 20 of 50 MF patients and in 3 of 5 saliva specimens.
  • Three of 8 sequenced tax-like amplimers were identical and 5 of 8 contained 1-2 substitutions. tax transcripts and antibodies to p40(tax) were detected in some 'PCR-tax'-positive MF patients.
  • Defective HTLV-1 genomes were demonstrated in 2 of 50 MF patients.
  • Phylogenetic analysis of the defective genome 5'-LTR sequence revealed a relationship with HTLV-1a sequences from the transcontinental subgroup of HTLV-1.
  • CONCLUSIONS: HTLV-1 tax-like sequences were revealed in blood and for the first time in saliva from MF patients living in an HTLV-1 nonendemic region.
  • [MeSH-major] Blood / virology. Genes, pX. HTLV-I Antibodies / blood. Human T-lymphotropic virus 1 / genetics. Mycosis Fungoides / virology. Saliva / virology. Skin Neoplasms / virology
  • [MeSH-minor] Adult. Amino Acid Substitution. Blotting, Southern. Blotting, Western. DNA, Viral / chemistry. DNA, Viral / genetics. Defective Viruses. Female. Genome, Viral. Humans. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Russia. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16024940.001).
  • [ISSN] 0300-5526
  • [Journal-full-title] Intervirology
  • [ISO-abbreviation] Intervirology
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF515451
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / HTLV-I Antibodies
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8. Hilgendorf I, Wilhelm S, Prall F, Junghanss C, Steiner B, Wolff D, Freund M, Casper J: Headache after hematopoietic stem cell transplantation: being aware of chronic bilateral subdural hematoma. Leuk Lymphoma; 2006 Oct;47(10):2247-9
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  • [Title] Headache after hematopoietic stem cell transplantation: being aware of chronic bilateral subdural hematoma.
  • [MeSH-major] Headache. Hematoma, Subdural, Chronic / diagnosis. Hematoma, Subdural, Chronic / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Lymphoma, T-Cell / therapy
  • [MeSH-minor] Adult. Brain / pathology. Humans. Male. Subarachnoid Hemorrhage / pathology

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  • [CommentIn] Leuk Lymphoma. 2007 Apr;48(4):835-6 [17454650.001]
  • (PMID = 17071502.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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9. Nakayama T, Hieshima K, Arao T, Jin Z, Nagakubo D, Shirakawa AK, Yamada Y, Fujii M, Oiso N, Kawada A, Nishio K, Yoshie O: Aberrant expression of Fra-2 promotes CCR4 expression and cell proliferation in adult T-cell leukemia. Oncogene; 2008 May 22;27(23):3221-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of Fra-2 promotes CCR4 expression and cell proliferation in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a mature CD4+ T-cell malignancy etiologically associated with human T-cell leukemia virus type 1 (HTLV-1).
  • Primary ATL cells frequently express CCR4 at high levels.
  • Since HTLV-1 Tax does not induce CCR4 expression, transcription factor(s) constitutively active in ATL may be responsible for its strong expression.
  • We identified an activator protein-1 (AP-1) site in the CCR4 promoter as the major positive regulatory element in ATL cells.
  • Among the AP-1 family members, Fra-2, JunB and JunD are highly expressed in fresh primary ATL cells.
  • Furthermore, Fra-2 small interfering RNA (siRNA) or JunD siRNA, but not JunB siRNA, effectively reduced CCR4 expression and cell growth in ATL cells.
  • Conversely, Fra-2 or JunD overexpression promoted cell growth in Jurkat cells.
  • We identified 49 genes, including c-Myb, BCL-6 and MDM2, which were downregulated by Fra-2 siRNA in ATL cells. c-Myb, BCL-6 and MDM2 were also downregulated by JunD siRNA.
  • As Fra-2, these proto-oncogenes were highly expressed in primary ATL cells but not in normal CD4+ T cells.
  • Collectively, aberrantly expressed Fra-2 in association with JunD may play a major role in CCR4 expression and oncogenesis in ATL.
  • [MeSH-major] Cell Proliferation. Fos-Related Antigen-2 / genetics. Gene Expression Regulation, Leukemic. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, CCR4 / genetics
  • [MeSH-minor] Binding Sites. Cell Culture Techniques. Cell Line, Tumor. Gene Expression Profiling. Humans. Jurkat Cells. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Protein Binding. Proto-Oncogene Proteins c-jun / antagonists & inhibitors. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. RNA, Small Interfering / pharmacology

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  • (PMID = 18071306.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / FOSL2 protein, human; 0 / Fos-Related Antigen-2; 0 / Proto-Oncogene Proteins c-jun; 0 / RNA, Small Interfering; 0 / Receptors, CCR4
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10. Ohsugi T, Kumasaka T, Okada S, Ishida T, Yamaguchi K, Horie R, Watanabe T, Umezawa K: Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines. Cancer Lett; 2007 Nov 18;257(2):206-15
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  • [Title] Dehydroxymethylepoxyquinomicin (DHMEQ) therapy reduces tumor formation in mice inoculated with tax-deficient adult T-cell leukemia-derived cell lines.
  • Adult T-cell leukemia (ATL) is an aggressive neoplasm caused by human T-cell leukemia virus type I (HTLV-I), which induces nuclear factor-kappaB (NF-kappaB), a molecule central to the ensuing neoplasia.
  • The NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) has been shown to inhibit NF-kappaB activation in Tax-expressing HTLV-I-infected cells.
  • In this study, we used NOD/SCID beta2-microglobulin(null) mice to show that intraperitoneal inoculation with Tax-deficient ATL cell lines caused rapid death, whereas DHMEQ-treated mice survived.
  • Furthermore, DHMEQ treatment after subcutaneous inoculation inhibited the growth of transplanted ATL cells.
  • These results demonstrate that DHMEQ has therapeutic efficacy on ATL cells, regardless of Tax expression.
  • [MeSH-major] Benzamides / pharmacology. Cyclohexanones / pharmacology. Gene Products, tax / deficiency. Leukemia, T-Cell / prevention & control. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Adult. Animals. Apoptosis / drug effects. Cell Line, Tumor. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Tumor Burden. beta 2-Microglobulin / genetics. beta 2-Microglobulin / metabolism

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  • (PMID = 17764832.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzamides; 0 / Cyclohexanones; 0 / Gene Products, tax; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / beta 2-Microglobulin; 0 / dehydroxymethylepoxyquinomicin
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11. Feldman AL, Law ME, Inwards DJ, Dogan A, McClure RF, Macon WR: PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus. Mod Pathol; 2010 Apr;23(4):593-602
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  • [Title] PAX5-positive T-cell anaplastic large cell lymphomas associated with extra copies of the PAX5 gene locus.
  • Cell lineage is the major criterion by which lymphomas are classified.
  • Immunohistochemistry has greatly facilitated lymphoma diagnosis by detecting expression of lineage-associated antigens.
  • Anaplastic large cell lymphoma is a T-cell lymphoma that shows morphologic and phenotypic overlap with classical Hodgkin's lymphoma, which is a tumor of B-cell derivation.
  • Staining for the B-cell transcription factor, paired box 5 (PAX5), has been suggested to be helpful in this differential, as it is positive in most classical Hodgkin's lymphomas, but absent in anaplastic large cell lymphomas.
  • In this study we report four systemic T-cell anaplastic large cell lymphomas that were positive for PAX5 by immunohistochemistry, with weak staining intensity similar to that observed in classical Hodgkin's lymphoma.
  • All diagnoses were confirmed by a combination of morphologic, phenotypic, and molecular criteria.
  • Three cases were anaplastic lymphoma kinase (ALK) negative and one was ALK positive.
  • PAX5 immunohistochemistry was negative in 198 additional peripheral T-cell lymphomas, including 66 anaplastic large cell lymphomas.
  • Unexpectedly, although PAX5 translocations were absent, all evaluable PAX5-positive anaplastic large cell lymphomas showed extra copies of the PAX5 gene locus by fluorescence in situ hybridization (FISH).
  • In contrast, only 4% of PAX5-negative peripheral T-cell lymphomas had extra copies of PAX5.
  • We conclude that aberrant expression of PAX5 occurs rarely in T-cell anaplastic large cell lymphomas, and may be associated with extra copies of the PAX5 gene.
  • PAX5-positive lymphomas with morphologic features overlapping different lymphoma types should be evaluated with an extensive immunohistochemical panel and/or molecular studies to avoid diagnostic errors that could lead to inappropriate treatment.
  • As PAX5 overexpression causes T-cell neoplasms in experimental models, PAX5 may have contributed to lymphomagenesis in our cases.

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  • (PMID = 20118907.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-08; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ NIHMS167829; NLM/ PMC2848697
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12. Strupp C, Germing U, Aivado M, Kündgen A, Fenk R, Hünerlitürkoglu A, Kobbe G, Haas R, Gattermann N: The ratio between CD4+ and CD8+ cells in the peripheral blood of patients with hematological malignancies is not altered by thalidomide. Leuk Lymphoma; 2005 Jul;46(7):999-1006
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  • Thalidomide is thought to have anti-angiogenic and immunomodulatory properties, including suppression of tumor necrosis factor-alpha, effects on interleukins and interferons, down-regulation of some cell adhesion molecules, and changes in the proportion of lymphocyte subsets.
  • It is unclear whether the clinical response to thalidomide in patients with multiple myeloma (MM), idiopathic myelofibrosis (IM), and myelodysplastic syndromes (MDS) is related to its ability to inhibit angiogenesis or its immunomodulatory effects.
  • We examined the effect of thalidomide on T-lymphocyte subsets in 18 patients with MDS, 6 patients with MM, 4 patients with IM, and 3 patients with angioimmunoblastic lymphoma (AILD).
  • These patients had either a relapse or progressive disease following cytotoxic chemotherapy including high-dose chemotherapy with autologous stem cell support.
  • T-lymphocyte subsets (CD4+, CD8+) were measured by fluorescence-activated cell sorter (FACS) before and during treatment with thalidomide.
  • Our findings show that an effect of thalidomide on the T lymphocytes studied is unlikely to be of major importance for the clinical effects.
  • [MeSH-minor] Adult. Aged. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Female. Humans. Male. Middle Aged. Stem Cell Transplantation

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  • (PMID = 16019550.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
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13. Ramuz O, Bouabdallah R, Devilard E, Borie N, Groulet-Martinec A, Bardou VJ, Brousset P, Bertucci F, Birg F, Birnbaum D, Xerri L: Identification of TCL1A as an immunohistochemical marker of adverse outcome in diffuse large B-cell lymphomas. Int J Oncol; 2005 Jan;26(1):151-7
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  • [Title] Identification of TCL1A as an immunohistochemical marker of adverse outcome in diffuse large B-cell lymphomas.
  • We used a combination of DNA-microarray and tissue-microarray (TMA) analyses to identify markers that could be routinely used to predict the outcome of diffuse large-B-cell lymphoma (DLCL) patients.
  • Gene expression profiling was performed using DNA-microarrays on 52 tumour biopsy samples [31 DLCL and 21 follicular lymphomas (FL)] from 48 patients (28 DLCL and 20 FL).
  • T-cell leukemia/lymphoma-1A (TCL1A) mRNA overexpression was correlated with relapse in DLCL patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Proto-Oncogene Proteins / analysis
  • [MeSH-minor] Adult. Aged. Female. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. Tissue Array Analysis. Transcriptional Activation

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  • (PMID = 15586235.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins; 0 / TCL1A protein, human
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14. 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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  • [Title] A network biology approach evaluating the anticancer effects of bortezomib identifies SPARC as a therapeutic target in adult T-cell leukemia 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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  • (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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15. van den Heuvel MJ, Jefferson BJ, Jacobs RM: Isolation of a bovine plasma fibronectin-containing complex which inhibits the expression of bovine leukemia virus p24. J Virol; 2005 Jul;79(13):8164-70
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  • [Title] Isolation of a bovine plasma fibronectin-containing complex which inhibits the expression of bovine leukemia virus p24.
  • Bovine leukemia virus (BLV) is a deltaretrovirus that infects cattle worldwide.
  • Like the human T-cell leukemia virus (HTLV), there is a lengthy period of viral quiescence after initial infection with BLV.
  • Unlike HTLV, BLV resides predominantly in B cells.
  • Lymphoma is observed in less than 10% of BLV-infected adult cattle.
  • [MeSH-major] Fibronectins / blood. Leukemia Virus, Bovine / physiology. Viral Core Proteins / blood
  • [MeSH-minor] Animals. Cattle. Serum Albumin, Bovine. Virus Replication / physiology

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  • (PMID = 15956561.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fibronectins; 0 / Serum Albumin, Bovine; 0 / Viral Core Proteins; 0 / core protein p24, bovine leukemia virus
  • [Other-IDs] NLM/ PMC1143752
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16. Jia Y, Hikim AP, Lue YH, Swerdloff RS, Vera Y, Zhang XS, Hu ZY, Li YC, Liu YX, Wang C: Signaling pathways for germ cell death in adult cynomolgus monkeys (Macaca fascicularis) induced by mild testicular hyperthermia and exogenous testosterone treatment. Biol Reprod; 2007 Jul;77(1):83-92
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  • [Title] Signaling pathways for germ cell death in adult cynomolgus monkeys (Macaca fascicularis) induced by mild testicular hyperthermia and exogenous testosterone treatment.
  • Male contraception has focused, to a great extent, on approaches that induce azoospermia or severe oligospermia through accelerated germ cell apoptosis.
  • Understanding the specific steps in the germ cell apoptotic pathways that are affected by male contraceptives will allow more specific targeting in future contraceptive development.
  • In this study, we have used a nonhuman primate model to characterize the key apoptotic pathway(s) in germ cell death after mild testicular hyperthermia, hormonal deprivation, or combined interventions.
  • Groups of 8 adult (7- to 10-year-old) cynomolgus monkeys (Macaca fascicularis) received one of the following treatments:.
  • Activation of MAPK1/3 and MAPK14 were accompanied by an increase in B-cell leukemia/lymphoma (BCL) 2 levels in both cytosolic and mitochondrial fractions of testicular lysates (BAX levels remained unaffected) and cytochrome c and DIABLO release from mitochondria.
  • We conclude that the serine phosphorylation of BCL2 and activation of the MAPK14-mediated mitochondria-dependent pathway are critical for male germ cell death in monkeys.

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  • (PMID = 17377139.001).
  • [ISSN] 0006-3363
  • [Journal-full-title] Biology of reproduction
  • [ISO-abbreviation] Biol. Reprod.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD39293
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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17. Kotoula V, Bobos M, Kostopoulos I, Kaloutsi V, Koletsa T, Karayannopoulou G, Papadimitriou CS: In situ detection of hTERT variants in anaplastic large cell lymphoma. Leuk Lymphoma; 2006 Aug;47(8):1639-50
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  • [Title] In situ detection of hTERT variants in anaplastic large cell lymphoma.
  • The expression of hTERT and its isoforms is difficult to assess in lymphoma tissues with the commonly used reverse transcription-polymerase chain reaction (RT-PCR) methods, because non-neoplastic lymphocytes expressing hTERT are always present in the lymphomatous infiltrates.
  • The present study aimed to investigate hTERT mRNA variants in anaplastic large cell lymphoma (ALCL) (n = 38) with in situ hybridization (ISH), along with the immunodetection of hTERT protein.
  • Although all ALCL examined were found positive for hTERT expression with RT-PCR, hTERT mRNAs were identified in 68% of these tumors with ISH, with a higher incidence in the group bearing ALK translocations (10 out of 11; 90.9%) compared to the ALK negative group (17 out of 27; 59.3%) (PPearson's = 0.002).
  • In approximately 50% of cases, only Bplus positive cells were identified, again with a higher incidence in the ALK positive compared to the ALK negative group (PPearson's = 0.016).
  • In conclusion, ISH for hTERT mRNAs appears to be a valuable tool for the investigation of hTERT expression in lymphomas.
  • Aberrations in hTERT variant profiles and a decline in the expression of the B deleted isoform may be associated with the pathogenesis of ALCL, especially with respect to ALK positive tumors.
  • [MeSH-major] Genetic Variation. In Situ Hybridization / methods. Lymphoma, Large-Cell, Anaplastic / genetics. Telomerase / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Immunohistochemistry. Lymphocytes / metabolism. Male. Middle Aged. Neoplasm Proteins / genetics. RNA, Messenger / analysis. RNA, Messenger / genetics

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  • (PMID = 16966278.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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18. O'Mahony D, Morris JC, Stetler-Stevenson M, Matthews H, Brown MR, Fleisher T, Pittaluga S, Raffeld M, Albert PS, Reitsma D, Kaucic K, Hammershaimb L, Waldmann TA, Janik JE: EBV-related lymphoproliferative disease complicating therapy with the anti-CD2 monoclonal antibody, siplizumab, in patients with T-cell malignancies. Clin Cancer Res; 2009 Apr 1;15(7):2514-22
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  • [Title] EBV-related lymphoproliferative disease complicating therapy with the anti-CD2 monoclonal antibody, siplizumab, in patients with T-cell malignancies.
  • PURPOSE: We report an increased incidence of EBV-induced B-cell lymphoproliferative disease (LPD) in patients treated with siplizumab, an anti-CD2 antibody.
  • The development of EBV-LPD has been associated with the use of immunosuppressive agents used in solid organ, bone marrow, and stem cell transplantation and in certain congenital immunodeficiencies.
  • EXPERIMENTAL DESIGN: We conducted a single-institution phase I dose-escalation trial of siplizumab, a humanized monoclonal antibody to CD2, in 29 patients with T-cell malignancies.
  • Reductions in CD4(+) and CD8(+) cell count numbers in response to therapy were seen in all patients, but in those patients developing EBV-LPD a significantly greater reduction in natural killer (NK) cell number and CD2 expression on T cells was seen.
  • These findings highlight the importance of NK-cell depletion and CD2 expression in addition to T-cell depletion in the etiology of EBV-LPD.
  • CONCLUSIONS: The emergence of EBV-LPD may be associated with the ability of siplizumab to deplete both T and NK cells without affecting B cells.
  • Agents that deplete T- and NK-cell populations without affecting B cell number should be screened for this potentially serious adverse event.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Epstein-Barr Virus Infections / immunology. Leukemia, Large Granular Lymphocytic / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoproliferative Disorders / immunology. Sialic Acid Binding Ig-like Lectin 2 / immunology

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  • [CommentIn] Clin Cancer Res. 2009 Apr 1;15(7):2205-6 [19293254.001]
  • (PMID = 19293260.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / siplizumab
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19. Smith SM, van Besien K, Karrison T, Dancey J, McLaughlin P, Younes A, Smith S, Stiff P, Lester E, Modi S, Doyle LA, Vokes EE, Pro B: Temsirolimus has activity in non-mantle cell non-Hodgkin's lymphoma subtypes: The University of Chicago phase II consortium. J Clin Oncol; 2010 Nov 01;28(31):4740-6
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  • [Title] Temsirolimus has activity in non-mantle cell non-Hodgkin's lymphoma subtypes: The University of Chicago phase II consortium.
  • PURPOSE: Despite high initial remission rates, most lymphomas relapse and require further therapy.
  • The mammalian target of rapamycin (mTOR) pathway is a validated target in mantle cell lymphoma, but has not been extensively evaluated in other lymphomas.
  • PATIENTS AND METHODS: We performed a phase II trial of single-agent temsirolimus 25-mg weekly in patients with relapsed aggressive and indolent lymphomas.
  • Patients were stratified by histology: group A (diffuse large B-cell lymphoma, transformed follicular lymphoma), group B (follicular lymphoma), and group C (chronic lymphocytic leukemia/small lymphocytic lymphoma, and other indolent lymphomas).
  • CONCLUSIONS: Single-agent temsirolimus has significant activity in both diffuse large B-cell lymphoma and follicular lymphoma, although the durability of responses and PFS are longer for patients with follicular lymphoma.
  • This is the first report of substantial activity of temsirolimus in lymphomas other than mantle cell lymphoma, and supports further evaluation of mTOR as a target in these diseases.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Serine-Threonine Kinases / metabolism. Sirolimus / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow / drug effects. Chicago. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Male. Middle Aged. Mucositis / chemically induced. Pneumonia / chemically induced. Remission Induction. TOR Serine-Threonine Kinases. Treatment Outcome

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  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00290472
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-17102
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Kinase Inhibitors; 624KN6GM2T / temsirolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3020703
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20. Semmes OJ: Adult T cell leukemia: a tale of two T cells. J Clin Invest; 2006 Apr;116(4):858-60
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  • [Title] Adult T cell leukemia: a tale of two T cells.
  • Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent for the development of an aggressive hematologic neoplasia termed adult T cell leukemia/lymphoma (ATLL).
  • Although the virus infects T cell subsets that display either CD4 or CD8 cell surface markers, the leukemic cell is exclusively of the CD4+ subtype.
  • In the article by Sibon et al. in this issue of the JCI, the authors demonstrate that the molecular basis for clonal expansion differs between these 2 infected T cell populations (see the related article beginning on page 974).
  • The molecular events associated with a preleukemic state, such as genomic instability, polynucleation, and cell cycle redistribution, were only observed in CD4+ T cells.
  • This finding provides a molecular-based mechanism for the restriction of the leukemic phenotype to the CD4+ T cell subtype.
  • [MeSH-major] CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Gene Products, tax / metabolism. Humans. Models, Biological. Phenotype

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  • [ISO-abbreviation] J. Clin. Invest.
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21. Taylor JM, Nicot C: HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches. Apoptosis; 2008 Jun;13(6):733-47
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  • [Title] HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches.
  • A universal cellular defense mechanism against viral invasion is the elimination of infected cells through apoptotic cell death.
  • To counteract host defenses many viruses have evolved complex apoptosis evasion strategies.
  • The oncogenic human retrovirus HTLV-1 is the etiological agent of adult-T-cell leukemia/lymphoma (ATLL) and the neurodegenerative disease known as HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
  • The poor prognosis in HTLV-1-induced ATLL is linked to the resistance of neoplastic T cells against conventional therapies and the immuno-compromised state of patients.
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  • A better understanding of the molecular mechanisms employed by HTLV-1 to counteract cellular death pathways remains an important challenge for future therapies and the treatment of HTLV-1-associated diseases.

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  • (PMID = 18421579.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115398-01A2; United States / NCI NIH HHS / CA / CA106258-05; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / R01 CA106258-05; United States / NCI NIH HHS / CA / R01 CA115398-01A2; United States / NCI NIH HHS / CA / CA106258; United States / NCI NIH HHS / CA / CA115398; United States / NCI NIH HHS / CA / R01 CA106258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; 0 / Retroviridae Proteins; 0 / STAT Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Viral Regulatory and Accessory Proteins; 0 / p12I protein, Human T-lymphotropic virus 1; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; 5688UTC01R / Tretinoin; EC 2.7.10.2 / Janus Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.10 / I-kappa B Kinase
  • [Number-of-references] 201
  • [Other-IDs] NLM/ NIHMS81007; NLM/ PMC2633601
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22. Alizadeh AA, Bohen SP, Lossos C, Martinez-Climent JA, Ramos JC, Cubedo-Gil E, Harrington WJ Jr, Lossos IS: Expression profiles of adult T-cell leukemia-lymphoma and associations with clinical responses to zidovudine and interferon alpha. Leuk Lymphoma; 2010 Jul;51(7):1200-16
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  • [Title] Expression profiles of adult T-cell leukemia-lymphoma and associations with clinical responses to zidovudine and interferon alpha.
  • Adult T-cell leukemia-lymphoma (ATLL) is an HTLV-1-associated lymphoproliferative malignancy that is frequently fatal.
  • We compared gene expression profiles (GEPs) of leukemic specimens from nine patients with ATLL at the time of diagnosis and immediately after combination therapy with zidovudine (AZT) and interferon alpha (IFNalpha).
  • We identified several genes anomalously over-expressed in the ATLL leukemic cells at the mRNA level, including LYN, CSPG2, and LMO2, and confirmed LMO2 expression in ATLL cells at the protein level.
  • In vivo AZT-IFNalpha therapy evoked a marked induction of interferon-induced genes accompanied by repression of cell-cycle regulated genes, including those encoding ribosomal proteins.
  • Demonstration of specific gene expression signatures associated with response to AZT-IFNalpha therapy may provide novel insights into the mechanisms of action in ATLL.
  • [MeSH-major] Anti-HIV Agents / therapeutic use. Biomarkers, Tumor / genetics. Gene Expression Profiling. Interferon-alpha / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Zidovudine / therapeutic use
  • [MeSH-minor] Adult. Comparative Genomic Hybridization. Drug Therapy, Combination. Humans. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • [CommentIn] Leuk Lymphoma. 2010 Jul;51(7):1157-8 [20388057.001]
  • (PMID = 20370541.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P30 AI073961; United States / NCI NIH HHS / CA / P30 CA124435; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA122105
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Biomarkers, Tumor; 0 / Interferon-alpha; 0 / RNA, Messenger; 4B9XT59T7S / Zidovudine
  • [Other-IDs] NLM/ NIHMS636985; NLM/ PMC4296320
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23. Lu Y, Zhao X, Wang E, Chen W, Huang Q: ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase". Leuk Res; 2010 Apr;34(4):475-82
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  • [Title] ALK-negative anaplastic large cell lymphoma with extensive peripheral blood and bone marrow involvements manifested as "leukemic phase".
  • CD30-positive anaplastic large cell lymphoma (ALCL) is a distinctive malignant large cell lymphoma of T-cell lineage, often presenting in lymph node or extranodal sites.
  • ALCL cases with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase" are extremely rare and the most of those cases reported are anaplastic large cell lymphoma kinase (ALK) positive ALCL in childhood population.
  • Here we report four adult cases of ALK-negative ALCL with extensive bone marrow and peripheral blood involvement manifested as "leukemic phase".
  • Circulating large lymphoma cells varied from 20 to 80% in peripheral blood and bone marrow biopsy showed various nodular or interstitial infiltrates.
  • By reviewing the clinicopathologic data of previously reported ALCL cases with extensive bone marrow and peripheral blood involvement, there appears to be of large variations in regard to the patient's age, morphologic variants, immunophenotypic or genotypic characteristics of the disease.
  • While most cases of ALCL with peripheral blood and bone marrow involvement were ALK-positive or carrying t(2;5) translocation, rare ALK-negative cases were also present.
  • [MeSH-major] Bone Marrow Neoplasms / secondary. Lymphoma, Large-Cell, Anaplastic / pathology. Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adult. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Receptor Protein-Tyrosine Kinases

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19695703.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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24. Gui W, Zhao ZQ, Zhang Z, Guo YR, Zhang QH, Su W: [Analysis of pathological type and clinical features of lymphoma cell leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Oct;30(10):662-6
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  • [Title] [Analysis of pathological type and clinical features of lymphoma cell leukemia].
  • OBJECTIVE: To analyze the pathological type and clinical features of patients with lymphoma cell leukemia (LML).
  • METHODS: According to the 2008 WHO classification of tumors of hematopoietic and lymphoid tissue, the pathological type and clinical features of 127 LML cases were analyzed retrospectively.
  • The incidence in frequent order of them was B-lymphoblastic lymphoma, CLL/small lymphocytic lymphoma (SLL) and T-lymphoblastic lymphoma.
  • The LML of T and B cell subtypes were 45 and 74, respectively.
  • Eighty one patients presented LML at the same time of the NHL diagnosis and 46 during the course (1 - 88 months) of disease.
  • The clinical manifestations of LBL and SLL patients differed from that of ALL and CLL patients.
  • The clinical features of LML patients are somewhat special, especially for primary extranodal LML patients.
  • [MeSH-major] Leukemia, Lymphoid / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Lymphoma, Non-Hodgkin / pathology. Male. Middle Aged. Retrospective Studies. Young Adult

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  • (PMID = 19954660.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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25. Uphoff CC, Denkmann SA, Steube KG, Drexler HG: Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines. J Biomed Biotechnol; 2010;2010:904767
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  • [Title] Detection of EBV, HBV, HCV, HIV-1, HTLV-I and -II, and SMRV in human and other primate cell lines.
  • The high prevalence of contaminated cell cultures suggests that viral contaminations might be distributed among cultures.
  • We investigated more than 460 primate cell lines for Epstein-Barr (EBV), hepatitis B (HBV), hepatitis C (HCV), human immunodeficiency virus type 1 (HIV-1), human T-cell leukemia/lymphoma virus I and II (HTLV-I/-II), and squirrel monkey retrovirus (SMRV) infections for risk assessment.
  • None of the cell lines were infected with HCV, HIV-1, or HTLV-I/-II.
  • However, one cell line displayed reverse transcriptase activity.
  • Thirty-nine cell lines harbored EBV DNA sequences.
  • Studies on the lytic phase of EBV revealed that five cell lines produce EBV particles and six further cell lines produced EBV upon stimulation.
  • One cell line contained an integrated HBV genome fragment but showed no virus production.
  • Six cell lines were SMRV-infected.
  • Newly established cell lines should be tested for EBV infections to detect B-lymphoblastoid cell lines (B-LCL).
  • B-LCLs established with EBV from cell line B95-8 should be tested for SMRV infections.
  • [MeSH-major] Primates / virology. Viruses / genetics. Viruses / isolation & purification
  • [MeSH-minor] Animals. Blotting, Southern. Cell Line. DNA, Circular / analysis. HIV-1 / genetics. HIV-1 / isolation & purification. Hepacivirus / genetics. Hepacivirus / isolation & purification. Hepatitis B virus / genetics. Hepatitis B virus / isolation & purification. Herpesvirus 4, Human / genetics. Herpesvirus 4, Human / isolation & purification. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / genetics. Human T-lymphotropic virus 2 / isolation & purification. Humans. In Situ Hybridization, Fluorescence. Polymerase Chain Reaction. Retroviruses, Simian / genetics. Retroviruses, Simian / isolation & purification. Saimiri / virology. Viral Proteins / analysis

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  • (PMID = 20454443.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Circular; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2861168
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26. Hasegawa H, Sawa H, Lewis MJ, Orba Y, Sheehy N, Yamamoto Y, Ichinohe T, Tsunetsugu-Yokota Y, Katano H, Takahashi H, Matsuda J, Sata T, Kurata T, Nagashima K, Hall WW: Thymus-derived leukemia-lymphoma in mice transgenic for the Tax gene of human T-lymphotropic virus type I. Nat Med; 2006 Apr;12(4):466-72
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  • [Title] Thymus-derived leukemia-lymphoma in mice transgenic for the Tax gene of human T-lymphotropic virus type I.
  • Adult T-cell leukemia-lymphoma (ATLL) is a group of T-cell malignancies caused by infection with human T-lymphotropic virus type I (HTLV-I).
  • Although the pathogenesis of ATLL remains incompletely understood, the viral regulatory protein Tax is centrally involved in cellular transformation.
  • Here we describe the generation of HTLV-I Tax transgenic mice using the Lck proximal promoter to restrict transgene expression to developing thymocytes.
  • After prolonged latency periods, transgenic mice developed diffuse large-cell lymphomas and leukemia with clinical, pathological and immunological features characteristic of acute ATLL.
  • Fulminant disease also developed rapidly in SCID mice after engraftment of lymphomatous cells from transgenic mice.
  • This phenotype is indicative of a thymus-derived pre-T-cell phenotype, and disease development was associated with the constitutive activation of NF-kappaB.
  • Our model accurately reproduces human disease and will provide a tool for analysis of the molecular events in transformation and for the development of new therapeutics.
  • [MeSH-major] Genes, pX. Human T-lymphotropic virus 1 / genetics. Leukemia, Lymphoid / pathology. Thymus Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, CD3 / immunology. Antigens, CD3 / metabolism. Biomarkers. Chromosome Mapping. Chromosomes. Disease Models, Animal. Electrophoretic Mobility Shift Assay. Flow Cytometry. Fluorescent Antibody Technique, Indirect. Humans. Immunohistochemistry. Mice. Mice, Inbred C57BL. Mice, SCID. Mice, Transgenic. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction. Transgenes. Transplantation, Homologous


27. Hartmann EM, Rosenwald A: Gene expression signatures of adult T-cell leukemia: is treatment response prediction on the horizon? Leuk Lymphoma; 2010 Jul;51(7):1157-8
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  • [Title] Gene expression signatures of adult T-cell leukemia: is treatment response prediction on the horizon?
  • [MeSH-major] Antiviral Agents / therapeutic use. Biomarkers, Tumor / genetics. Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adult. Humans. Treatment Outcome

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  • [CommentOn] Leuk Lymphoma. 2010 Jul;51(7):1200-16 [20370541.001]
  • (PMID = 20388057.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Biomarkers, Tumor
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28. O'Neil J, Tchinda J, Gutierrez A, Moreau L, Maser RS, Wong KK, Li W, McKenna K, Liu XS, Feng B, Neuberg D, Silverman L, DeAngelo DJ, Kutok JL, Rothstein R, DePinho RA, Chin L, Lee C, Look AT: Alu elements mediate MYB gene tandem duplication in human T-ALL. J Exp Med; 2007 Dec 24;204(13):3059-66
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  • [Title] Alu elements mediate MYB gene tandem duplication in human T-ALL.
  • Recent studies have demonstrated that the MYB oncogene is frequently duplicated in human T cell acute lymphoblastic leukemia (T-ALL).
  • We find that the human MYB locus is flanked by 257-bp Alu repeats and that the duplication is mediated somatically by homologous recombination between the flanking Alu elements on sister chromatids.
  • We conclude that Alu-mediated MYB tandem duplication occurs at low frequency during normal thymocyte development and is clonally selected during the molecular pathogenesis of human T-ALL.

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  • (PMID = 18070937.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE7615
  • [Grant] United States / NCI NIH HHS / CA / P01 CA109901; United States / NIGMS NIH HHS / GM / R37 GM050237; United States / NCI NIH HHS / CA / CA11560; United States / NIGMS NIH HHS / GM / GM067055; United States / NIGMS NIH HHS / GM / R01 GM067055; United States / NIGMS NIH HHS / GM / R01 GM050237; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / R21 CA115853; United States / NIGMS NIH HHS / GM / GM050237; United States / NCI NIH HHS / CA / CA115853; United States / NCI NIH HHS / CA / CA68484-11; United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / CA109901
  • [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 / Proto-Oncogene Proteins c-myb
  • [Other-IDs] NLM/ PMC2150982
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29. Aref S, Mabed M, El-Sherbiny M, Selim T, Metwaly A: Cyclin D1 expression in acute leukemia. Hematology; 2006 Feb;11(1):31-4
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  • [Title] Cyclin D1 expression in acute leukemia.
  • BACKGROUND: Disorders of the cell cycle regulatory machinery play a key role in the pathogenesis of cancer.
  • Over expression of cyclin D1 protein has been reported in several solid tumors and certain lymphoid malignancies, but little is known about the involvement of cyclin D1 in acute leukemia.
  • PATIENTS AND METHODS: In this study, we analyzed the expression of cyclin D1 at protein level in, 40 newly diagnosed patients with acute myeloid leukemia (AML), 10 patients with acute lymphoblastic leukemia (ALL), and 11 normal controls using flow cytometry.
  • The ALL cases with cyclin D1 over expression were significantly correlated to blast cell counts in the peripheral blood and bone marrow (BM) but not with hemoglobin level, WBC, and platelets count.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Cyclin D1 / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood
  • [MeSH-minor] Adult. Bone Marrow / metabolism. Bone Marrow / pathology. Female. Humans. Male. Middle Aged

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  • (PMID = 16522546.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 136601-57-5 / Cyclin D1
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30. Peloponese JM, Yeung ML, Jeang KT: Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation. Immunol Res; 2006;34(1):1-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of nuclear factor-kappaB by human T cell leukemia virus type 1 Tax protein: implications for oncogenesis and inflammation.
  • Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM).
  • HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses.
  • [MeSH-major] Cell Transformation, Neoplastic / immunology. Gene Products, tax / immunology. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Inflammation / immunology. NF-kappa B / immunology

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  • (PMID = 16720895.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B
  • [Number-of-references] 102
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31. Sargent JT, Smith OP: Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders. Br J Haematol; 2010 May;149(4):465-77
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  • Hypercalcaemia is a common metabolic complication of malignant disease often requiring emergency intervention.
  • Although it is more frequently associated with solid tumours, malignancy-associated hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.
  • Its association with myeloma and adult T-cell leukaemia/lymphoma is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.
  • Haematologists need to be familiar with the clinical manifestations of, the differential diagnosis to be considered and the most effective management strategies that are currently available for MAH.
  • [MeSH-minor] Adult. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans

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  • (PMID = 20377591.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 96
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32. Miyano-Kurosaki N, Kira J, Barnor JS, Maeda N, Misawa N, Kawano Y, Tanaka Y, Yamamoto N, Koyanagi Y: Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients. Microbiol Immunol; 2007;51(2):235-42
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  • [Title] Autonomous proliferation of HTLV-CD4+ T cell clones derived from human T cell leukemia virus type I (HTLV-I)-associated myelopathy patients.
  • That HTLV-I infects CD4(+) T cells and enhances their cell growth has been shown as successful long-term in vitro proliferation in the presence of IL-2.
  • It is known that T cells isolated from HAM patients possess strong ability for cell proliferation in vitro and mRNA of various cytokines are abundantly expressed in CNS tissues of HAM patients.
  • In this study, we examined the relationship between cell proliferation and ability of in vitro cytokine production of CD4(+) T cell clones isolated from HAM patients.
  • We started a culture from a single cell to isolate cell clones immediately after drawing blood from the patients using limiting dilution method, which could allow the cell to avoid in vitro HTLV-I infection after initiation of culture.
  • Many cell clones were obtained and the rate of proliferation efficiency from a single cell was as high as 80%, especially in the 4 weeks' culture cells from HAM patients.
  • Our results indicate that the ability of cell proliferation in HAM patients is not restricted in HTLV-I-infected T cells.
  • HTLV-Iuninfected CD4(+) T cells, mainly Th0 cells, also have a strong ability to respond to IL-2-stimulation, showing that unusual immune activation on T cells has been observed in HAM patients.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / immunology. Paraparesis, Tropical Spastic / immunology
  • [MeSH-minor] Adult. Aged. Clone Cells. Cytokines / genetics. Cytokines / immunology. DNA, Viral / chemistry. DNA, Viral / genetics. Female. Humans. Lymphocyte Activation. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Antigen, T-Cell / immunology

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  • (PMID = 17310092.001).
  • [ISSN] 0385-5600
  • [Journal-full-title] Microbiology and immunology
  • [ISO-abbreviation] Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA, Viral; 0 / Receptors, Antigen, T-Cell
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33. Du JW, Gu JY, Liu J, Cen XN, Zhang Y, Ou Y, Chu B, Zhu P: TCR spectratyping revealed T lymphocytes associated with graft-versus-host disease after allogeneic hematopoietic stem cell transplantation. Leuk Lymphoma; 2007 Aug;48(8):1618-27
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  • [Title] TCR spectratyping revealed T lymphocytes associated with graft-versus-host disease after allogeneic hematopoietic stem cell transplantation.
  • Clonal expansion of T cells after allogeneic hematopoietic stem cell transplantation (allo-HSCT) has been observed, but their characteristics remain to be fully elucidated.
  • We report here that CD8(+) T cells were the dominant T lymphocytes seen and T-cell repertoire diversity decreased dramatically during the first 3 months after allo-HSCT.
  • Patients with GVHD grade II - IV had significantly lower T-cell repertoire diversity compared with non-GVHD patients.
  • These findings suggest that TCR spectratyping is helpful for revealing GVHD-related T cells and may have utility in early diagnosis.
  • [MeSH-major] Graft vs Host Disease / diagnosis. Hematopoietic Stem Cell Transplantation. Receptors, Antigen, T-Cell / metabolism. T-Lymphocytes / immunology. Transplantation, Homologous
  • [MeSH-minor] Adolescent. Adult. Amino Acid Motifs. CD8-Positive T-Lymphocytes. Child. Complementarity Determining Regions / analysis. DNA Primers / chemistry. Female. Graft vs Leukemia Effect / immunology. Humans. Immunoglobulin Variable Region. Leukemia / therapy. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 17701594.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / DNA Primers; 0 / Immunoglobulin Variable Region; 0 / Receptors, Antigen, T-Cell
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34. Jiao Y, Zhang W, Liu J, Ni W, Xu W, Jin J, Qian W: Telomere attrition and chromosome instability via downregulation of TRF2 contributes to arsenic trioxide-induced apoptosis of human T-Cell leukemia cell line molt-4 cells. Cancer Biol Ther; 2007 Aug;6(8):1186-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomere attrition and chromosome instability via downregulation of TRF2 contributes to arsenic trioxide-induced apoptosis of human T-Cell leukemia cell line molt-4 cells.
  • Overexpression of human telomere repeat binding factor 2 (TRF2), which may play an important role in the fate of cancer cells, has been observed in adult T-cell leukemia.
  • In this study, we demonstrated that arsenic trioxide (As2O3) induced in vitro growth inhibition and/or apoptosis of human T-cell leukemia cell line Molt-4 in a caspase-independent manner.
  • Telomerase activity was not inhibited, although the level of the reverse transcriptase subunit of the human telomerase gene (hTERT) mRNA expression was down regulated during the early times and then recovered to the level found in untreated controls about 48 hours after treatment with As2O3.
  • Inc ontrast, the alteration of telomere length did not occur after exposure to higher concentration of As2O3 (10 microM) for 24 hours and 48 hours, respectively, suggesting that the shortening of telomeres induced by As2O3 is dependent of a series of cell division cycles.
  • Chromosomal analysis showed that As2O3 exposure caused chromosomal end-to-end fusion in human T-cell leukemia cells while downregulation of TRF2 was observed.
  • Finally, the inhibition of TRF2 protein expression and the sensitivity to As2O3 in a panel of leukemia cell lines were checked.
  • The data revealed that inhibition of TRF2 rendered leukemia cells more susceptible to As2O3.
  • In conclusion, the downregulation of TRF2 by As2O3 contribute to chromosomal end-to-end fusion, and apoptosis in leukemia cells, suggesting that TRF2 could be an attractive target for new therapies of leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Chromosomal Instability. Leukemia-Lymphoma, Adult T-Cell / metabolism. Oxides / pharmacology. Telomere / drug effects. Telomeric Repeat Binding Protein 2 / antagonists & inhibitors
  • [MeSH-minor] Apoptosis. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Telomerase / antagonists & inhibitors. Telomerase / genetics. Telomerase / metabolism

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  • (PMID = 17643074.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Telomeric Repeat Binding Protein 2; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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35. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study. Blood; 2009 Apr 23;113(17):3918-24
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  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Adult. Genotype. Humans. Mutation / genetics. Phenotype. Prognosis. Societies, Medical. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 19109228.001).
  • [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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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41. Toulza F, Nosaka K, Takiguchi M, Pagliuca T, Mitsuya H, Tanaka Y, Taylor GP, Bangham CR: FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia. Int J Cancer; 2009 Nov 15;125(10):2375-82
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  • [Title] FoxP3+ regulatory T cells are distinct from leukemia cells in HTLV-1-associated adult T-cell leukemia.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATLL).
  • It has been postulated that ATLL cells might act as regulatory T cells (T(regs)) which, in common with ATLL cells, express both CD25 and FoxP3, and so contribute to the severe immune suppression typical of ATLL.
  • We report here that the frequency of CD25(+) cells varied independently of the frequency of FoxP3(+) cells in both a cross-sectional study and in a longitudinal study of 2 patients with chronic ATLL.
  • Furthermore, the capacity of ATLL cells to suppress proliferation of heterologous CD4(+)CD25(-) cells correlated with the frequency of CD4(+) FoxP3(+) cells but was independent of CD25 expression.
  • Finally, the frequency of CD4(+)FoxP3(+) cells was inversely correlated with the lytic activity of HTLV-1-specific CTLs in patients with ATLL.
  • We conclude that ATLL is not a tumor of FoxP3(+) regulatory T cells, and that a population of FoxP3(+) cells distinct from ATLL cells has regulatory functions and may impair the cell-mediated immune response to HTLV-1 in patients with ATLL.
  • [MeSH-major] Forkhead Transcription Factors / metabolism. HTLV-I Infections / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD4-Positive T-Lymphocytes / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Cell Proliferation. Chronic Disease. Female. Flow Cytometry. Follow-Up Studies. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate

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  • (PMID = 19544530.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
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42. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • RESULTS: As assessed by serial section staining, 2D7(+) cells were found to co-express myeloperoxidase, histidine decarboxylase, CD9, and CD43, but did not express B cell or T cell restricted antigens.
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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43. Paulsson K, Jonson T, Ora I, Olofsson T, Panagopoulos I, Johansson B: Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemias. Br J Haematol; 2007 Jul;138(2):196-201
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  • [Title] Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemias.
  • The t(1;19)(q23;p13), one of the most common translocations in childhood and adult acute lymphoblastic leukaemias (ALLs), usually results in fusion of exons 1-16 of TCF3 (previously E2A) and exons 3-9 of PBX1.
  • However, some t(1;19)-positive ALLs are negative for this chimaera.
  • We here report an alternative TCF3/PBX1 transcript, fusing exon 17 of TCF3 with exon 5 of PBX1, in a paediatric t(1;19)-positive ALL.
  • Hence, ALLs with t(1;19) that test negative for TCF3/PBX1 should be analysed further before excluding this alternative fusion.
  • Furthermore, we have characterised the genomic translocation breakpoints in eight TCF3/PBX1-positive ALLs; four cases with a balanced t(1;19) and four with an unbalanced der(19)t(1;19).
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. DNA-Binding Proteins / genetics. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Child. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 19 / genetics. Exons / genetics. Gene Rearrangement / genetics. Humans. Male. Oncogene Proteins, Fusion / genetics. RNA, Messenger / genetics. RNA, Neoplasm / genetics

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  • (PMID = 17593026.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TCF3 protein, human; 0 / pbx1 protein, human
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44. Lagacé-Wiens PR, Harding GK: A Canadian immigrant with coinfection of Strongyloides stercoralis and human T-lymphotropic virus 1. CMAJ; 2007 Aug 28;177(5):451-3
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  • [Title] A Canadian immigrant with coinfection of Strongyloides stercoralis and human T-lymphotropic virus 1.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / complications. Strongyloides stercoralis / isolation & purification. Strongyloidiasis / complications
  • [MeSH-minor] Animals. Diagnosis, Differential. Emigration and Immigration. Fatal Outcome. Humans. Male. Manitoba. Middle Aged. United States Virgin Islands

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  • [Cites] Clin Microbiol Rev. 2004 Jan;17(1):208-17 [14726461.001]
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  • (PMID = 17724322.001).
  • [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/ PMC1950173
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45. Kawano N, Shimoda K, Ishikawa F, Taketomi A, Yoshizumi T, Shimoda S, Yoshida S, Uozumi K, Suzuki S, Maehara Y, Harada M: Adult T-cell leukemia development from a human T-cell leukemia virus type I carrier after a living-donor liver transplantation. Transplantation; 2006 Sep 27;82(6):840-3
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  • [Title] Adult T-cell leukemia development from a human T-cell leukemia virus type I carrier after a living-donor liver transplantation.
  • Adult T-cell leukemia (ATL) develops in a human T-cell leukemia virus type I (HTLV-I) carrier.
  • We describe the development of three cases of ATL in eight HTLV-I carriers within 164 living-donor liver transplant recipients undergoing immunosuppressive treatment.
  • Acute-type ATL was diagnosed at 6, 9, and 25 months after living-donor liver transplantation, based on increased numbers of CD4+25+ lymphocytes exhibiting "flower-like" nuclei, and the elevation of lactate dehydrogenase.
  • Southern blot analysis demonstrated the clonal proliferation of ATL cells in peripheral blood.
  • The ATL cells originated from the recipient, as demonstrated by fluorescence in situ hybridization analysis using sex chromosomal markers.
  • Our observations suggest that immunosuppressive treatment for the prevention of graft rejection after living-donor liver transplantation may induce the development of ATL in an HTLV-I carrier.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / virology. Liver Transplantation / adverse effects. Living Donors
  • [MeSH-minor] Adult. Aged. Carrier State. Cell Division. Female. Humans. Male. Middle Aged


46. Bacigalupo A, Lamparelli T, Gualandi F, Occhini D, Bregante S, Raiola AM, Ibatici A, di Grazia C, Dominietto A, Piaggio G, Podesta M, Bruno B, Lombardi A, Frassoni F, Viscoli C, Sacchi N, Van Lint MT: Allogeneic hemopoietic stem cell transplants for patients with relapsed acute leukemia: long-term outcome. Bone Marrow Transplant; 2007 Mar;39(6):341-6
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  • [Title] Allogeneic hemopoietic stem cell transplants for patients with relapsed acute leukemia: long-term outcome.
  • We assessed the long-term outcome of patients with relapsed acute myeloid (n=86) or acute lymphoid leukemia (n=66), undergoing an allogeneic hemopoietic stem cell transplantation in our unit.
  • Twenty-two patients (15%) survive disease free, with a median follow-up of 14 years: 18 are off medications.
  • In multivariate analysis of survival, favorable predictors were chronic graft-versus-host disease (GvHD) (P=0.0003), donor other than family mismatched (P=0.02), donor age less than 34 years (P=0.02) and blast count less than 30% (P=0.07).
  • This study confirms that a fraction of relapsed leukemias is cured with an allogeneic transplant: selection of patients with a blast count <30%, identification of young, human leukocyte antigen-matched donors and the use of total body radiation may significantly improve the outcome.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Bone Marrow Examination. Child. Female. Follow-Up Studies. Graft Survival. Graft vs Host Disease. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Patient Selection. Prognosis. Survivors. Transplantation, Homologous

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  • (PMID = 17277788.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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47. Giebel S, Dziaczkowska J, Wysoczanska B, Wojnar J, Krawczyk-Kulis M, Lange A, Holowiecki J: Lymphocyte reconstitution after allogeneic bone marrow transplantation in a previously thymectomized patient--no evidence of extrathymic T-cell maturation. Bone Marrow Transplant; 2007 Oct;40(7):705-6
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  • [Title] Lymphocyte reconstitution after allogeneic bone marrow transplantation in a previously thymectomized patient--no evidence of extrathymic T-cell maturation.
  • [MeSH-minor] Adult. Graft vs Host Disease / immunology. Graft vs Host Disease / prevention & control. Humans. Immunosuppressive Agents / therapeutic use. Lymphocyte Activation. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Thymectomy. Thymoma / surgery. Thymus Gland / immunology. Thymus Neoplasms / surgery. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17680024.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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48. Tözsér J, Weber IT: The protease of human T-cell leukemia virus type-1 is a potential therapeutic target. Curr Pharm Des; 2007;13(12):1285-94
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  • [Title] The protease of human T-cell leukemia virus type-1 is a potential therapeutic target.
  • Human T-cell leukemia virus type-1 (HTLV-1) is associated with a number of human diseases.
  • Although the mechanism by which the virus causes diseases is still not known, studies indicate that viral replication is critical for the development of HTLV-1 associated myelopathy, and initial studies suggested that blocking replication with reverse transcriptase inhibitors had a therapeutic effect.
  • Therefore, based on the success of HIV-1 protease inhibitors, the HTLV-1 protease is also a potential target for chemotherapy.
  • Furthermore, mutated residues in HIV-1 protease that confer drug resistance are frequently seen in equivalent positions of other retroviral proteases, like HTLV-1 protease.
  • Therefore, comparison of HTLV-1 and HIV-1 proteases is expected to aid the rational design of broad spectrum inhibitors effective against various retroviral proteases, including the mutant HIV-1 enzymes appearing in drug resistance.
  • This review describes the characteristics of HTLV-1 protease, makes comparison with HIV-1 protease, and discusses the status of inhibitor development for the HTLV-1 protease.

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  • (PMID = 17504236.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM062920; United States / NIGMS NIH HHS / GM / GM 062920; United States / FIC NIH HHS / TW / TW01001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protease Inhibitors; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.- / HTLV-1 protease
  • [Number-of-references] 45
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49. Chevallier P, Robillard N, Houille G, Ayari S, Guillaume T, Delaunay J, Harousseau JL, Avet-Loiseau H, Mohty M, Garand R: Simultaneous study of five candidate target antigens (CD20, CD22, CD33, CD52, HER2) for antibody-based immunotherapy in B-ALL: a monocentric study of 44 cases. Leukemia; 2009 Apr;23(4):806-7
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  • [MeSH-major] Antibodies / therapeutic use. Antigens, CD / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunophenotyping. Male. Middle Aged. Young Adult

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  • (PMID = 18971949.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD
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50. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15921375.001).
  • [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 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
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51. Tseliou PM, Spanakis N, Spiliotakara A, Markogiannakis A, Legakis NJ, Tsakris A: Prevalence of infection by HTLV-I/II among pregnant women and high-risk groups in the Peloponnese peninsula, Greece. Int J STD AIDS; 2006 Aug;17(8):543-6
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  • [Title] Prevalence of infection by HTLV-I/II among pregnant women and high-risk groups in the Peloponnese peninsula, Greece.
  • Although screening for human T-cell lymphotropic virus types I and II (HTLV-I/II) antibodies in volunteer blood donors has been systematic in Greece since 1995, the epidemiology and the determinants of HTLV-I/II infection are not well defined among population groups.
  • During 1997-2005, the prevalence of HTLV-I/II infection was investigated in a sample of 2016 pregnant women, 102 multitransfused haematologic and oncologic patients, 93 thalassaemic patients and 57 intravenous drug users originating from four geographic areas of Pelopennese peninsula, Greece.
  • One recipient of HTLV-I infected blood and the relatives of a woman died from adult T-cell leukaemia/lymphoma (ATTL) related to HTLV-I have also been tested.
  • The subjects were initially screened by an enzyme immunoassay whereas Western blot, INNO-LIA HTLV, polymerase chain reaction and nucleotide sequencing confirmed the infection.
  • One thalassaemic patient had proved HTLV-I infection giving an overall prevalence of 11 per 1000.
  • In the recipient of the infected blood and in two of the five relatives of the woman died from ATTL, HTLV-I infection was also detected.
  • In none of the pregnant women, multitransfused patients and intravenous drug users HTLV-I/II infection was confirmed.
  • These data suggest that HTLV-I is present in Greece among populations at high-risk.
  • However, they would not support the need for HTLV-I/II antenatal screening in Greece.
  • [MeSH-major] Human T-lymphotropic virus 1. Human T-lymphotropic virus 2. Leukemia, T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Pregnancy Complications, Infectious / epidemiology. Pregnancy Complications, Infectious / virology

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  • (PMID = 16925902.001).
  • [ISSN] 0956-4624
  • [Journal-full-title] International journal of STD & AIDS
  • [ISO-abbreviation] Int J STD AIDS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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52. Meier M, den Boer ML, Meijerink JP, Broekhuis MJ, Passier MM, van Wering ER, Janka-Schaub GE, Pieters R: Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia. Leukemia; 2006 Aug;20(8):1377-84
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  • [Title] Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia.
  • The T-lineage phenotype of childhood acute lymphoblastic leukaemia (ALL) is associated with an increased relapse-risk and in vitro resistance to drugs as compared to a precursor B phenotype.
  • Our results suggest that childhood T-ALL is associated with a high expression of DeltaTA-p73.
  • These isoforms may play a role in cellular resistance to DNA-damaging drugs in children at initial diagnosis of T-ALL.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Cell Lineage. Child. Child, Preschool. DNA Methylation. Drug Resistance, Neoplasm. Genes, Tumor Suppressor. Humans. Infant. Loss of Heterozygosity. Protein Isoforms. RNA, Messenger / analysis. Tumor Suppressor Proteins

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  • (PMID = 16791269.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
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53. Bouaziz JD, Cordel N, Hickman G, Fieschi C, Ortonne N, Bagot M: Cutaneous tumor lysis syndrome in a patient with HTLV-1 adult T-cell lymphoma/leukemia. Blood; 2009 Nov 5;114(19):4320-1
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  • [Title] Cutaneous tumor lysis syndrome in a patient with HTLV-1 adult T-cell lymphoma/leukemia.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Skin Diseases / pathology. Tumor Lysis Syndrome / pathology

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  • (PMID = 19892727.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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54. Chiarini F, Del Sole M, Mongiorgi S, Gaboardi GC, Cappellini A, Mantovani I, Follo MY, McCubrey JA, Martelli AM: The novel Akt inhibitor, perifosine, induces caspase-dependent apoptosis and downregulates P-glycoprotein expression in multidrug-resistant human T-acute leukemia cells by a JNK-dependent mechanism. Leukemia; 2008 Jun;22(6):1106-16
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  • [Title] The novel Akt inhibitor, perifosine, induces caspase-dependent apoptosis and downregulates P-glycoprotein expression in multidrug-resistant human T-acute leukemia cells by a JNK-dependent mechanism.
  • Also, upregulation of the phosphatidylinositol 3-kinase (PI3K)/Akt-signaling pathway is known to play an important role in drug resistance, and has been implicated in the aggressiveness of a number of different cancers, including T-acute lymphoblastic leukemia (T-ALL).
  • We have investigated the therapeutic potential of the novel Akt inhibitor, perifosine (a synthetic alkylphospholipid), on human T-ALL CEM cells (CEM-R), characterized by both overexpression of P-gp and constitutive upregulation of the PI3K/Akt network.
  • [MeSH-major] Apoptosis / drug effects. Caspases / metabolism. JNK Mitogen-Activated Protein Kinases / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. P-Glycoprotein / metabolism. Phosphorylcholine / analogs & derivatives. Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. BH3 Interacting Domain Death Agonist Protein / metabolism. Blotting, Western. Cell Survival / drug effects. Cytochromes c / metabolism. Down-Regulation. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Electrophoretic Mobility Shift Assay. Enzyme Activation. Flow Cytometry. Humans. Immunoenzyme Techniques. Membrane Microdomains / metabolism. Mitochondria / drug effects. Mitochondria / metabolism. Phosphatidylinositol 3-Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Vinblastine / pharmacology

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  • (PMID = 18385752.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA090125
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 107-73-3 / Phosphorylcholine; 2GWV496552 / perifosine; 5V9KLZ54CY / Vinblastine; 9007-43-6 / Cytochromes c; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
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55. Van Vlierberghe P, Meijerink JP, Stam RW, van der Smissen W, van Wering ER, Beverloo HB, Pieters R: Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias. Blood; 2005 Dec 15;106(13):4414-5
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  • [Title] Activating FLT3 mutations in CD4+/CD8- pediatric T-cell acute lymphoblastic leukemias.
  • [MeSH-major] CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / metabolism. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [CommentOn] Blood. 2004 Jul 15;104(2):558-60 [15044257.001]
  • (PMID = 16326981.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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56. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
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  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • We investigated the expression of HTLV-I antigens in fresh ATL cells by using both in vitro and in vivo assays.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Concomitantly with HTLV-I-expression, these ATL cells expressed co-stimulatory molecules such as CD80, CD86 and OX40, and showed elevated levels of antigenicity against allogeneic T cells and HTLV-I Tax-specific cytotoxic T-lymphocytes (CTL).
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [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 / DNA Primers
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57. Ikezoe T, Yang Y, Bandobashi K, Saito T, Takemoto S, Machida H, Togitani K, Koeffler HP, Taguchi H: Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways. Mol Cancer Ther; 2005 Apr;4(4):578-86
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  • This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.
  • Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin's lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.
  • Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.
  • [MeSH-major] Cell Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western. Cell Line. Cell Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells. Leukemia / drug therapy. Leukemia / pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein

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  • (PMID = 15827331.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine
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58. Aiello A, Fattorusso E, Luciano P, Menna M, Calzado MA, Muñoz E, Bonadies F, Guiso M, Sanasi MF, Cocco G, Nicoletti R: Synthesis of structurally simplified analogues of aplidinone A, a pro-apoptotic marine thiazinoquinone. Bioorg Med Chem; 2010 Jan 15;18(2):719-27
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  • The study evidenced one of the synthetic analogues (11) as a potent cytotoxic and pro-apoptotic agent against several tumor cell lines which also inhibits the TNFalpha-induced NF-kappaB activation in a human leukemia T cell line.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Computer Simulation. Drug Screening Assays, Antitumor. Humans. Molecular Structure. NF-kappa B / metabolism. Structure-Activity Relationship. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / pharmacology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20031419.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha; 0 / aplidinone A
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59. 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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  • [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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  • (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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60. Gillet N, Florins A, Boxus M, Burteau C, Nigro A, Vandermeers F, Balon H, Bouzar AB, Defoiche J, Burny A, Reichert M, Kettmann R, Willems L: Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human. Retrovirology; 2007;4:18
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  • [Title] Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.
  • In 1871, the observation of yellowish nodules in the enlarged spleen of a cow was considered to be the first reported case of bovine leukemia.
  • The etiological agent of this lymphoproliferative disease, bovine leukemia virus (BLV), belongs to the deltaretrovirus genus which also includes the related human T-lymphotropic virus type 1 (HTLV-1).
  • Recently, the BLV model has also cast light onto novel prospects for therapies of HTLV induced diseases, for which no satisfactory treatment exists so far.
  • [MeSH-major] Anti-Retroviral Agents / therapeutic use. Disease Models, Animal. Enzootic Bovine Leukosis / drug therapy. Leukemia Virus, Bovine / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sheep Diseases / drug therapy
  • [MeSH-minor] Animals. B-Lymphocytes / pathology. B-Lymphocytes / physiology. B-Lymphocytes / virology. Cattle. Cytokines / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Humans. Leukocytes, Mononuclear / pathology. Leukocytes, Mononuclear / physiology. Leukocytes, Mononuclear / virology. Sheep. Viral Proteins / genetics. Viral Proteins / metabolism

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  • (PMID = 17362524.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Retroviral Agents; 0 / Cytokines; 0 / Viral Proteins
  • [Number-of-references] 358
  • [Other-IDs] NLM/ PMC1839114
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61. Hieshima K, Nagakubo D, Nakayama T, Shirakawa AK, Jin Z, Yoshie O: Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells. J Immunol; 2008 Jan 15;180(2):931-9
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  • [Title] Tax-inducible production of CC chemokine ligand 22 by human T cell leukemia virus type 1 (HTLV-1)-infected T cells promotes preferential transmission of HTLV-1 to CCR4-expressing CD4+ T cells.
  • Adult T cell leukemia is a mature CD4+ T cell malignancy which predominantly expresses CCR4 and is etiologically associated with human T cell leukemia virus type 1 (HTLV-1).
  • Because HTLV-1 transmission depends on close cell-cell contacts, HTLV-1-infected T cells may preferentially interact with CCR4+CD4+ T cells for efficient viral transmission.
  • In terms of gene expression and protein secretion, we found a strong correlation between HTLV-1 Tax oncoprotein and CCL22, a CCR4 ligand, in HTLV-1-infected T cells.
  • Transient Tax expression in an HTLV-1-negative T cell line activated the CCL22 promoter and induced CCL22.
  • In chemotaxis assays, the culture supernatants of HTLV-1-infected T cells selectively attracted CCR4+CD4+ T cells in PBMCs.
  • Finally, anti-CCL22 Ab treatment also blocked HTLV-1 transmission to primary CD4+ T cells in coculture experiments with HTLV-1 producer cells.
  • Thus, HTLV-1-infected T cells produce CCL22 through Tax and selectively interact with CCR4+CD4+ T cells, resulting in preferential transmission of HTLV-1 to CCR4+CD4+ T cells.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Chemokine CCL22 / genetics. Gene Expression Regulation, Viral. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / physiology. Virus Internalization
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Adhesion / genetics. Cell Line. Humans. Pertussis Toxin / pharmacology. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Receptors, CCR4 / antagonists & inhibitors. Receptors, CCR4 / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / virology

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

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  • (PMID = 15761473.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 100730; United States / FIC NIH HHS / TW / TW005705-03; United States / FIC NIH HHS / TW / TW 05705; United States / FIC NIH HHS / TW / R03 TW005705; United States / FIC NIH HHS / TW / R03 TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-01A1; United States / FIC NIH HHS / TW / TW005705-02; United States / FIC NIH HHS / TW / R03 TW005705-03; United States / FIC NIH HHS / TW / R03 TW005705-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Retroviridae Proteins; 0 / rof protein, Human T-lymphotropic virus 1; 0 / tof protein, Human T-lymphotropic virus 1; SY7Q814VUP / Calcium
  • [Number-of-references] 84
  • [Other-IDs] NLM/ NIHMS183534; NLM/ PMC3057663
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63. Zubair AC, Rymer R, Young J, Keeton U, Befort R, Nolot B, Evans C, Bleach T, Torloni A: Multiple myeloma patients receiving large volume leukapheresis efficiently yield enough CD34+ cells to allow double transplants. J Clin Apher; 2009;24(1):6-11
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  • The median total CD34+ cell yield/kg was 6.4 x 10(6) for LVL and 5.2 x 10(6) for SVL.
  • Because the target CD34+ cell dose for a single transplant was 3 x 10(6)/kg at our institution, overall the LVL yields enough CD34+ cells that could allow for two transplants.
  • Because of the reserved cells for a second transplant, LVL patients received significantly less CD34+ cell/kg per transplant than the patients in SVL group (P = <0.001).

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
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  • (PMID = 19156756.001).
  • [ISSN] 1098-1101
  • [Journal-full-title] Journal of clinical apheresis
  • [ISO-abbreviation] J Clin Apher
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102824-05; United States / NCI NIH HHS / CA / K23 CA102824; United States / NCI NIH HHS / CA / CA102824; United States / NCI NIH HHS / CA / K23 CA102824-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Other-IDs] NLM/ NIHMS101366; NLM/ PMC2678026
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64. Lyell V, Khatamzas E, Allain T: Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report. J Med Case Rep; 2007;1:56
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  • [Title] Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
  • Human T cell lymphotrophic virus type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.
  • Although there is a long latency, carriers have a 1-5% chance of developing adult T cell leukaemia/lymphoma, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.
  • We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have lymphoma and was positive for HTLV-1.

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  • (PMID = 17651486.001).
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65. Sugita K, Shimauchi T, Kabashima R, Nakashima D, Hino R, Kabashima K, Nakamura M, Tokura Y: Loss of tumor cell CCR4 expression upon leukemic change in adult T-cell leukemia/lymphoma. J Am Acad Dermatol; 2009 Jul;61(1):163-4
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  • [Title] Loss of tumor cell CCR4 expression upon leukemic change in adult T-cell leukemia/lymphoma.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / metabolism. Receptors, CCR4 / biosynthesis
  • [MeSH-minor] Aged. Fatal Outcome. Gene Expression. Humans. Leukemia / pathology. Male. Skin Neoplasms / pathology

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  • (PMID = 19539864.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Receptors, CCR4
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66. Ratner L, Harrington W, Feng X, Grant C, Jacobson S, Noy A, Sparano J, Lee J, Ambinder R, Campbell N, Lairmore M, AIDS Malignancy Consortium: Human T cell leukemia virus reactivation with progression of adult T-cell leukemia-lymphoma. PLoS One; 2009;4(2):e4420
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  • [Title] Human T cell leukemia virus reactivation with progression of adult T-cell leukemia-lymphoma.
  • BACKGROUND: Human T-cell leukemia virus-associated adult T-cell leukemia-lymphoma (ATLL) has a very poor prognosis, despite trials of a variety of different treatment regimens.
  • Virus expression has been reported to be limited or absent when ATLL is diagnosed, and this has suggested that secondary genetic or epigenetic changes are important in disease pathogenesis.
  • METHODS AND FINDINGS: We prospectively investigated combination chemotherapy followed by antiretroviral therapy for this disorder.
  • Nineteen patients were prospectively enrolled between 2002 and 2006 at five medical centers in a phase II clinical trial of infusional chemotherapy with etoposide, doxorubicin, and vincristine, daily prednisone, and bolus cyclophosphamide (EPOCH) given for two to six cycles until maximal clinical response, and followed by antiviral therapy with daily zidovudine, lamivudine, and alpha interferon-2a for up to one year.
  • Seven patients were on study for less than one month due to progressive disease or chemotherapy toxicity.
  • During chemotherapy induction, viral RNA expression increased (median 190-fold), and virus replication occurred, coincident with development of disease progression.
  • CONCLUSIONS: EPOCH chemotherapy followed by antiretroviral therapy is an active therapeutic regimen for adult T-cell leukemia-lymphoma, but viral reactivation during induction chemotherapy may contribute to treatment failure.
  • Alternative therapies are sorely needed in this disease that simultaneously prevent virus expression, and are cytocidal for malignant cells.
  • [MeSH-major] Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Virus Activation
  • [MeSH-minor] Adult. Antiviral Agents / pharmacology. Antiviral Agents / therapeutic use. DNA-Directed RNA Polymerases / metabolism. Disease Progression. Disease-Free Survival. Humans. Middle Aged. RNA, Viral / metabolism. Time Factors. Treatment Outcome

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  • (PMID = 19204798.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00041327
  • [Grant] United States / NCI NIH HHS / CA / U01 CA070058; United States / NCI NIH HHS / CA / U01 CA070019; United States / NCI NIH HHS / CA / U01 CA083038; United States / NCI NIH HHS / CA / U01 CA071375; United States / NCI NIH HHS / CA / U01 CA070054; United States / NCI NIH HHS / CA / CA10521; United States / NCI NIH HHS / CA / U01 CA070062; United States / NCI NIH HHS / CA / P01 CA100730-07
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / RNA, Viral; EC 2.7.7.6 / DNA-Directed RNA Polymerases
  • [Other-IDs] NLM/ PMC2636875
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67. De Braekeleer E, Douet-Guilbert N, Morel F, Le Bris MJ, Basinko A, Berthou C, Morice P, Férec C, De Braekeleer M: Philadelphia chromosome-positive acute lymphoblastic leukemia: a cytogenetic study of 33 patients diagnosed between 1981 and 2008. Anticancer Res; 2010 Feb;30(2):569-73
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  • [Title] Philadelphia chromosome-positive acute lymphoblastic leukemia: a cytogenetic study of 33 patients diagnosed between 1981 and 2008.
  • BACKGROUND: The Philadelphia (Ph) chromosome, resulting from a t(9;22)(q34;q11), is one of the most frequent chromosomal abnormalities observed among patients with acute lymphoblastic leukemia (ALL).
  • Main of study: To analyze the distribution of Ph chromosome-positive ALL patients.
  • PATIENTS AND METHODS: Conventional cytogenetic analysis was performed on bone marrow cells at the time of diagnosis and/or relapse of 208 patients shown to have B-cell ALL.
  • RESULTS: Thirty-three Ph chromosome-positive ALL patients were identified between 1981 and 2008.
  • CONCLUSION: Ph chromosome-positive ALL patients show cytogenetic characteristics that differ from those of other ALL patients.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, B-Cell / diagnosis. Leukemia, B-Cell / genetics. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Survival Rate. Time Factors. Translocation, Genetic. Treatment Outcome. Young Adult

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  • (PMID = 20332472.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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68. Schlecht-Louf G, Renard M, Mangeney M, Letzelter C, Richaud A, Ducos B, Bouallaga I, Heidmann T: Retroviral infection in vivo requires an immune escape virulence factor encrypted in the envelope protein of oncoretroviruses. Proc Natl Acad Sci U S A; 2010 Feb 23;107(8):3782-7
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  • Here, we genetically "switched off' the envelope-mediated immunosuppression of an infectious retrovirus, the Friend murine leukemia virus, while preserving mutant envelope infectivity both ex vivo and in vivo, thus allowing us to test the functional importance of envelope-mediated immunosuppression in retrovirus physiology.
  • Remarkably, we show, in vivo, that the non-IS mutant virus displays the same propagation kinetics as its WT counterpart in irradiated immunocompromised mice but that it is rapidly and totally cleared from normal immunocompetent mice, which become fully protected against a challenge with the WT retrovirus.
  • Using cell depletion strategies, we further establish that envelope-mediated immunosuppression enables the retrovirus to escape innate (natural killer cells) and adaptive (CD8 T cells) antiviral effectors.
  • In conclusion, our work demonstrates the critical role of Env-induced immunosuppression for retrovirus propagation in vivo and identifies a unique definite target for antiretroviral therapies and vaccine strategies, also characterized in the human T-cell leukemia virus (HTLV) and xenotropic murine leukemia virus-related virus (XMRV) retroviruses, opening unprecedented prospects for the treatment of retroviral diseases.
  • [MeSH-major] Friend murine leukemia virus / immunology. Immune Tolerance. Leukemia, Experimental / immunology. Retroviridae Infections / immunology. Tumor Virus Infections / immunology. Viral Envelope Proteins / immunology. Virulence Factors / immunology

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  • (PMID = 20142478.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Viral Envelope Proteins; 0 / Viral Vaccines; 0 / Virulence Factors
  • [Other-IDs] NLM/ PMC2840525
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69. Nicot C, Harrod RL, Ciminale V, Franchini G: Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions. Oncogene; 2005 Sep 5;24(39):6026-34
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  • [Title] Human T-cell leukemia/lymphoma virus type 1 nonstructural genes and their functions.
  • The human T-cell leukemia/lymphoma virus (HTLV) genome, in addition to the structural Gag and Env proteins and retroviral enzymes, carries a region at its 3' end originally designated pX.
  • To date, we know that this region encodes two essential transcriptional and post-transcriptional positive regulators of viral expression, the Tax and Rex proteins, respectively (reviewed elsewhere in this issue).
  • [MeSH-major] Human T-lymphotropic virus 1 / genetics. Viral Nonstructural Proteins / genetics

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  • (PMID = 16155609.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI058944; United States / NCI NIH HHS / CA / R01 CA106258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Viral Nonstructural Proteins
  • [Number-of-references] 54
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70. Jiang XJ, Wang JS, Fang Q: [Gene expression of breast cancer resistance protein in adult acute lymphocytic leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Feb;16(1):31-4
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  • [Title] [Gene expression of breast cancer resistance protein in adult acute lymphocytic leukemia and its clinical significance].
  • The objective of this study was to investigate the relationship between the expressions of breast cancer resistance protein (BCRP) gene and drug resistance as well as prognosis in adult patients with acute lymphocytic leukemia (ALL).
  • Semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of BCRP gene in 97 adult patients with acute lymphocytic leukemia (ALL) and 30 normal subjects.
  • BCRP/beta(2)-MG ratio >or= 0.48 was defined as BCRP positive.
  • The results showed that the positive ratio of BCRP gene expression in untreated group was 28.7%, in contrast that in refractory and relapsed patients was 51.2%.
  • The first complete remission rates in patients with negative and positive expression were 71.7% and 29.7% respectively.
  • In immune types the BCRP gene expression of B-ALL was higher than that of T cell type, especially in mature B cell type with obviously statistical significance (p<0.01).
  • It is concluded that the high expression of BCRP gene may induce clinical drug resistance, and may be an unfavorable factor for prognosis in adult patients with acute lymphocytic leukemia.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Drug Resistance, Neoplasm / genetics. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 18315895.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Neoplasm Proteins
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71. Klingebiel T, Cornish J, Labopin M, Locatelli F, Darbyshire P, Handgretinger R, Balduzzi A, Owoc-Lempach J, Fagioli F, Or R, Peters C, Aversa F, Polge E, Dini G, Rocha V, Pediatric Diseases and Acute Leukemia Working Parties of the European Group for Blood and Marrow Transplantation (EBMT): Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group. Blood; 2010 Apr 29;115(17):3437-46
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  • [Title] Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group.
  • T cell-depleted haploidentical hematopoietic stem cell transplantation (haploHSCT) is an option to treat children with very high-risk acute lymphoblastic leukemia (ALL) lacking an HLA-identical donor.
  • The 5-year leukemia-free survival (LFS) was 30%, 34%, 22%, and 0%, respectively.
  • In a multivariate analysis, haploHSCT performed in larger centers (performing > or = 231 allotransplantations in the studied period) was associated with improved LFS rate and decreased RI (adjusted P = .01 and P = .04, respectively), adjusting for different patient-, disease-, and transplant-related factors such as number of previous autotransplantations, cytomegalovirus serology status, type of T-cell depletion, and use of total body irradiation and antithymocyte globulin.
  • In conclusion, higher CD34(+) cell dose and better patient selection may improve outcomes of children with ALL who undergo a haploHSCT.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Hospitals, Pediatric. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Europe. Female. Humans. Infant. Male. Remission Induction. Risk Factors. Survival Rate. Transplantation, Homologous


72. Ernst T, Gruber FX, Pelz-Ackermann O, Maier J, Pfirrmann M, Müller MC, Mikkola I, Porkka K, Niederwieser D, Hochhaus A, Lange T: A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib. Haematologica; 2009 Sep;94(9):1227-35
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  • [Title] A co-operative evaluation of different methods of detecting BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia on second-line dasatinib or nilotinib therapy after failure of imatinib.
  • BACKGROUND: Various techniques have been employed to detect BCR-ABL kinase domain mutations in patients with chronic myeloid leukemia who are resistant to imatinib.
  • This has led to different reported frequencies of mutations and the finding of a heterogeneous pattern of individual mutations.
  • DESIGN AND METHODS: We compared direct sequencing alone and in combination with denaturing high-performance liquid chromatography and two high-sensitivity allele-specific oligonucleotide polymerase chain reaction approaches for analysis of BCR-ABL mutations in 200 blinded cDNA samples prior to and during second-line dasatinib or nilotinib therapy in patients with chronic myeloid leukemia in whom imatinib treatment had failed.
  • The clinical impact of such low-level mutations remains uncertain and requires further investigation.
  • Allele-specific oligonucleotide polymerase chain reaction allows detection of defined mutations at a lower level than does denaturing high performance liquid chromatography combined with direct sequencing and may, therefore, provide clinical benefit by permitting early reconsideration of therapeutic strategies.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Protein Kinase Inhibitors / administration & dosage. Protein-Tyrosine Kinases / genetics. Pyrimidines / administration & dosage. Thiazoles / administration & dosage
  • [MeSH-minor] Adult. Aged. Benzamides. DNA Mutational Analysis. Dasatinib. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Polymerase Chain Reaction. Protein Structure, Tertiary / genetics

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  • (PMID = 19608684.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC2738714
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73. Hara T, Tsurumi H, Goto N, Kanemura N, Yoshikawa T, Kasahara S, Yamada T, Sawada M, Goto H, Fukuno K, Kitagawa J, Yasuda I, Katsumura N, Takemura M, Takahashi T, Takami T, Moriwaki H: Serum soluble Fas level determines clinical outcome of patients with diffuse large B-cell lymphoma treated with CHOP and R-CHOP. J Cancer Res Clin Oncol; 2009 Oct;135(10):1421-8
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  • [Title] Serum soluble Fas level determines clinical outcome of patients with diffuse large B-cell lymphoma treated with CHOP and R-CHOP.
  • INTRODUCTION: We previously reported that serum concentrations of soluble Fas (sFas) predict the clinical outcome of patients with diffuse large B cell lymphoma (DLBCL) after treatment with CHOP but without rituximab (R).
  • [MeSH-major] Antigens, CD95 / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / blood. Lymphoma, Large B-Cell, Diffuse / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prednisone / therapeutic use. Prognosis. Prospective Studies. Rituximab. Treatment Outcome. Vincristine / therapeutic use. Young Adult

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  • (PMID = 19381687.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD95; 0 / FAS protein, human; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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74. Wrzesień-Kuś A, Robak T, Pluta A, Zwolińska M, Wawrzyniak E, Wierzbowska A, Skotnicki A, Jakubas B, Hołowiecki J, Nowak K, Kuliczkowski K, Mazur G, Haus O, Dmoszyńska A, Adamczyk-Cioch M, Jedrzejczak WW, Paluszewska M, Konopka L, Pałynyczko G: Outcome of treatment in adults with Philadelphia chromosome-positive and/or BCR-ABL--positive acute lymphoblastic leukemia-retrospective analysis of Polish Adult Leukemia Group (PALG). Ann Hematol; 2006 Jun;85(6):366-73
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  • [Title] Outcome of treatment in adults with Philadelphia chromosome-positive and/or BCR-ABL--positive acute lymphoblastic leukemia-retrospective analysis of Polish Adult Leukemia Group (PALG).
  • Patients with Philadelphia chromosome-positive (Ph+) and/or BCR-ABL+ acute lymphoblastic leukemia (ALL) have extremely poor prognoses.
  • Most of these patients have additional, heterogenous karyotype abnormalities, the majority of which have uncertain clinical significance.
  • In this study we analyzed the clinical characteristics, karyotype abnormalities, and outcome of 77 patients with Ph+ and/or BCR-ABL+ ALL registered in Poland in 1997-2004.
  • In 31/55 patients with known karyotype, the sole t(9;22)(q34;q11) abnormality had been diagnosed; in one patient, variant translocation t(4;9;22)(q21q31.1;q34;q11), and additional abnormalities in 23 (42%) patients, had been diagnosed.
  • The overall survival (OS) probability of 2 years was 63, 43, and 17% for patients treated with allogeneic stem cell transplantation (alloSCT), autologous SCT, and chemotherapy, respectively (log rank p=0.002).
  • There were no significant differences in CR rate, disease-free survival (DFS), and OS for patients with t(9;22) and additional abnormalities compared with the whole group.
  • Only WBC >20 G/l at diagnosis adversely influenced OS probability (log rank p=0.0017).
  • We have shown that additional karyotype abnormalities did not influence the clinical characteristics of the patients; however, their influence on treatment results needs to be further assessed.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Disease-Free Survival. Female. Hematopoietic Stem Cell Transplantation. Humans. Karyotyping. Male. Methotrexate / administration & dosage. Middle Aged. Poland. Remission Induction. Retrospective Studies. Treatment Outcome

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  • (PMID = 16523310.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; E7WED276I5 / 6-Mercaptopurine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; YL5FZ2Y5U1 / Methotrexate
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75. Talaulikar D, Dahlstrom JE, Shadbolt B, Broomfield A, McDonald A: Role of immunohistochemistry in staging diffuse large B-cell lymphoma (DLBCL). J Histochem Cytochem; 2008 Oct;56(10):893-900
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  • [Title] Role of immunohistochemistry in staging diffuse large B-cell lymphoma (DLBCL).
  • The use of immunohistochemistry (IHC) in staging bone marrow in non-Hodgkin's lymphoma (NHL) is largely limited to ambiguous cases, particularly those with lymphoid aggregates.
  • Its role in routine clinical practice remains unestablished.
  • This study aimed to determine whether the routine use of IHC in diffuse large B-cell lymphoma (DLBCL) would improve the detection of lymphomatous involvement in the bone marrow.
  • It also sought to determine the impact of IHC on predicting survival compared with routine histological diagnosis using hematoxylin and eosin (H&E), Giemsa, and reticulin staining.
  • The bone marrow trephines of 156 histologically proven DLBCL cases were assessed on routine histology, and IHC using two T-cell markers (CD45RO and CD3), two B-cell markers (CD20 and CD79a), and kappa and lambda light chains.
  • IHC performed routinely on bone marrow trephines has the ability to improve detection of occult lymphoma in experienced hands.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow / pathology. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Staging. Proportional Hazards Models

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  • (PMID = 18574254.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2544620
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76. Aifantis I, Raetz E, Buonamici S: Molecular pathogenesis of T-cell leukaemia and lymphoma. Nat Rev Immunol; 2008 May;8(5):380-90
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  • [Title] Molecular pathogenesis of T-cell leukaemia and lymphoma.
  • T-cell acute lymphoblastic leukaemia (T-ALL) is induced by the transformation of T-cell progenitors and mainly occurs in children and adolescents.
  • Although treatment outcome in patients with T-ALL has improved in recent years, patients with relapsed disease continue to have a poor prognosis.
  • It is therefore important to understand the molecular pathways that control both the induction of transformation and the treatment of relapsed disease.
  • In this Review, we focus on the molecular mechanisms responsible for disease induction and maintenance.
  • We also compare the physiological progression of T-cell differentiation with T-cell transformation, highlighting the close relationship between these two processes.

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  • (PMID = 18421304.001).
  • [ISSN] 1474-1741
  • [Journal-full-title] Nature reviews. Immunology
  • [ISO-abbreviation] Nat. Rev. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / R01CA105129; United States / NCI NIH HHS / CA / T32 CA-09161
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / Receptor, Notch1; 0 / Transcription Factors; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 101
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77. Shiratori S, Yasumoto A, Tanaka J, Shigematsu A, Yamamoto S, Nishio M, Hashino S, Morita R, Takahata M, Onozawa M, Kahata K, Kondo T, Ota S, Wakasa K, Sugita J, Koike T, Asaka M, Kasai M, Imamura M: A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect. Biol Blood Marrow Transplant; 2008 Jul;14(7):817-23
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  • [Title] A retrospective analysis of allogeneic hematopoietic stem cell transplantation for adult T cell leukemia/lymphoma (ATL): clinical impact of graft-versus-leukemia/lymphoma effect.
  • Adult T cell leukemia/lymphoma (ATL) is a highly aggressive T cell malignancy, and has a poor prognosis.
  • Recently, allogeneic-hematopoietic stem cell transplantation (allo-HSCT) has been suggested to improve the outcome.
  • We retrospectively analyzed 15 patients with ATL who had received allo-HSCT in 2 institutions in Hokkaido, Japan.
  • Calcineurin inhibitor dosage was reduced and administration was discontinued abruptly in 6 of the 15 patients for disease control; as a result, 4 (66.7%) of the 6 patients achieved complete response (CR) or partial response.
  • Therefore, a graft-versus-leukemia/lymphoma (GVL) effect might be induced by discontinuation of immunosuppression.
  • Thirteen of the 15 patients were followed up by monitoring HTLV-1 proviral DNA levels.
  • In 10 of the 11 patients with positive HTLV-1 proviral DNA before allo-HSCT, HTLV-1 proviral DNA became undetectable at least once after allo-HSCT, and only 1 of the 5 patients in whom HTLV-1 proviral DNA became detectable after allo-HSCT relapsed.
  • Compared to the results of past studies, these results show that allo-HSCT greatly improved the prognosis of ATL and suggest a contribution of the induction of a GVL effect.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Follow-Up Studies. HTLV-I Infections / blood. HTLV-I Infections / therapy. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Retrospective Studies. Transplantation, Homologous. Viral Load

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  • [ErratumIn] Biol Blood Marrow Transplant. 2008 Sep;14(9):1079
  • (PMID = 18541202.001).
  • [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] Journal Article; Multicenter Study
  • [Publication-country] United States
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78. Crowley JA, Butler MS, Ronnenburg MJ, Ament CN, Meekins JS, Ning Y: Development of a dual-color fluorescence in situ hybridization probe set on chromosome 6q to improve cytogenetic diagnosis of lymphoid malignancies. Cancer Genet Cytogenet; 2005 Feb;157(1):78-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a dual-color fluorescence in situ hybridization probe set on chromosome 6q to improve cytogenetic diagnosis of lymphoid malignancies.
  • Deletions in the long arm of chromosome 6 are one of the most commonly observed chromosome aberrations in lymphoid malignancies and have been identified as an adverse prognostic factor in subsets of leukemia and lymphoma.
  • We have also demonstrated its potential for clinical applications.
  • While applying this new probe set to clinical cytogenetic studies, we identified a unique t(6;14) translocation in a patient with acute lymphoid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 14. In Situ Hybridization, Fluorescence / methods. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Artificial, Bacterial. Chromosomes, Human, Pair 6. Humans

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  • (PMID = 15676153.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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79. Ohkura S, Yamashita M, Ishida T, Babu PG, Koyanagi Y, Yamamoto N, Miura T, Hayami M: Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A. AIDS Res Hum Retroviruses; 2005 Apr;21(4):325-30
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  • [Title] Phylogenetic heterogeneity of new HTLV type 1 isolates from southern India in subgroup A.
  • Seven isolates of human T cell leukemia virus type 1 (HTLV-1) were taken in southern India and phylogenetically analyzed to gain new insights into the origin and dissemination of HTLV-1 in the subcontinent.
  • The new Indian HTLV-1s were found to be members of subgroup A (Transcontinental subgroup) of the Cosmopolitan group.
  • These results demonstrate that Indian HTLV-1s are genetically heterogeneous and include the most divergent strain of subgroup A.
  • On the basis of these results, we speculate that subgroup A HTLV- 1s may have been present for thousands of years in India.
  • [MeSH-major] HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Polymorphism, Genetic
  • [MeSH-minor] Adult. Child. DNA, Viral / chemistry. Female. Humans. India. Male. Middle Aged. Molecular Sequence Data. Phylogeny. Sequence Analysis, DNA. Terminal Repeat Sequences / genetics

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  • (PMID = 15943577.001).
  • [ISSN] 0889-2229
  • [Journal-full-title] AIDS research and human retroviruses
  • [ISO-abbreviation] AIDS Res. Hum. Retroviruses
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY607576/ AY607577/ AY607578/ AY607579/ AY607580/ AY607581/ AY607582
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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80. Tong H, Zhang J, Lu C, Liu Z, Zheng Y: Immunophenotypic, cytogenetic and clinical features of 113 acute lymphoblastic leukaemia patients in China. Ann Acad Med Singapore; 2010 Jan;39(1):49-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotypic, cytogenetic and clinical features of 113 acute lymphoblastic leukaemia patients in China.
  • INTRODUCTION: The analysis of immunophenotype of the leukaemic cells has been of great importance for the diagnosis, classification and prognosis of acute lymphoblastic leukaemia (ALL).
  • MyAg positivity was higher in adult with ALL (47.6%) than in children with ALL (26.6%).
  • The clinical and biological characteristics of ALL patients between MyAg+ and MyAg- groups showed that increased white blood count (WBC) (>50 x 109/L), higher CD34 positivity and higher percentage of adult patients were found to be correlated with MyAg+ ALL.
  • CONCLUSION: Our results indicate that the immunophenotype did have relevance to the abnormal cytogenetic changes and clinical features in ALL.
  • Flow cytometry immunophenotype has become the most important method for diagnosis and typing of ALL.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. China / epidemiology. Cytogenetic Analysis. Diploidy. Female. Humans. Immunophenotyping. Infant. Male. Middle Aged. Translocation, Genetic. Young Adult

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  • (PMID = 20126815.001).
  • [ISSN] 0304-4602
  • [Journal-full-title] Annals of the Academy of Medicine, Singapore
  • [ISO-abbreviation] Ann. Acad. Med. Singap.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
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81. Micklethwaite KP, Savoldo B, Hanley PJ, Leen AM, Demmler-Harrison GJ, Cooper LJ, Liu H, Gee AP, Shpall EJ, Rooney CM, Heslop HE, Brenner MK, Bollard CM, Dotti G: Derivation of human T lymphocytes from cord blood and peripheral blood with antiviral and antileukemic specificity from a single culture as protection against infection and relapse after stem cell transplantation. Blood; 2010 Apr 1;115(13):2695-703
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Derivation of human T lymphocytes from cord blood and peripheral blood with antiviral and antileukemic specificity from a single culture as protection against infection and relapse after stem cell transplantation.
  • Viral infections and leukemic relapse account for the majority of treatment failures in patients with B-cell acute lymphoblastic leukemia (B-ALL) receiving allogeneic hematopoietic stem cell (HSC) or cord blood (CB) transplants.
  • Adoptive transfer of virus-specific cytotoxic T lymphocytes (CTLs) provides protection against common viruses causing serious infections after HSC transplantation without concomitant graft-versus-host disease.
  • We have now generated CTL lines from peripheral blood (PB) or CB units that recognize multiple common viruses and provide antileukemic activity by transgenic expression of a chimeric antigen receptor (CAR) targeting CD19 expressed on B-ALL.
  • PB-derived CAR(+) CTLs produced interferon-gamma (IFNgamma) in response to cytomegalovirus-pp65, adenovirus-hexon, and Epstein-Barr virus pepmixes (from 205 +/- 104 to 1034 +/- 304 spot-forming cells [SFCs]/10(5) T cells) and lysed primary B-ALL blasts in (51)Cr-release assays (mean, 66% +/- 5% specific lysis; effector-target [E/T] ratio, 40:1) and the CD19(+) Raji cell line (mean, 78% +/- 17%) in contrast to nontransduced controls (8% +/- 8% and 3% +/- 2%).
  • CB-derived CAR(+) CTLs showed similar antiviral and antitumor function and both PB and CB CAR(+) CTLs completely eliminated B-ALL blasts over 5 days of coculture.

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  • (PMID = 20110422.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA141303; United States / NCI NIH HHS / CA / R01 CA124782; United States / NCI NIH HHS / CA / P01CA94237; United States / NCI NIH HHS / CA / P50 CA126752; United States / NCI NIH HHS / CA / P50CA126752; United States / NCI NIH HHS / CA / R01CA131027; United States / NCI NIH HHS / CA / R01 CA131027; United States / NCI NIH HHS / CA / P01 CA094237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; R