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1. Platzbecker U, Thiede C, Füssel M, Geissler G, Illmer T, Mohr B, Hänel M, Mahlberg R, Krümpelmann U, Weissinger F, Schaich M, Theuser C, Ehninger G, Bornhäuser M: Reduced intensity conditioning allows for up-front allogeneic hematopoietic stem cell transplantation after cytoreductive induction therapy in newly-diagnosed high-risk acute myeloid leukemia. Leukemia; 2006 Apr;20(4):707-14
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  • [Title] Reduced intensity conditioning allows for up-front allogeneic hematopoietic stem cell transplantation after cytoreductive induction therapy in newly-diagnosed high-risk acute myeloid leukemia.
  • There is substantial need to improve the outcome of patients with high-risk acute myeloid leukemia (AML).
  • The clinical trial reported here investigated a new approach of up-front allogeneic hematopoietic stem cell transplantation (HSCT), provided a median of 40 days (range 22-74) after diagnosis, in twenty-six consecutive patients with newly-diagnosed high-risk AML characterized by poor-risk cytogenetics (n = 19) or inadequate blast clearance by induction chemotherapy (IC, n = 7).
  • During IC-induced aplasia after the 1st (n = 11) or 2nd (n = 15) cycle, patients received allogeneic peripheral blood stem cells (PBSC) from related (n = 11) or unrelated (n = 15) donors following a fludarabine-based reduced-intensity regimen.
  • Grades II to IV acute GvHD occurred in 14 (56%) and extensive chronic GvHD was documented in 8 (35%) patients.
  • The probability of disease-free survival was 61% with only three patients relapsing 5, 6 and 7 months after transplantation, respectively.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chimerism. Female. Graft vs Host Disease / prevention & control. Graft vs Host Disease / therapy. Humans. Male. Middle Aged. Recurrence. Remission Induction. Risk Factors. Survival Rate. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16482208.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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2. Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA: A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3525-31
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  • [Title] A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia.
  • PURPOSE: Polyunsaturated fatty acids (PUFA) and the sulfur-substituted fatty acid tetradecylthioacetic acid (TTA) inhibit proliferation and induce apoptosis in lymphoma and leukemic cell lines, but it is unknown if they can modify leukemogenesis in the intact organism.
  • EXPERIMENTAL DESIGN: We now examined the effects of PUFA and TTA in rats transplanted with either acute promyelocytic leukemia or acute T-cell leukemia.
  • RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat leukemia, n-3 PUFA had no significant effect compared with controls.
  • Only TTA inhibited (P < 0.05) leukemic infiltration in the bone marrow and spleen, probably due to apoptosis of the leukemic cells.
  • CONCLUSIONS: Dietary intake of TTA, but not of n-3 PUFA, in rats with acute leukemia, prolonged their survival.
  • TTA intake was also associated with reduced leukemic cell burden as well as diminished extramedullar dissemination.
  • TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with acute leukemias.
  • [MeSH-major] Fatty Acids, Unsaturated / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sulfides / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Diet. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration / diagnosis. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16740779.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
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3. Huguet F, Leguay T, Raffoux E, Thomas X, Beldjord K, Delabesse E, Chevallier P, Buzyn A, Delannoy A, Chalandon Y, Vernant JP, Lafage-Pochitaloff M, Chassevent A, Lhéritier V, Macintyre E, Béné MC, Ifrah N, Dombret H: Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study. J Clin Oncol; 2009 Feb 20;27(6):911-8
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  • [Title] Pediatric-inspired therapy in adults with Philadelphia chromosome-negative acute lymphoblastic leukemia: the GRAALL-2003 study.
  • PURPOSE: Retrospective comparisons have suggested that adolescents or teenagers with acute lymphoblastic leukemia (ALL) benefit from pediatric rather than adult chemotherapy regimens.
  • Thus, the aim of the present phase II study was to test a pediatric-inspired treatment, including intensified doses of nonmyelotoxic drugs, such as prednisone, vincristine, or L-asparaginase, in adult patients with ALL up to the age of 60 years.
  • PATIENTS AND METHODS: Between 2003 and 2005, 225 adult patients (median age, 31 years; range, 15 to 60 years) with Philadelphia chromosome-negative ALL were enrolled onto the Group for Research on Adult Acute Lymphoblastic Leukemia 2003 protocol, which included several pediatric options.
  • Some adult options, such as allogeneic stem-cell transplantation for patients with high-risk ALL, were nevertheless retained.
  • RESULTS: were retrospectively compared with the historical France-Belgium Group for Lymphoblastic Acute Leukemia in Adults 94 (LALA-94) trial experience in 712 patients age 15 to 55 years.
  • CONCLUSION: These results suggest that pediatric-inspired therapy markedly improves the outcome of adult patients with ALL, at least until the age of 45 years.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Female. Humans. Male. Middle Aged. Patient Selection. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome. Young Adult

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  • [ErratumIn] J Clin Oncol. 2009 May 20;27(15):2574. Dosage error in article text
  • (PMID = 19124805.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Druley TE, Hayashi R, Mansur DB, Zhang QJ, Barnes Y, Trinkaus K, Witty S, Thomas T, Klein EE, DiPersio JF, Adkins D, Shenoy S: Early outcomes after allogeneic hematopoietic SCT in pediatric patients with hematologic malignancies following single fraction TBI. Bone Marrow Transplant; 2009 Feb;43(4):307-14
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  • Overall survival and disease-free survival at 1 year were 60 and 47%, respectively.
  • Acute toxicities included grade 3-4 mucositis (18%), invasive infections (11%), multiorgan failure/shock (11%), hemolytic anemia (7%), veno-occlusive disease (4%) and renal failure (4%).
  • The regimen was well tolerated even in heavily pretreated children and supported donor cell engraftment; long-term follow up is in progress.

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  • [Cites] Leukemia. 2005 Dec;19(12):2130-8 [16304572.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2101-16 [16136167.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4961-7 [16493003.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Nov;13(11):1338-45 [17950920.001]
  • [Cites] Bone Marrow Transplant. 2007 Nov;40(10):951-5 [17873916.001]
  • [Cites] J Clin Oncol. 2007 Dec 20;25(36):5800-7 [18089878.001]
  • [Cites] Pediatr Transplant. 2008 Feb;12(1):24-31 [18186885.001]
  • [Cites] Bone Marrow Transplant. 2008 Jan;41(2):141-8 [18176616.001]
  • [Cites] Biol Blood Marrow Transplant. 2001;7(6):352-8 [11464978.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):340-7 [10637248.001]
  • [Cites] Bone Marrow Transplant. 2008 Jun;41(11):941-5 [18264141.001]
  • [Cites] J Pediatr Hematol Oncol. 2002 Feb;24(2):115-9 [11990696.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1996 Jan 1;34(1):71-7 [12118567.001]
  • [Cites] Biol Blood Marrow Transplant. 2002;8(11):608-18 [12463480.001]
  • [Cites] Pediatr Transplant. 2003 Jun;7(3):168-78 [12756040.001]
  • [Cites] Bone Marrow Transplant. 2003 Sep;32(6):543-8 [12953124.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 May;10(5):310-9 [15111930.001]
  • [Cites] Blood. 1991 Feb 1;77(3):661-9 [1991176.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Mar;20(3):631-4 [1995552.001]
  • [Cites] Br J Haematol. 1991 Apr;77(4):529-34 [2025579.001]
  • [Cites] Blood. 1994 Jun 1;83(11):3384-9 [8193376.001]
  • [Cites] J Clin Oncol. 1994 Jun;12(6):1217-22 [8201385.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Apr 30;32(1):69-73 [7536723.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Bone Marrow Transplant. 1999 May;23(10):1049-53 [10373072.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3035-41 [15126314.001]
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 2):7164s-7170s [16203817.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Dec 1;63(5):1568-75 [15990246.001]
  • [Cites] Br J Haematol. 2006 Mar;132(6):755-69 [16487177.001]
  • (PMID = 19011666.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / HD007499-09; United States / NICHD NIH HHS / HD / T32 HD007499; United States / NICHD NIH HHS / HD / T32 HD 007499; United States / NICHD NIH HHS / HD / T32 HD007499-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS80149; NLM/ PMC2792985
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5. Andrikovics H, Szilvási A, Meggyesi N, Király V, Halm G, Lueff S, Nahajevszky S, Mikala G, Sipos A, Lovas N, Csukly Z, Mátrai Z, Tamáska J, Tordai A, Masszi T: [Role of the activating mutation Val617Phe of Janus kinase 2 gene in myeloproliferative diseases and significance of its detection]. Orv Hetil; 2007 Feb 4;148(5):203-10
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  • [Transliterated title] A 2-es típusú Janus tirozin kináz Val617Phe aktiváló pontmutáció szerepe és kimutatásának jelentosége myeloproliferatív szindrómában.
  • The Val617Phe point mutation of Janus kinase 2 gene is believed to participate in the pathogenesis of myeloproliferative syndrome characterised by the clonal alteration of hematopoietic stem cells.
  • We found significantly elevated hemoglobin levels and white blood cell counts (measured at the time of diagnosis) in Val617Phe-positive polycythemia vera and essential thrombocythemia patient groups compared to Val617Phe-negative patients.
  • However, the frequencies of splenomegaly and other complications (thrombosis, bleeding, transformation to acute leukemia) were not significantly different between the mutation-positive and negative groups.
  • [MeSH-minor] Adult. Aged. Biopsy. Bone Marrow / pathology. Female. Gene Expression Regulation. Gene Frequency. Humans. Male. Middle Aged. Phenotype. Phenylalanine. Polycythemia Vera / genetics. Polymerase Chain Reaction. Primary Myelofibrosis / genetics. Thrombocytosis / genetics. Valine

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  • (PMID = 17344140.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 47E5O17Y3R / Phenylalanine; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; HG18B9YRS7 / Valine
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6. Kufner S, Zitzelsberger H, Kroell T, Pelka-Fleischer R, Salem A, de Valle F, Schweiger C, Nuessler V, Schmid C, Kolb HJ, Schmetzer HM: Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions. Scand J Immunol; 2005 Jul;62(1):86-98
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  • [Title] Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions.
  • Functional dendritic cells (DC) are professional antigen-presenting cells (APC) and can be generated in vitro from healthy as well as from leukaemic cells from acute myeloid leukemia (AML) patients giving rise to APC of leukaemic origin-presenting leukaemic antigens.
  • We describe the generation and characterization of DC from different mononuclear cell (MNC) fractions from 50 AML patients under different serum-free culture conditions, determine the optimal culture conditions and compare the results with that from 23 healthy donors.
  • In parallel cultures, we compared DC harvests after 7- or 14-day culture, with total or adherent MNC or T-cell depleted MNC or peripheral blood (PB) or bone marrow-MNC (BM-MNC), thawn or fresh MNC, in Xvivo or CellGro serum-free media, +/-10% autologous plasma or +/-FL.
  • In detail, we could show that AML-DC harvests were higher after 10-14 days culture (healthy DC: 7 days); total or adherent PB or BM-MNC fractions yield comparable DC counts, however, from magnetic cell sorting (MACS)-depleted MNC fractions or thawn MNC lower DC counts can be generated.
  • Autologous T-cell activation of leukaemia-derived DC was demonstrated in cases with AML.
  • Autologous T cells proliferate and upregulate DC-contact-relevant antigens.
  • We demonstrate that the generation of leukaemia-derived DC is feasable in AML under serum-free culture conditions giving rise to DC with comparable characteristics as healthy DC and offering an anti-leukaemia-directed immunotherapeutical vaccination strategy in AML.
  • [MeSH-major] Bone Marrow Cells / immunology. Cell Culture Techniques. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Middle Aged. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology. Vaccination / methods

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  • (PMID = 16091128.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Culture Media, Serum-Free; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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7. Al Khabori M, Samiee S, Fung S, Xu W, Brandwein J, Patterson B, Brien W, Chang H: Adult precursor T-lymphoblastic leukemia/lymphoma with myeloid-associated antigen expression is associated with a lower complete remission rate following induction chemotherapy. Acta Haematol; 2008;120(1):5-10
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  • [Title] Adult precursor T-lymphoblastic leukemia/lymphoma with myeloid-associated antigen expression is associated with a lower complete remission rate following induction chemotherapy.
  • Prognostic studies of T-cell lymphoblastic leukemia/lymphoma (T-ALL) have been performed in small patient cohorts with conflicting results.
  • We systematically reviewed 67 adult T-ALL patients diagnosed and treated at our institute to identify clinical and pathologic prognostic factors.
  • Our study indicates that expression of myeloid-associated antigens is associated with a lower CR rate in adult T-ALL and may be considered in risk stratification for induction chemotherapy.
  • [MeSH-major] Antigens, Differentiation, Myelomonocytic / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neprilysin / metabolism. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Survival Rate

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • [CommentIn] Expert Rev Hematol. 2009 Feb;2(1):27-9 [21082991.001]
  • (PMID = 18635939.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13; EC 3.4.24.11 / Neprilysin
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8. Matsumoto K, Murao K, Imachi H, Nishiuchi T, Cao W, Yu X, Li J, Ahmed RA, Iwama H, Kobayashi R, Tokumitsu H, Ishida T: The role of calcium/calmodulin-dependent protein kinase cascade on MIP-1alpha gene expression of ATL cells. Exp Hematol; 2008 Apr;36(4):390-400
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  • [Title] The role of calcium/calmodulin-dependent protein kinase cascade on MIP-1alpha gene expression of ATL cells.
  • OBJECTIVE: Adult T-cell leukemia (ATL) is a mature CD4(+) T-cell malignancy caused by infection with human T-lymphotrophic virus type-1 and is associated with a marked hypercalcemia in many patients.
  • In this study, we investigated the effect of extracellular calcium on MIP-1alpha secretion in ATL cells and the role of Ca(2+)/calmodulin (CaM)-dependent protein kinase (CaM-K) cascade in transcriptional activation of MIP-1alpha.
  • MATERIALS AND METHODS: MIP-1alpha protein levels in the culture supernatant collected from ATL cells were measured by enzyme-linked immunosorbent assay.
  • Reporter plasmid containing the MIP-1alpha promoter was transfected to ATL cells, and the promoter activity was measured by luciferase assay.
  • RESULTS: The addition of calcium to the culture medium enhanced the secretion of MIP-1alpha from ATL cells, which was inhibited by the CaM-KK inhibitor.
  • CONCLUSION: Hypercalcemia enhances MIP-1alpha secretion in ATL cells, and this mechanism requires the involvement of CaM-KK/CaM-KIV cascade through the CRE.
  • [MeSH-major] Calcium-Calmodulin-Dependent Protein Kinases / metabolism. Chemokine CCL3 / metabolism. Gene Expression Regulation, Leukemic / drug effects. Leukemia, T-Cell / metabolism. Signal Transduction / drug effects
  • [MeSH-minor] Benzimidazoles / pharmacology. Calcium / pharmacology. Calcium-Calmodulin-Dependent Protein Kinase Kinase / antagonists & inhibitors. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Humans. Isoquinolines / pharmacology. Naphthalimides / pharmacology. Phosphorylation / drug effects. Promoter Regions, Genetic

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  • (PMID = 18249060.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzimidazoles; 0 / Chemokine CCL3; 0 / Enzyme Inhibitors; 0 / Isoquinolines; 0 / Naphthalimides; 0 / STO 609; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Kinase; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; SY7Q814VUP / Calcium
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9. Beck C, Humpe A, Harder S, Schmid M, Horst HA: Myelodysplastic syndrome of donor origin subsequent to successful treatment of myeloid/NK-cell precursor leukaemia with allogeneic PBSCT: two very rare conditions in one patient. Ann Hematol; 2005 Sep;84(9):616-8
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  • [Title] Myelodysplastic syndrome of donor origin subsequent to successful treatment of myeloid/NK-cell precursor leukaemia with allogeneic PBSCT: two very rare conditions in one patient.
  • We report a 36-year-old male with myeloid/natural killer (NK)-cell precursor acute leukaemia with a complex aberrant karyotype, who was treated according to an acute-myeloid-leukaemia (AML) treatment protocol (idarubicine, cytarabine, and etoposide) followed by high-dose cytarabine consolidation and achieved complete remission.
  • He underwent allogeneic matched unrelated donor (MUD) peripheral blood stem-cell transplantation (PBSCT) and remained in remission throughout his remaining life.
  • This patient represents one of the few cases published achieving remission for a significant period of time after being diagnosed with myeloid/NK-cell precursor acute leukaemia, a very rare malignant disease.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Myeloid / pathology. Leukemia, Myeloid / therapy. Leukemia, Prolymphocytic, T-Cell / pathology. Myelodysplastic Syndromes / etiology. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Fatal Outcome. Humans. Infection. Male. Remission Induction / methods. Thrombocytopenia. Tissue Donors. Transplantation, Homologous. Treatment Outcome


10. Ersvaer E, Hampson P, Wendelbo Ø, Lord JM, Gjertsen BT, Bruserud Ø: Circulating T cells in patients with untreated acute myelogenous leukemia are heterogeneous and can be activated through the CD3/TCR complex. Hematology; 2007 Jun;12(3):199-207
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Circulating T cells in patients with untreated acute myelogenous leukemia are heterogeneous and can be activated through the CD3/TCR complex.
  • T lymphocyte defects may contribute to the immune insufficiency seen in acute myelogenous leukemia (AML).
  • We therefore characterized the T cell system for untreated AML patients.
  • The in vitro interferon-gamma (IFNgamma) release in response to stimulation with anti-CD3 plus anti-CD28 in the presence of autologous AML cells was examined for 31 patients.
  • The majority of circulating lymphocytes were CD3(+)T cells, and CD19(+)B cells usually constituted < 10% of the lymphocytes.
  • Most T cells expressed the alphabeta T cell receptor (TCRalphabeta(+)), and only a minority of the cells was TCRgammadelta(+).
  • Both CD4(+) and CD8(+)T cells were detected, the CD4:CD8 ratio showed a wide variation but was generally >1.0.
  • The majority of CD4(+) and CD8(+)T cells were CD45RA(+) cells.
  • The T cells could be stimulated to release IFNgamma in response to anti-CD3 plus anti-CD28 ligation even in the presence of excess autologous AML blasts, and for a subset of patients (6 of 27) these IFNgamma levels could be further increased by the novel protein kinase C (PKC) agonist PEP005.
  • In conclusion, circulating T cells in patients with untreated AML are mainly CD4(+) or CD8(+) TCRalphabeta(+); both CD45RA(+) and CD45R0(+) can be detected, and these cells can be activated through the CD3/TCR complex even in the presence of excess AML cells.
  • For a subset of patients T cell responsiveness can be further increased by targeting PKC and these data therefore suggest that T cell function is not inhibited in AML patients.
  • [MeSH-major] Antigens, CD3 / immunology. Leukemia, Myeloid, Acute / immunology. Lymphocyte Activation / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blood Cells. Female. Flow Cytometry. Humans. Immunophenotyping. Male. Middle Aged. Protein Kinase C. Receptors, Antigen, T-Cell / immunology. T-Lymphocyte Subsets / immunology

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  • (PMID = 17558695.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Receptors, Antigen, T-Cell; EC 2.7.11.13 / Protein Kinase C
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11. Klopfenstein KJ, Clayton J, Rosselet R, Kerlin B, Termuhlen A, Gross T: Prevalence of abnormal bone density of pediatric patients prior to blood or marrow transplant. Pediatr Blood Cancer; 2009 Oct;53(4):675-7
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  • [MeSH-major] Bone Diseases, Metabolic / epidemiology. Bone Marrow Transplantation. Osteoporosis / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Bone Density. Child. Child, Preschool. Female. Humans. Infant. Male. Prevalence

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  • (PMID = 19533650.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Yoshino A, Katayama Y, Yokoyama T, Watanabe T, Ogino A, Ota T, Komine C, Fukushima T, Kusama K: Therapeutic implications of interferon regulatory factor (IRF)-1 and IRF-2 in diffusely infiltrating astrocytomas (DIA): response to interferon (IFN)-beta in glioblastoma cells and prognostic value for DIA. J Neurooncol; 2005 Sep;74(3):249-60
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  • [Title] Therapeutic implications of interferon regulatory factor (IRF)-1 and IRF-2 in diffusely infiltrating astrocytomas (DIA): response to interferon (IFN)-beta in glioblastoma cells and prognostic value for DIA.
  • To gain a better insight into these mechanisms, we investigated the signaling pathways focusing particularly on interferon regulatory factor 1 (IRF-1) and IRF-2 in glioblastoma cell lines.
  • We first assessed the cytotoxic effects of IFN-beta based on a cell growth study and modified MTT assay, and then quantified the apoptosis using a sandwich enzyme immunoassay following IFN-beta treatment in the cell lines, U-87MG, T98G, and A-172.
  • Furthermore, we assessed the expression of type I IFN receptor, IRF-1, and IRF-2 using immunohistochemical techniques in 63 DIA (15 of WHO grade II, 18 of grade III, and 30 of grade IV), and analyzed their impact on prognosis.
  • IFN-beta treatment for 6 h significantly enhanced the expression of IRF-1 in all three cell lines.
  • While minimal processing of caspase-8 was noted in the three cell lines throughout the experiment, caspase-9 activation was observed in the apoptosis-detected T98G after 48 h of treatment, as indicated by a 1.33-fold increase (P=0.037).
  • Thus, IRF-1 and IRF-2 could represent one of the therapeutic target sites for the regulation of cell growth in DIA.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Enzyme Activation / physiology. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Receptors, Interferon / metabolism

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  • [Cites] Acta Neurochir (Wien). 1994;127(1-2):55-9 [7942182.001]
  • [Cites] J Biol Chem. 1998 Jan 2;273(1):194-9 [9417064.001]
  • [Cites] Cancer Chemother Pharmacol. 2000;45(3):199-206 [10663637.001]
  • [Cites] Science. 1993 Feb 12;259(5097):971-4 [8438157.001]
  • [Cites] Nature. 1991 Jun 6;351(6326):453-6 [2046748.001]
  • [Cites] Cell. 1998 Sep 18;94(6):739-50 [9753321.001]
  • [Cites] J Biol Chem. 1992 Mar 15;267(8):5017-20 [1371992.001]
  • [Cites] Cancer Res. 2003 Jan 15;63(2):513-21 [12543810.001]
  • [Cites] J Biol Chem. 1998 Oct 23;273(43):28378-83 [9774464.001]
  • [Cites] Oncogene. 1994 Nov;9(11):3313-20 [7936656.001]
  • [Cites] Nature. 1996 Aug 29;382(6594):816-8 [8752276.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5673-80 [11059759.001]
  • [Cites] J Cell Biol. 1999 Jan 25;144(2):281-92 [9922454.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]
  • [Cites] Cell. 1998 Aug 7;94(3):339-52 [9708736.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7133-41 [11156422.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1309-12 [9721092.001]
  • [Cites] Annu Rev Cell Dev Biol. 1999;15:269-90 [10611963.001]
  • [Cites] Toxicol Lett. 1998 Dec 28;102-103:121-9 [10022243.001]
  • [Cites] J Neurooncol. 2003 Jan;61(2):171-6 [12622456.001]
  • [Cites] J Biol Chem. 1999 Feb 19;274(8):5053-60 [9988752.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] Science. 1991 Jul 5;253(5015):49-53 [1905840.001]
  • [Cites] Trends Cell Biol. 1996 Jul;6(7):245-8 [15157443.001]
  • [Cites] Biochimie. 1998 Aug-Sep;80(8-9):641-50 [9865486.001]
  • [Cites] Eur Cytokine Netw. 1998 Dec;9(4):619-31 [9889406.001]
  • [Cites] Immunol Today. 1988 Dec;9(12):393-400 [2475121.001]
  • [Cites] Ann Oncol. 2000 Jun;11(6):707-14 [10942060.001]
  • [Cites] Oncogene. 1998 Dec 24;17(25):3237-45 [9916986.001]
  • [Cites] Cell. 1996 Oct 18;87(2):171 [8861900.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):416-23 [10652435.001]
  • [Cites] Nature. 1995 Aug 17;376(6541):596-9 [7637809.001]
  • [Cites] Ann Surg Oncol. 1999 Sep;6(6):604-8 [10493631.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Cancer Res. 1996 May 15;56(10):2417-21 [8625321.001]
  • [Cites] J Biol Chem. 1999 Apr 23;274(17):11549-56 [10206961.001]
  • [Cites] Cell. 1997 Nov 14;91(4):443-6 [9390553.001]
  • [Cites] Cancer Res. 1993 Sep 15;53(18):4164-8 [8364909.001]
  • [Cites] Oncogene. 2000 Jul 13;19(30):3372-83 [10918594.001]
  • [Cites] Clin Chem. 1996 Jun;42(6 Pt 1):858-68 [8665676.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1821-31 [11410525.001]
  • [Cites] Cell. 1998 Sep 18;94(6):695-8 [9753316.001]
  • [Cites] Mol Cell. 1998 Jun;1(7):949-57 [9651578.001]
  • [Cites] Cancer Invest. 1996;14(1):25-53 [8597888.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 21;257(3):672-7 [10208842.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1293-8 [11350897.001]
  • [Cites] Leukemia. 1997 Jul;11(7):933-9 [9204971.001]
  • [Cites] Trends Biochem Sci. 1995 May;20(5):198-202 [7610484.001]
  • [Cites] Ann Surg. 2001 May;233(5):623-9 [11323500.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4453-60 [9766678.001]
  • [Cites] J Biol Chem. 1997 Jun 27;272(26):16351-7 [9195941.001]
  • [Cites] Genes Dev. 1998 Jun 1;12(11):1551-70 [9620844.001]
  • [Cites] J Biol Chem. 2000 Mar 10;275(10):7337-42 [10702305.001]
  • [Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):1-16 [9337844.001]
  • [Cites] J Interferon Cytokine Res. 2002 Jan;22(1):39-47 [11846974.001]
  • [Cites] J Natl Cancer Inst. 1996 Oct 16;88(20):1442-55 [8841019.001]
  • (PMID = 16187022.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Regulatory Factor-1; 0 / Interferon Regulatory Factor-2; 0 / Receptors, Interferon; 77238-31-4 / Interferon-beta; EC 3.4.22.- / Caspases
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13. Baseggio L, Berger F, Morel D, Delfau-Larue MH, Goedert G, Salles G, Magaud JP, Felman P: Identification of circulating CD10 positive T cells in angioimmunoblastic T-cell lymphoma. Leukemia; 2006 Feb;20(2):296-303
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  • [Title] Identification of circulating CD10 positive T cells in angioimmunoblastic T-cell lymphoma.
  • Here, we evaluated if the analysis of blood smears may suggest the blood dissemination of angioimmunoblastic T-cell lymphoma (AITL) and if CD10 expression on neoplastic T cells, as recently reported on AITL, may contribute to the diagnosis.
  • According to previous results, a fraction of T cells expressed CD10 in 10/11 lymph nodes.
  • Interestingly, all blood smears showed atypical lymphoid cells and a fraction of T cells expressed CD10 with a mean percentage of 18.75% (range 5.00-47.00%), regardless of lymphocytosis level and of rate of CD10 T cells in corresponding lymph node.
  • In contrast, in all control samples (100), none CD10-positive T cell was identified.
  • This is to our knowledge the first description of circulating CD10 neoplastic T cells in AITL.
  • Therefore, they ought to be explored in further studies when aggressive lymphoma, in particular with lymphopenia and circulating atypical cells, is suspected.
  • [MeSH-major] Lymphoma, T-Cell / diagnosis. Neoplastic Cells, Circulating / immunology. Neoplastic Cells, Circulating / pathology. Neprilysin / biosynthesis. T-Lymphocytes / immunology. T-Lymphocytes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Flow Cytometry. Gene Rearrangement. Genes, T-Cell Receptor gamma / genetics. Humans. Immunoglobulin Heavy Chains / genetics. Immunohistochemistry. Immunophenotyping. Male. Middle Aged. Sensitivity and Specificity

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  • (PMID = 16341050.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; EC 3.4.24.11 / Neprilysin
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14. Torelli GF, Guarini A, Maggio R, Alfieri C, Vitale A, Foà R: Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission. Haematologica; 2005 Jun;90(6):785-92
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  • [Title] Expansion of natural killer cells with lytic activity against autologous blasts from adult and pediatric acute lymphoid leukemia patients in complete hematologic remission.
  • BACKGROUND AND OBJECTIVES: Natural killer (NK) cells constitute an important area of research for hematologic malignancies.
  • The anti-leukemic activity of NK cells against acute myeloid leukemia (AML) blasts has been described, but very few data are available for acute lymphoid leukemia (ALL).
  • The present study was designed to investigate whether: (i) NK effectors could be expanded from adult and pediatric ALL patients in complete remission;.
  • (ii) the signal transduction machinery of these cells was preserved;.
  • (iii) NK cells showed cytotoxic activity against autologous blasts;.
  • (v) any differences in cytotoxic activity could be found between expanded effectors from adult and pediatric patients.
  • DESIGN AND METHODS: We co-cultured patients' peripheral blood mononuclear cells (PBMC) with the feeder cell line RPMI 8866 and analyzed the NK cells' expansion capacity by cell count and cytofluorimetric analyses.
  • Signal transduction of expanded effector cells was evaluated by Western blot.
  • 51Cr release assays, before and after stimulation with activating cytokines, were performed to analyze the cytotoxic potential of effector cells against tumor cell lines and autologous blast cells.
  • RESULTS: We obtained an average 40-fold increase in NK cells.
  • Patients' expanded cells showed cytotoxic activity against target cell lines comparable to that of normal donors.
  • More significantly, these cells also exerted a lytic effect against autologous blasts.
  • No differences in expansion and cytotoxic activity were found between pediatric and adult patients.
  • INTERPRETATION AND CONCLUSIONS: These findings document for the first time the possibility of expanding ex vivo cytotoxic effectors with autologous killing capacity from ALL patients in remission, and suggest a new potential immunotherapeutic strategy for the management of early disease recurrence or of residual disease.
  • [MeSH-major] Immunotherapy / methods. Killer Cells, Natural / cytology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adult. Child. Coculture Techniques. Cytokines / metabolism. Flow Cytometry. Humans. Interleukin-15 / metabolism. Interleukin-2 / metabolism. Receptors, IgG / metabolism. Remission Induction. Signal Transduction

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  • (PMID = 15951291.001).
  • [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 / Cytokines; 0 / Interleukin-15; 0 / Interleukin-2; 0 / Receptors, IgG
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15. Ozçelik T, Ozkalemkaş F, Kocaeli H, Altundal Y, Ener B, Ali R, Ozkocaman V, Hakyemez B, Tunali A: [Successful treatment of neuroaspergillosis in a patient with acute lymphoblastic leukemia: role of surgery, systemic antifungal therapy and intracavitary therapy]. Mikrobiyol Bul; 2009 Jul;43(3):499-506
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  • [Title] [Successful treatment of neuroaspergillosis in a patient with acute lymphoblastic leukemia: role of surgery, systemic antifungal therapy and intracavitary therapy].
  • We report here a case of cerebral aspergillosis in a 34-years-old man with acute lymphoblastic leukaemia who was successfully treated with a combination of aggressive neurosurgery, intracavitary instillation of amphotericin B and voriconazole.
  • Due to disease progression during combination therapy, the patient had a second surgical resection resulting in a 75% reduction in lesion size.
  • However, leukemia relapsed.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillus flavus / isolation & purification. Neuroaspergillosis / drug therapy. Neuroaspergillosis / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adult. Amphotericin B / administration & dosage. Amphotericin B / therapeutic use. Chemotherapy, Adjuvant. Drug Therapy, Combination. Echinocandins / administration & dosage. Echinocandins / therapeutic use. Fatal Outcome. Humans. Injections, Intraventricular. Male. Pyrimidines / administration & dosage. Pyrimidines / therapeutic use. Triazoles / administration & dosage. Triazoles / therapeutic use. Voriconazole

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  • (PMID = 19795628.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; F0XDI6ZL63 / caspofungin; JFU09I87TR / Voriconazole
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16. Friedrisch JR, Prá D, Maluf SW, Bittar CM, Mergener M, Pollo T, Kayser M, da Silva MA, Henriques JA, da Rocha Silla LM: DNA damage in blood leukocytes of individuals with sickle cell disease treated with hydroxyurea. Mutat Res; 2008 Jan 8;649(1-2):213-20
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  • [Title] DNA damage in blood leukocytes of individuals with sickle cell disease treated with hydroxyurea.
  • Hydroxyurea (HU) plays an important role in the treatment of patients with sickle cell disease (SCD).
  • Although HU has been associated with an increased risk of leukemia in some patients with myeloproliferative disorders, the mutagenic and carcinogenic potential of HU has not been established.
  • [MeSH-major] Anemia, Sickle Cell / drug therapy. DNA Damage. Hydroxyurea / adverse effects. Leukocytes / drug effects
  • [MeSH-minor] Adolescent. Adult. Antisickling Agents / adverse effects. Antisickling Agents / therapeutic use. Child. Child, Preschool. Comet Assay. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged

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  • (PMID = 17988936.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antisickling Agents; X6Q56QN5QC / Hydroxyurea
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17. Hsiao HH, Tsai HJ, Liu YC, Lee CP, Lin SF: Allo-SCT in a rare t(8;21) evolution of CML. Bone Marrow Transplant; 2010 Aug;45(8):1365-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Translocation, Genetic
  • [MeSH-minor] Adult. Benzamides. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Imatinib Mesylate. Male. Piperazines / pharmacology. Piperazines / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Transplantation, Homologous

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  • (PMID = 20023710.001).
  • [ISSN] 1476-5365
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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18. Lv L, Kerzic P, Lin G, Schnatter AR, Bao L, Yang Y, Zou H, Fu H, Ye X, Gross SA, Armstrong TW, Irons RD: The TNF-alpha 238A polymorphism is associated with susceptibility to persistent bone marrow dysplasia following chronic exposure to benzene. Leuk Res; 2007 Nov;31(11):1479-85
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  • Chronic exposure to benzene can result in transient hematotoxicity (benzene poisoning, BP) or persistent bone marrow pathology including dysplasia and/or acute myeloid leukemia.
  • Leuk Res 2005;29:1371-80].
  • In this study we investigated the association of single nucleotide polymorphisms (SNP) (-863 (C-->A), -857 (C-->T), -308 (G-->A), -238 (G-->A)) in the promoter region of the cytokine, tumor necrosis factor-alpha (TNF-alpha) on the development of BP, persistent BID and de novo myelodysplastic syndrome (MDS) in 394 individuals.
  • 1.23-44.7) and was specific for BID and not de novo MDS or BP.
  • These findings are consistent with a role for inflammation in the development of BID and suggest that cell-specific alterations in TNF-alpha expression may promote clonal selection in the evolution of neoplastic hematopoietic disease.
  • [MeSH-minor] Adult. Aged. Base Sequence. DNA Primers. Female. Humans. Male. Middle Aged

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  • (PMID = 17367855.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Tumor Necrosis Factor-alpha; J64922108F / Benzene
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19. Sonmez M, Akagun T, Cobanoglu U, Topbas M, Erkut N, Yilmaz M, Ovali E, Omay SB: Effect of LMO2 protein expression on survival in chronic myeloid leukemia patients treated with imatinib mesylate. Hematology; 2009 Aug;14(4):220-3
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  • [Title] Effect of LMO2 protein expression on survival in chronic myeloid leukemia patients treated with imatinib mesylate.
  • LIM domain only-2 (LMO2) is an important regulator of hematopoietic stem cell development.
  • Chronic myeloid leukemia (CML) is a malignant clonal myeloproliferative disorder in which the terminal differentiation is not altered until the appearance of an accelerated or blast phase.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Metalloproteins / biosynthesis. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Benzamides. Female. Humans. Imatinib Mesylate. LIM Domain Proteins. Male. Middle Aged. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins / biosynthesis. Survival Rate. Young Adult

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  • (PMID = 19635185.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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20. Moskowitz AJ, Yahalom J, Kewalramani T, Maragulia JC, Vanak JM, Zelenetz AD, Moskowitz CH: Pretransplantation functional imaging predicts outcome following autologous stem cell transplantation for relapsed and refractory Hodgkin lymphoma. Blood; 2010 Dec 2;116(23):4934-7
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  • [Title] Pretransplantation functional imaging predicts outcome following autologous stem cell transplantation for relapsed and refractory Hodgkin lymphoma.
  • One hundred fifty-three patients with chemosensitive disease after ICE (ifosfamide, carboplatin, and etoposide)-based salvage therapy (ST) proceeded to high-dose chemoradiotherapy followed by autologous stem cell transplantation (ASCT).
  • Studies evaluating novel STs, conditioning regimens, post-ASCT maintenance, or allogeneic stem cell transplantation are warranted for patients who fail to normalize pre-ASCT functional imaging.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Hodgkin Disease / radiography. Hodgkin Disease / radionuclide imaging. Hodgkin Disease / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Combined Modality Therapy. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Ifosfamide / administration & dosage. Kaplan-Meier Estimate. Male. Middle Aged. Neoplasm Recurrence, Local / surgery. Positron-Emission Tomography. Prognosis. Radiotherapy. Salvage Therapy / methods. Tomography, X-Ray Computed. Transplantation Conditioning. Transplantation, Autologous. Treatment Outcome. Young Adult

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  • [Cites] Blood. 2001 Feb 1;97(3):616-23 [11157476.001]
  • [Cites] Lancet. 2002 Jun 15;359(9323):2065-71 [12086759.001]
  • [Cites] Blood. 2003 Jul 1;102(1):53-9 [12609836.001]
  • [Cites] Lancet. 1993 Apr 24;341(8852):1051-4 [8096958.001]
  • [Cites] Blood. 2006 Jan 1;107(1):52-9 [16150944.001]
  • [Cites] Blood. 2007 Jan 15;109(2):486-91 [17003382.001]
  • [Cites] Leukemia. 2002 Feb;16(2):260-7 [11840293.001]
  • [Cites] Cancer. 2007 Jun 15;109(12):2481-9 [17497648.001]
  • [Cites] J Clin Oncol. 2007 Aug 20;25(24):3746-52 [17646666.001]
  • [Cites] Leuk Lymphoma. 2008 Apr;49(4):727-33 [18398740.001]
  • [Cites] Ann Oncol. 2008 Jul;19(7):1312-9 [18356139.001]
  • [Cites] J Clin Oncol. 2008 Nov 10;26(32):5240-7 [18809615.001]
  • [Cites] Br J Haematol. 2010 Mar;148(6):890-7 [20085577.001]
  • [Cites] Clin Lymphoma Myeloma. 2006 Nov;7(3):217-25 [17229338.001]
  • (PMID = 20733154.001).
  • [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] 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; UM20QQM95Y / Ifosfamide
  • [Other-IDs] NLM/ PMC3799204
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21. Arisawa K, Soda M, Akahoshi M, Fujiwara S, Uemura H, Hiyoshi M, Takeda H, Kashino W, Suyama A: Human T-cell lymphotropic virus type-1 infection and risk of cancer: 15.4 year longitudinal study among atomic bomb survivors in Nagasaki, Japan. Cancer Sci; 2006 Jun;97(6):535-9
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  • [Title] Human T-cell lymphotropic virus type-1 infection and risk of cancer: 15.4 year longitudinal study among atomic bomb survivors in Nagasaki, Japan.
  • The objective of the present study was to investigate the association between human T-lymphotropic virus type-1 (HTLV-1) infection and cancer risk in a longitudinal study.
  • The baseline survey, including analysis of antibody to HTLV-1, took place during 1985-1987 and follow-up was performed until the end of 2001.
  • After adjustment for sex, age and other variables, HTLV-1 infection was not associated with the risk of developing cancers of all sites, excluding adult T-cell leukemia (rate ratio 1.0, 95% confidence interval [CI] 0.76-1.4), stomach, colon and rectum, lung, female breast or other minor sites, but was associated with increased risk of liver cancer (rate ratio 2.1, 95%CI 1.0-4.6).
  • The point estimate of the rate ratio for thyroid cancer was 3.0, but this was not significantly higher than 1 because of the small number of events (n = 11) and low prevalence of HTLV-1 seropositivity.
  • These findings support the idea that HTLV-1 infection is not associated with an increased general cancer risk.
  • Confounding by hepatitis C virus (HCV) and the interaction between HTLV-1 and HCV may explain the increased risk of liver cancer among HTLV-1 carriers.
  • Further follow-up may be required to determine if HTLV-1 carriers are at increased risk of thyroid cancer.
  • [MeSH-major] HTLV-I Infections / epidemiology. Neoplasms / epidemiology. Neoplasms / virology. Nuclear Warfare. Survivors / statistics & numerical data

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  • (PMID = 16734733.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radioactive Fallout
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22. Schüler F, Dölken L, Hirt C, Kiefer T, Berg T, Fusch G, Weitmann K, Hoffmann W, Fusch C, Janz S, Rabkin CS, Dölken G: Prevalence and frequency of circulating t(14;18)-MBR translocation carrying cells in healthy individuals. Int J Cancer; 2009 Feb 15;124(4):958-63
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  • [Title] Prevalence and frequency of circulating t(14;18)-MBR translocation carrying cells in healthy individuals.
  • The significance of low level circulating t(14;18)-positive cells in healthy individuals as clonal lymphoma precursors or indicators of risk is still unclear.
  • These results were compared with number of circulating t(14;18)-positive cells in 108 FL patients at initial presentation.
  • Specifically, among individuals up to 10 years old, none had detectable circulating t(14;18)-positive cells.
  • Four percent (31/715) of individuals carried more than one t(14;18)-positive cell per 25,000 peripheral blood mononuclear cells (PBMNCs).
  • In comparison, 108 stage III/IV FL patients had a median number of circulating t(14;18)-positive malignant FL cells of about 9200/1 million PBMNCs (range 7-1,000,000).
  • These findings will further improve the understanding of the relevance of t(14;18)-positive cells in healthy individuals as a risk marker toward the development into lymphoma precursors.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Child. Child, Preschool. Humans. Infant. Infant, Newborn. Lymphoma, Follicular / genetics. Middle Aged. Prevalence. Proto-Oncogene Proteins c-bcl-2 / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19030176.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA151354
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2
  • [Other-IDs] NLM/ NIHMS638971; NLM/ PMC4216731
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23. Röth A, de Beer D, Nückel H, Sellmann L, Dührsen U, Dürig J, Baerlocher GM: Significantly shorter telomeres in T-cells of patients with ZAP-70+/CD38+ chronic lymphocytic leukaemia. Br J Haematol; 2008 Nov;143(3):383-6
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  • [Title] Significantly shorter telomeres in T-cells of patients with ZAP-70+/CD38+ chronic lymphocytic leukaemia.
  • In contrast to other B-cell neoplasias, chronic lymphocytic leukaemia (CLL) is characterized by increased non-leukaemic T-cells.
  • Naive and memory T-cells from ZAP-70(+)/CD38(+) patients exhibited significantly shorter average telomere lengths than ZAP-70(-)/CD38(-) patients.
  • Compared to the age-related percentiles of telomere length values from healthy individuals practically all values of the naive and memory T-cells from the ZAP-70(+)/CD38(+) CLL patients fell below the 50th percentile.
  • This indicated an extensive expansion and a role for T-cells in ZAP-70(+)/CD38(+) CLL patients.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / immunology. T-Lymphocytes / ultrastructure. Telomere / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD38 / blood. Antigens, Neoplasm / blood. Cell Proliferation. Female. Humans. Immunologic Memory. Male. Membrane Glycoproteins / blood. Middle Aged. Retrospective Studies. ZAP-70 Protein-Tyrosine Kinase / blood

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  • (PMID = 18759763.001).
  • [ISSN] 1365-2141
  • [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 / Antigens, Neoplasm; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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24. Imamura M, Asano S, Harada M, Ikeda Y, Kato K, Kato S, Kawa K, Kojima S, Morishima Y, Morishita Y, Nakahata T, Okamura J, Okamoto S, Shiobara S, Tanimoto M, Tsuchida M, Atsuta Y, Yamamoto K, Tanaka J, Hamajima N, Kodera Y: Current status of hematopoietic cell transplantation for adult patients with hematologic diseases and solid tumors in Japan. Int J Hematol; 2006 Feb;83(2):164-78
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  • [Title] Current status of hematopoietic cell transplantation for adult patients with hematologic diseases and solid tumors in Japan.
  • A nationwide survey of hematopoietic cell transplantation (HCT) was started in Japan in 1991, and the analyzed survey data have been presented as the annual report of the Japan Society for Hematopoietic Cell Transplantation.
  • The 10-year overall survival (OS) rates after HCT for each disease are as follows: acute myelogenous leukemia, 44.2%; acute lymphocytic leukemia, 33.7%; adult T-cell leukemia, 24.6%; chronic myelogenous leukemia, 53.3%; myelodysplastic syndrome, 37.3%; non-Hodgkin's lymphoma, 41.5%; Hodgkin's lymphoma, 50.8%; aplastic anemia, 72.5%; breast cancer, 37.1%; germ cell tumor, 52.6%; and ovarian cancer, 44.2%.
  • The respective frequencies of acute graft-versus-host disease (GVHD) and chronic GVHD were 41.1% and 34.9% for related bone marrow transplantation (BMT), 66.8% and 34.5% for unrelated BMT, 52.9% and 36.0% for allogeneic peripheral blood stem cell transplantation, and 53.3% and 32.1% for allogeneic cord blood transplantation.
  • OS for each disease was analyzed by patient age, stem cell source, donor type, disease status, and disease type.
  • [MeSH-major] Hematologic Diseases / therapy. Hematopoietic Stem Cell Transplantation / methods. Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Female. Graft Survival. Graft vs Host Disease. Humans. Japan / epidemiology. Male. Middle Aged. Survival Rate

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  • [Cites] Blood. 2002 Aug 1;100(3):799-803 [12130489.001]
  • [Cites] Bone Marrow Transplant. 2005 Aug;36(3):205-13 [15937505.001]
  • [Cites] Bone Marrow Transplant. 1988 Nov;3(6):531-5 [3063321.001]
  • [Cites] N Engl J Med. 1998 Oct 22;339(17):1177-85 [9780337.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] N Engl J Med. 1995 Jan 26;332(4):217-23 [7808487.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2816-25 [15254049.001]
  • [Cites] Bone Marrow Transplant. 1998 Feb;21(3):255-61 [9489648.001]
  • [Cites] Am J Med. 2001 Apr 1;110(5):339-46 [11286947.001]
  • [Cites] Bone Marrow Transplant. 2004 Oct;34(8):711-9 [15361916.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(10):821-6 [9404921.001]
  • [Cites] N Engl J Med. 1995 Dec 7;333(23):1540-5 [7477169.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1606-13 [7632970.001]
  • [Cites] Bone Marrow Transplant. 1996 May;17 Suppl 3:S5-6 [8769690.001]
  • [Cites] Br J Haematol. 2000 Oct;111(1):6-17 [11091178.001]
  • [Cites] N Engl J Med. 1998 Dec 3;339(23):1649-56 [9834301.001]
  • [Cites] Ann Oncol. 1998;9 Suppl 1:S1-3 [9581234.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1541-7 [12714500.001]
  • [Cites] J Clin Oncol. 1996 Feb;14(2):572-8 [8636773.001]
  • [Cites] Leukemia. 1998 Sep;12 Suppl 1:S25-9 [9777891.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1295-303 [11870172.001]
  • [Cites] Blood. 1997 Feb 1;89(3):789-93 [9028309.001]
  • [Cites] Hum Immunol. 1997 Aug-Sep;56(1-2):1-5 [9455488.001]
  • [Cites] N Engl J Med. 2003 May 8;348(19):1875-83 [12736280.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3829-36 [12881308.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2490-7 [14656884.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):95-103 [10595758.001]
  • [Cites] Semin Hematol. 2001 Jul;38(3):243-9 [11486312.001]
  • [Cites] Blood. 2004 Jan 1;103(1):20-32 [12969978.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1997-2004 [12200358.001]
  • [Cites] Blood. 1996 Aug 1;88(3):795-802 [8704232.001]
  • [Cites] Stem Cells. 2002;20(1):3-10 [11796917.001]
  • [Cites] J Clin Oncol. 1994 Apr;12(4):759-63 [8151319.001]
  • [Cites] Bone Marrow Transplant. 1992;10 Suppl 1:102-6 [1521081.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3447-54 [12855572.001]
  • [Cites] Lancet. 1998 Mar 7;351(9104):700-8 [9504514.001]
  • [Cites] N Engl J Med. 2000 Sep 14;343(11):750-8 [10984562.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1943-51 [11877264.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4200-6 [12010826.001]
  • [Cites] Ann Oncol. 2003 May;14(5):737-44 [12702528.001]
  • [Cites] Biol Blood Marrow Transplant. 2004 Mar;10(3):195-203 [14993885.001]
  • [Cites] Lancet Oncol. 2000 Dec;1:227-34 [11905640.001]
  • [Cites] Blood. 1989 Nov 1;74(6):2252-6 [2804362.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3515-20 [9808542.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3586-92 [15173064.001]
  • [Cites] N Engl J Med. 1993 Mar 4;328(9):593-602 [8429851.001]
  • [Cites] J Clin Oncol. 2001 Dec 1;19(23):4314-21 [11731514.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1955-60 [14604976.001]
  • [Cites] N Engl J Med. 1996 Jul 11;335(2):91-7 [8649495.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:111-35 [12446421.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):423-9 [10458261.001]
  • [Cites] Springer Semin Immunopathol. 2004 Nov;26(1-2):31-56 [15368078.001]
  • [Cites] Bone Marrow Transplant. 2005 Oct;36(7):575-90 [16086045.001]
  • [Cites] N Engl J Med. 1998 Apr 2;338(14):962-8 [9521984.001]
  • [Cites] J Clin Oncol. 1996 Apr;14(4):1291-6 [8648386.001]
  • (PMID = 16513537.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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25. Aswald JM, Wang XH, Aswald S, Lutynski A, Minden MD, Messner HA, Keating A: Flow cytometric assessment of autologous gammadelta T cells in patients with acute myeloid leukemia: potential effector cells for immunotherapy? Cytometry B Clin Cytom; 2006 Nov 15;70(6):379-90
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  • [Title] Flow cytometric assessment of autologous gammadelta T cells in patients with acute myeloid leukemia: potential effector cells for immunotherapy?
  • BACKGROUND: Gammadelta T cells are a rare component of the circulating innate immune system capable of exerting anti-neoplastic activity.
  • This population may be suitable for the adoptive immunotherapy of acute myeloid leukemia (AML).
  • Little is known however, about the frequency and function of circulating gammadelta T cells in AML.
  • The aim of the study was to enumerate peripheral blood gammadelta T cells in patients with AML and explore the feasibility of their use clinically.
  • METHODS: We compared the absolute circulating gammadelta T cell levels in 33 AML patients before and after treatment versus 20 healthy volunteers using flow cytometry.
  • The function of gammadelta T cells was assessed by detection of intracelluar interferon-gamma (IFN-gamma) and cytotoxicity against leukemic blasts.
  • RESULTS: AML patients with high blast counts prior to induction chemotherapy had marginally decreased gammadelta T cell levels compared with healthy controls: median 38/microL versus 83/microL; P = 0.051.
  • Sequential gammadelta T cell enumeration after induction showed significantly decreased counts in patients with a persistently high blast burden compared to patients with reduced but detectable residual disease (molecular maker or borderline bone marrow infiltration): median 7/microL versus 105/microL; P = 0.008.
  • Patients with residual disease had significantly higher gammadelta T cell counts compared to those retested after they had achieved complete remission (CR); P = 0.0025.
  • In CR, gammadelta T cell counts remained lower than those of healthy individuals: median 33/microL versus 83/microL, P = 0.030.
  • We detected a sharp increase (on average, four-fold higher than values in CR) of gammadelta T cells in patients in very early morphologic or molecular relapse.
  • We also tested the functional properties of gammadelta T cells from patients with AML in CR.
  • Flow cytometric assessment of IFN-gamma revealed similar numbers of gammadelta T cells expressing the T1 cytokine compared with healthy controls.
  • We also showed that gammadelta T cells were able to kill leukemic target cells in vitro.
  • CONCLUSION: Flow cytometric assessment of gammadelta T cells in patients with AML revealed quantitative shifts with respect to disease status.
  • Our data suggest that gammadelta T cells warrant further investigation as potential therapeutic agents.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Myeloid / immunology. Receptors, Antigen, T-Cell, gamma-delta / immunology. T-Lymphocytes / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Count. Feasibility Studies. Female. Humans. Immunotherapy. Male. Middle Aged. Neoplasm, Residual / immunology. Recurrence. Remission Induction. Sensitivity and Specificity

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  • [Copyright] Copyright 2006 International Society for Analytical Cytology.
  • (PMID = 16977635.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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26. Burkhardt B, Reiter A, Landmann E, Lang P, Lassay L, Dickerhoff R, Lakomek M, Henze G, von Stackelberg A: Poor outcome for children and adolescents with progressive disease or relapse of lymphoblastic lymphoma: a report from the berlin-frankfurt-muenster group. J Clin Oncol; 2009 Jul 10;27(20):3363-9
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  • [Title] Poor outcome for children and adolescents with progressive disease or relapse of lymphoblastic lymphoma: a report from the berlin-frankfurt-muenster group.
  • PURPOSE: Little is known about the outcome of pediatric patients with lymphoblastic lymphoma (LBL) who suffer from progressive disease or relapse.
  • Relapse therapy was according to acute lymphoblastic leukemia (ALL) -Relapse-BFM protocols or ALL-BFM protocols for high-risk patients.
  • RESULTS: Twenty-eight (11%) of 251 registered patients with precursor T-cell LBL (T-LBL) and six (8%) of 73 patients with precursor B-cell LBL (pB-LBL) suffered from relapse.
  • Of the 28 patients with T-LBL, one died from infection during relapse chemotherapy, 18 failed to achieve stable remission and died from disease progression, and nine reached allogeneic stem-cell transplantation (SCT).
  • Two of these nine patients who underwent SCT died from transplantation-associated toxicity, three died from disease progression, and four are still alive.
  • Of the six patients with pB-LBL who experienced relapse, one patient died as a result of toxicity of relapse chemotherapy, two died from disease progression after chemotherapy, and three received allogeneic SCT.
  • Of these, two died from subsequent disease progression, and one is still alive 57 months after allogeneic SCT.
  • CONCLUSION: Using modern conventional therapy in the frontline treatment of LBL, 10% of patients suffer from progressive disease or relapse.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Analysis of Variance. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Disease Progression. Female. Germany. Humans. Kaplan-Meier Estimate. Male. Multicenter Studies as Topic. Prognosis. Recurrence. Stem Cell Transplantation / adverse effects. Stem Cell Transplantation / methods. Switzerland. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • (PMID = 19433688.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Sanda T, Asamitsu K, Ogura H, Iida S, Utsunomiya A, Ueda R, Okamoto T: Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor. Leukemia; 2006 Apr;20(4):590-8
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  • [Title] Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor.
  • NF-kappaB is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.
  • In this study, we demonstrate that NF-kappaB is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IkappaBalpha and p65 subunit of NF-kappaB, activation of NF-kappaB DNA binding, and upregulation of various target genes including bcl-xL, bcl-2, XIAP, c-IAP1, survivin, cyclinD1, ICAM-1 and VCAM-1.
  • The effects of a novel IkappaB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.
  • We found that ACHP could inhibit the phosphorylation of IkappaBalpha and p65, as well as NF-kappaB DNA-binding, associated with downregulation of the NF-kappaB target genes and induce cell growth arrest and apoptosis in these cells.
  • When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.
  • Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.
  • These findings indicate that ACHP and its derivatives are effective in inducing ATL cell death and thus feasible candidates for the treatment of ATL.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / metabolism. Nicotinic Acids / pharmacology. Nitriles / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Binding Sites. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Gene Expression Regulation, Enzymologic / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. In Vitro Techniques. Phosphorylation. Protein Subunits / antagonists & inhibitors. Protein Subunits / genetics. Protein Subunits / metabolism. Structure-Activity Relationship. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism

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  • (PMID = 16453001.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-6-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-4-piperidin-4-yl nicotinonitrile; 0 / Enzyme Inhibitors; 0 / Nicotinic Acids; 0 / Nitriles; 0 / Protein Subunits; 0 / Transcription Factor RelA; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase
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28. Stern M, Ruggeri L, Mancusi A, Bernardo ME, de Angelis C, Bucher C, Locatelli F, Aversa F, Velardi A: Survival after T cell-depleted haploidentical stem cell transplantation is improved using the mother as donor. Blood; 2008 Oct 1;112(7):2990-5
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  • [Title] Survival after T cell-depleted haploidentical stem cell transplantation is improved using the mother as donor.
  • We hypothesized that transplacental leukocyte trafficking during pregnancy, which induces long-term, stable, reciprocal microchimerism in mother and child, might influence outcome of patients with acute leukemia given parental donor haploidentical hematopoietic stem cell transplantation (HSCT).
  • We analyzed the outcome of 118 patients who received transplants for acute leukemia in 2 centers.
  • Patients received highly T cell-depleted haploidentical grafts after myelo-ablative conditioning.
  • Incidences of rejection and acute graft-versus-host disease were not significantly influenced.


29. Urnowey S, Ansai T, Bitko V, Nakayama K, Takehara T, Barik S: Temporal activation of anti- and pro-apoptotic factors in human gingival fibroblasts infected with the periodontal pathogen, Porphyromonas gingivalis: potential role of bacterial proteases in host signalling. BMC Microbiol; 2006 Mar 08;6:26
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  • BACKGROUND: Porphyromonas gingivalis is the foremost oral pathogen of adult periodontitis in humans.
  • RESULTS: We report host-P. gingivalis interactions in primary human gingival fibroblast (HGF) cells.
  • Use of inhibitors revealed an anti-apoptotic function of NF-kappa B and PI3 kinase in P. gingivalis-infected HGF cells.

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  • [Cites] Oral Microbiol Immunol. 1991 Aug;6(4):209-15 [1667433.001]
  • [Cites] Oral Microbiol Immunol. 2004 Apr;19(2):121-3 [14871353.001]
  • [Cites] J Biol Chem. 1995 Jun 16;270(24):14255-8 [7782278.001]
  • [Cites] Infect Immun. 1995 Oct;63(10):3878-85 [7558295.001]
  • [Cites] Microbiology. 1995 Sep;141 ( Pt 9):2047-52 [7496515.001]
  • [Cites] Biochem J. 1996 Nov 1;319 ( Pt 3):683-90 [8920967.001]
  • [Cites] Infect Immun. 1997 May;65(5):1980-4 [9125593.001]
  • [Cites] Virology. 1997 Jun 9;232(2):369-78 [9191851.001]
  • [Cites] Mol Microbiol. 1997 Jun;24(6):1179-87 [9218767.001]
  • [Cites] J Virol. 1998 Jul;72(7):5610-8 [9621019.001]
  • [Cites] Methods Mol Biol. 2000;144:219-23 [10818766.001]
  • [Cites] Leukemia. 2000 Sep;14(9):1695-703 [10995018.001]
  • [Cites] J Cell Biochem. 2001;80(3):441-54 [11135374.001]
  • [Cites] Infect Immun. 2001 Mar;69(3):1364-72 [11179300.001]
  • [Cites] Infect Immun. 2001 May;69(5):3048-56 [11292723.001]
  • [Cites] J Periodontol. 2001 May;72(5):641-50 [11394400.001]
  • [Cites] FEMS Microbiol Lett. 2001 Jun 25;200(2):145-9 [11425466.001]
  • [Cites] Biol Chem. 2001 May;382(5):727-33 [11517925.001]
  • [Cites] Biol Chem. 2001 May;382(5):817-24 [11517936.001]
  • [Cites] Infect Immun. 2001 Dec;69(12):7527-34 [11705929.001]
  • [Cites] Microsc Res Tech. 2002 Jan 1;56(1):15-31 [11810703.001]
  • [Cites] Proteins. 2002 Mar 1;46(4):355-67 [11835511.001]
  • [Cites] Infect Immun. 2002 May;70(5):2512-8 [11953390.001]
  • [Cites] Cell Microbiol. 2002 May;4(5):305-14 [12027958.001]
  • [Cites] Infect Immun. 2002 Oct;70(10):5846-56 [12228316.001]
  • [Cites] J Periodontol. 2003 Jan;74(1):90-6 [12593602.001]
  • [Cites] J Periodontol. 2003 Jan;74(1):119-22 [12593606.001]
  • [Cites] J Biol Chem. 2003 Mar 21;278(12):10458-64 [12533545.001]
  • [Cites] J Biol Chem. 2003 Apr 18;278(16):14162-7 [12576481.001]
  • [Cites] Infect Immun. 2003 Aug;71(8):4742-8 [12874356.001]
  • [Cites] Int J Parasitol. 2004 Mar 9;34(3):381-91 [15003498.001]
  • [Cites] J Periodontol. 2004 Mar;75(3):370-9 [15088874.001]
  • [Cites] Semin Cell Dev Biol. 2004 Apr;15(2):177-82 [15209377.001]
  • [Cites] Infect Immun. 2004 Jul;72(7):3743-51 [15213114.001]
  • [Cites] Infect Immun. 2004 Jul;72(7):3752-8 [15213115.001]
  • [Cites] BMC Microbiol. 2004 Jul 15;4:28 [15256003.001]
  • [Cites] Infect Immun. 2004 Aug;72(8):4689-98 [15271930.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] Genes Dev. 2004 Sep 15;18(18):2195-224 [15371334.001]
  • [Cites] J Periodontol. 1992 Jan;63(1):44-51 [1313102.001]
  • [Cites] Eur J Oral Sci. 1998 Aug;106(4):863-71 [9708689.001]
  • [Cites] FEBS Lett. 1998 Dec 28;441(3):361-5 [9891971.001]
  • [Cites] Arch Oral Biol. 1999 Apr;44(4):337-42 [10348360.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17955-60 [10364243.001]
  • [Cites] EMBO J. 1999 Oct 15;18(20):5453-62 [10523290.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Nov;5(11):897-907 [15520809.001]
  • [Cites] J Dent Res. 2005 Jan;84(1):9-20 [15615869.001]
  • [Cites] Microb Pathog. 2004 Dec;37(6):303-12 [15619426.001]
  • [Cites] Infect Immun. 2005 Mar;73(3):1543-52 [15731052.001]
  • [Cites] Curr Top Microbiol Immunol. 2005;289:131-50 [15791954.001]
  • [Cites] Microbes Infect. 2005 Mar;7(3):448-56 [15811635.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):7383-92 [15905586.001]
  • [Cites] J Dent Res. 2003 Oct;82(10):796-801 [14514759.001]
  • [Cites] Oral Microbiol Immunol. 2003 Dec;18(6):398-400 [14622347.001]
  • [Cites] Oncogene. 2003 Dec 8;22(56):8961-82 [14663476.001]
  • [Cites] Curr Protein Pept Sci. 2003 Dec;4(6):389-95 [14683425.001]
  • [Cites] Curr Protein Pept Sci. 2003 Dec;4(6):397-407 [14683426.001]
  • [Cites] Oral Microbiol Immunol. 1993 Aug;8(4):203-7 [8247606.001]
  • (PMID = 16524480.001).
  • [ISSN] 1471-2180
  • [Journal-full-title] BMC microbiology
  • [ISO-abbreviation] BMC Microbiol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY013826; United States / NIAID NIH HHS / AI / AI045803; United States / NIAID NIH HHS / AI / R01 AI045803; United States / NEI NIH HHS / EY / R01 EY013826; United States / NCRR NIH HHS / RR / C06 RR11174
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.- / Peptide Hydrolases
  • [Other-IDs] NLM/ PMC1431544
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30. Christopoulos P, Follo M, Fisch P, Veelken H: The peripheral helper T-cell repertoire in untreated indolent B-cell lymphomas: evidence for antigen-driven lymphomagenesis. Leukemia; 2008 Oct;22(10):1952-4
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  • [Title] The peripheral helper T-cell repertoire in untreated indolent B-cell lymphomas: evidence for antigen-driven lymphomagenesis.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / immunology. T-Lymphocytes, Helper-Inducer / immunology
  • [MeSH-minor] Adult. Aged. Complementarity Determining Regions. Female. Humans. Male. Middle Aged. Receptors, Antigen, T-Cell / analysis

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  • (PMID = 18385751.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Complementarity Determining Regions; 0 / Receptors, Antigen, T-Cell
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31. Chen B, Zhao WL, Jin J, Xue YQ, Cheng X, Chen XT, Cui J, Chen ZM, Cao Q, Yang G, Yao Y, Xia HL, Tong JH, Li JM, Chen J, Xiong SM, Shen ZX, Waxman S, Chen Z, Chen SJ: Clinical and cytogenetic features of 508 Chinese patients with myelodysplastic syndrome and comparison with those in Western countries. Leukemia; 2005 May;19(5):767-75
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  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic stem cell disorder characterized by ineffective hematopoiesis and leukemia progression.
  • (2) a strong predictive value of cytogenetic abnormalities on disease outcome and involvement of genomic instability in leukemia clone development.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. China. Cytogenetic Analysis / methods. Developed Countries. Female. Humans. Male. Middle Aged. Reproducibility of Results. Retrospective Studies. Survival Analysis. Treatment Outcome


32. Suneetha KJ, Nancy KN, Rajalekshmy KR, Sagar TG, Rajkumar T: Role of GSTM1 (Present/Null) and GSTP1 (Ile105Val) polymorphisms in susceptibility to acute lymphoblastic leukemia among the South Indian population. Asian Pac J Cancer Prev; 2008 Oct-Dec;9(4):733-6
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  • [Title] Role of GSTM1 (Present/Null) and GSTP1 (Ile105Val) polymorphisms in susceptibility to acute lymphoblastic leukemia among the South Indian population.
  • Acute lymphoblastic leukaemia (ALL) is the most common pediatric malignancy worldwide.
  • The origin of this disease may be explained by a combination of genetic and environmental factors.
  • [MeSH-major] Genetic Predisposition to Disease / epidemiology. Glutathione S-Transferase pi / genetics. Glutathione Transferase / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Age Distribution. Case-Control Studies. Chi-Square Distribution. Child. Child, Preschool. Confidence Intervals. Female. Gene Expression Regulation, Neoplastic. Genotype. Humans. Incidence. India / epidemiology. Male. Odds Ratio. Polymerase Chain Reaction. Probability. Prognosis. Risk Assessment. Severity of Illness Index. Sex Distribution. Survival Analysis. Young Adult

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  • (PMID = 19256768.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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33. Sirohi B, Powles R, Treleaven J, Kulkarni S, Saso R, Potter M, Ethell M, Morgan G, Singhal S, Mehta J: The role of maintenance chemotherapy after autotransplantation for acute lymphoblastic leukemia in first remission: single-center experience of 100 patients. Bone Marrow Transplant; 2008 Jul;42(2):105-12
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  • [Title] The role of maintenance chemotherapy after autotransplantation for acute lymphoblastic leukemia in first remission: single-center experience of 100 patients.
  • A total of 100 adults with ALL in first CR received melphalan (110 mg/m(2)) with TBI followed by autologous marrow (n=35) or single-agent melphalan (200 mg/m(2)) followed by autologous blood stem cells (n=65).
  • The 7-year probabilities of disease-free survival (DFS) and overall survival were 45 and 48%.
  • Maintenance chemotherapy after autotransplantation reduces relapse and improves outcome in adult patients with ALL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Transplantation, Autologous


34. Ishii T, Ishida T, Utsunomiya A, Inagaki A, Yano H, Komatsu H, Iida S, Imada K, Uchiyama T, Akinaga S, Shitara K, Ueda R: Defucosylated humanized anti-CCR4 monoclonal antibody KW-0761 as a novel immunotherapeutic agent for adult T-cell leukemia/lymphoma. Clin Cancer Res; 2010 Mar 1;16(5):1520-31
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  • [Title] Defucosylated humanized anti-CCR4 monoclonal antibody KW-0761 as a novel immunotherapeutic agent for adult T-cell leukemia/lymphoma.
  • PURPOSE: Adult T-cell leukemia/lymphoma (ATLL) has a very poor prognosis.
  • EXPERIMENTAL DESIGN: The antitumor activity of KW-0761 against ATLL cell lines was evaluated in vitro using human cells and in mice in vivo.
  • Primary ATLL cells from 23 patients were evaluated for susceptibility to autologous ADCC with KW-0761 by two independent methods.
  • RESULTS: KW-0761 showed potent antitumor activity against ATLL cell lines both in vitro and in the ATLL mouse model in vivo.
  • In addition, KW-0761 showed potent antitumor activity mediated by highly enhanced ADCC against primary ATLL cells both in vitro and ex vivo in an autologous setting.
  • The degree of KW-0761 ADCC against primary ATLL cells in an autologous setting was mainly determined by the amount of effector natural killer cells present, but not the amount of the target molecule CCR4 on the ATLL cell surface.
  • In addition, combination treatment strategies that augment natural killer cell activity should be promising for amplifying the effect of KW-0761.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotherapy / methods. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Animals. Antibodies, Monoclonal, Humanized. Antibody-Dependent Cell Cytotoxicity / drug effects. Antibody-Dependent Cell Cytotoxicity / immunology. Biosensing Techniques. Cell Separation. Flow Cytometry. Humans. Male. Mice. Mice, SCID. Receptors, CCR4 / immunology

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  • (PMID = 20160057.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / mogamulizumab
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35. Franzoi AC, Araújo AQ: Disability and determinants of gait performance in tropical spastic paraparesis/HTLV-I associated myelopathy (HAM/TSP). Spinal Cord; 2007 Jan;45(1):64-8
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  • [Title] Disability and determinants of gait performance in tropical spastic paraparesis/HTLV-I associated myelopathy (HAM/TSP).
  • OBJECTIVES: The aim of this survey is to describe the disability profile in a group of tropical spastic paraparesis/HTLV-I-associated myelopathy patients, identifying the requirements for community ambulation.
  • SETTING: Tertiary care unit, Rio de Janeiro, Brazil.
  • RESULTS: The sample had an average age of 40 years and an average of 137 months of duration of the disease.
  • Strength, age, low-back pain, duration of disease, asymmetric onset of the symptoms and spasticity interfered in the ability to walk (P<0.05).
  • [MeSH-major] Disability Evaluation. Gait / physiology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Paraparesis, Tropical Spastic / epidemiology. Paraparesis, Tropical Spastic / physiopathology
  • [MeSH-minor] Activities of Daily Living. Adult. Brazil / epidemiology. Cross-Sectional Studies. Female. Humans. Male. Middle Aged. Neurologic Examination


36. van Besien K, Artz A, Smith S, Cao D, Rich S, Godley L, Jones D, Del Cerro P, Bennett D, Casey B, Odenike O, Thirman M, Daugherty C, Wickrema A, Zimmerman T, Larson RA, Stock W: Fludarabine, melphalan, and alemtuzumab conditioning in adults with standard-risk advanced acute myeloid leukemia and myelodysplastic syndrome. J Clin Oncol; 2005 Aug 20;23(24):5728-38
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  • [Title] Fludarabine, melphalan, and alemtuzumab conditioning in adults with standard-risk advanced acute myeloid leukemia and myelodysplastic syndrome.
  • PURPOSE: This prospective phase II study evaluated toxicity, relapse rate, progression-free survival, and overall survival after allogeneic transplantation and conditioning with fludarabine, melphalan, and alemtuzumab in patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Median age was 52 years (range, 17 to 71 years) and the majority of patients had high-risk disease, comorbidities, and/or modest reduction in performance status.
  • The cumulative probability of extensive chronic graft-versus-host disease (GVHD) was only 18% (95% CI, 8% to 40%); extensive chronic GVHD was only observed in recipients of unrelated donor transplants.
  • Performance score and disease status were the major predictors of outcome.
  • High-risk disease (ie, active AML or MDS with > 5% blasts) or even modest decreases in performance status were associated with poor outcomes.
  • Patients with standard-risk leukemia (first or second complete remission) or MDS (< 5% blasts) had excellent outcomes despite unfavorable disease characteristics.
  • For patients with active disease, this regimen provides at best modest palliation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / prevention & control. Humans. Male. Melphalan / administration & dosage. Middle Aged. Proportional Hazards Models. Prospective Studies. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 16009946.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 101337
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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37. Uberti JP, Ayash L, Ratanatharathorn V, Silver S, Reynolds C, Becker M, Reddy P, Cooke KR, Yanik G, Whitfield J, Jones D, Hutchinson R, Braun T, Ferrara JL, Levine JE: Pilot trial on the use of etanercept and methylprednisolone as primary treatment for acute graft-versus-host disease. Biol Blood Marrow Transplant; 2005 Sep;11(9):680-7
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  • [Title] Pilot trial on the use of etanercept and methylprednisolone as primary treatment for acute graft-versus-host disease.
  • Clinical and preclinical data indicate that tumor necrosis factor (TNF)-alpha is an important mediator of acute graft-versus-host disease (aGVHD) after allogeneic bone marrow transplantation.
  • Fourteen patients with grade II aGVHD (11 family donors and 3 unrelated donors) and 6 patients with grade III aGVHD (3 family donors and 3 unrelated donors) were treated.
  • Reasons for not completing all doses of etanercept included progression of aGVHD (n = 4), relapsed leukemia (n = 2), progression of pulmonary and central nervous system lesions (n = 1), and perforated duodenal ulcer (n = 1).
  • [MeSH-major] Anti-Inflammatory Agents / administration & dosage. Bone Marrow Transplantation. Graft vs Host Disease / drug therapy. Immunoglobulin G / administration & dosage. Lymphoproliferative Disorders / therapy. Methylprednisolone / administration & dosage. Receptors, Tumor Necrosis Factor / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Child. Drug Therapy, Combination. Etanercept. Female. Humans. Immunosuppressive Agents. Male. Middle Aged. Pilot Projects. Receptors, Tumor Necrosis Factor, Type I / blood. Tacrolimus / administration & dosage. Transplantation, Homologous. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16125638.001).
  • [ISSN] 1083-8791
  • [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
  • [Grant] United States / FDA HHS / FD / FD-R-002020; United States / NCI NIH HHS / CA / K23 CA88930; United States / NCI NIH HHS / CA / P01 CA 039542
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept; WM0HAQ4WNM / Tacrolimus; X4W7ZR7023 / Methylprednisolone
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38. Horie R: NF-kappaB in pathogenesis and treatment of adult T-cell leukemia/lymphoma. Int Rev Immunol; 2007 Sep-Dec;26(5-6):269-81
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  • [Title] NF-kappaB in pathogenesis and treatment of adult T-cell leukemia/lymphoma.
  • Human T-cell leukemia/lymphoma virus type 1 (HTLV-1) induces aberrant nuclear factor-kappaB (NF-kappaB) activation.
  • Although Tax is thought to play major roles in NF-kappaB activation, cells expressing Tax become a target of cytotoxic T cells.
  • Accordingly, HTLV-1-infected cells lose Tax expression and acquire Tax-independent NF-kappaB activation.
  • Blocking NF-kappaB not only induces apoptosis in adult T-cell leukemia/lymphoma (ATL) cells but also reduces the number of HTLV-1-infected cells in virus carriers.
  • Therefore, because constitutively activated NF-kappaB appears to be the common biological basis shared between HTLV-1-infected untransformed cells and ATL cells, blocking NF-kappaB might be a potential strategy for treating and preventing ATL.
  • [MeSH-major] Human T-lymphotropic virus 1 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / therapy. NF-kappa B / metabolism
  • [MeSH-minor] Cell Proliferation. Gene Products, tax / metabolism. Humans

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  • (PMID = 18027201.001).
  • [ISSN] 0883-0185
  • [Journal-full-title] International reviews of immunology
  • [ISO-abbreviation] Int. Rev. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / NF-kappa B
  • [Number-of-references] 46
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39. Mami NB, Mohty M, Aurran-Schleinitz T, Olive D, Gaugler B: Blood dendritic cells in patients with chronic lymphocytic leukaemia. Immunobiology; 2008;213(6):493-8
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  • [Title] Blood dendritic cells in patients with chronic lymphocytic leukaemia.
  • Myeloid and plasmacytoid dendritic cells (MDC, PDC) play a key role in the initiation of immune responses.
  • We found a reduction of both DC subsets in 42 patients with chronic lymphocytic leukaemia (CLL) at diagnosis (P<0.0001 and 0.0001 vs. controls, respectively), likely related to the high secretion of CCL22 and CXCL12 (P=0.04 and 0.008 vs. controls, respectively) by leukaemic cells.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cytokines / metabolism. Dendritic Cells / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Lymphocyte Subsets / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

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  • (PMID = 18514751.001).
  • [ISSN] 0171-2985
  • [Journal-full-title] Immunobiology
  • [ISO-abbreviation] Immunobiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytokines
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40. Matsuda R, Nikaido Y, Yamada T, Mishima H, Tamaki R: [High-dose radiation-induced meningioma following prophylactic cranial irradiation for acute lymphoblastic leukaemia]. No Shinkei Geka; 2005 Mar;33(3):277-80
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  • [Title] [High-dose radiation-induced meningioma following prophylactic cranial irradiation for acute lymphoblastic leukaemia].
  • A 12 year-old girl was treated with prophylatic cranial irradiation for acute lymphoblastic leukaemia (ALL).
  • [MeSH-major] Cranial Irradiation / adverse effects. Meningeal Neoplasms / etiology. Meningioma / etiology. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy
  • [MeSH-minor] Adult. Central Nervous System Neoplasms / prevention & control. Female. Humans. Radiotherapy Dosage

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  • (PMID = 15773318.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 11
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41. Meuleman N, Tondreau T, Ahmad I, Kwan J, Crokaert F, Delforge A, Dorval C, Martiat P, Lewalle P, Lagneaux L, Bron D: Infusion of mesenchymal stromal cells can aid hematopoietic recovery following allogeneic hematopoietic stem cell myeloablative transplant: a pilot study. Stem Cells Dev; 2009 Nov;18(9):1247-52
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  • [Title] Infusion of mesenchymal stromal cells can aid hematopoietic recovery following allogeneic hematopoietic stem cell myeloablative transplant: a pilot study.
  • Mesenchymal stromal cells (MSCs) are important in the support of hematopoiesis.
  • In this pilot study, we evaluated the safety and efficiency of donor-expanded MSC infusion after allogeneic hematopoietic stem cell transplantation (HSCT) in six patients with poor hematopoietic recovery.
  • One patient developed cytomegalovirus (CMV) reactivation 12 days following the MSC infusion and died from CMV disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Mesenchymal Stem Cell Transplantation / methods. Stromal Cells / transplantation. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Cytomegalovirus Infections / etiology. Graft Rejection / prevention & control. Hematopoiesis. Humans. Leukemia / blood. Leukemia / therapy. Male. Middle Aged. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / therapy. Pilot Projects. Pulmonary Aspergillosis / etiology. Recovery of Function. Remission Induction. Time Factors. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • [CommentIn] Stem Cells Dev. 2009 Nov;18(9):1243-6 [19905962.001]
  • (PMID = 19309241.001).
  • [ISSN] 1557-8534
  • [Journal-full-title] Stem cells and development
  • [ISO-abbreviation] Stem Cells Dev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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42. Li S, Wang T, Wang J, Li J, Zhang L: [Dynamic detection of FLT3 gene in patients with AML and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):705-8
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  • Minimal residual disease (MRD) is an important cause of relapse and disease-free survival time decrease in patients with acute myeloid leukemia (AML).
  • Using genomic PCR, 125 AML patients were detected for FLT3 gene expression before and after chemical therapy and allogeneic hematopoietic stem cell transplantation (allo-HSCT), meantime the AML patients with FLT3 positive expression were observed by follow-up.
  • It is concluded that FLT3 gene expression is related to leukemia pathogenesis; the dynamic levels of FLT3 expression before and after treatment can be used for estimating prognosis of AML patients and detecting MRD.

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  • (PMID = 17708787.001).
  • [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] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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43. Chen AI, McMillan A, Negrin RS, Horning SJ, Laport GG: Long-term results of autologous hematopoietic cell transplantation for peripheral T cell lymphoma: the Stanford experience. Biol Blood Marrow Transplant; 2008 Jul;14(7):741-7
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  • [Title] Long-term results of autologous hematopoietic cell transplantation for peripheral T cell lymphoma: the Stanford experience.
  • The peripheral T cell lymphomas (PTCL) carry a worse prognosis compared to B cell non-Hodgkin lymphoma.
  • There is no uniform standard therapy for PTCL, and autologous hematopoietic cell transplant (AHCT) is often offered as consolidation in first remission or at relapse because of the poor outcomes with conventional therapy.
  • Fifty-three cases were identified consisting of systemic anaplastic large cell (n = 18), PTCL unspecified (n = 17), angioimmunoblastic (n = 9), nasal type extranodal NK/T (n = 7), hepatosplenic (n = 2), and adult T cell leukemia/lymphoma (n = 1).
  • Fifteen patients were transplanted in first complete or partial response (CR1/PR1), 32 in second or beyond CR or PR (CR2/PR2+), and 11 with primary refractory disease (REF).
  • Disease status at AHCT had a significant impact on PFS and OS.
  • The pretransplant factors that impacted survival were disease status and the number of prior regimens.


44. Park HH, Kim M, Lee BH, Lim J, Kim Y, Lee EJ, Min WS, Kang CS, Kim WI, Shim SI, Han K: Intracellular IL-4, IL-10, and IFN-gamma levels of leukemic cells and bone marrow T cells in acute leukemia. Ann Clin Lab Sci; 2006;36(1):7-15
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  • [Title] Intracellular IL-4, IL-10, and IFN-gamma levels of leukemic cells and bone marrow T cells in acute leukemia.
  • The quantitative levels of intracellular cytokines IL-4, IL-10, and IFN-gamma (ie, the number of bound PE-conjugated antibody molecules/cell) of leukemic cells and bone marrow T cells (bmT cells) of acute leukemia patients were analyzed by flow cytometry.
  • The leukemic cell IL-4 level was highest in the monocytic AML group (1735 +/- 1056) and lowest in the dysplastic AML group (960 +/- 545).
  • The IFN-gamma level was highest in the acute promyelocytic leukemia (APL) group (495 +/- 159), and lowest in the ALL group (252 +/- 119).
  • In bmT cells, the IL-10 level was highest in the dysplastic AML group (972 +/- 1049) and lowest in the APL group (397 +/- 352).
  • The leukemic cell cytokine levels were lowest and bmT cell cytokine levels were highest in the dysplastic AML group.
  • The cytokine levels of bmT cells at the time of CR became normal and were not different among the diagnosis groups.
  • In summary, leukemic cell and bmT cell cytoplasmic expression profiles of IL-4, IL-10, and IFN-gamma are characteristic for each diagnostic group of acute leukemia patients and the profiles of bmT cells are normal at the time of CR.
  • [MeSH-major] Bone Marrow Cells / metabolism. Interferon-gamma / blood. Interleukin-10 / blood. Interleukin-4 / blood. Leukemia / metabolism. T-Lymphocytes / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Remission Induction

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  • (PMID = 16501231.001).
  • [ISSN] 0091-7370
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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45. Kawamura M, Kaku H, Ito T, Funata N, Taki T, Shimada A, Hayashi Y: FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia. Cancer Genet Cytogenet; 2010 Dec;203(2):292-6
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  • [Title] FLT3-internal tandem duplication in a pediatric patient with t(8;21) acute myeloid leukemia.
  • Patients diagnosed with t(8;21)-acute myeloid leukemia (AML) are currently considered to have good prognoses, but about half of these patients relapse.
  • Expression of the neural cell-adhesion molecule (CD56) is also associated with a significantly shorter complete remission duration and survival in patients with t(8;21)-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD56 / biosynthesis. Fatal Outcome. Female. Humans. Jaundice, Obstructive / mortality. Jaundice, Obstructive / pathology. Male. Middle Aged. Proto-Oncogene Proteins c-kit / metabolism. Recurrence. Remission Induction

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 21156247.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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46. Wada T, Yoshinaga E, Oiso N, Kawara S, Kawada A, Kozuka T: Adult T-cell leukemia-lymphoma associated with follicular mucinosis. J Dermatol; 2009 Dec;36(12):638-42
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  • [Title] Adult T-cell leukemia-lymphoma associated with follicular mucinosis.
  • Follicular mucinosis (alopecia mucinosa) is often associated with malignancies including mycosis fungoides and Sézary syndrome, but not adult T-cell leukemia-lymphoma (ATLL).
  • The patient showed 11% of flower-shaped atypical lymphocytes in blood examination and positive human T-cell leukemia virus type 1 antibody in serology, consistent with the chronic type of ATLL.
  • This case seems to be a very rare association of follicular mucinosis and chronic ATLL, suggesting that malignant T cells may have a feature of folliculotropism as well as epidermotropism.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Mucinosis, Follicular / complications

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  • (PMID = 19958447.001).
  • [ISSN] 1346-8138
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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47. Olteanu H, Schur BC, Bredeson C, Atallah E, Kroft SH: Expression of natural killer receptors in T- and NK-cells: comparison of healthy individuals, patients with prior stem cell transplant, and patients undergoing chemotherapy. Leuk Lymphoma; 2010 Mar;51(3):481-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of natural killer receptors in T- and NK-cells: comparison of healthy individuals, patients with prior stem cell transplant, and patients undergoing chemotherapy.
  • We studied the expression of natural killer receptors (NKRs) on peripheral blood cytotoxic T lymphocytes and NK cells in patients who underwent an allogeneic stem cell transplant (SCT), and compared these findings with results from healthy individuals (CTRL) and patients undergoing chemotherapy (CHEMO), respectively.
  • Peripheral blood mononuclear cells were analyzed by flow cytometry with antibodies against the NKRs CD158a, CD158b, CD158e (known as killer immunoglobulin-like receptors, KIRs), and CD94.
  • Expression of NKRs was evaluated separately in CD56+, CD57+, and CD56/CD57 (double +) subsets of T and NK cells.
  • Our results provide a comprehensive overview of KIR and CD94 expression in T and NK cells following SCT and chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gene Expression Regulation. Killer Cells, Natural / metabolism. Lymphoproliferative Disorders / drug therapy. Receptors, Natural Killer Cell / metabolism. Stem Cell Transplantation. T-Lymphocytes, Cytotoxic / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, CD / metabolism. Female. Humans. Immunophenotyping. Male. Middle Aged. Transplantation, Homologous. Young Adult

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  • (PMID = 20141431.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Receptors, Natural Killer Cell
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48. Kashima K, Daa T, Yokoyama S: Detection of HTLV-1 gene on cytologic smear slides. Methods Mol Biol; 2005;304:183-9
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  • [Title] Detection of HTLV-1 gene on cytologic smear slides.
  • In this chapter we describe a method for the detection of human T-cell leukemia virus type 1 (HTLV-1) genes in cytologic smears by polymerase chain reaction (PCR).
  • If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes, cells of interest are isolated by microdissection.
  • Second, microdissected cells are collected in microtubes and digested with proteinase K.
  • The cells that did not undergo the microdissection are digested and dissolve in the proteinase K solution on the slides.
  • We use two sets of primers for detection of HTLV-1 genes, and the products of amplification by PCR that correspond to the pX and tax regions are expected to be 127 and 159 base pairs long, respectively.
  • Although this method does not provide proof of the monoclonal integration of HTLV-1 genes, it can be applied when adult T-cell leukemia/lymphoma is suspected cytologically but fresh samples for Southern blotting are unavailable.
  • [MeSH-major] Cytodiagnosis / methods. Genes, Viral. Human T-lymphotropic virus 1 / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Polymerase Chain Reaction / methods

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  • (PMID = 16061975.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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49. Kashanchi F, Brady JN: Transcriptional and post-transcriptional gene regulation of HTLV-1. Oncogene; 2005 Sep 5;24(39):5938-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional and post-transcriptional gene regulation of HTLV-1.
  • Adult T-cell leukemia (ATL) is an aggressive hematologic malignancy caused by human T-cell leukemia virus type I (HTLV-1).
  • Tax, encoded by the HTLV-1 pX region, has been recognized by its pleiotropic actions to play a critical role in leukemogenesis.
  • Tax transactivation has been attributed to the protein's interaction with transcription factors, chromatin remodeling complexes, cell cycle and repair genes.
  • In this review, we will discuss some of the latest findings on this fascinating viral activator and highlight its regulation of cellular factors including CREB, p300/CBP and their effect on RNA polymerase II and chromatin remodeling, as well as its role in cytoplasmic and nuclear function.
  • It is quite obvious that, collectively, Tax's effects on a wide variety of cellular targets cooperate in promoting cell proliferation and leukemogenesis.

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  • (PMID = 16155601.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / PHS HHS / / 13969; United States / NIAID NIH HHS / AI / AI43894; United States / NIAID NIH HHS / AI / AI44357
  • [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 / Gene Products, rex; 0 / Gene Products, tax; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
  • [Number-of-references] 157
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50. Usui T, Yanagihara K, Tsukasaki K, Murata K, Hasegawa H, Yamada Y, Kamihira S: Characteristic expression of HTLV-1 basic zipper factor (HBZ) transcripts in HTLV-1 provirus-positive cells. Retrovirology; 2008;5:34
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  • [Title] Characteristic expression of HTLV-1 basic zipper factor (HBZ) transcripts in HTLV-1 provirus-positive cells.
  • BACKGROUND: HTLV-1 causes adult T-cell leukemia (ATL).
  • Recently, a new viral factor, HTLV-1 basic Zip factor (HBZ), encoded from the minus strand mRNA was discovered and the current models of Tax-centered ATL cell pathogenesis are in conflict with this discovery.
  • HBZs consisting of non-spliced and spliced isoforms (HBZ-SI) are thought to be implicated in viral replication and T-cell proliferation but there is little evidence on the HBZ expression profile on a large scale.
  • RESULTS: To investigate the role of HBZ-SI in HTLV-1 provirus-positive cells, the HBZ-SI and Tax mRNA loads in samples with a mixture of infected and non-infected cells were measured and then adjusted by dividing by the HTLV-I proviral load.
  • We show here that the HBZ-SI mRNA level is 4-fold higher than non-spliced HBZ and is expressed by almost all cells harboring HTLV-1 provirus with variable intensity.
  • The proviral-adjusted HBZ-SI and Tax quantification revealed a characteristic imbalanced expression feature of high HBZ and low Tax expression levels in primary ATL cells or high HBZ and very high Tax levels in HTLV-1-related cell lines (cell lines) compared with a standard expression profile of low HBZ and low Tax in infected cells.
  • Interestingly, according to the mutual Tax and HBZ expression status, HTLV-1-related cell lines were subcategorized into two groups, an ATL cell type with high HBZ and low Tax levels and another type with high Tax and either high or low HBZ, which was closely related to its cell origin.
  • CONCLUSION: This is the first comprehensive study to evaluate the mutual expression profile of HBZ and Tax in provirus-positive cells, revealing that there are quantitative and relative characteristic features among infected cells, primary ATL cells, and cell lines.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. HTLV-I Infections / virology. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. Proviruses / isolation & purification. Viral Proteins / genetics
  • [MeSH-minor] Alternative Splicing. Cell Line. Gene Order. Gene Products, tax / genetics. Gene Products, tax / metabolism. Genome, Viral. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Viral / genetics. RNA, Viral / metabolism. T-Lymphocytes / virology. Viral Load

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  • [Cites] Rev Med Virol. 2007 Sep-Oct;17(5):301-11 [17621367.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Int J Hematol. 2007 Aug;86(2):107-12 [17875522.001]
  • [Cites] Retrovirology. 2007;4:92 [18078517.001]
  • [Cites] Int J Hematol. 2000 Jul;72(1):79-84 [10979214.001]
  • [Cites] Blood. 2002 Jan 1;99(1):88-94 [11756157.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Clin Lab Haematol. 2003 Apr;25(2):111-7 [12641615.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Blood. 1995 Apr 1;85(7):1865-70 [7703492.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4265-72 [9596675.001]
  • [Cites] J Exp Med. 1999 Apr 5;189(7):1063-71 [10190897.001]
  • [Cites] Br J Haematol. 2005 Jan;128(2):253-65 [15638862.001]
  • [Cites] Lab Hematol. 2005;11(1):8-13 [15790547.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Clin Lab Haematol. 2005 Aug;27(4):235-41 [16048490.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Mar;80(5):2495-505 [16474156.001]
  • [Cites] Blood. 2006 May 15;107(10):3976-82 [16424388.001]
  • [Cites] Retrovirology. 2006;3:15 [16512901.001]
  • [Cites] Front Biosci. 2007;12:1496-507 [17127397.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] Int J Hematol. 2007 Aug;86(2):101-6 [17875521.001]
  • (PMID = 18426605.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Other-IDs] NLM/ PMC2386809
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51. Blaise D, Vey N, Faucher C, Mohty M: Current status of reduced-intensity-conditioning allogeneic stem cell transplantation for acute myeloid leukemia. Haematologica; 2007 Apr;92(4):533-41
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  • [Title] Current status of reduced-intensity-conditioning allogeneic stem cell transplantation for acute myeloid leukemia.
  • Allogeneic stem cell transplantation (allo-SCT) is the most efficient antileukemic treatment for acute myeloblastic leukemia (AML).
  • Such RIC regimens aim primarily to provide the immune graft-versus-leukemia effect while causing little toxicity.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / surgery. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antilymphocyte Serum / administration & dosage. Antilymphocyte Serum / adverse effects. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Diseases / chemically induced. Bone Marrow Diseases / prevention & control. Clinical Trials as Topic / statistics & numerical data. Combined Modality Therapy. Disease-Free Survival. Female. Graft vs Leukemia Effect. Humans. Lymphocyte Depletion. Male. Middle Aged. Recurrence. Remission Induction. Survival Analysis. T-Lymphocytes. Time Factors. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / adverse effects. Vidarabine / analogs & derivatives

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  • (PMID = 17488664.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents, Alkylating; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 60
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52. Lengfelder E, Haferlach C, Saussele S, Haferlach T, Schultheis B, Schnittger S, Ludwig WD, Staib P, Aul C, Grüneisen A, Kern W, Reichle A, Serve H, Berdel WE, Braess J, Spiekermann K, Wörmann B, Sauerland MC, Heinecke A, Hiddemann W, Hehlmann R, Büchner T, German AML Cooperative Group: High dose ara-C in the treatment of newly diagnosed acute promyelocytic leukemia: long-term results of the German AMLCG. Leukemia; 2009 Dec;23(12):2248-58
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  • [Title] High dose ara-C in the treatment of newly diagnosed acute promyelocytic leukemia: long-term results of the German AMLCG.
  • The objective of this study for newly diagnosed acute promyelocytic leukemia (APL) was to evaluate the efficacy of an intensified double induction chemotherapy including high dose ara-C (HD) and all-trans retinoic acid (ATRA) followed by consolidation and 3 years maintenance therapy.
  • In contrast to APL studies stratifying therapy according to pretreatment white blood cell (WBC) count < and > or =10 x 10(9)/l (low/intermediate and high risk according to the Sanz score), our patients received uniform therapy.
  • [MeSH-major] Cytarabine / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Germany. Humans. Longitudinal Studies. Lymphocyte Count. Middle Aged. Prognosis. Remission Induction. Survival Analysis. Treatment Outcome. Tretinoin / administration & dosage. Young Adult

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  • (PMID = 19741727.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin
  • [Investigator] Ittel T; Fuss H; Mayr A; Grüneisen A; Arnold R; Dörken B; Maschmeyer G; Notter M; Thiel E; Ludwig WD; Schöndube D; Weh AJ; Zumsprekel A; Teschendorf C; Stechstor M; Trenn G; Wörmann B; Hertenstein B; Thomssen H; Peyn A; Pielken H; Hindahl H; Wehmeyer A; Heyll A; Flasshove M; Karow J; Aul C; Giagounidis; Fuchs R; Schlegel F; Seeber S; Meckenstock G; Giagounidis G; Haase D; Trümper L; Griesinger F; Gropp C; Depenbusch R; Eimermacher H; Schütte W; Haak U; Braumann D; Balleisen L; Kirchner H; Lange JG; Schmitz-Hübner U; Fauser A; Fricke HJ; Wolf M; Ritter B; Kneba M; Hallek M; Staib P; Dormann A; Frieling T; Planker M; Hartmann F; Middeke H; Gründgens C; Constantin C; Niederle N; Wagner T; Fetscher S; Schmielau J; Uppenkamp M; Hoffmann M; Hehlmann R; Lengfelder E; Schwonzen M; Spangenberg H; Graeven D; Kohl D; Heuer T; Emmerich B; Dengler R; Schlag B; Hiddemann W; Nibler K; Fleckenstein D; Büchner T; Berdel WE; Serve H; Hartlapp J; Hegge T; Peceny R; Koch O; Innig G; Südhoff T; Wagner T; Reichle A; Andreesen R; Gassmann W; Gaska T; Frickhofen N; Fuhr HG; Kreibich U; Schott G; Sommer S; Zschille W
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53. Sundberg TB, Swenson L, Wahl DR, Opipari AW Jr, Glick GD: Apoptotic signaling activated by modulation of the F0F1-ATPase: implications for selective killing of autoimmune lymphocytes. J Pharmacol Exp Ther; 2009 Nov;331(2):437-44
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  • 7-Chloro-5-(4-hydroxyphenyl)-1-methyl-3-(napthalen-2-ylmetyl)-4,5,-dihydro-1H-benzo[b][1,4]diazepin-2(3H)-one (Bz-423) is a proapoptotic 1,4-benzodiazepine that potently suppresses disease in the murine model of lupus by selectively killing pathogenic lymphocytes.
  • In MRL/MpJ-Fas(lpr) (MRL-lpr) mice, Bz-423 overcomes deficient expression of the Fas death receptor and hyperactivation of antiapoptotic phosphatidylinositol 3-kinase (PI3K)-Akt signaling to specifically kill pathogenic CD4(+) T cells.
  • To gain insight into how apoptotic signaling activated by Bz-423-induced superoxide contributes to the selective depletion of MRL-lpr CD4(+) T cells, we characterized the death mechanism in a CD4(+) T cell leukemia line (Jurkat).
  • Although Bz-423-induced superoxide indirectly inactivates Akt, this response is not required for T cell death.
  • By directly up-regulating proteins that trigger loss of mitochondrial outer membrane integrity, Bz-423 bypasses defective Fas function and antiapoptotic PI3K-Akt signaling in MRL-lpr CD4(+) T cells.
  • Moreover, because disease-associated abnormalities should sensitize autoreactive CD4(+) T cells to transcriptional up-regulation of Noxa by redox signals and to Bak-dependent apoptosis, the apoptotic mechanism elucidated in Jurkat cells provides important clues into the cell-type- and disease-selective effects of Bz-423 in MRL-lpr mice.

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  • [Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]
  • [Cites] EMBO J. 2007 Feb 7;26(3):825-34 [17235284.001]
  • [Cites] Nat Rev Immunol. 2007 Mar;7(3):191-201 [17290298.001]
  • [Cites] Curr Opin Cell Biol. 2007 Apr;19(2):142-9 [17303404.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59 [18097445.001]
  • [Cites] Mol Cell Endocrinol. 2008 Jan 16;281(1-2):47-55 [18035477.001]
  • [Cites] J Biol Chem. 2008 Feb 8;283(6):3357-64 [18056701.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3035-40 [18287039.001]
  • [Cites] Curr Mol Med. 2008 Mar;8(2):138-47 [18336294.001]
  • [Cites] Free Radic Biol Med. 2008 Nov 1;45(9):1232-42 [18718527.001]
  • [Cites] Microbiol Mol Biol Rev. 2008 Dec;72(4):590-641, Table of Contents [19052322.001]
  • [Cites] Arthritis Rheum. 2009 Jan;60(1):207-18 [19116915.001]
  • [Cites] Carcinogenesis. 2009 Sep;30(9):1517-27 [19578044.001]
  • [Cites] Biochem Pharmacol. 2009 Oct 15;78(8):966-73 [19481066.001]
  • [Cites] J Inorg Biochem. 2001 Jun;85(2-3):201-8 [11410240.001]
  • [Cites] Trends Immunol. 2001 Sep;22(9):490-6 [11525939.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13681-6 [11717429.001]
  • [Cites] J Clin Invest. 2002 Oct;110(8):1123-32 [12393848.001]
  • [Cites] Arthritis Rheum. 2003 Mar;48(3):757-66 [12632430.001]
  • [Cites] Cell Death Differ. 2003 Jan;10(1):36-44 [12655294.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] Autoimmun Rev. 2004 Jan;3(1):33-9 [14871647.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 11;1697(1-2):3-16 [15023346.001]
  • [Cites] Science. 2004 Apr 23;304(5670):554 [15016963.001]
  • [Cites] Clin Immunol. 2004 Oct;113(1):4-13 [15380523.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 May 24;91(11):4708-12 [8197123.001]
  • [Cites] J Immunol. 1997 Nov 1;159(9):4197-204 [9379013.001]
  • [Cites] Arch Biochem Biophys. 1999 Mar 1;363(1):91-7 [10049502.001]
  • [Cites] Chem Biol. 2005 Apr;12(4):485-96 [15850986.001]
  • [Cites] Immunol Rev. 2005 Jun;205:158-69 [15882352.001]
  • [Cites] Oncogene. 2005 May 26;24(23):3797-809 [15782127.001]
  • [Cites] Oncogene. 2005 Jun 2;24(24):3954-63 [15782121.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] Nat Med. 2005 Sep;11(9):933-5 [16127435.001]
  • [Cites] Science. 2006 Feb 10;311(5762):847-51 [16469926.001]
  • [Cites] Mol Cell. 2006 Mar 17;21(6):749-60 [16543145.001]
  • [Cites] Oncogene. 2006 Nov 16;25(54):7192-200 [16732318.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3967-75 [16926289.001]
  • [Cites] Neuropharmacology. 2007 Feb;52(2):536-41 [17027047.001]
  • [Cites] Cell Death Differ. 2007 Mar;14(3):534-47 [16888645.001]
  • (PMID = 19706792.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI047450; United States / NIAID NIH HHS / AI / R21 AI047450; United States / NIAID NIH HHS / AI / AI47450; United States / NCI NIH HHS / CA / CA10456
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bz-423; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / bcl-2 Homologous Antagonist-Killer Protein; 12794-10-4 / Benzodiazepines; 8L70Q75FXE / Adenosine Triphosphate; 9007-49-2 / DNA; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.6.3.14 / Proton-Translocating ATPases
  • [Other-IDs] NLM/ PMC2775264
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54. Khandanpour C, Thiede C, Valk PJ, Sharif-Askari E, Nückel H, Lohmann D, Horsthemke B, Siffert W, Neubauer A, Grzeschik KH, Bloomfield CD, Marcucci G, Maharry K, Slovak ML, van der Reijden BA, Jansen JH, Schackert HK, Afshar K, Schnittger S, Peeters JK, Kroschinsky F, Ehninger G, Lowenberg B, Dührsen U, Möröy T: A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia. Blood; 2010 Mar 25;115(12):2462-72
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  • [Title] A variant allele of Growth Factor Independence 1 (GFI1) is associated with acute myeloid leukemia.
  • In the mouse, Gfi1 deficiency causes neutropenia and an accumulation of granulomonocytic precursor cells that is reminiscent of a myelodysplastic syndrome.
  • We report here that a variant allele of GFI1 (GFI1(36N)) is associated with acute myeloid leukemia (AML) in white subjects with an odds ratio of 1.6 (P < 8 x 10(-5)).
  • [MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. COS Cells. Cell Nucleus / metabolism. Cercopithecus aethiops. Core Binding Factor Alpha 2 Subunit / metabolism. Female. Gene Frequency. Genetic Variation. HeLa Cells. Humans. Linkage Disequilibrium. Male. Mice. Middle Aged. NIH 3T3 Cells. Oncogene Proteins, Fusion / metabolism. Translocation, Genetic. Young Adult

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  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10338-51 [16287849.001]
  • [Cites] Blood. 2009 May 28;113(22):5466-75 [19346496.001]
  • [Cites] EMBO Rep. 2006 Mar;7(3):326-33 [16397623.001]
  • [Cites] Nat Immunol. 2006 Aug;7(8):859-67 [16819553.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Aug;59(2):85-97 [16716599.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] J Cell Physiol. 2006 Dec;209(3):935-42 [16972259.001]
  • [Cites] Nat Genet. 2006 Nov;38(11):1269-77 [17041602.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18214-9 [17116877.001]
  • [Cites] Mol Cell. 2007 Aug 17;27(4):562-72 [17707228.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2611-20 [17694175.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14882-7 [10611307.001]
  • [Cites] EMBO J. 2000 Nov 1;19(21):5845-55 [11060035.001]
  • [Cites] Br J Haematol. 2001 Feb;112(2):300-7 [11167822.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Nat Genet. 2002 Mar;30(3):295-300 [11810106.001]
  • [Cites] Science. 2002 Jun 21;296(5576):2225-9 [12029063.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • [Cites] Immunity. 2003 Jan;18(1):109-20 [12530980.001]
  • [Cites] J Clin Oncol. 2003 Feb 15;21(4):615-23 [12586797.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):308-12 [12778173.001]
  • [Cites] J Cell Biochem. 2003 Aug 1;89(5):1005-18 [12874834.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] Nucleic Acids Res. 2004;32(8):2508-19 [15131254.001]
  • [Cites] J Biol Chem. 2004 Sep 24;279(39):40906-17 [15252036.001]
  • [Cites] EMBO J. 2004 Oct 13;23(20):4116-25 [15385956.001]
  • [Cites] Nature. 2004 Oct 21;431(7011):1002-7 [15457180.001]
  • [Cites] Mol Cell Biol. 1993 Mar;13(3):1759-68 [8441411.001]
  • [Cites] J Natl Cancer Inst. 1993 Dec 15;85(24):1994-2003 [8246285.001]
  • [Cites] Oncogene. 1996 Apr 18;12(8):1789-801 [8622900.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11895-900 [8876234.001]
  • [Cites] Biometrics. 1997 Dec;53(4):1253-61 [9423247.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Science. 2005 Apr 15;308(5720):385-9 [15761122.001]
  • [Cites] Immunity. 2005 Jun;22(6):717-28 [15963786.001]
  • [Cites] Cancer Causes Control. 2005 Jun;16(5):489-500 [15986104.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):5869-79 [15988004.001]
  • [Cites] Cell. 2005 Aug 26;122(4):633-44 [16122429.001]
  • [Cites] Pediatr Blood Cancer. 2008 Mar;50(3):630-2 [17096407.001]
  • [Cites] Cancer Cell. 2008 Apr;13(4):299-310 [18394553.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] J Immunol. 2008 Nov 1;181(9):6222-9 [18941212.001]
  • [Cites] Curr Opin Hematol. 2006 Jan;13(1):1-6 [16319680.001]
  • (PMID = 20075157.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA101140
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2919174
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55. Sharma P, Asthana B, Tyagi S: Triphenotypic acute leukemia with TRAP-positive blasts: A pathological rarity. Leuk Res; 2009 Jul;33(7):e83-4
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  • [Title] Triphenotypic acute leukemia with TRAP-positive blasts: A pathological rarity.
  • [MeSH-major] Acid Phosphatase / metabolism. Isoenzymes / metabolism. Leukemia, Myeloid, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Blast Crisis. Flow Cytometry. Humans. Male. Prognosis

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  • (PMID = 19237193.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
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56. Wu T, Li ZJ, Qiu LG: Complications of chronic lymphocytic leukemia: analysis of 203 cases in China. Leuk Res; 2010 Feb;34(2):e64-5
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  • [Title] Complications of chronic lymphocytic leukemia: analysis of 203 cases in China.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. China. Female. Humans. Incidence. Male. Middle Aged. Prognosis

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  • (PMID = 19699521.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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57. Miyahara H, Itou H, Sekine A, Taniyama D, Katsui T, Tanaka W, Satou R, Kurihara A, Satou Y, Sakamaki F: [A case of adult T-cell leukemia/lymphoma with primary lung cancer]. Nihon Kokyuki Gakkai Zasshi; 2009 Apr;47(4):342-6
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  • [Title] [A case of adult T-cell leukemia/lymphoma with primary lung cancer].
  • The mass was pathologically diagnosed as adult T-cell leukemia/lymphoma (ATLL) because of a high HTLV-1 antibody titer, and radiation therapy was started.
  • [MeSH-major] Adenocarcinoma / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary

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  • (PMID = 19455967.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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58. Yoshida M: Molecular approach to human leukemia: isolation and characterization of the first human retrovirus HTLV-1 and its impact on tumorigenesis in adult T-cell leukemia. Proc Jpn Acad Ser B Phys Biol Sci; 2010;86(2):117-30
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  • [Title] Molecular approach to human leukemia: isolation and characterization of the first human retrovirus HTLV-1 and its impact on tumorigenesis in adult T-cell leukemia.
  • A human retrovirus was established during 1980-1982 in linkage with a unique human leukemia, concurrently in Japan and USA.
  • This review covers our efforts on the discovery of new retrovirus, Human T-cell Leukemia Virus Type 1 (HTLV-1), first introducing to a new class of retroviruses with a unique regulatory factors, Tax and Rex.
  • Then it is followed by analyses of molecular interaction of the vial Tax with cellular machineries involved in the pathogenesis of Adult T-cell Leukemia (ATL).
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adult. Humans. Virus Replication

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  • [Cites] Nature. 1988 Jun 9;333(6173):504 [2836736.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3351-5 [2541443.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Cell. 1978 Feb;13(2):381-6 [203405.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Blood. 1981 Sep;58(3):645-7 [6455129.001]
  • [Cites] Cancer Genet Cytogenet. 1981 Apr;3(3):251-9 [6974589.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Gan. 1981 Dec;72(6):978-81 [6281119.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Int J Cancer. 1982 Jun 15;29(6):631-5 [6980846.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Nov;79(22):6899-902 [6294664.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Science. 1983 Dec 16;222(4629):1178 [6316504.001]
  • [Cites] Virology. 1984 Feb;133(1):238-41 [6322435.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] Nature. 1984 Jun 14-20;309(5969):640-2 [6328324.001]
  • [Cites] Hematol Oncol. 1983 Jul-Sep;1(3):193-204 [6329935.001]
  • [Cites] Science. 1984 Jul 27;225(4660):381-5 [6330891.001]
  • [Cites] Gan. 1984 Sep;75(9):747-51 [6094295.001]
  • [Cites] EMBO J. 1984 Dec 20;3(13):3231-7 [6098469.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2277-81 [2986109.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 May;82(10):3101-5 [2582407.001]
  • [Cites] Science. 1985 Jun 28;228(4707):1532-4 [2990031.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Virology. 1985 Jul 15;144(1):59-65 [2998047.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8359-63 [3001699.001]
  • [Cites] Jpn J Cancer Res. 1985 Dec;76(12):1127-31 [3005203.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4524-8 [3012571.001]
  • [Cites] EMBO J. 1986 Nov;5(11):2883-8 [3024966.001]
  • [Cites] FEBS Lett. 1986 Dec 15;209(2):187-90 [3025015.001]
  • [Cites] Cell. 1987 Jan 30;48(2):343-50 [3026643.001]
  • [Cites] J Virol. 1989 Aug;63(8):3234-9 [2545901.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5620-4 [2787512.001]
  • [Cites] Mol Cell Biol. 1990 Jan;10(1):413-7 [2403646.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1071-5 [2300570.001]
  • [Cites] Science. 1990 Mar 2;247(4946):1082-4 [2309119.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):5011-5 [1711215.001]
  • [Cites] Oncogene. 1992 Sep;7(9):1737-42 [1501885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3584-8 [8170951.001]
  • [Cites] Nature. 1994 Jul 21;370(6486):223-6 [7913207.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5967-72 [10557085.001]
  • [Cites] Virology. 2000 May 10;270(2):291-8 [10792988.001]
  • [Cites] J Virol. 2001 Jul;75(13):6086-94 [11390610.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] J Mol Biol. 1976 Mar 5;101(3):349-65 [176368.001]
  • [Cites] AIDS Res Hum Retroviruses. 1994 Oct;10(10):1259-68 [7531462.001]
  • [Cites] Oncogene. 1995 Mar 16;10(6):1199-207 [7700645.001]
  • [Cites] EMBO J. 1996 Apr 1;15(7):1607-14 [8612584.001]
  • [Cites] Virology. 1997 Apr 28;231(1):135-40 [9143312.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Virology. 1999 Jan 20;253(2):155-61 [9918874.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17402-5 [10364167.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4137-43 [10435595.001]
  • [Cites] J Virol. 1999 Oct;73(10):7981-7 [10482545.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5926-30 [16155599.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5931-7 [16155600.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] Retrovirology. 2009;6:71 [19650892.001]
  • [Cites] AIDS Res. 1986 Dec;2 Suppl 1:S71-8 [3030350.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Annu Rev Immunol. 1987;5:541-59 [2885015.001]
  • [Cites] Biochim Biophys Acta. 1987 Jul 8;907(2):145-61 [2885029.001]
  • [Cites] Science. 1987 Sep 11;237(4820):1324-9 [2888190.001]
  • [Cites] EMBO J. 1988 Feb;7(2):519-23 [2835230.001]
  • (PMID = 20154469.001).
  • [ISSN] 1349-2896
  • [Journal-full-title] Proceedings of the Japan Academy. Series B, Physical and biological sciences
  • [ISO-abbreviation] Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 68
  • [Other-IDs] NLM/ PMC3417562
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59. Yasunaga J, Matsuoka M: Leukaemogenic mechanism of human T-cell leukaemia virus type I. Rev Med Virol; 2007 Sep-Oct;17(5):301-11
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  • [Title] Leukaemogenic mechanism of human T-cell leukaemia virus type I.
  • Adult T-cell leukaemia (ATL) is a neoplastic disease derived from CD4(+) T-lymphocytes and etiologically associated with human T-cell leukaemia virus type I (HTLV-I).
  • In addition to structural genes, HTLV-I encodes regulatory and accessory genes in the pX region.
  • However, since Tax is a major target of the host immune system, its expression is often lost in ATL cells, indicating Tax is dispensable in the last phase of leukaemogenesis.
  • The HTLV-I bZIP factor (HBZ), encoded on the HTLV-I minus strand, was recently shown to be expressed in all ATL cells, and to support growth of human T-cell lines.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Cell Transformation, Neoplastic. Human T-lymphotropic virus 1 / physiology. Leukemia / virology

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  • (PMID = 17621367.001).
  • [ISSN] 1052-9276
  • [Journal-full-title] Reviews in medical virology
  • [ISO-abbreviation] Rev. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Viral Proteins
  • [Number-of-references] 94
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60. Maggio R, Peragine N, Calabrese E, De Propris MS, Intoppa S, Della Starza I, Ariola C, Vitale A, Foà R, Guarini A: Generation of functional dendritic cells (DC) in adult acute lymphoblastic leukemia: rationale for a DC-based vaccination program for patients in complete hematological remission. Leuk Lymphoma; 2007 Feb;48(2):302-10
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  • [Title] Generation of functional dendritic cells (DC) in adult acute lymphoblastic leukemia: rationale for a DC-based vaccination program for patients in complete hematological remission.
  • The capacity to generate effective dendritic cells (DC) from adult acute lymphoblastic leukemia (ALL) patients in complete remission (CR) and off-therapy was investigated.
  • DC loaded with leukemia-derived apoptotic bodies increased their ability to stimulate both allogeneic and autologous lymphocytes, and to generate specific anti-leukemic CD3 + cells.
  • These findings offer a rationale for the design of DC-based vaccine programs for adult ALL patients in CR with the aim of controlling/eradicating the disease.
  • [MeSH-major] Apoptosis. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Vaccination
  • [MeSH-minor] Adult. Aged. Cancer Vaccines / therapeutic use. Cell Proliferation. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Immunophenotyping. Interferon-gamma / metabolism. Interleukin-12 / metabolism. Interleukin-4 / pharmacology. Killer Cells, Natural / immunology. Male. Middle Aged. Phagocytosis. Remission Induction. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. T-Lymphocytes / pathology. T-Lymphocytes, Cytotoxic / immunology. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • [CommentIn] Leuk Lymphoma. 2007 Feb;48(2):217-8 [17325876.001]
  • (PMID = 17325890.001).
  • [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 / Cancer Vaccines; 0 / Tumor Necrosis Factor-alpha; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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61. Rhee CK, Rhee JH, Kim HJ, Choi SM, Kim YJ, Kim DW, Lee JW, Min WS, Shin WS, Kim CC, Ahn KJ: T-cell lymphoproliferative disorder following a full haplotype-mismatched haematopoietic stem cell transplant in a patient with acute myeloid leukaemia. Bone Marrow Transplant; 2005 Sep;36(5):461-3
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  • [Title] T-cell lymphoproliferative disorder following a full haplotype-mismatched haematopoietic stem cell transplant in a patient with acute myeloid leukaemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Living Donors. T-Lymphocytes
  • [MeSH-minor] Adult. Haplotypes. Histocompatibility Testing. Humans. Lymphoproliferative Disorders / etiology. Lymphoproliferative Disorders / pathology. Male. Transplantation, Homologous

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  • (PMID = 15968275.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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62. Takami A, Shimadoi S, Sugimori C, Takemoto K, Shibayama M, Yoshida T, Murayama T, Nagai K, Miyamura K, Asakura H, Nakao S: Successful treatment of minimal residual disease-positive Philadelphia chromosome-positive acute lymphoblastic leukemia with imatinib followed by reduced-intensity unrelated cord blood transplantation after allogeneic peripheral blood stem cell transplantation. Int J Hematol; 2006 Aug;84(2):170-3
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  • [Title] Successful treatment of minimal residual disease-positive Philadelphia chromosome-positive acute lymphoblastic leukemia with imatinib followed by reduced-intensity unrelated cord blood transplantation after allogeneic peripheral blood stem cell transplantation.
  • We describe a 35-year-old woman with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) who received allogeneic sibling donor peripheral blood stem cell transplantation (PBSCT) and entered a second complete remission.
  • Following the failure of donor leukocyte infusions, she underwent reduced-intensity unrelated cord blood transplantation (RI-UCBT), and has continued durable molecular remission for more than 30 months without substantial graft-versus-host disease.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Cord Blood Stem Cell Transplantation. Peripheral Blood Stem Cell Transplantation. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Combined Modality Therapy. Female. Humans. Imatinib Mesylate. Neoplasm, Residual. Transplantation, Homologous

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  • [Cites] Blood. 2004 Feb 15;103(4):1495-8 [14576058.001]
  • [Cites] Bone Marrow Transplant. 1997 Feb;19(4):393-4 [9051252.001]
  • [Cites] Bone Marrow Transplant. 2000 Jan;25(2):213-5 [10673684.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):433-44 [9053463.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Mar;15(1):91-103 [11987918.001]
  • [Cites] N Engl J Med. 2004 Nov 25;351(22):2276-85 [15564544.001]
  • [Cites] Blood. 2005 Jul 15;106(2):458-63 [15817679.001]
  • [Cites] J Clin Oncol. 2001 Aug 15;19(16):3675-84 [11504749.001]
  • [Cites] J Formos Med Assoc. 1997 Mar;96(3):205-8 [9080760.001]
  • [Cites] Bone Marrow Transplant. 2002 Jan;29(1):63-6 [11840146.001]
  • [Cites] Leukemia. 1999 Jun;13(6):957-64 [10360386.001]
  • [Cites] N Engl J Med. 2001 Jun 14;344(24):1815-22 [11407342.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1965-71 [12200353.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1915-9 [12738676.001]
  • [Cites] Jpn J Clin Oncol. 2001 Jun;31(6):290-3 [11463810.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 May;86(10):3828-32 [2566997.001]
  • [Cites] Blood. 1997 Apr 1;89(7):2602-9 [9116308.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2332-8 [11588027.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3586-92 [15173064.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(9):773-7 [9384480.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2357-66 [12239143.001]
  • [Cites] N Engl J Med. 2004 Nov 25;351(22):2265-75 [15564543.001]
  • [Cites] Leukemia. 2003 Feb;17(2):290-7 [12592325.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3813-20 [15280199.001]
  • [Cites] Blood. 1992 Mar 1;79(5):1366-70 [1371420.001]
  • (PMID = 16926141.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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63. Strefford JC, Worley H, Barber K, Wright S, Stewart AR, Robinson HM, Bettney G, van Delft FW, Atherton MG, Davies T, Griffiths M, Hing S, Ross FM, Talley P, Saha V, Moorman AV, Harrison CJ: Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization. Oncogene; 2007 Jun 21;26(29):4306-18
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  • [Title] Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization.
  • Chromosomal abnormalities are important for the classification and risk stratification of patients with acute lymphoblastic leukemia (ALL).
  • However, approximately 30% of childhood and 50% of adult patients lack abnormalities with clinical relevance.
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Profiling. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Gene Dosage. Humans. Infant. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 17237825.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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64. Lamvik J, Waage A, Wahl SG, Naess I, Paulsen PQ, Hammerstrøm J: Adult acute lymphoblastic leukemia, Burkitt's lymphoma and lymphoblastic lymphoma in middle Norway 1985-2004. Haematologica; 2006 Oct;91(10):1428-9
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  • [Title] Adult acute lymphoblastic leukemia, Burkitt's lymphoma and lymphoblastic lymphoma in middle Norway 1985-2004.
  • We report a population-based investigation on adult acute precursor B lymphoblastic leukemia, Burkitt's lymphoma and T lymphoblastic lymphoma in a defined geographic area.
  • [MeSH-major] Burkitt Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Hematopoietic Stem Cells / pathology. Humans. Incidence. Male. Middle Aged. Norway / epidemiology


65. Sirohi B, Powles R, Singhal S, Smith K, Jones RL, Saso R, Kulkarni S, Treleaven J, Swansbury GJ, Potter M, Morgan G, Mehta J: Outcome of high-dose cytarabine-based induction therapy followed by hematopoietic stem cell transplantation in acute myeloid leukemia: influence of karyotype. Leuk Lymphoma; 2008 Dec;49(12):2284-90
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  • [Title] Outcome of high-dose cytarabine-based induction therapy followed by hematopoietic stem cell transplantation in acute myeloid leukemia: influence of karyotype.
  • One-hundred-twenty consecutive adult patients aged 15-69 years (median 40) with acute myeloid leukemia (AML) excluding t(15;17) received induction therapy comprising idarubicin, high-dose cytarabine and etoposide.
  • Planned post-induction treatment included two courses of moderate-intensity consolidation therapy followed by stem cell transplantation.
  • The overall CR rate, after salvage chemotherapy but excluding allogeneic transplantation for primary refractory disease, was 82%.
  • Overall, 84 of 98 patients (86%) attaining CR underwent autologous (n=59), allogeneic (n=23) or syngeneic (n=2) hematopoietic stem cell transplantation in first CR.
  • [MeSH-major] Cytarabine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Etoposide. Humans. Idarubicin. Karyotyping. Middle Aged. Remission Induction / methods. Survival Rate. Treatment Outcome

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  • [CommentIn] Leuk Lymphoma. 2008 Dec;49(12):2227-8 [19052964.001]
  • (PMID = 19052975.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
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66. Conrad DM, Furlong SJ, Doucette CD, West KA, Hoskin DW: The Ca(2+) channel blocker flunarizine induces caspase-10-dependent apoptosis in Jurkat T-leukemia cells. Apoptosis; 2010 May;15(5):597-607
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  • [Title] The Ca(2+) channel blocker flunarizine induces caspase-10-dependent apoptosis in Jurkat T-leukemia cells.
  • Flunarizine is a Ca(2+) channel blocker that can be either cytoprotective or cytotoxic, depending on the cell type that is being examined.
  • We show here that flunarizine was cytotoxic for Jurkat T-leukemia cells, as well as for other hematological maligancies, but not for breast or colon carcinoma cells.
  • Treatment of Jurkat cells with flunarizine resulted in caspase-3 activation, poly (ADP-ribose) polymerase cleavage, and laddering of DNA fragments, all of which are hallmarks of apoptosis.
  • Flunarizine-induced DNA fragmentation was inhibited by the caspase-3 inhibitor z-DEVD-fmk, the caspase-8/caspase-10 inhibitor z-IETD-fmk, and the caspase-10 inhibitor z-AEVD-fmk, but was not reduced in caspase-8-deficient Jurkat cells, indicating the involvement of caspase-10 upstream of caspase-3 activation.
  • Interestingly, FADD recruitment to a death receptor was not involved since flunarizine caused DNA fragmentation in FADD-deficient Jurkat cells.
  • Flunarizine treatment of Jurkat cells also resulted in reactive oxygen species production, dissipation of mitochondrial transmembrane potential, release of cytochrome c from mitochondria, and caspase-9 activation, although none of these events were necessary for apoptosis induction.
  • Collectively, these findings indicate that flunarizine triggers apoptosis in Jurkat cells via FADD-independent activation of caspase-10.
  • [MeSH-minor] Caspase Inhibitors. Cysteine Proteinase Inhibitors / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Jurkat Cells. Membrane Potential, Mitochondrial / drug effects. Oligopeptides / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reactive Oxygen Species / metabolism

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  • (PMID = 20094800.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Oligopeptides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Reactive Oxygen Species; 0 / benzyloxycarbonyl-alanyl-glutamyl-valyl-aspartic acid fluoromethyl ketone; 0 / benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone; EC 3.4.22.- / Caspase 10; R7PLA2DM0J / Flunarizine
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67. Schnittger S, Kern W, Tschulik C, Weiss T, Dicker F, Falini B, Haferlach C, Haferlach T: Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML. Blood; 2009 Sep 10;114(11):2220-31
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  • [Title] Minimal residual disease levels assessed by NPM1 mutation-specific RQ-PCR provide important prognostic information in AML.
  • Nucleophosmin (NPM1)-mutated acute myeloid leukemia (AML), which is recognized as a provisional entity in the World Health Organization 2008 classification of myeloid neoplasms, accounts for 30% of AML.
  • Paired diagnostic/relapse samples of 84 patients revealed stable NPM1 mutations in all cases, suggesting that they are pathogenetically early events and thus applicable for minimal residual disease detection.
  • Univariate analyses, including age, white blood cell count, blast count, CD34 positivity, FLT3 mutations status, FAB type, karyotype, NPM1 mutation type, and pretreatment NPM1 mutational level, showed that, besides NPM1 mutation level, only age and FLT3-LM mutation status were prognostically significant for EFS.
  • Similar results were obtained in patients undergoing second-line chemotherapy or allogeneic stem cell transplantation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. Polymerase Chain Reaction
  • [MeSH-minor] Adult. Age Factors. Aged. Antigens, CD34 / genetics. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Leukocyte Count. Male. Middle Aged. Neoplasm, Residual. Prognosis. Proto-Oncogene Proteins c-abl / genetics. Proto-Oncogene Proteins c-abl / metabolism. Recurrence. Stem Cell Transplantation. Transplantation, Homologous. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 19587375.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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68. 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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69. Huang Y, Lin TY, Wu QL, Su ZL, Huang HQ, Xia ZJ, Sun XF, Jiang WQ, Guan ZZ: [Survival outcomes of T-cell non-Hodgkin's lymphoma: a report of 111 cases]. Ai Zheng; 2005 Apr;24(4):470-4
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  • [Title] [Survival outcomes of T-cell non-Hodgkin's lymphoma: a report of 111 cases].
  • BACKGROUND & OBJECTIVE: T-cell non-Hodgkin's lymphoma (NHL) is a group of heterogeneous malignancies with poor prognosis, and without ideal therapeutic regimen.
  • This study was to summarize clinical and pathologic features of T-cell NHL.
  • METHODS: Records of 111 patients with T-cell NHL, treated from Jan. 1994 to Dec.
  • Among all histological type subgroups, the prognosis of NK/T-cell lymphoma was the worst with the 3-year survival rate of only 25%u the 3-year survival rate was 40% in unspecified peripheral T-cell lymphoma group,and 85% in angioimmunoblast T-cell lymphoma group.
  • CONCLUSIONS: Present treatment modalities for T-cell NHL patients, especially the high risk patients, can't achieve satisfactory outcomes.
  • [MeSH-major] Lymphoma, T-Cell / drug therapy. Lymphoma, T-Cell / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Combined Modality Therapy. Female. Follow-Up Studies. Humans. L-Lactate Dehydrogenase / blood. Lymphoma, T-Cell, Peripheral / drug therapy. Lymphoma, T-Cell, Peripheral / mortality. Lymphoma, T-Cell, Peripheral / pathology. Lymphoma, T-Cell, Peripheral / radiotherapy. Male. Middle Aged. Neoplasm Staging. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 15820072.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
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70. Li LL, Liu HG, Piao YS, He CY, Zhou Q, Zhang Y: [Clinicopathologic study of malignant tumors in head and neck region complicated by fungal infection]. Zhonghua Bing Li Xue Za Zhi; 2010 Aug;39(8):508-12
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  • The primary tumors in such cases included leukemia (n = 7) and nasopharyngeal carcinoma (n = 1).
  • Fourteen patients had follow-up information available and six of them died of the disease.
  • Invasive fungal sinusitis (due to Zygomycetes and Aspergillus) often occurs in patients with leukemia, tends to involve orbit and is associated with poor prognosis.
  • [MeSH-major] Head and Neck Neoplasms / microbiology. Head and Neck Neoplasms / pathology. Leukemia / pathology. Mycoses / pathology. Sinusitis / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Aspergillosis / microbiology. Aspergillosis / pathology. Aspergillus / isolation & purification. Candida / isolation & purification. Candidiasis / drug therapy. Candidiasis / microbiology. Candidiasis / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / microbiology. Carcinoma, Squamous Cell / pathology. Child. Female. Follow-Up Studies. Humans. Lymphoma, Extranodal NK-T-Cell / drug therapy. Lymphoma, Extranodal NK-T-Cell / microbiology. Lymphoma, Extranodal NK-T-Cell / pathology. Male. Middle Aged. Retrospective Studies. Young Adult. Zygomycosis / drug therapy. Zygomycosis / microbiology. Zygomycosis / pathology


71. Tsagarakis NJ, Kentrou NA, Papadimitriou KA, Pagoni M, Kokkini G, Papadaki H, Pappa V, Marinakis T, Anagnostopoulos NI, Vadikolia C, Anagnostopoulos A, Angelopoulou MK, Terpos E, Poziopoulos C, Anargyrou K, Rontogianni D, Papadaki T, Psarra A, Kontopidou FN, Skoumi D, Papadhimitriou SI, Paterakis G, Hellenic Dendritic Cell Leukemia Study Group: Acute lymphoplasmacytoid dendritic cell (DC2) leukemia: results from the Hellenic Dendritic Cell Leukemia Study Group. Leuk Res; 2010 Apr;34(4):438-46
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  • [Title] Acute lymphoplasmacytoid dendritic cell (DC2) leukemia: results from the Hellenic Dendritic Cell Leukemia Study Group.
  • We present a cohort of 22 patients with type 2 dendritic cell (DC2) acute leukemia (or blastic plasmacytoid dendritic cell neoplasm-BPDCN, as it has been recently named), diagnosed in Greece over the past 12-year period, according to the main clinical and immunophenotypic features of this entity.
  • Four additional cases are discussed, classified as leukemia of ambiguous lineage (LAL), because of the simultaneous detection of a CD56 negative DC2 population and of a second myeloid precursor cell population.
  • Acute lymphoblastic leukemia-type chemotherapeutic regimens were more efficient in controlling the disease.
  • Immunophenotyping of typical BPDCN cases revealed CD4(+), CD56(+), HLA-DR(+) and CD123(bright) neoplastic cells, in the absence of major B-, T- and myeloid-associated markers, while the phenotype of the four cases characterized as LAL highlights the risk of misdiagnosis.
  • Based on our experience, we propose a flow cytometric algorithmic approach for the distinction of typical BPDCN from certain types of acute myeloid leukemia, but also for the identification of acute myeloid leukemia, admixed with CD56 negative DC2 cells, which could be misdiagnosed as BPDCN.
  • [MeSH-major] Dendritic Cells / pathology. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Diagnosis, Differential. Female. Greece. Humans. Immunophenotyping / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Male. Middle Aged. Skin Neoplasms / diagnosis. Skin Neoplasms / genetics. Skin Neoplasms / immunology. Skin Neoplasms / pathology

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19793612.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study
  • [Publication-country] England
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72. Ochenrider MG, Patterson DJ, Aboulafia DM: Hepatosplenic T-cell lymphoma in a young man with Crohn's disease: case report and literature review. Clin Lymphoma Myeloma Leuk; 2010 Apr;10(2):144-8
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  • [Title] Hepatosplenic T-cell lymphoma in a young man with Crohn's disease: case report and literature review.
  • Hepatosplenic T-cell lymphoma (HSTCL) is a rare form of peripheral T-cell lymphoma.
  • Recent reports suggest an excessive number of cases of HSTCL in young patients with Crohn's disease who are treated with thiopurines (azathioprine or 6-mercaptopurine [6-MP]) either in conjunction with or without agents that inhibit tumor necrosis factor-alpha (TNF-alpha).
  • Herein, we describe the case of an 18-year-old man with Crohn's disease who developed HSTCL after 5 years of 6-MP treatment.
  • Additional research is needed to better understand the role of thiopurines and TNF-alpha inhibitors in promoting HSTCL and what can be done to prevent and treat this devastating malignancy in young patients with Crohn's disease.
  • [MeSH-major] Antibodies, Monoclonal. Crohn Disease / drug therapy. Liver Neoplasms / chemically induced. Lymphoma, T-Cell / chemically induced. Splenic Neoplasms / chemically induced
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Adalimumab. Adolescent. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Azathioprine / therapeutic use. Fatal Outcome. Humans. Infliximab. Leukemia-Lymphoma, Adult T-Cell / chemically induced. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell, Peripheral / chemically induced. Lymphoma, T-Cell, Peripheral / drug therapy. Male. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 20371449.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; E7WED276I5 / 6-Mercaptopurine; FYS6T7F842 / Adalimumab; MRK240IY2L / Azathioprine
  • [Number-of-references] 24
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73. Pankiv S, Lamark T, Bruun JA, Øvervatn A, Bjørkøy G, Johansen T: Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies. J Biol Chem; 2010 Feb 19;285(8):5941-53
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  • [Title] Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies.
  • It is also suggested to shuttle ubiquitinated proteins for proteasomal degradation. p62 is commonly found in cytosolic protein inclusions in patients with protein aggregopathies, it is up-regulated in several forms of human tumors, and mutations in the gene are linked to classical adult onset Paget disease of the bone.
  • The protein is also found in nuclear promyelocytic leukemia bodies.
  • We found p62 to be essential for accumulation of polyubiquitinated proteins in promyelocytic leukemia bodies upon inhibition of nuclear protein export.
  • [MeSH-minor] Active Transport, Cell Nucleus / genetics. Ataxin-1. Ataxins. HeLa Cells. Humans. Peptides / genetics. Peptides / metabolism. Proteasome Endopeptidase Complex / genetics. Proteasome Endopeptidase Complex / metabolism

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  • [Cites] Exp Cell Res. 2007 May 15;313(9):1735-44 [17428466.001]
  • [Cites] Annu Rev Biochem. 2007;76:647-71 [17506639.001]
  • [Cites] J Biol Chem. 2007 Aug 17;282(33):24131-45 [17580304.001]
  • [Cites] J Biol Chem. 2007 Sep 7;282(36):26245-56 [17616529.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Mar 16;269(2):521-5 [10708586.001]
  • [Cites] EMBO J. 2000 Apr 3;19(7):1576-86 [10747026.001]
  • [Cites] Structure. 2000 Mar 15;8(3):329-38 [10745017.001]
  • [Cites] Exp Cell Res. 2000 Apr 10;256(1):213-24 [10739668.001]
  • [Cites] Mol Cell Biol. 2000 Jul;20(13):4494-504 [10848576.001]
  • [Cites] Oncogene. 2000 Jun 1;19(24):2870-6 [10851091.001]
  • [Cites] Nat Cell Biol. 2000 Sep;2(9):653-60 [10980707.001]
  • [Cites] Mol Biol Cell. 2001 May;12(5):1431-43 [11359933.001]
  • [Cites] Science. 2001 Nov 30;294(5548):1895-901 [11729309.001]
  • [Cites] Am J Pathol. 2002 Jan;160(1):255-63 [11786419.001]
  • [Cites] Am J Hum Genet. 2002 Jun;70(6):1582-8 [11992264.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5319-36 [12101228.001]
  • [Cites] Mol Biol Cell. 2002 Aug;13(8):2771-82 [12181345.001]
  • [Cites] Hum Mol Genet. 2002 Oct 15;11(22):2735-9 [12374763.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 1;31(1):393-6 [12520031.001]
  • [Cites] Oncogene. 2003 Apr 17;22(15):2322-33 [12700667.001]
  • [Cites] Mol Cell. 2003 Jul;12(1):39-50 [12887891.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):34568-81 [12813044.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Dec;62(12):1241-53 [14692700.001]
  • [Cites] Mol Cell Biol. 2004 Sep;24(18):8055-68 [15340068.001]
  • [Cites] J Neurochem. 2004 Oct;91(1):57-68 [15379887.001]
  • [Cites] Cell. 1995 Aug 11;82(3):475-83 [7543368.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5991-5 [8650207.001]
  • [Cites] Anal Chem. 1996 Mar 1;68(5):850-8 [8779443.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20235-7 [8702753.001]
  • [Cites] Curr Biol. 1996 Aug 1;6(8):1025-7 [8805337.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Mar 6;232(1):33-7 [9125146.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6191-6 [9177193.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Dec 8;241(1):157-63 [9405250.001]
  • [Cites] Nat Genet. 1998 Jun;19(2):148-54 [9620770.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7288-93 [9819415.001]
  • [Cites] Genes Dev. 1998 Nov 15;12(22):3499-511 [9832503.001]
  • [Cites] Nature. 1999 Mar 11;398(6723):160-5 [10086358.001]
  • [Cites] EMBO J. 1999 Jun 1;18(11):3044-53 [10356400.001]
  • [Cites] J Biol Chem. 1999 Oct 1;274(40):28708-15 [10497241.001]
  • [Cites] Trends Cell Biol. 2005 Mar;15(3):121-4 [15752974.001]
  • [Cites] Nat Struct Mol Biol. 2005 Aug;12(8):708-14 [16007098.001]
  • [Cites] J Cell Sci. 2005 Nov 15;118(Pt 22):5231-42 [16249232.001]
  • [Cites] J Cell Biol. 2005 Nov 21;171(4):603-14 [16286508.001]
  • [Cites] Histopathology. 2006 Jan;48(2):157-61 [16405664.001]
  • [Cites] J Virol. 2006 Feb;80(4):1979-91 [16439554.001]
  • [Cites] Cell Metab. 2006 Mar;3(3):211-22 [16517408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5391-6 [16565220.001]
  • [Cites] J Cell Biol. 2006 Jul 3;174(1):65-76 [16818720.001]
  • [Cites] Hum Mol Genet. 2007 Oct 15;16 Spec No. 2:R115-23 [17911155.001]
  • [Cites] Science. 2007 Nov 30;318(5855):1412-6 [18048681.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1149-63 [18083104.001]
  • [Cites] J Cell Biol. 2008 Feb 25;180(4):697-704 [18283109.001]
  • [Cites] Neuropathol Appl Neurobiol. 2008 Apr;34(2):169-80 [17961133.001]
  • [Cites] Cancer Cell. 2008 Apr;13(4):343-54 [18394557.001]
  • [Cites] J Neuropathol Exp Neurol. 2008 Apr;67(4):280-98 [18379439.001]
  • [Cites] J Biol Chem. 2008 Aug 15;283(33):22847-57 [18524774.001]
  • [Cites] Mol Cell. 2009 Feb 27;33(4):505-16 [19250911.001]
  • [Cites] Cell. 2009 May 15;137(4):721-35 [19427028.001]
  • [Cites] Mol Cell. 2009 May 15;34(3):259-69 [19450525.001]
  • [Cites] Cell. 2009 Jun 12;137(6):1062-75 [19524509.001]
  • [Cites] Cell Cycle. 2009 Jul 1;8(13):1986-90 [19502794.001]
  • [Cites] Autophagy. 2006 Jul-Sep;2(3):189-99 [16874109.001]
  • [Cites] Cell. 2006 Nov 3;127(3):635-48 [17081983.001]
  • [Cites] Autophagy. 2007 Mar-Apr;3(2):85-92 [17204844.001]
  • [Cites] J Biol Chem. 2007 Feb 23;282(8):5101-5 [17170104.001]
  • [Cites] Endocr Relat Cancer. 2007 Mar;14(1):73-80 [17395976.001]
  • (PMID = 20018885.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATXN1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Ataxin-1; 0 / Ataxins; 0 / Nerve Tissue Proteins; 0 / Nuclear Localization Signals; 0 / Nuclear Proteins; 0 / Peptides; 0 / SQSTM1 protein, human; 26700-71-0 / polyglutamine; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2820819
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74. Wilhelm C, Neubauer A, Brendel C: Discordant results of flow cytometric ZAP-70 expression status in B-CLL samples if different gating strategies are applied. Cytometry B Clin Cytom; 2006 Jul 15;70(4):242-50
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  • BACKGROUND: Recent studies have identified ZAP-70 expression status as an excellent prognostic parameter in chronic lymphocytic leukemia (CLL).
  • RESULTS: Applying either T-/NK-cell isotype or healthy control analysis strategies on patient samples that were processed in parallel revealed discrepant results in 48% (12/25) of all cases.
  • We demonstrate that high variances in ZAP-70 T-/NK-cell staining within B-CLL patients, paired with a close proximity of ZAP-70 B-cell values to the suggested cut-off levels, may lead to interpretation difficulties of ZAP-70 status.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. ZAP-70 Protein-Tyrosine Kinase / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / immunology. Humans. Immunophenotyping. Kaplan-Meier Estimate. Killer Cells, Natural / immunology. Middle Aged. Reference Values. Reproducibility of Results. Survival Rate. T-Lymphocytes / immunology

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  • [Copyright] (c) 2006 International Society for Analytical Cytology.
  • (PMID = 16906574.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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75. Geng SX, Li YQ, Chen SH, Yang LJ, Yin QS, Wu XL, Zhang XL: [Peripheral blood naive T cell level and its T cell receptor Vbeta repertoire usage profile in patients with chronic myelogenous leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jul;26(7):413-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Peripheral blood naive T cell level and its T cell receptor Vbeta repertoire usage profile in patients with chronic myelogenous leukemia].
  • OBJECTIVE: To analyze peripheral blood naive T cell level, its T cell receptor (TCR) Vbeta repertoire usage profile and clonality for evaluating the recent thymic output function and the expansion feature of TCR Vbeta subfamily T cells in patients with chronic myelogenous leukemia (CML).
  • METHODS: Quantitative detection of T-cell receptor excision DNA circles (TRECs) in peripheral blood mononuclear cells (PBMNC) from 20 cases of CML was preformed by real-time PCR (TaqMan) analysis, and TRECs-number in T-cells was calculated from peripheral blood CD3-positive cell rate.
  • The mean value of TRECs was 0.06 +/- 0.16 copy/1000 CD3(+) cells in CML patients while 6.84 +/- 4.71 copies/1000 CD3(+) cells in normal controls (P < 0.01).
  • Genescan analysis identified clonal expanded T cells of some Vbeta subfamily from 13 cases.
  • Vbeta3, Vbeta10, Vbeta19, Vbeta21 and Vbeta22 subfamilies clonal T cells were more frequently seen.
  • CONCLUSION: There is a prominent reduction of recent thymic output naive T cells function in CML.
  • The predominant usage and clonal expansion of TCR Vbeta subfamily T cells could be identified, indicating that CML patients have specific immune response to leukemia associated antigen, in spite of their T cell immunodeficiency.
  • [MeSH-major] Genes, T-Cell Receptor beta / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Receptors, Antigen, T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Gene Expression Regulation, Leukemic. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / immunology. Thymus Gland / immunology

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  • (PMID = 16251024.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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76. Lu G, Kong Y, Yue C: Genetic and immunophenotypic profile of IGH@ rearrangement detected by fluorescence in situ hybridization in 149 cases of B-cell chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2010 Jan 1;196(1):56-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic and immunophenotypic profile of IGH@ rearrangement detected by fluorescence in situ hybridization in 149 cases of B-cell chronic lymphocytic leukemia.
  • Recent studies have shown a higher frequency of immunoglobulin heavy (IGH@) locus rearrangement in B-cell chronic lymphocytic leukemia (B-CLL) than previously reported.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Adult. Aged. Female. Flow Cytometry. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged


77. Wlodarski MW, Nearman Z, Jiang Y, Lichtin A, Maciejewski JP: Clonal predominance of CD8(+) T cells in patients with unexplained neutropenia. Exp Hematol; 2008 Mar;36(3):293-300
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  • [Title] Clonal predominance of CD8(+) T cells in patients with unexplained neutropenia.
  • OBJECTIVE: T-cell-mediated autoimmunity may be involved in some cases of idiopathic neutropenia.
  • We hypothesized that a precise T-cell receptor repertoire analysis may uncover cytotoxic T-cell (CTL) expansions that are less pronounced than those seen in T large granular lymphocyte leukemia (T-LGL), but are pathophysiologically analogous and thus can serve as markers of a T-cell-mediated process.
  • MATERIALS AND METHODS: Using rational algorithms for T-cell receptor analysis and in vivo tracking of CTL responses previously established in our laboratory, we studied patients with unexplained chronic neutropenia (n = 20), T-LGL (n = 15), and healthy controls (n = 12).
  • To determine the level of immune activation, we studied interferon-gamma expression in CD8(+)cells using Taqman polymerase chain reaction.
  • In comparison to LGL leukemia, these clones were less immunodominant, but clearly discernible from subclinical lymphoproliferations in controls.

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  • [Cites] Blood. 1993 Jul 1;82(1):1-14 [8324214.001]
  • [Cites] Blood. 1991 Aug 15;78(4):1096-104 [1678288.001]
  • [Cites] Blood. 1994 Jul 15;84(2):625-31 [7517722.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1620-7 [8068951.001]
  • [Cites] Blood. 1997 Jan 1;89(1):256-60 [8978299.001]
  • [Cites] J Immunol. 1997 May 1;158(9):4493-9 [9127016.001]
  • [Cites] Br J Haematol. 1997 Apr;97(1):123-6 [9136951.001]
  • [Cites] Blood. 1998 Jan 1;91(1):181-6 [9414283.001]
  • [Cites] N Engl J Med. 1999 Jan 28;340(4):278-84 [9920952.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1797-802 [10477706.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:63-79 [15561677.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):863-76 [15755293.001]
  • [Cites] Br J Haematol. 2005 May;129(3):411-9 [15842666.001]
  • [Cites] Autoimmun Rev. 2005 Jun;4(5):315-21 [15990080.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2769-80 [15914562.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2632-41 [16614248.001]
  • [Cites] Blood. 2001 Jul 1;98(1):165-73 [11418476.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):765-73 [11544283.001]
  • [Cites] Eur J Haematol. 2001 Jul;67(1):35-44 [11553265.001]
  • [Cites] Am J Pathol. 2001 Nov;159(5):1861-8 [11696446.001]
  • [Cites] J Intern Med. 2001 Dec;250(6):476-91 [11902816.001]
  • [Cites] Semin Hematol. 2002 Apr;39(2):75-81 [11957188.001]
  • [Cites] Semin Hematol. 2002 Apr;39(2):113-20 [11957194.001]
  • [Cites] Semin Hematol. 2002 Apr;39(2):121-7 [11957195.001]
  • [Cites] Autoimmun Rev. 2003 Jun;2(4):218-23 [12848949.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1123-4 [12937414.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] J Immunol. 2004 Feb 1;172(3):1960-9 [14734782.001]
  • [Cites] In Silico Biol. 2004;4(1):17-29 [15089751.001]
  • [Cites] Lancet. 2004 Jul 24-30;364(9431):355-64 [15276395.001]
  • [Cites] Exp Hematol. 2004 Oct;32(10):1010-22 [15504556.001]
  • [Cites] N Engl J Med. 1975 Oct 9;293(15):748-53 [1172188.001]
  • [Cites] Clin Exp Immunol. 1980 Feb;39(2):307-14 [7389203.001]
  • [Cites] J Clin Invest. 1985 Jan;75(1):119-23 [3838096.001]
  • [Cites] Br J Haematol. 1986 May;63(1):59-67 [3085703.001]
  • [Cites] Blood. 1986 Nov;68(5):1095-100 [3490286.001]
  • [Cites] J Exp Med. 1986 Dec 1;164(6):2089-94 [3023520.001]
  • [Cites] Medicine (Baltimore). 1987 Sep;66(5):397-405 [3626848.001]
  • [Cites] Blood. 1988 Mar;71(3):822-4 [3345349.001]
  • [Cites] Nature. 1988 Aug 4;334(6181):395-402 [3043226.001]
  • [Cites] J Clin Invest. 1989 May;83(5):1676-81 [2523415.001]
  • [Cites] J Clin Invest. 1989 Nov;84(5):1688-91 [2478590.001]
  • [Cites] Blood. 1990 Jan 1;75(1):213-7 [2136803.001]
  • [Cites] Blood. 1990 Feb 1;75(3):736-43 [2297575.001]
  • [Cites] Science. 1993 Oct 15;262(5132):422-4 [8211163.001]
  • (PMID = 18279717.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113972-04; United States / NCRR NIH HHS / RR / U54 RR 019391; United States / NCRR NIH HHS / RR / U54 RR019397-05S16959; United States / NCI NIH HHS / CA / CA 113972-01; United States / NHLBI NIH HHS / HL / R01 HL 73429; United States / NCI NIH HHS / CA / R01 CA113972; United States / NCRR NIH HHS / RR / RR019397-05S16959; United States / NHLBI NIH HHS / HL / R01 HL073429-04; United States / NCI NIH HHS / CA / R01 CA113972-04; United States / NHLBI NIH HHS / HL / HL073429-04; United States / NCRR NIH HHS / RR / U54 RR019397; United States / NHLBI NIH HHS / HL / R01 HL073429; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ NIHMS83525; NLM/ PMC2643087
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78. Nakashima Y, Tagawa H, Suzuki R, Karnan S, Karube K, Ohshima K, Muta K, Nawata H, Morishima Y, Nakamura S, Seto M: Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type. Genes Chromosomes Cancer; 2005 Nov;44(3):247-55
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  • [Title] Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type.
  • Natural killer (NK) cell lymphomas/leukemias are highly aggressive lymphoid malignancies, but little is known about their genomic alterations, and thus there is an urgent need for identification and analysis of NK cell lymphomas/leukemias.
  • We performed an array CGH analysis for 27 NK-cell lymphoma/leukemia cases that were classified into two disease groups based on the World Health Organization Classification (10 aggressive NK-cell leukemia cases and 17 extranodal NK/T-cell [NK/T] lymphomas, nasal type).
  • The recurrent regions characteristic of the aggressive NK-cell leukemia group compared with those of the extranodal NK/T lymphoma, nasal-type group, were gain of 1q and loss of 7p15.1-p22.3 and 17p13.1.
  • Our results can be expected to provide further insights into the genetic basis of lymphomagenesis and the clinicopathologic features of NK-cell lymphomas/leukemias.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Genome, Human. Killer Cells, Natural / pathology. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Nose Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Karyotyping. Male. Middle Aged. Nucleic Acid Hybridization


79. Ohashi H, Kato C, Fukami S, Saito H, Hamaguchi M: Leukemic relapse in the central nervous system after allogeneic stem cell transplantation with complete remission in the bone marrow and donor-type chimerism: report of two cases. Am J Hematol; 2005 Jun;79(2):142-6
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  • [Title] Leukemic relapse in the central nervous system after allogeneic stem cell transplantation with complete remission in the bone marrow and donor-type chimerism: report of two cases.
  • We studied two cases with leukemia that relapsed in the central nervous system (CNS) after allogeneic stem cell transplantation.
  • One patient underwent peripheral blood stem cell transplantation (SCT) from a related, yet haplotype-mismatched, donor for chronic myelomonocytic leukemia.
  • In the other patient, with acute lymphoblastic leukemia, systemic relapse occurred when he was still on immunosuppression 6 months after SCT from an unrelated donor.
  • Chimerism status in the BM mononuclear cells and fractionated peripheral blood (PB) cells (granulocytes, T-lymphocytes, and the others) was assessed by short tandem repeat analysis.
  • In both patients, the BM cells and all the fractions of the PB cells proved donor-type chimeras.
  • These results seem to suggest that the graft-versus-leukemia effects might not be as effective in the CNS as in the BM, even when complete T-lymphoid chimerism is achieved.
  • [MeSH-major] Bone Marrow / pathology. Central Nervous System Neoplasms / therapy. Leukemia / therapy. Neoplasm Recurrence, Local. Peripheral Blood Stem Cell Transplantation. Tissue Donors. Transplantation Chimera
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelomonocytic, Chronic / pathology. Leukemia, Myelomonocytic, Chronic / therapy. Male. Middle Aged. Remission Induction. Transplantation, Homologous

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  • (PMID = 15929112.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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80. de Witte T, Suciu S, Brand R, Muus P, Kröger N: Autologous stem cell transplantation in myelodysplastic syndromes. Semin Hematol; 2007 Oct;44(4):274-7
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  • [Title] Autologous stem cell transplantation in myelodysplastic syndromes.
  • Allogeneic stem cell transplantation (SCT) is the treatment of choice for the majority of young patients with myelodysplasia (MDS) who have a histocompatible donor (sibling or unrelated donor).
  • For some patients lacking a human leukocyte antigen (HLA)-compatible donor, chemotherapy followed by autologous SCT may be a reasonable alternative, especially for patients with therapy-related MDS/acute myeloid leukemia (AML).
  • A substantial number of candidates may not be eligible for autologous SCT due to failure to induce remission or failure to collect sufficient numbers of stem cells.
  • Mobilized peripheral blood stem cells are the preferred stem cell source for young patients, especially in view of the more rapid hematopoietic recovery after transplantation with mobilized stem cells, but bone marrow stem cells also may be considered for patients older than 50 years.
  • [MeSH-major] Bone Marrow Transplantation. Hematopoietic Stem Cell Transplantation. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Disease-Free Survival. Evidence-Based Medicine. Hematopoietic Stem Cell Mobilization. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Middle Aged. Peripheral Blood Stem Cell Transplantation. Remission Induction. Risk Assessment. Transplantation, Autologous / methods. Transplantation, Homologous / methods


81. Arnold J, Zimmerman B, Li M, Lairmore MD, Green PL: Human T-cell leukemia virus type-1 antisense-encoded gene, Hbz, promotes T-lymphocyte proliferation. Blood; 2008 Nov 1;112(9):3788-97
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  • [Title] Human T-cell leukemia virus type-1 antisense-encoded gene, Hbz, promotes T-lymphocyte proliferation.
  • Human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) is dispensable for HTLV-1-mediated cellular transformation in cell culture, but is required for efficient viral infectivity and persistence in rabbits.
  • In most adult T-cell leukemia (ATL) cells, Tax oncoprotein expression is typically low or undetectable, whereas Hbz gene expression is maintained, suggesting that Hbz expression may support infected cell survival and, ultimately, leukemogenesis.
  • Herein, lentiviral vectors that express Hbz-specific short hairpin (sh)-RNA effectively decreased both Hbz mRNA and HBZ protein expression in transduced HTLV-1-transformed SLB-1 T cells.
  • Hbz knockdown correlated with a significant decrease in T-cell proliferation in culture.
  • Both SLB-1 and SLB-1-Hbz knockdown cells engrafted into inoculated NOD/SCID(gammachain-/-) mice to form solid tumors that also infiltrated multiple tissues.
  • However, tumor formation and organ infiltration were significantly decreased in animals challenged with SLB-1-Hbz knockdown cells.
  • Our data indicate that Hbz expression enhances the proliferative capacity of HTLV-1-infected T cells, playing a critical role in cell survival and ultimately HTLV-1 tumorigenesis in the infected host.

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  • [Cites] Blood. 2002 Nov 1;100(9):3175-82 [12384415.001]
  • [Cites] Retrovirology. 2007;4:92 [18078517.001]
  • [Cites] J Virol. 2003 May;77(9):5286-94 [12692230.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] J Gen Virol. 2003 Dec;84(Pt 12):3177-89 [14645900.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):165-70 [15044019.001]
  • [Cites] J Virol. 2004 Oct;78(20):11077-83 [15452228.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] Virology. 1994 Nov 1;204(2):656-64 [7941334.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 14;92(4):1057-61 [7862633.001]
  • [Cites] J Virol. 1996 Aug;70(8):5194-202 [8764028.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] Blood. 1998 Jun 15;91(12):4701-7 [9616168.001]
  • [Cites] J Virol. 1999 Jun;73(6):4856-65 [10233947.001]
  • [Cites] J Virol. 1999 Oct;73(10):8112-9 [10482560.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5996-6004 [16155606.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6026-34 [16155609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Virol. 2006 Mar;80(5):2495-505 [16474156.001]
  • [Cites] J Virol. 2000 Feb;74(3):1094-100 [10627519.001]
  • [Cites] J Virol. 2000 Mar;74(6):2655-62 [10684280.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1683-8 [11080810.001]
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Jun-Sep;12(2-3):207-17 [11325603.001]
  • [Cites] J Virol. 2002 Mar;76(6):2648-53 [11861831.001]
  • [Cites] Mol Cell Biol. 2002 May;22(10):3327-38 [11971966.001]
  • [Cites] Leukemia. 2002 Jun;16(6):1069-85 [12040438.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):204-9 [12077246.001]
  • [Cites] J Virol. 2002 Sep;76(18):9389-97 [12186921.001]
  • [Cites] J Virol. 2006 Apr;80(7):3469-76 [16537614.001]
  • [Cites] Blood. 2006 May 15;107(10):3976-82 [16424388.001]
  • [Cites] Retrovirology. 2006;3:15 [16512901.001]
  • [Cites] J Virol. 2006 Nov;80(21):10683-91 [16943297.001]
  • [Cites] Blood. 2006 Dec 15;108(13):3979-82 [16917009.001]
  • [Cites] J Virol. 2007 Feb;81(4):1543-53 [17151132.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] J Virol Methods. 2007 Jun;142(1-2):159-68 [17337070.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • (PMID = 18689544.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA100730-06; United States / NCI NIH HHS / CA / P01 CA100730-06; United States / NCI NIH HHS / CA / CA077566; United States / NIAID NIH HHS / AI / AI064440; United States / NIAID NIH HHS / AI / R21 AI064440
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / DNA, Antisense; 0 / DNA, Viral; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Messenger; 0 / RNA, Viral; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2572803
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82. Brioschi M, Fischer J, Cairoli R, Rossetti S, Pezzetti L, Nichelatti M, Turrini M, Corlazzoli F, Scarpati B, Morra E, Sacchi N, Beghini A: Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits. Neoplasia; 2010 Nov;12(11):866-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down-regulation of microRNAs 222/221 in acute myelogenous leukemia with deranged core-binding factor subunits.
  • Core-binding factor leukemia (CBFL) is a subgroup of acute myeloid leukemia (AML) characterized by genetic mutations involving the subunits of the core-binding factor (CBF).
  • The leukemogenesis model for CBFL posits that one, or more, gene mutations inducing increased cell proliferation and/or inhibition of apoptosis cooperate with CBF mutations for leukemia development.
  • Here, we show that MIR-222/221 expression is upregulated after myeloid differentiation of normal bone marrow AC133(+) stem progenitor cells.
  • Because of the highly conserved sequence homology, we demonstrated concomitant MIR-222/221 down-regulation and KIT up-regulation in the 32D/WT1 mouse cell model carrying the AML1-MTG16 fusion protein.
  • [MeSH-major] Core Binding Factor alpha Subunits / genetics. Leukemia, Myeloid / genetics. MicroRNAs / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Animals. Antigens, CD / genetics. Antigens, CD / metabolism. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Line, Tumor. Cells, Cultured. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. Down-Regulation. Erythropoietin / pharmacology. Female. Flow Cytometry. Glycoproteins / genetics. Glycoproteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Humans. Male. Middle Aged. Mutation. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Peptides / genetics. Peptides / metabolism. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells

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  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • [Cites] J Natl Cancer Inst. 2010 May 19;102(10):706-21 [20388878.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1369-75 [15855281.001]
  • [Cites] Oncogene. 2005 Aug 11;24(34):5325-32 [16007222.001]
  • [Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Leukemia. 2001 Apr;15(4):664-5 [11368373.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Leukemia. 2001 Nov;15(11):1685-8 [11681407.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2449-56 [12239155.001]
  • [Cites] Oncogene. 2002 Sep 26;21(43):6703-12 [12242670.001]
  • [Cites] Crit Rev Oncol Hematol. 2003 Feb;45(2):129-50 [12604126.001]
  • [Cites] Br J Haematol. 2003 Nov;123(4):749-50 [14616987.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Clin Chim Acta. 2004 May;343(1-2):85-92 [15115679.001]
  • [Cites] Genomics. 2004 Jul;84(1):1-9 [15203199.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Blood. 1990 Aug 15;76(4):801-7 [2200539.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Blood. 1994 Mar 15;83(6):1603-11 [8123851.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1911-8 [8946930.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):322-33 [9418879.001]
  • [Cites] Blood. 1998 Mar 15;91(6):1924-33 [9490675.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4028-37 [9596646.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9 [15650049.001]
  • [Cites] Cell. 2005 Dec 2;123(5):819-31 [16325577.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):18081-6 [16330772.001]
  • [Cites] Blood. 2006 May 1;107(9):3463-8 [16384925.001]
  • [Cites] BMC Genomics. 2007;8:38 [17266773.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):457-66 [17996649.001]
  • [Cites] Leukemia. 2008 Feb;22(2):303-7 [17960171.001]
  • [Cites] Neoplasia. 2009 Feb;11(2):167-76 [19177201.001]
  • [Cites] BMC Bioinformatics. 2005;6:79 [15799782.001]
  • (PMID = 21076613.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / AML1-ETO fusion protein, human; 0 / Antigens, CD; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor alpha Subunits; 0 / Glycoproteins; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Fusion; 0 / Peptides; 11096-26-7 / Erythropoietin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC2978910
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83. Cooley S, Trachtenberg E, Bergemann TL, Saeteurn K, Klein J, Le CT, Marsh SG, Guethlein LA, Parham P, Miller JS, Weisdorf DJ: Donors with group B KIR haplotypes improve relapse-free survival after unrelated hematopoietic cell transplantation for acute myelogenous leukemia. Blood; 2009 Jan 15;113(3):726-32
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  • [Title] Donors with group B KIR haplotypes improve relapse-free survival after unrelated hematopoietic cell transplantation for acute myelogenous leukemia.
  • Survival for patients with acute myeloid leukemia (AML) is limited by treatment-related mortality (TRM) and relapse after unrelated donor (URD) hematopoietic cell transplantation (HCT).
  • Natural killer (NK)-cell alloreactivity, determined by donor killer-cell immunoglobulin-like receptors (KIRs) and recipient HLA, correlates with successful HCT for AML.
  • Hypothesizing that donor KIR genotype (A/A: 2 A KIR haplotypes; B/x: at least 1 B haplotype) would affect outcomes, we genotyped donors and recipients from 209 HLA-matched and 239 mismatched T-replete URD transplantations for AML.
  • B/x donors were associated with a higher incidence of chronic graft-versus-host disease (GVHD; RR: 1.51 [95% CI: 1.01-2.18]; P = .03), but not of acute GVHD, relapse, or TRM.

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  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] Am J Transplant. 2008 Jun;8(6):1312-7 [18444913.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13483-8 [14597723.001]
  • [Cites] J Immunol. 2004 Jan 1;172(1):644-50 [14688377.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1521-6 [14504099.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1923-30 [15191952.001]
  • [Cites] Immunol Today. 1990 Jul;11(7):237-44 [2201309.001]
  • [Cites] Nature. 1997 Apr 3;386(6624):510-4 [9087412.001]
  • [Cites] Nat Rev Immunol. 2005 Mar;5(3):201-14 [15719024.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2594-600 [15536148.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4878-84 [15731175.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1446-51 [15973456.001]
  • [Cites] Hum Immunol. 2005 Jul;66(7):836-41 [16112031.001]
  • [Cites] Curr Top Microbiol Immunol. 2006;298:259-77 [16323418.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4370-6 [16131567.001]
  • [Cites] J Exp Med. 2006 Mar 20;203(3):633-45 [16533882.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):828-36 [16864053.001]
  • [Cites] Biol Blood Marrow Transplant. 2006 Aug;12(8):876-84 [16864058.001]
  • [Cites] Bone Marrow Transplant. 2006 Sep;38(6):437-44 [16892071.001]
  • [Cites] Transplantation. 2006 Oct 27;82(8):1024-30 [17060849.001]
  • [Cites] Tissue Antigens. 2007 Apr;69 Suppl 1:42-5 [17445161.001]
  • [Cites] Tissue Antigens. 2007 Apr;69 Suppl 1:92-5 [17445176.001]
  • [Cites] Hum Immunol. 2007 May;68(5):309-23 [17462498.001]
  • [Cites] Clin Exp Immunol. 2007 Jun;148(3):520-8 [17493020.001]
  • [Cites] Blood. 2007 Jun 1;109(11):5058-61 [17317850.001]
  • [Cites] Clin Immunol. 2007 Jun;123(3):272-80 [17446137.001]
  • [Cites] Immunogenetics. 2007 Jul;59(7):525-37 [17464504.001]
  • [Cites] Blood. 2007 Jul 1;110(1):433-40 [17371948.001]
  • [Cites] J Exp Med. 2007 Nov 26;204(12):3027-36 [18025129.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4576-83 [17785583.001]
  • [Cites] Int J Immunogenet. 2008 Feb;35(1):1-8 [18093180.001]
  • [Cites] Blood. 2003 Aug 1;102(3):814-9 [12689936.001]
  • (PMID = 18945962.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA076518; United States / PHS HHS / / P01 111412; United States / NCI NIH HHS / CA / U24-CA76518
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / Receptors, KIR
  • [Other-IDs] NLM/ PMC2628378
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84. Appel IM, den Boer ML, Meijerink JP, Veerman AJ, Reniers NC, Pieters R: Up-regulation of asparagine synthetase expression is not linked to the clinical response L-asparaginase in pediatric acute lymphoblastic leukemia. Blood; 2006 Jun 1;107(11):4244-9
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  • [Title] Up-regulation of asparagine synthetase expression is not linked to the clinical response L-asparaginase in pediatric acute lymphoblastic leukemia.
  • L-asparaginase (L-Asp) is an effective drug for treatment of children with acute lymphoblastic leukemia (ALL).
  • The effectiveness is generally thought to result from a rapid depletion of asparagine in serum and cells.
  • We monitored AS mRNA levels in leukemic cells before and during 5 days after intravenous administration of 1000 IU/m(2) pegylated L-asparaginase (PEG-Asp) in a therapeutic window in children with ALL at initial diagnosis.
  • [MeSH-major] Asparaginase / pharmacology. Aspartate-Ammonia Ligase / genetics. Polyethylene Glycols / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Up-Regulation / drug effects
  • [MeSH-minor] Adolescent. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Female. Humans. Infant. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / pathology. Male. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Neoplasm / analysis. RNA, Neoplasm / drug effects. Treatment Outcome

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  • (PMID = 16497975.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Neoplasm; 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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85. Naghashpour M, Lancet J, Moscinski L, Zhang L: Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report. Am J Hematol; 2010 Jun;85(6):451-4
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  • [Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
  • The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.
  • A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.
  • These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].
  • They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).
  • The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].
  • Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.
  • Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
  • Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
  • [MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20513125.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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86. Akagi T, Shih LY, Kato M, Kawamata N, Yamamoto G, Sanada M, Okamoto R, Miller CW, Liang DC, Ogawa S, Koeffler HP: Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations. Blood; 2009 Feb 19;113(8):1741-8
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  • [Title] Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations.
  • Acute promyelocytic leukemia (APL) is a hematopoietic malignant disease characterized by the chromosomal translocation t(15;17), resulting in the formation of the PML-RARA gene.
  • Here, we showed for the first time hidden abnormalities and novel disease-related genomic changes in t(15;17) APL.

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  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Haematologica. 2009 Feb;94(2):213-23 [19144660.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3188-97 [12515727.001]
  • [Cites] Cancer. 2003 Sep 15;98(6):1206-16 [12973844.001]
  • [Cites] Blood. 1984 Feb;63(2):254-9 [6362749.001]
  • [Cites] Nature. 1990 Oct 11;347(6293):558-61 [2170850.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]
  • [Cites] Haematologica. 2000 Jan;85(1):31-4 [10629588.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):744-57 [11886377.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] N Engl J Med. 1993 Jul 15;329(3):177-89 [8515790.001]
  • [Cites] Blood. 1997 Jan 15;89(2):376-87 [9002938.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2551-6 [9122233.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Blood. 2005 May 1;105(9):3699-706 [15650056.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4792-9 [15718420.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4129-37 [15806161.001]
  • [Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1153-60 [15889156.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2113-9 [15951308.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Oncogene. 2006 Mar 13;25(11):1594-601 [16550159.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1708-15 [16675706.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1202-10 [17053054.001]
  • [Cites] Br J Haematol. 2007 Apr;137(1):64-75 [17359372.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Br J Haematol. 2007 Sep;138(5):603-15 [17686054.001]
  • [Cites] Blood. 2008 Jan 15;111(2):776-84 [17890455.001]
  • [Cites] Cancer. 2008 Mar 15;112(6):1296-305 [18246537.001]
  • [Cites] Blood. 2008 Aug 1;112(3):814-21 [18490517.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Sep;47(9):729-39 [18506749.001]
  • [Cites] Leuk Lymphoma. 2008 Jun;49(6):1178-83 [18452069.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Nov;35(3):261-70 [12353268.001]
  • (PMID = 19109227.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / 5R01CA026038-30
  • [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 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2647673
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87. Hishizawa M, Kanda J, Utsunomiya A, Taniguchi S, Eto T, Moriuchi Y, Tanosaki R, Kawano F, Miyazaki Y, Masuda M, Nagafuji K, Hara M, Takanashi M, Kai S, Atsuta Y, Suzuki R, Kawase T, Matsuo K, Nagamura-Inoue T, Kato S, Sakamaki H, Morishima Y, Okamura J, Ichinohe T, Uchiyama T: Transplantation of allogeneic hematopoietic stem cells for adult T-cell leukemia: a nationwide retrospective study. Blood; 2010 Aug 26;116(8):1369-76
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  • [Title] Transplantation of allogeneic hematopoietic stem cells for adult T-cell leukemia: a nationwide retrospective study.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is increasingly used as a curative option for adult T-cell leukemia (ATL), an intractable mature T-cell neoplasm causally linked with human T-cell leukemia virus type I (HTLV-I).
  • Treatment-related mortality rate was higher among patients given cord blood transplants; disease-associated mortality was higher among male recipients or those given transplants not in remission.
  • Among patients who received related transplants, donor HTLV-I seropositivity adversely affected disease-associated mortality.
  • [MeSH-major] Graft vs Leukemia Effect / immunology. Hematopoietic Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy
  • [MeSH-minor] Adult. Disease Progression. Female. Follow-Up Studies. Graft Survival. Human T-lymphotropic virus 1 / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Humans. Japan / epidemiology. Male. Middle Aged. Retrospective Studies. Survival Rate. Transplantation, Homologous

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  • (PMID = 20479287.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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88. Ogata S, Hamada N, Maeyama T, Takayama K, Inoue H, Nakanishi Y: [A case of interstitial pneumonia with smoldering adult T-cell leukemia]. Nihon Kokyuki Gakkai Zasshi; 2010 Apr;48(4):293-7
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  • [Title] [A case of interstitial pneumonia with smoldering adult T-cell leukemia].
  • Then, ATL cells appeared in her peripheral blood, and the number of lymphocytes in BALF increased.
  • Inverse PCR for HTLV-1 clonality of the peripheral blood revealed a polyclonal pattern, and she was given a diagnosis of smoldering adult T-cell leukemia.
  • Using BALF flow cytometry, both CD4- and CD25-positive cells accounted for only 0.8%.
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / complications. Leukemia-Lymphoma, Adult T-Cell / complications. Lung Diseases, Interstitial / etiology

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  • (PMID = 20432970.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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89. Thompson BJ, Buonamici S, Sulis ML, Palomero T, Vilimas T, Basso G, Ferrando A, Aifantis I: The SCFFBW7 ubiquitin ligase complex as a tumor suppressor in T cell leukemia. J Exp Med; 2007 Aug 6;204(8):1825-35
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  • [Title] The SCFFBW7 ubiquitin ligase complex as a tumor suppressor in T cell leukemia.
  • Recent studies have shown that activating mutations of NOTCH1 are responsible for the majority of T cell acute lymphoblastic leukemia (T-ALL) cases.
  • Furthermore, we identify inactivating FBW7 mutations in a large fraction of human T-ALL lines and primary leukemias.
  • Our data suggest that FBW7 is a novel tumor suppressor in T cell leukemia, and implicate the loss of FBW7 function as a potential mechanism of drug resistance in T-ALL.

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  • [Cites] Mol Cell. 2003 Aug;12(2):381-92 [14536078.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):9417-23 [14672936.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3338-45 [14766969.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9085-90 [15150404.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cancer Res. 1984 Oct;44(10):4594-601 [6331881.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34371-8 [11425854.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35847-53 [11461910.001]
  • [Cites] Nature. 2001 Sep 20;413(6853):316-22 [11565034.001]
  • [Cites] Science. 2001 Oct 5;294(5540):173-7 [11533444.001]
  • [Cites] Nature. 2001 Nov 29;414(6863):514-21 [11734846.001]
  • [Cites] Cell. 2003 Jan 24;112(2):243-56 [12553912.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11400-6 [8876147.001]
  • [Cites] Genes Dev. 1997 Dec 1;11(23):3182-93 [9389650.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Mol Cell. 2004 Nov 19;16(4):509-20 [15546612.001]
  • [Cites] Nature. 2004 Dec 9;432(7018):775-9 [15592418.001]
  • [Cites] J Biol Chem. 2005 Mar 4;280(9):7654-8 [15611062.001]
  • [Cites] Annu Rev Immunol. 2005;23:601-49 [15771582.001]
  • [Cites] Annu Rev Immunol. 2005;23:945-74 [15771590.001]
  • [Cites] Semin Cell Dev Biol. 2005 Jun;16(3):323-33 [15840441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9649-54 [15980150.001]
  • [Cites] Cancer Cell. 2005 Jul;8(1):25-33 [16023596.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Blood. 2006 May 15;107(10):4115-21 [16449526.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9262-7 [16751266.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6261-71 [16880534.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nat Med. 2007 Jan;13(1):70-7 [17173050.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1687-9 [16015384.001]
  • [Cites] EMBO Rep. 2005 Dec;6(12):1120-5 [16299468.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11361-6 [16357143.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • (PMID = 17646408.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-02; United States / NCI NIH HHS / CA / R01 CA105129; United States / NCI NIH HHS / CA / CA120196; United States / NCI NIH HHS / CA / R01 CA120196-02; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / R01CA105129
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Stem Cell Factor; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2118676
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90. Osuji N, Matutes E, Catovsky D, Lampert I, Wotherspoon A: Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review. Am J Surg Pathol; 2005 Jul;29(7):935-41
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  • [Title] Histopathology of the spleen in T-cell large granular lymphocyte leukemia and T-cell prolymphocytic leukemia: a comparative review.
  • We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies.
  • Moderate splenic enlargement with red pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia.
  • Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red pulp T cells.
  • Unlike in hairy cell leukemia, the main differential diagnosis for red pulp lymphocytosis, the white pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones.
  • By comparison, T-PLL spleens showed marked red pulp lymphoid infiltration by medium-sized cells with irregular nuclei and prominent eosinophilic nucleoli.
  • T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-.
  • Expression of CD4 and CD8 in these cells mirrored that of circulating T-PLL cells.
  • These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
  • [MeSH-major] Leukemia, Prolymphocytic / pathology. Leukemia, T-Cell / pathology. Spleen / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 15958859.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 23
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91. Chetaille B: [Mediastinal lymphomas: histopathology]. Rev Pneumol Clin; 2010 Feb;66(1):28-31
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  • Three main entities summarize this pathology: T lymphoblastic lymphoma, mediastinal (thymic) diffuse large B cell lymphoma, and classical Hodgkin lymphoma.
  • [MeSH-major] Hodgkin Disease / pathology. Lymphoma, Non-Hodgkin / pathology. Mediastinal Neoplasms / pathology
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / analysis. Child. Humans. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / surgery. Mediastinum / pathology. Mediastinum / surgery. Neoplasm Invasiveness. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Prognosis. Thymus Neoplasms / diagnosis. Thymus Neoplasms / pathology. Young Adult

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  • [Copyright] Copyright (c) 2010. Published by Elsevier Masson SAS.
  • (PMID = 20207293.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 2
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92. Nabeshi H, Yoshikawa T, Kamada H, Shibata H, Sugita T, Abe Y, Nagano K, Nomura T, Minowa K, Tsunoda S, Tsutsumi Y: Arsenic trioxide induces down-regulation of gp46 via protein oxidation: proteomics analysis of oxidative modified proteins in As2O3-treated HTLV-1-infected cells. Pharmazie; 2010 Sep;65(9):702-7
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  • [Title] Arsenic trioxide induces down-regulation of gp46 via protein oxidation: proteomics analysis of oxidative modified proteins in As2O3-treated HTLV-1-infected cells.
  • Adult T-cell leukemia (ATL) is a severe chemotherapy-resistant malignancy associated with prolonged infection by the human T cell-lymphotropic virus 1 (HTLV-1) retrovirus.
  • Epidemiology studies strongly indicate that an increase in HTLV-1 virus load is an important factor during the onset of ATL.
  • Therefore, inhibition of the growth/transmission of HTLV-1 infected cells is a promising strategy in preventing the disease.
  • In our previous study, we revealed that arsenic trioxide (As2O3), a drug used to treat acute promyelocytic leukemia (APL), exerts an inhibitory effect on syncytium formation between HTLV-1 infected cells and HeLa cells via suppression of HTLV-1 envelope protein gp46 expression at low concentrations.
  • We postulate that AS2O3 exerts an inhibitory effect on HTLV-1 virus transmission via down-regulation of gp46-production, which might be caused by oxidative modification of various proteins such as chaperones.
  • [MeSH-major] Arsenicals / pharmacology. Gene Products, env / biosynthesis. HTLV-I Infections / metabolism. Oxides / pharmacology. Retroviridae Proteins, Oncogenic / biosynthesis
  • [MeSH-minor] Cell Fusion. Down-Regulation / drug effects. Electrophoresis, Gel, Two-Dimensional. Gels. HeLa Cells. Humans. Hydrolysis. Immunoprecipitation. Oxidation-Reduction. Proteomics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Trypsin / chemistry

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  • (PMID = 21038850.001).
  • [ISSN] 0031-7144
  • [Journal-full-title] Die Pharmazie
  • [ISO-abbreviation] Pharmazie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Gels; 0 / Gene Products, env; 0 / Oxides; 0 / Retroviridae Proteins, Oncogenic; 0 / gp46 protein, Human T-cell leukemia virus type I; EC 3.4.21.4 / Trypsin; S7V92P67HO / arsenic trioxide
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93. van Imhoff GW, van der Holt B, MacKenzie MA, Ossenkoppele GJ, Wijermans PW, Kramer MH, van 't Veer MB, Schouten HC, van Marwijk Kooy M, van Oers MH, Raemaekers JM, Sonneveld P, Meulendijks LA, Kluin PM, Kluin-Nelemans HC, Verdonck LF, Dutch-Belgian Hemato-Oncology Cooperative Group (HOVON): Short intensive sequential therapy followed by autologous stem cell transplantation in adult Burkitt, Burkitt-like and lymphoblastic lymphoma. Leukemia; 2005 Jun;19(6):945-52
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  • [Title] Short intensive sequential therapy followed by autologous stem cell transplantation in adult Burkitt, Burkitt-like and lymphoblastic lymphoma.
  • The feasibility and efficacy of up-front high-dose sequential chemotherapy followed by autologous stem cell transplantation (ASCT) in previously untreated adults (median age 33 years; range 15-64) with Burkitt lymphoma (BL), Burkitt-like lymphoma (BLL) or lymphoblastic lymphoma (LyLy), both without central nervous system or extensive bone marrow involvement was investigated in a multicenter phase II study.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Burkitt Lymphoma / drug therapy. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / adverse effects. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Prednisone / administration & dosage. Prednisone / adverse effects. Transplantation, Autologous

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  • (PMID = 15800666.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; VB0R961HZT / Prednisone
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94. Mattei D, Bassan R, Mordini N, Rapezzi D, Rambaldi A, Strola G, Peretti C, Del Grosso F, Ferraris AM, Castellino C, Gallamini A: Expansion of B cell precursors after unrelated cord blood transplantation for an adult patient. Bone Marrow Transplant; 2007 Aug;40(3):283-5
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  • [Title] Expansion of B cell precursors after unrelated cord blood transplantation for an adult patient.
  • [MeSH-major] Cell Proliferation. Cord Blood Stem Cell Transplantation. Leukemia-Lymphoma, Adult T-Cell / complications. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cells, B-Lymphoid / pathology
  • [MeSH-minor] Adult. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antigens, CD / genetics. Antigens, CD / immunology. Chromosomes, Human, X / genetics. Chromosomes, Human, X / immunology. Cyclosporine / administration & dosage. Cyclosporine / adverse effects. Diarrhea / drug therapy. Diarrhea / etiology. Diarrhea / genetics. Diarrhea / immunology. Fatal Outcome. Female. Gastrointestinal Agents / administration & dosage. Gastrointestinal Agents / adverse effects. Graft Survival / immunology. Graft vs Host Disease / genetics. Graft vs Host Disease / immunology. Graft vs Host Disease / pathology. Graft vs Host Disease / prevention & control. Humans. Ileus / drug therapy. Ileus / etiology. Ileus / genetics. Ileus / immunology. Immunosuppressive Agents / administration & dosage. Immunosuppressive Agents / adverse effects. Infliximab. Neoplasm, Residual. Transplantation Chimera / genetics. Transplantation Chimera / immunology. Transplantation Conditioning

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  • (PMID = 17529999.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Gastrointestinal Agents; 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; B72HH48FLU / Infliximab
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95. Hütter G, Nowak D, Mossner M, Ganepola S, Müssig A, Allers K, Schneider T, Hofmann J, Kücherer C, Blau O, Blau IW, Hofmann WK, Thiel E: Long-term control of HIV by CCR5 Delta32/Delta32 stem-cell transplantation. N Engl J Med; 2009 Feb 12;360(7):692-8
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  • [Title] Long-term control of HIV by CCR5 Delta32/Delta32 stem-cell transplantation.
  • We transplanted stem cells from a donor who was homozygous for CCR5 delta32 in a patient with acute myeloid leukemia and HIV-1 infection.
  • [MeSH-major] HIV Infections / therapy. HIV-1. Receptors, CCR5 / genetics. Stem Cell Transplantation
  • [MeSH-minor] Adult. Anti-Retroviral Agents / therapeutic use. Antigens, CD4. CD4 Lymphocyte Count. CD4-Positive T-Lymphocytes / immunology. DNA, Viral / blood. Genetic Predisposition to Disease. Homozygote. Humans. Male. RNA, Viral / blood. Transplantation Chimera. Transplantation, Homologous. Viral Load


96. Sharma VM, Calvo JA, Draheim KM, Cunningham LA, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco AJ, Kelliher MA: Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc. Mol Cell Biol; 2006 Nov;26(21):8022-31
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  • [Title] Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
  • Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).
  • To identify Notch1 target genes in leukemia, we developed mouse T-cell leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
  • Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-cell leukemia. c-myc mRNA levels are increased in primary mouse T-cell tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic cell growth.
  • Consistent with these findings, retroviral insertional mutagenesis screening of our T-cell leukemia mouse model revealed common insertions in either notch1 or c-myc genes.

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  • [Cites] J Biol Chem. 2005 May 13;280(19):19331-42 [15743767.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9262-7 [16751266.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Future Oncol. 2005 Aug;1(4):511-9 [16556027.001]
  • [Cites] Blood. 2006 May 15;107(10):4115-21 [16449526.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Mol Cell Biol. 2000 Jan;20(1):273-85 [10594030.001]
  • [Cites] J Biol Chem. 2000 Jun 2;275(22):17211-20 [10747963.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] J Biol Chem. 2000 Nov 17;275(46):35734-7 [10940313.001]
  • [Cites] Nat Immunol. 2000 Aug;1(2):138-44 [11248806.001]
  • [Cites] Oncogene. 2001 Jun 28;20(29):3897-905 [11439353.001]
  • [Cites] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(22):7761-74 [11604511.001]
  • [Cites] Science. 2001 Dec 7;294(5549):2179-81 [11679632.001]
  • [Cites] Dev Biol. 2001 Oct 1;238(1):110-9 [11783997.001]
  • [Cites] Genes Dev. 2002 Jun 1;16(11):1397-411 [12050117.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Mol Cell Biol. 2002 Nov;22(22):7812-9 [12391150.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):44754-9 [12223485.001]
  • [Cites] J Immunol. 2003 Jun 15;170(12):5834-41 [12794108.001]
  • [Cites] J Biol Chem. 2003 Jun 20;278(25):23196-203 [12682059.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):551-64 [12842084.001]
  • [Cites] J Immunol. 2003 Sep 15;171(6):2896-903 [12960312.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3338-45 [14766969.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4936-41 [15044701.001]
  • [Cites] J Biol Chem. 2004 Jun 11;279(24):24986-93 [15067010.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Mol Cell Biol. 2004 Oct;24(20):8813-22 [15456857.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1994 Dec 2;79(5):885-92 [8001125.001]
  • [Cites] Development. 1995 Aug;121(8):2633-44 [7671825.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2424-33 [9694806.001]
  • [Cites] Immunity. 1998 Dec;9(6):777-86 [9881968.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):518-22 [10206645.001]
  • [Cites] Curr Opin Immunol. 1999 Apr;11(2):167-71 [10322160.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):5025-35 [10373552.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2112-20 [10473095.001]
  • [Cites] Mol Cell. 2004 Nov 19;16(4):509-20 [15546612.001]
  • [Cites] J Biol Chem. 2005 Mar 11;280(10):9313-9 [15611067.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7159-68 [16103066.001]
  • (PMID = 16954387.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC1636748
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97. Kishi Y, Kami M, Murashige N, Tanaka Y, Haraguchi K, Fujisaki G, Kusumoto S, Mori SI, Takaue Y, Tanosaki R: Hyperacute GVHD and emergence of peripheral CD3+CD56+ T cells and activated natural killer cells are useful markers for early diagnosis of post-transplant hemophagocytic syndrome. Bone Marrow Transplant; 2005 Feb;35(4):415-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hyperacute GVHD and emergence of peripheral CD3+CD56+ T cells and activated natural killer cells are useful markers for early diagnosis of post-transplant hemophagocytic syndrome.
  • [MeSH-major] Graft vs Host Disease. Histiocytosis, Non-Langerhans-Cell / diagnosis. Stem Cell Transplantation
  • [MeSH-minor] Adult. Antigens, CD3 / blood. Antigens, CD56 / blood. Biomarkers / blood. Humans. Killer Cells, Natural. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / therapy. Lymphocyte Activation. Male. T-Lymphocytes

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  • (PMID = 15640826.001).
  • [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 / Antigens, CD3; 0 / Antigens, CD56; 0 / Biomarkers
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98. Zhao XY, Chang YJ, Xu LP, Liu DH, Liu KY, Huang XJ: Association of natural killer cells in allografts with transplant outcomes in patients receiving G-CSF-mobilized PBSC grafts and G-CSF-primed BM grafts from HLA-haploidentical donors. Bone Marrow Transplant; 2009 Dec;44(11):721-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of natural killer cells in allografts with transplant outcomes in patients receiving G-CSF-mobilized PBSC grafts and G-CSF-primed BM grafts from HLA-haploidentical donors.
  • The aim of this study was to investigate the effects of natural killer (NK) cells on transplant outcomes in patients receiving G-CSF-mobilized PBSC grafts and G-CSF-primed BM grafts from HLA-haploidentical donors.
  • Forty-one haploidentical allogeneic hematopoietic SCT patients were analyzed according to the NK cell concentration in relation to acute GVHD (aGVHD), chronic GVHD (cGVHD), TRM and leukemia-free survival.
  • The patients receiving a higher dose of CD56(bright) NK cells (>1.9 x 10(6)/kg) showed a higher incidence of grades II-IV aGVHD (hazard risk (HR), 2.872; P=0.022) and cGVHD (HR, 2.884; P=0.039).
  • A higher CD56(dim)/CD56(bri) NK cell ratio (>8.0) was correlated with a decreased risk of III-IV aGVHD (HR, 0.290; P=0.065) and TRM (HR, 0.072; P=0.012), thereby increasing the rate of leukemia-free survival (HR, 0.174; P=0.007) after haploidentical transplantation without in vitro T-cell depletion.
  • Our results suggest that a high allograft CD56(dim)/CD56(bright) NK cell ratio (>8.0) plays an important role in improving transplant outcomes.
  • A higher dose of CD56(bright) NK cells might be a predictor for a higher incidence of GVHD.