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1. McCormack MP, Hall MA, Schoenwaelder SM, Zhao Q, Ellis S, Prentice JA, Clarke AJ, Slater NJ, Salmon JM, Jackson SP, Jane SM, Curtis DJ: A critical role for the transcription factor Scl in platelet production during stress thrombopoiesis. Blood; 2006 Oct 1;108(7):2248-56
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  • Quantitative real-time polymerase chain reaction showed that Scl-null platelets lacked NF-E2, and chromatin immunoprecipitation analysis demonstrated Scl binding to the NF-E2 promoter in the human megakaryoblastic-cell line Meg-01, along with its binding partners E47, Lmo2, and the cofactors Ldb1 and GATA-2.

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  • [Cites] Blood. 2005 Aug 15;106(4):1223-31 [15860665.001]
  • [Cites] J Thromb Haemost. 2003 Jun;1(6):1174-82 [12871316.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3037-47 [10556187.001]
  • [Cites] J Cell Biol. 1999 Dec 13;147(6):1299-312 [10601342.001]
  • [Cites] J Biol Chem. 2000 Apr 7;275(14):10567-76 [10744751.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1366-73 [10942379.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3970-9 [12907454.001]
  • [Cites] Genes Dev. 2003 Dec 1;17(23):2864-9 [14665668.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):11-24 [14725896.001]
  • [Cites] Blood. 2004 May 1;103(9):3342-8 [14726374.001]
  • [Cites] EMBO J. 2004 Jul 21;23(14):2841-52 [15215894.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1327-34 [15059849.001]
  • [Cites] Blood. 1980 Jan;55(1):164-6 [7350937.001]
  • [Cites] Blood. 1982 Jul;60(1):213-9 [7082839.001]
  • [Cites] Blood. 1984 Apr;63(4):768-78 [6704539.001]
  • [Cites] J Cell Biol. 1986 Nov;103(5):1903-10 [3782288.001]
  • [Cites] EMBO J. 1994 Oct 17;13(20):4831-9 [7957052.001]
  • [Cites] Blood. 1995 Jan 15;85(2):402-13 [7529062.001]
  • [Cites] Nature. 1995 Feb 2;373(6513):432-4 [7830794.001]
  • [Cites] Cell. 1995 Jun 2;81(5):695-704 [7774011.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):7075-9 [7624372.001]
  • [Cites] Exp Hematol. 1995 Aug;23(9):996-1001 [7635185.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1427-9 [7660125.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8690-4 [7567998.001]
  • [Cites] Blood. 1997 Feb 1;89(3):823-33 [9028313.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] EMBO J. 1997 Jul 1;16(13):3965-73 [9233806.001]
  • [Cites] EMBO J. 1997 Sep 15;16(18):5654-61 [9312024.001]
  • [Cites] J Histochem Cytochem. 1998 Jan;46(1):49-57 [9405494.001]
  • [Cites] Genes Dev. 1998 Feb 15;12(4):473-9 [9472016.001]
  • [Cites] Blood. 1998 Sep 1;92(5):1608-16 [9716588.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11897-902 [9751762.001]
  • [Cites] Blood. 1999 May 1;93(9):2760-70 [10216069.001]
  • [Cites] Blood. 1999 May 1;93(9):2867-75 [10216081.001]
  • [Cites] Development. 1999 Jun;126(12):2799-811 [10331989.001]
  • [Cites] Development. 1999 Oct;126(20):4603-15 [10498694.001]
  • [Cites] Biochem J. 1999 Nov 1;343 Pt 3:615-20 [10527940.001]
  • [Cites] J Biol Chem. 2004 Dec 10;279(50):52183-90 [15466856.001]
  • [Cites] Nat Med. 2005 May;11(5):507-14 [15834429.001]
  • [Cites] Mol Cell Biol. 2005 Aug;25(15):6355-62 [16024775.001]
  • [Cites] Exp Hematol. 2000 Oct;28(10):1113-9 [11027829.001]
  • [Cites] Curr Biol. 2001 Apr 17;11(8):579-86 [11369202.001]
  • [Cites] Mol Cell. 2001 Aug;8(2):465-71 [11545748.001]
  • [Cites] Stem Cells. 2001;19(5):397-407 [11553848.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3359-67 [12032774.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11760-5 [12193659.001]
  • [Cites] Nature. 2003 Jan 30;421(6922):547-51 [12540851.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):992-7 [12552125.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4789-96 [12586623.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10235-50 [16287841.001]
  • (PMID = 16763211.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 237011; United States / PHS HHS / / 282400; United States / NHLBI NIH HHS / HL / P01 HL53749-03
  • [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 / NF-E2 Transcription Factor, p45 Subunit; 0 / Nfe2 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 9014-42-0 / Thrombopoietin
  • [Other-IDs] NLM/ PMC1895552
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2. Mansour MR, Sulis ML, Duke V, Foroni L, Jenkinson S, Koo K, Allen CG, Gale RE, Buck G, Richards S, Paietta E, Rowe JM, Tallman MS, Goldstone AH, Ferrando AA, Linch DC: Prognostic implications of NOTCH1 and FBXW7 mutations in adults with T-cell acute lymphoblastic leukemia treated on the MRC UKALLXII/ECOG E2993 protocol. J Clin Oncol; 2009 Sep 10;27(26):4352-6
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  • [Title] Prognostic implications of NOTCH1 and FBXW7 mutations in adults with T-cell acute lymphoblastic leukemia treated on the MRC UKALLXII/ECOG E2993 protocol.
  • PURPOSE: Notch pathway activation by mutations in either NOTCH1 and/or FBXW7 is one of the most common molecular events in T-cell acute lymphoblastic leukemia (T-ALL) and, in pediatric disease, predicts for favorable outcome.
  • We sought to evaluate the outcome according to mutation status of patients with adult T-ALL treated on the United Kingdom Acute Lymphoblastic Leukaemia XII (UKALLXII)/Eastern Cooperative Oncology Group (ECOG) E2993 protocol.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Adolescent. Adult. Chromatography, High Pressure Liquid / methods. DNA Mutational Analysis. Disease-Free Survival. Female. Follow-Up Studies. Gene Frequency. Genotype. Humans. Male. Middle Aged. Multivariate Analysis. Prognosis. Treatment Outcome. United Kingdom. Young Adult

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  • [Cites] Blood. 2006 Feb 1;107(3):1116-23 [16195338.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3760-7 [16105981.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [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] Blood. 2007 Feb 1;109(3):910-5 [17023577.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3189-97 [17170120.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5611-6 [17575125.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1262-70 [17456725.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1827-33 [18048644.001]
  • [Cites] Leuk Res. 2008 Nov;32(11):1751-5 [18485478.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4386-93 [12036866.001]
  • [Cites] Haematologica. 2002 Nov;87(11):1126-34 [12414341.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2149-56 [14576730.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Blood. 1988 Jan;71(1):123-31 [3422030.001]
  • [Cites] Leukemia. 1998 Apr;12(4):463-73 [9557602.001]
  • [Cites] Leukemia. 2006 Mar;20(3):537-9 [16424867.001]
  • (PMID = 19635999.001).
  • [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
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002514
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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 / Receptor, Notch1; EC 2.3.2.27 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / FBXW7 protein, human
  • [Other-IDs] NLM/ PMC2744275
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3. Igarashi N, Chou T, Hirose T, Imai Y, Ishiguro T, Nemoto K: Donor cell-derived acute lymphocytic leukemia after allogeneic stem cell transplantation for multiple myeloma. Int J Hematol; 2009 Oct;90(3):378-82
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  • [Title] Donor cell-derived acute lymphocytic leukemia after allogeneic stem cell transplantation for multiple myeloma.
  • Donor cell leukemia (DCL) is a rare, but well-known, complication after allogeneic hematopoietic cell transplantation.
  • We report a case of donor cell-derived acute lymphocytic leukemia (ALL) occurring in a 55-year-old man after allogeneic bone marrow transplantation (allo-BMT) from an HLA-matched unrelated donor for refractory multiple myeloma (MM).
  • However, he died from severe graft-versus-host disease four months after the second transplantation.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Multiple Myeloma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Dexamethasone / therapeutic use. Fatal Outcome. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Male. Middle Aged. Pyrazines / therapeutic use. Tissue Donors. Transplantation, Homologous


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4. Chalandon Y, Passweg JR, Schmid C, Olavarria E, Dazzi F, Simula MP, Ljungman P, Schattenberg A, de Witte T, Lenhoff S, Jacobs P, Volin L, Iacobelli S, Finke J, Niederwieser D, Guglielmi C, Chronic Leukemia Working Party of European Group for Blood and Marrow Transplantation: Outcome of patients developing GVHD after DLI given to treat CML relapse: a study by the Chronic Leukemia Working Party of the EBMT. Bone Marrow Transplant; 2010 Mar;45(3):558-64
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  • [Title] Outcome of patients developing GVHD after DLI given to treat CML relapse: a study by the Chronic Leukemia Working Party of the EBMT.
  • We analyzed GVHD by clinical presentation (acute or chronic GVHD) and onset time after the first DLI (early (< or =45 days) or late (>45 days)).
  • Some form of GVHD occurred at a median of 104 days, acute GVHD at 45 days and chronic GVHD at 181 days after DLI.
  • The clinical presentation was acute GVHD in 71 patients, of whom 31 subsequently developed chronic GVHD subsequently.
  • De novo chronic GVHD was seen in 51 patients.
  • OS for all patients was 69% (95% confidence interval (CI) 63-75) at 5 years, DLI-related mortality was 11% (95% CI 8-15) and disease-related mortality was 20% (95% CI 16-25).
  • Risk factors for developing GVHD after DLI were T-cell dose at first DLI, the time interval from transplant to DLI and donor type.
  • Clinical presentation as acute GVHD and early onset GVHD were associated with increased mortality.
  • [MeSH-major] Graft vs Host Disease / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion / adverse effects
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Multivariate Analysis. Proportional Hazards Models. Recurrence. Risk Factors. Survival Rate. Time Factors. Tissue Donors. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • (PMID = 19633691.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ G0802523
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Investigator] Olavarria E; Schattenberg A; Jacobs P; Ljungman P; Finke J; Lenhoff S; Volin L; Jacobsen N; Passweg J; Jouet JP; de Souza CA; Michallet M; Ferrant A; Harousseau JL; Milligan D; Liakopoulou E; Bron D; Hamladji R; Koza V; Bandini B; Leblond V; Haas R; Beguin Y; Mufti G; Bornhäuser M; Boogaerts M; Davies JM; Sierra J; Pihkala U; Zander A; Pretnar J
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5. Xiong H, Zhang YD, Hu Q, Sun Y, Liu SY, Zhang LQ, Liu AG, Wang GL: [Biological characteristics of T-lineage acute lymphoblastic leukemia in 23 children]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Aug;12(8):605-8
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  • [Title] [Biological characteristics of T-lineage acute lymphoblastic leukemia in 23 children].
  • OBJECTIVE: To investigate the biological characteristics of childhood T-lineage acute lymphoblastic leukemia (T-ALL) and their clinical significance.
  • RESULTS: CD3(+) expression of T-lineage antigens was apparently higher than CD7(+) and CD5(+) expression.
  • CD19(+) expression of B-lineage antigens was apparently higher than CD22(+), CD10(+) and CD20(+) expression.
  • Myeloid antigen was expressed in 4 cases (17%).
  • CONCLUSIONS: Immunophenotyping is an important tool for diagnosis of T-ALL.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 20704789.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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6. Indraccolo S, Minuzzo S, Masiero M, Pusceddu I, Persano L, Moserle L, Reboldi A, Favaro E, Mecarozzi M, Di Mario G, Screpanti I, Ponzoni M, Doglioni C, Amadori A: Cross-talk between tumor and endothelial cells involving the Notch3-Dll4 interaction marks escape from tumor dormancy. Cancer Res; 2009 Feb 15;69(4):1314-23
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  • Here, we report that escape of human T-cell acute lymphoblastic leukemia (T-ALL) cells or colorectal cancer cells from dormancy is associated with Dll4 expression in the tumor microenvironment and increased Notch3 signaling in tumor cells.
  • [MeSH-major] Cell Communication / physiology. Colorectal Neoplasms / physiopathology. Endothelial Cells / physiology. Intercellular Signaling Peptides and Proteins / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Receptors, Notch / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Coculture Techniques. Female. Gene Expression Regulation, Neoplastic. Gene Silencing. Genes, Reporter. Humans. Jurkat Cells. Mice. Mice, Inbred NOD. Mice, SCID. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19208840.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DLL4 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / NOTCH3 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Notch
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7. Roman-Gomez J, Jimenez-Velasco A, Agirre X, Castillejo JA, Navarro G, Calasanz MJ, Garate L, San Jose-Eneriz E, Cordeu L, Prosper F, Heiniger A, Torres A: CpG island methylator phenotype redefines the prognostic effect of t(12;21) in childhood acute lymphoblastic leukemia. Clin Cancer Res; 2006 Aug 15;12(16):4845-50
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  • [Title] CpG island methylator phenotype redefines the prognostic effect of t(12;21) in childhood acute lymphoblastic leukemia.
  • PURPOSE: To examine cancer genes undergoing epigenetic inactivation in a set of ETV6/RUNX1-positive acute lymphoblastic leukemias in order to define the CpG island methylator phenotype (CIMP) in the disease and evaluate its relationship with clinical features and outcome.
  • EXPERIMENTAL DESIGN: Methylation-specific PCR was used to analyze the methylation status of 38 genes involved in cell immortalization and transformation in 54 ETV6/RUNX1-positive samples in comparison with 190 ETV6/RUNX1-negative samples.
  • Estimated disease-free survival and overall survival at 9 years were 92% and 100% for the CIMP- group and 33% and 73% for the CIMP+ group (P = 0.002 and P = 0.04, respectively).
  • Multivariate analysis showed that methylation profile was an independent prognostic factor in predicting disease-free survival (P = 0.01) and overall survival (P = 0.05).
  • CONCLUSION: Our results suggest that methylation profile may be a potential new biomarker of risk prediction in ETV6/RUNX1-positive acute lymphoblastic leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 21 / genetics. DNA Methylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [CommentIn] Clin Cancer Res. 2006 Aug 15;12(16):4787-9 [16914562.001]
  • (PMID = 16914570.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
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8. Simon M, Grandage VL, Linch DC, Khwaja A: Constitutive activation of the Wnt/beta-catenin signalling pathway in acute myeloid leukaemia. Oncogene; 2005 Mar 31;24(14):2410-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive activation of the Wnt/beta-catenin signalling pathway in acute myeloid leukaemia.
  • Wnt stimulation leads to beta-catenin accumulation, nuclear translocation and interaction with T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors to regulate genes important for embryonic development and proliferation.
  • Wnt/beta-catenin can promote stem cell self-renewal and is dysregulated in colon carcinoma.
  • We have examined the role of the Wnt pathway in the development of acute myeloid leukaemia (AML) and find that the beta-catenin protein is readily detected in primary AML samples.
  • Using transfection of a TCF/LEF reporter construct into primary AML cells and normal human progenitors, we find increased reporter activity in 16/25 leukaemia samples.
  • [MeSH-major] Cytoskeletal Proteins / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Leukemia, Myeloid / metabolism. Signal Transduction. Trans-Activators / metabolism
  • [MeSH-minor] Acute Disease. Base Sequence. Cell Survival. DNA Primers. Humans. Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Wnt Proteins. Wnt1 Protein. beta Catenin

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  • (PMID = 15735743.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA Primers; 0 / Intercellular Signaling Peptides and Proteins; 0 / Trans-Activators; 0 / WNT1 protein, human; 0 / Wnt Proteins; 0 / Wnt1 Protein; 0 / beta Catenin
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9. Schlaeger TM, Mikkola HK, Gekas C, Helgadottir HB, Orkin SH: Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development. Blood; 2005 May 15;105(10):3871-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tie2Cre-mediated gene ablation defines the stem-cell leukemia gene (SCL/tal1)-dependent window during hematopoietic stem-cell development.
  • The stem-cell leukemia gene (SCL/tal1) is essential for the formation of all blood lineages.
  • [MeSH-major] Cell Differentiation. DNA-Binding Proteins / metabolism. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Integrases / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, TIE-2 / metabolism. Transcription Factors / metabolism. Viral Proteins / metabolism


10. Schetelig J, van Biezen A, Brand R, Caballero D, Martino R, Itala M, García-Marco JA, Volin L, Schmitz N, Schwerdtfeger R, Ganser A, Onida F, Mohr B, Stilgenbauer S, Bornhäuser M, de Witte T, Dreger P: Allogeneic hematopoietic stem-cell transplantation for chronic lymphocytic leukemia with 17p deletion: a retrospective European Group for Blood and Marrow Transplantation analysis. J Clin Oncol; 2008 Nov 1;26(31):5094-100
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  • [Title] Allogeneic hematopoietic stem-cell transplantation for chronic lymphocytic leukemia with 17p deletion: a retrospective European Group for Blood and Marrow Transplantation analysis.
  • PURPOSE: Patients with chronic lymphocytic leukemia (CLL) and 17p deletion (17p-) have a poor prognosis.
  • Although allogeneic hematopoietic stem-cell transplantation (HCT) has the potential to cure patients with advanced CLL, it is not known whether this holds true for patients with 17p-CLL.
  • Acute, grade 2 to 4 graft-versus-host disease (GVHD) occurred in 43% of patients, and extensive chronic GVHD occurred in 53% of patients.
  • The cumulative incidence of progressive disease at 4 years was 34%.
  • CONCLUSION: Allogeneic HCT has the potential to induce long-term disease-free survival in patients with 17p-CLL.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 17. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / surgery
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Europe. Female. Graft vs Host Disease / etiology. Humans. Male. Middle Aged. Registries. Retrospective Studies. Surveys and Questionnaires. Time Factors. Transplantation, Homologous. Treatment Failure. Treatment Outcome

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  • (PMID = 18711173.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Zhou GB, Zhang J, Wang ZY, Chen SJ, Chen Z: Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy. Philos Trans R Soc Lond B Biol Sci; 2007 Jun 29;362(1482):959-71
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  • [Title] Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy.
  • To turn a disease from highly fatal to highly curable is extremely difficult, especially when the disease is a type of cancer.
  • However, we can gain some insight into how this can be done by looking back over the 50-year history of taming acute promyelocytic leukaemia (APL).
  • APL is the M3 type of acute myeloid leukaemia characterized by an accumulation of abnormal promyelocytes in bone marrow, a severe bleeding tendency and the presence of the chromosomal translocation t(15;17) or variants.
  • APL was considered the most fatal type of acute leukaemia five decades ago and the treatment of APL was a nightmare for physicians.
  • Great efforts have been made by scientists worldwide to conquer this disease.
  • Of note, both ATRA and ATO trigger catabolism of the PML-RARalpha fusion protein which is the key player in APL leukaemogenesis generated from t(15;17), targeting the RARalpha (retinoic acid receptor alpha) or promyelocytic leukaemia (PML) moieties, respectively.
  • Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease.
  • Thus, the story of APL can serve as a model for the development of curative approaches for disease; it suggests that molecularly synergistic targeted therapies are powerful tools in cancer, and dissection of disease pathogenesis or anatomy of the cancer genome is critical in developing molecular target-based therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

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  • [Cites] Semin Hematol. 2001 Jan;38(1):26-36 [11172537.001]
  • [Cites] J Exp Med. 2001 Feb 19;193(4):531-43 [11181704.001]
  • [Cites] Nat Med. 2001 Jun;7(6):680-6 [11385504.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3919-24 [11389035.001]
  • [Cites] J Exp Med. 2001 Jun 18;193(12):1361-71 [11413191.001]
  • [Cites] J Clin Oncol. 2001 Sep 15;19(18):3852-60 [11559723.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7223-33 [11704850.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7257-65 [11704854.001]
  • [Cites] Blood. 2002 Feb 1;99(3):759-67 [11806975.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1014-22 [11807007.001]
  • [Cites] Cell. 2002 Jan 25;108(2):165-70 [11832207.001]
  • [Cites] Oncologist. 2002;7 Suppl 1:1-13 [11961204.001]
  • [Cites] Blood. 2002 May 1;99(9):3136-43 [11964275.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8283-8 [12060771.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3893-903 [12124315.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):705-13 [12209159.001]
  • [Cites] J Exp Med. 2002 Nov 18;196(10):1373-80 [12438428.001]
  • [Cites] Curr Drug Metab. 2003 Feb;4(1):1-10 [12570742.001]
  • [Cites] FEBS Lett. 2003 Mar 13;538(1-3):117-24 [12633864.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3188-97 [12515727.001]
  • [Cites] J Clin Oncol. 2003 Jun 15;21(12):2326-34 [12805334.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):539-53 [12899709.001]
  • [Cites] Cell. 2003 Oct 31;115(3):305-18 [14636558.001]
  • [Cites] Oncogene. 2003 Dec 8;22(56):9048-57 [14663483.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5328-35 [15044693.001]
  • [Cites] Cancer Cell. 2004 Apr;5(4):389-401 [15093545.001]
  • [Cites] J Exp Med. 2004 Apr 19;199(8):1163-74 [15096541.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1373-9 [15190260.001]
  • [Cites] Nature. 2004 Sep 9;431(7005):205-11 [15356634.001]
  • [Cites] Proc Natl Acad Sci U S A. 1970 Nov;67(3):1542-9 [5274478.001]
  • [Cites] Proc Natl Acad Sci U S A. 1973 Feb;70(2):343-6 [4510279.001]
  • [Cites] Blood. 1973 Apr;41(4):489-96 [4510926.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Lancet. 1977 Mar 5;1(8010):549-50 [65649.001]
  • [Cites] Cancer. 1978 Jun;41(6):2484-90 [274995.001]
  • [Cites] N Engl J Med. 1998 Nov 5;339(19):1341-8 [9801394.001]
  • [Cites] Nat Genet. 1998 Nov;20(3):259-65 [9806544.001]
  • [Cites] Cancer. 2003 Sep 15;98(6):1206-16 [12973844.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2003;:1-13 [14633774.001]
  • [Cites] Nature. 1978 Aug 10;274(5671):535-9 [307692.001]
  • [Cites] Br J Haematol. 1978 Dec;40(4):509-17 [365215.001]
  • [Cites] Br J Haematol. 1980 Jan;44(1):169-70 [6929699.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8428-32 [7915840.001]
  • [Cites] Oncogene. 1996 Jan 18;12(2):323-36 [8570209.001]
  • [Cites] EMBO J. 1996 Jan 2;15(1):110-24 [8598193.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3624-9 [8622986.001]
  • [Cites] Leukemia. 1996 Apr;10(4):735-40 [8618456.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1052-61 [8704214.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2826-32 [8874178.001]
  • [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] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3978-83 [9108090.001]
  • [Cites] Blood. 1997 May 1;89(9):3345-53 [9129041.001]
  • [Cites] Blood. 1997 May 1;89(9):3354-60 [9129042.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 May 13;94(10):5302-7 [9144232.001]
  • [Cites] N Engl J Med. 1997 Oct 9;337(15):1021-8 [9321529.001]
  • [Cites] EMBO J. 1998 Jan 2;17(1):61-70 [9427741.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4300-10 [9596679.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2244-51 [9746761.001]
  • [Cites] J Exp Med. 1999 Apr 5;189(7):1043-52 [10190895.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] J Natl Cancer Inst. 1999 May 5;91(9):772-8 [10328107.001]
  • [Cites] Med Oncol. 1999 Apr;16(1):58-64 [10382944.001]
  • [Cites] Leukemia. 1999 Jul;13(7):1062-70 [10400422.001]
  • [Cites] Hum Mol Genet. 1999 Sep;8(9):1741-9 [10441338.001]
  • [Cites] Acta Med Scand. 1957 Nov 29;159(3):189-94 [13508085.001]
  • [Cites] Schweiz Med Wochenschr. 1959 Jun 6;89:604-8 [13799642.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):143-53 [15710327.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7653-8 [15894607.001]
  • [Cites] PLoS Med. 2005 Jan;2(1):e12 [15696202.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3315-24 [10552940.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1541-50 [10688806.001]
  • [Cites] Cell Death Differ. 2000 May;7(5):447-60 [10800078.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 May;77(5):2936-40 [6930676.001]
  • [Cites] Med Pediatr Oncol. 1981;9(1):5-15 [6936607.001]
  • [Cites] Blood. 1981 Jun;57(6):1000-4 [6939451.001]
  • [Cites] Br J Haematol. 1982 Feb;50(2):201-14 [6949609.001]
  • [Cites] Cancer. 1985 Jan 1;55(1):18-25 [3855265.001]
  • [Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]
  • [Cites] Am J Med. 1986 May;80(5):789-97 [3458366.001]
  • [Cites] Cancer. 1988 Jan 1;61(1):7-13 [3422032.001]
  • [Cites] Blood. 1988 Aug;72(2):567-72 [3165295.001]
  • [Cites] Clin Exp Immunol. 1990 Mar;79(3):448-53 [2317949.001]
  • [Cites] Blood. 1990 Nov 1;76(9):1704-9 [2224119.001]
  • [Cites] N Engl J Med. 1991 May 16;324(20):1385-93 [1850498.001]
  • [Cites] Chin Med Sci J. 1991 Jun;6(2):65-70 [1804379.001]
  • [Cites] Blood. 1992 Apr 15;79(8):1916-9 [1562718.001]
  • [Cites] Ann Hematol. 1992 Jun;64(6):270-2 [1637880.001]
  • [Cites] EMBO J. 1993 Mar;12(3):1161-7 [8384553.001]
  • [Cites] J Korean Med Sci. 1991 Dec;6(4):299-307 [1844638.001]
  • [Cites] J Clin Invest. 1993 May;91(5):2260-7 [8387545.001]
  • [Cites] N Engl J Med. 1993 Jul 15;329(3):177-89 [8515790.001]
  • [Cites] Leukemia. 1994 Aug;8(8):1350-3 [8057672.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1371-7 [10942231.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1496-504 [10942397.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10173-8 [10954752.001]
  • [Cites] Blood. 2001 Jan 1;97(1):264-9 [11133770.001]
  • (PMID = 17317642.001).
  • [ISSN] 0962-8436
  • [Journal-full-title] Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • [ISO-abbreviation] Philos. Trans. R. Soc. Lond., B, Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 90
  • [Other-IDs] NLM/ PMC2435563
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12. Desmond JC, Raynaud S, Tung E, Hofmann WK, Haferlach T, Koeffler HP: Discovery of epigenetically silenced genes in acute myeloid leukemias. Leukemia; 2007 May;21(5):1026-34
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  • [Title] Discovery of epigenetically silenced genes in acute myeloid leukemias.
  • The demethylating 5-aza-2'deoxycytidine (DAC) and the histone deacetylase inhibitor (HDACi) suberoyl anilide bishydroxamide (SAHA) possess potent antitumorigenic properties in myeloid disorders.
  • We analyzed the transcriptional effects of DAC and SAHA in the AML cell line KG-1.
  • [MeSH-major] Epigenesis, Genetic. Genes, Tumor Suppressor. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 17330099.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / EHD3 protein, human; 0 / Hydroxamic Acids; 0 / alpha Catenin; 58IFB293JI / vorinostat; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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13. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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  • [Title] Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • Chronic GvHD was noted in 36% of the patients, which was extensive disease in 18%.
  • The 2-year estimated overall and disease-free survival was 36-34%, respectively.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


14. Nigten J, Breems-de Ridder MC, Erpelinck-Verschueren CA, Nikoloski G, van der Reijden BA, van Wageningen S, van Hennik PB, de Witte T, Löwenberg B, Jansen JH: ID1 and ID2 are retinoic acid responsive genes and induce a G0/G1 accumulation in acute promyelocytic leukemia cells. Leukemia; 2005 May;19(5):799-805
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  • [Title] ID1 and ID2 are retinoic acid responsive genes and induce a G0/G1 accumulation in acute promyelocytic leukemia cells.
  • Acute promyelocytic leukemia (APL) is uniquely sensitive to treatment with all-trans retinoic acid (ATRA), which results in the expression of genes that induce the terminal granulocytic differentiation of the leukemic blasts.
  • ATRA induced a rapid increase in ID1 and ID2, both in the APL cell line NB4 as well as in primary patient cells.
  • [MeSH-major] DNA-Binding Proteins. G0 Phase / drug effects. G1 Phase / drug effects. Leukemia, Promyelocytic, Acute / genetics. Repressor Proteins. Transcription Factors. Tretinoin / pharmacology
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Clone Cells / drug effects. Colony-Forming Units Assay. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Humans. Inhibitor of Differentiation Protein 1. Inhibitor of Differentiation Protein 2. Translocation, Genetic

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  • (PMID = 15744343.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ID1 protein, human; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 1; 0 / Inhibitor of Differentiation Protein 2; 0 / Repressor Proteins; 0 / TCF3 protein, human; 0 / Transcription Factors; 5688UTC01R / Tretinoin
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15. Lee E, Enomoto R, Suzuki C, Ohno M, Ohashi T, Miyauchi A, Tanimoto E, Maeda K, Hirano H, Yokoi T, Sugahara C: Wogonin, a plant flavone, potentiates etoposide-induced apoptosis in cancer cells. Ann N Y Acad Sci; 2007 Jan;1095:521-6
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  • Etoposide, a podophylotoxin anticancer agent, induces apoptotic cell death in normal and cancer cells.
  • Similarly, wogonin accelerated etoposide-induced cell death in lung cancer cells.
  • Since wogonin had no effect on the action of other anticancer agents, such as 5-FU and cisplatin, this flavone seems to accelerate only etoposide-induced apoptotic cell death in cancer cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Etoposide / pharmacology. Flavanones / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Leukemia, T-Cell / pathology

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  • (PMID = 17404065.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Flavanones; 632-85-9 / wogonin; 6PLQ3CP4P3 / Etoposide
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16. Phillips AA, Shapira I, Willim RD, Sanmugarajah J, Solomon WB, Horwitz SM, Savage DG, Bhagat G, Soff G, Zain JM, Alobeid B, Seshan VE, O'Connor OA: A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score. Cancer; 2010 Jul 15;116(14):3438-46
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  • [Title] A critical analysis of prognostic factors in North American patients with human T-cell lymphotropic virus type-1-associated adult T-cell leukemia/lymphoma: a multicenter clinicopathologic experience and new prognostic score.
  • BACKGROUND: To define the clinicopathologic and prognostic features of patients with human T-cell lymphotropic virus type-1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATLL) in North America, standard criteria were used to identify patients with ATLL.
  • The acute subtype predominated (68.5%).
  • Although the International Prognostic Index and Prognostic Index for peripheral T-cell lymphoma unspecified identified subsets of patients, these models were not completely predictive.
  • A recursive partitioning analysis was performed on the data, which successfully identified 3 prognostic categories based on Eastern Cooperative Oncology Group performance status, stage, age, and calcium level at diagnosis.
  • [MeSH-major] Human T-lymphotropic virus 1. Leukemia-Lymphoma, Adult T-Cell

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  • [Copyright] Copyright (c) 2010 American Cancer Society.
  • (PMID = 20564100.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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17. Owatari S, Otsuka M, Takeshita T, Mizukami K, Suzuki S, Uozumi K, Tashiro Y, Arima N, Hanada S: Uncommon cases of immature-type CD56+ natural killer (NK)-cell neoplasms, characterized by expression of myeloid antigen of blastic NK-cell lymphoma. Int J Hematol; 2009 Mar;89(2):188-94
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  • [Title] Uncommon cases of immature-type CD56+ natural killer (NK)-cell neoplasms, characterized by expression of myeloid antigen of blastic NK-cell lymphoma.
  • Immature-type CD56(+) natural killer (NK)-cell neoplasms are classified as either myeloid/NK-cell precursor acute leukemia or blastic NK-cell lymphoma.
  • We identified two cases of immature-type CD56(+) NK-cell neoplasms that were not categorizable as either of these entities.
  • Cell surface markers of malignant cells showed CD4(+), CD7(-), CD13(+), CD33(+), CD34(-), CD43(+), CD56(+), cyCD68(+), and HLA-DR(+).
  • The phenotypes of tumor cells in both cases were compatible with blastic NK-cell lymphoma, except for the expression of myeloid antigen.
  • Clinical presentations of these cases showed characteristics of both blastic NK-cell lymphoma and myeloid/NK-cell precursor acute leukemia.
  • [MeSH-major] Killer Cells, Natural / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Lymphoid / pathology. Leukemia, Myeloid, Acute / pathology


18. Dubielecka PM, Jaźwiec B, Potoczek S, Wróbel T, Miłoszewska J, Haus O, Kuliczkowski K, Sikorski AF: Changes in spectrin organisation in leukaemic and lymphoid cells upon chemotherapy. Biochem Pharmacol; 2005 Jan 1;69(1):73-85
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  • [Title] Changes in spectrin organisation in leukaemic and lymphoid cells upon chemotherapy.
  • The aim of the present study was to investigate changes in spectrin and protein kinase C theta; (PKC theta;) organisation in human lymphoid and leukaemic cells undergoing chemotherapeutically induced apoptosis.
  • An analysis of spectrin arrangement in human peripheral lymphoid (non-Hodgkin lymphoma) and leukaemic (acute lymphoblastic leukaemia) cells before and after chemotherapy revealed radical differences in the distribution of this protein.
  • In normal or malignant cells before chemotherapy spectrin was totally soluble, however it should be mentioned that in total cell extracts and supernatants (but not in pellets) apoptotic fragments of spectrin (in addition to intact alpha and beta chains) were also found.
  • Apoptotic phosphatidyloserine (PS) externalisation, as well as cell shrinkage, membrane protrusions and blebbing were observed in lymphocytes after chemotherapy and treatment with cytostatics in vitro.
  • The overall results may suggest that spectrin redistribution/aggregation is the phenomenon involved in programmed cell death (PCD) of normal and neoplastic lymphocytes and lymphoblasts, however molecular basis of this phenomenon should be further investigated.
  • [MeSH-major] Lymphocytes / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Spectrin / metabolism

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  • (PMID = 15588716.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 12634-43-4 / Spectrin
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19. Curtis DJ, McCormack MP: The molecular basis of Lmo2-induced T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2010 Dec 1;16(23):5618-23
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  • [Title] The molecular basis of Lmo2-induced T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is commonly caused by the overexpression of oncogenic transcription factors in developing T cells.
  • In a mouse model of one such oncogene, LMO2, the cellular effect is to induce self-renewal of committed T cells in the thymus, which persist long-term while acquiring additional mutations and eventually giving rise to leukemia.
  • However, they depend on an aberrantly expressed stem cell-like self-renewal program for their maintenance, in addition to a specialized thymic microenvironmental niche.
  • Here, we discuss potential approaches for targeting pre-CSCs in T-ALL by using therapies directed at oncogenic transcription factors themselves, downstream self-renewal pathways, and the supportive cell niche.
  • [MeSH-major] DNA-Binding Proteins / physiology. Metalloproteins / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cell Transformation, Neoplastic / genetics. Disease Models, Animal. Humans. LIM Domain Proteins. Mice. Mice, Knockout. Models, Biological. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Stem Cell Niche / metabolism. Stem Cell Niche / pathology

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  • [Copyright] ©2010 AACR.
  • (PMID = 20861166.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins
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20. Le Gouill S, Milpied N, Buzyn A, De Latour RP, Vernant JP, Mohty M, Moles MP, Bouabdallah K, Bulabois CE, Dupuis J, Rio B, Gratecos N, Yakoub-Agha I, Attal M, Tournilhac O, Decaudin D, Bourhis JH, Blaise D, Volteau C, Michallet M, Société Française de Greffe de Moëlle et de Thérapie Cellulaire: Graft-versus-lymphoma effect for aggressive T-cell lymphomas in adults: a study by the Société Francaise de Greffe de Moëlle et de Thérapie Cellulaire. J Clin Oncol; 2008 May 10;26(14):2264-71
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  • [Title] Graft-versus-lymphoma effect for aggressive T-cell lymphomas in adults: a study by the Société Francaise de Greffe de Moëlle et de Thérapie Cellulaire.
  • PURPOSE: Aggressive T-cell lymphomas (ATCLs) represent 10% to 15% of non-Hodgkin's lymphomas (NHLs) in adults.
  • ATCLs show a worse prognosis than B-cell lymphomas.
  • PATIENTS AND METHODS: On behalf of the Société Française de Greffe de Moëlle et de Thérapie Cellulaire, we conducted a retrospective analysis including 77 ATCL patients who underwent allogeneic stem-cell transplantation (alloSCT).
  • RESULTS: The different diagnosis included anaplastic large-cell lymphoma (ALCL; n = 27), peripheral T-cell lymphoma not otherwise specified (PTCL-NOS; n = 27), angioimmunoblastic T-cell lymphoma (AITL; n = 11), hepatosplenic gamma/delta lymphoma (HSL; n = 3), T-cell granular lymphocytic leukemia (T-GLL; n = 1), nasal natural killer (NK)/T-cell lymphoma (nasal-NK/L; n = 3) or non-nasal NK/T-cell lymphoma (non-nasal-NK/L; n = 2), enteropathy-type T-cell (n = 1), and human T-lymphotropic virus (HTLV)-1 lymphoma (n = 2).
  • In multivariate analysis, chemoresistant disease (stable, refractory, or progressing disease) at the time of alloSCT and the occurrence of severe grade 3 to 4 acute graft-versus-host disease (aGVHD) were the strongest adverse prognostic factors for OS (P = .03 and .03, respectively).
  • Disease status at transplantation significantly influenced the 5-year EFS (P = .003), and an HLA-mismatched donor increased TRM (P = .04).
  • [MeSH-major] Graft vs Tumor Effect / immunology. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Child. Disease-Free Survival. Female. Graft vs Host Disease / immunology. Humans. Male. Middle Aged. Retrospective Studies. Transplantation Conditioning. Transplantation, Homologous / immunology


21. O'Reilly RJ, Doubrovina E, Trivedi D, Hasan A, Kollen W, Koehne G: Adoptive transfer of antigen-specific T-cells of donor type for immunotherapy of viral infections following allogeneic hematopoietic cell transplants. Immunol Res; 2007;38(1-3):237-50
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  • [Title] Adoptive transfer of antigen-specific T-cells of donor type for immunotherapy of viral infections following allogeneic hematopoietic cell transplants.
  • Allogeneic marrow and cytokine-mobilized peripheral blood stem cells adequately depleted of T cells prevent acute and chronic forms of graft versus host disease in HLA-matched and non-identical hosts without any posttransplant immunosuppressive prophylaxis.
  • Early clinical trials already indicate the potential of such T cells to treat and prevent life threatening diseases caused by these pathogens, particularly in recipients of T cell depleted grafts who do not require ongoing treatment with immunosuppressive agents, and therefore provide a permissive environment for the expansion and persistence of the T cells following adoptive transfer.
  • [MeSH-major] Adoptive Transfer. Cytomegalovirus Infections / therapy. Epstein-Barr Virus Infections / therapy. Graft vs Host Disease / prevention & control. T-Lymphocytes / transplantation
  • [MeSH-minor] Adult. Child. Female. HLA Antigens / genetics. HLA Antigens / immunology. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Immunotherapy. Male. Tissue Donors. Transplantation, Homologous / adverse effects

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  • [Cites] Blood. 2003 Jul 15;102(2):756-62 [12663454.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1923-30 [15191952.001]
  • [Cites] Nat Biotechnol. 2000 Apr;18(4):405-9 [10748520.001]
  • [Cites] J Immunol. 2004 Jun 1;172(11):6783-9 [15153496.001]
  • [Cites] Transfusion. 2006 Jul;46(7):1248-55 [16836575.001]
  • [Cites] Blood. 1998 Feb 1;91(3):1083-90 [9446672.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:390-7 [17124088.001]
  • [Cites] Blood. 2001 Feb 15;97(4):835-43 [11159505.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2816-25 [15254049.001]
  • [Cites] Nat Med. 1996 May;2(5):551-5 [8616714.001]
  • [Cites] Science. 1997 Jun 13;276(5319):1719-24 [9180086.001]
  • [Cites] Blood. 2002 Feb 1;99(3):806-14 [11806980.001]
  • [Cites] Blood. 2004 May 1;103(9):3565-72 [14670917.001]
  • [Cites] Eur J Immunol. 2000 Jun;30(6):1676-82 [10898504.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2594-603 [8630428.001]
  • [Cites] Blood. 2003 Jan 15;101(2):407-14 [12393659.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2208-16 [10498590.001]
  • [Cites] Environ Health Perspect. 1990 Aug;88:225-30 [2176975.001]
  • [Cites] N Engl J Med. 1994 Sep 8;331(10):679-80 [8052285.001]
  • [Cites] Blood. 2001 Feb 15;97(4):994-1000 [11159528.001]
  • [Cites] Ann Intern Med. 1984 Sep;101(3):310-5 [6087703.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):114-23 [9045297.001]
  • [Cites] Lancet. 1984 Apr 7;1(8380):761-4 [6143084.001]
  • [Cites] Hum Immunol. 2004 May;65(5):550-7 [15172456.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2498-505 [12805061.001]
  • [Cites] N Engl J Med. 1994 Apr 28;330(17):1185-91 [8093146.001]
  • [Cites] Blood Rev. 2002 Jun;16(2):81-5 [12127951.001]
  • [Cites] J Virol. 2003 May;77(9):5226-40 [12692225.001]
  • [Cites] Lancet. 2002 Aug 10;360(9331):436-42 [12241714.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2793-801 [15514011.001]
  • [Cites] J Exp Med. 2005 Aug 1;202(3):379-86 [16061727.001]
  • [Cites] Science. 1992 Jul 10;257(5067):238-41 [1352912.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4397-406 [16123217.001]
  • [Cites] Lancet. 1981 Aug 15;2(8242):327-31 [6115110.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3447-54 [15753458.001]
  • [Cites] Blood. 1998 Sep 1;92(5):1549-55 [9716582.001]
  • [Cites] N Engl J Med. 1977 Dec 15;297(24):1311-8 [21351.001]
  • [Cites] Blood. 1992 Jun 15;79(12):3380-7 [1596577.001]
  • [Cites] Leukemia. 2003 May;17(5):841-8 [12750695.001]
  • [Cites] Springer Semin Immunopathol. 2004 Nov;26(1-2):119-32 [15452666.001]
  • [Cites] Lancet. 2003 Feb 15;361(9357):553-60 [12598139.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2235-42 [12200390.001]
  • [Cites] J Immunol. 1999 Feb 1;162(3):1827-35 [9973448.001]
  • [Cites] Blood. 1983 Feb;61(2):341-8 [6217853.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Apr;72(4):1622-6 [165518.001]
  • [Cites] J Virol. 1996 Nov;70(11):7569-79 [8892876.001]
  • [Cites] Hum Immunol. 2003 Apr;64(4):440-52 [12651070.001]
  • [Cites] Transplantation. 1998 Nov 27;66(10):1330-4 [9846518.001]
  • [Cites] Lancet. 1968 Dec 28;2(7583):1366-9 [4177932.001]
  • [Cites] Clin Exp Immunol. 1977 Apr;28(1):72-9 [193663.001]
  • [Cites] Blood. 2002 Dec 1;100(12):4059-66 [12393655.001]
  • [Cites] Blood. 1999 Jan 15;93(2):467-80 [9885208.001]
  • [Cites] Transpl Infect Dis. 2007 Dec;9(4):286-94 [17511819.001]
  • [Cites] N Engl J Med. 1999 Feb 18;340(7):508-16 [10021471.001]
  • [Cites] N Engl J Med. 1995 Oct 19;333(16):1038-44 [7675046.001]
  • (PMID = 17917029.001).
  • [ISSN] 0257-277X
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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22. Jaggi M, Prasad S, Singh AT, Praveen R, Dutt S, Mathur A, Sharma R, Gupta N, Ahuja R, Mukherjee R, Burman AC: Anticancer activity of a peptide combination in gastrointestinal cancers targeting multiple neuropeptide receptors. Invest New Drugs; 2008 Dec;26(6):489-504
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  • Screening a large panel of analogs to the four peptide hormones on tumor cell proliferation led to the identification of four cytotoxic analogs, the combination of which was code-named DRF7295.
  • Gastrointestinal tumor cells of the colon, pancreas and duodenum were found to be most sensitive to DRF7295 with moderate activity seen in glioblastoma, prostate, leukemia and those of oral cancer cells.
  • Acute and long-term toxicity studies as well as safety pharmacology studies conducted indicate the safety of the drug upon systemic administration with no significant adverse pharmacological effects.
  • [MeSH-minor] Animals. Bombesin / analogs & derivatives. Cell Line, Tumor. Drug Combinations. Female. Humans. Male. Mice. Mice, Nude. Rats. Rats, Wistar. Receptors, Bombesin / drug effects. Receptors, Bombesin / metabolism. Receptors, Neurokinin-1 / drug effects. Receptors, Neurokinin-1 / metabolism. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / metabolism. Receptors, Vasoactive Intestinal Peptide / drug effects. Receptors, Vasoactive Intestinal Peptide / metabolism. Somatostatin / analogs & derivatives. Substance P / analogs & derivatives. Toxicity Tests. Vasoactive Intestinal Peptide / analogs & derivatives. Xenograft Model Antitumor Assays

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  • [Cites] Am J Pathol. 1999 Dec;155(6):2067-76 [10595936.001]
  • [Cites] Pharmacol Rev. 2000 Jun;52(2):179-206 [10835099.001]
  • [Cites] Cancer Res. 1992 Mar 1;52(5):1114-22 [1310640.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12664-8 [7809097.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):49-50 [8769380.001]
  • [Cites] Int J Cancer. 1997 Jul 29;72(3):498-504 [9247295.001]
  • [Cites] J Immunoassay. 1994 May;15(2):129-46 [8040348.001]
  • [Cites] J Biol Chem. 1989 Sep 5;264(25):14691-7 [2475489.001]
  • [Cites] Amino Acids. 2003 Jul;25(1):1-40 [12836056.001]
  • [Cites] Biopolymers. 1995 Jan;35(1):11-20 [7696551.001]
  • [Cites] Cell Mol Life Sci. 2004 May;61(9):1042-68 [15112052.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Sep;310(3):1161-70 [15102928.001]
  • [Cites] J Surg Res. 1991 Mar;50(3):245-51 [1705618.001]
  • [Cites] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906.001]
  • [Cites] Biochem Biophys Res Commun. 1986 May 29;137(1):135-41 [2424443.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):389-427 [12920149.001]
  • [Cites] J Med Chem. 1988 Nov;31(11):2170-7 [2903246.001]
  • [Cites] Nat Rev Drug Discov. 2003 Dec;2(12):999-1017 [14654798.001]
  • [Cites] J Surg Res. 1995 Jan;58(1):111-5 [7830399.001]
  • [Cites] J Pept Res. 2001 Aug;58(2):91-107 [11532069.001]
  • [Cites] Chemotherapy. 2001;47 Suppl 2:1-29 [11275699.001]
  • [Cites] Bull Cancer. 2004 Jan;91(1):75-80 [14975808.001]
  • [Cites] Cancer. 2004 Apr 15;100(8):1558-77 [15073842.001]
  • [Cites] Anticancer Res. 2000 Sep-Oct;20(5A):3123-9 [11062732.001]
  • [Cites] Int J Pept Protein Res. 1996 Oct;48(4):312-8 [8919051.001]
  • [Cites] J Lancet. 1964 Apr;84:131-3 [14139576.001]
  • [Cites] Cancer Res. 1999 Mar 1;59(5):1152-9 [10070977.001]
  • [Cites] Eur J Pharmacol. 1992 Sep 1;227(1):1-18 [1330636.001]
  • [Cites] Am Rev Respir Dis. 1990 Dec;142(6 Pt 2):S11-5 [2174658.001]
  • [Cites] Biochemistry. 1990 Jul 24;29(29):6747-56 [2204420.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1859-63 [2450349.001]
  • (PMID = 18217205.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DRF 7295; 0 / Drug Combinations; 0 / Peptides; 0 / Receptors, Bombesin; 0 / Receptors, Neurokinin-1; 0 / Receptors, Somatostatin; 0 / Receptors, Vasoactive Intestinal Peptide; 33507-63-0 / Substance P; 37221-79-7 / Vasoactive Intestinal Peptide; 51110-01-1 / Somatostatin; PX9AZU7QPK / Bombesin
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23. van der Velden VH, de Bie M, van Wering ER, van Dongen JJ: Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease. Haematologica; 2006 May;91(5):679-82
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  • [Title] Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease.
  • We analyzed the frequency and characteristics of Vk-Jk and Vlambda-Jlambda rearrangements inpatients with precursor-B-acute lymphoblastic leukemia (ALL) and evaluated the applicability of these rearrangements as targets for minimal residual disease (MRD) detection.
  • Vk-Jk and Vlambda-Jlambda rearrangements showed a good stability between diagnosis and relapse and reached good sensitivities in real-time quantitative polymerase chain reaction analysis.
  • [MeSH-major] DNA, Neoplasm / genetics. Gene Rearrangement, B-Lymphocyte, Light Chain. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16627258.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / Immunoglobulin Variable Region
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24. Yang MZ, Yuan YH, Wu DP, Chang WR, He J, Di WY: [A clinical study of 31 patients with malignant hematopoietic disease treated with non-T cell-depleted HLA-haploidentical hematopoietic stem cell transplantation]. Zhonghua Nei Ke Za Zhi; 2007 Jun;46(6):482-5
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  • [Title] [A clinical study of 31 patients with malignant hematopoietic disease treated with non-T cell-depleted HLA-haploidentical hematopoietic stem cell transplantation].
  • OBJECTIVE: To investigate the effects and prognosis of malignant hematological disease after HLA haploidentical hematopoietic stem cell transplantation (H-HSCT) without T-cell depletion.
  • METHODS: The clinical data of 31 cases with malignant hemopoietic disease treated with H-HSCT from July 2002 to July 2006 were analyzed, including 11 cases of standard risk and 20 of high risk.
  • RESULTS: 30 patients achieved engraftment of a median of 13 and 22 days for neutrophil and platelet, with an accumulative incidence of II - IV grade acute graft-versus-host disease (GVHD) 61.3%, and an accumulative incidence of chronic GVHD 41.9%.
  • The CD(3)(+) T cells count of the graft and the disparity of HLA-A, B, DR loci were the major factors of impact on acute GVHD.
  • CONCLUSION: HLA H-HSCT is an effective therapeutic method for malignant hematological disease, CD(3)(+) T cells count of the graft and the disparity of HLA-A, B, DR loci are the major factors of impact on acute GVHD.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Hematopoietic Stem Cells / cytology. Leukemia / surgery
  • [MeSH-minor] Adolescent. Adult. Antigens, CD3 / analysis. Child. Female. Graft vs Host Disease / immunology. Graft vs Host Disease / pathology. HLA Antigens / analysis. Haploidy. Histocompatibility Testing. Humans. Kaplan-Meier Estimate. Lymphocyte Depletion. Male. Middle Aged. T-Lymphocytes / cytology. T-Lymphocytes / immunology. T-Lymphocytes / metabolism. Transplantation Conditioning

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  • (PMID = 17663825.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / HLA Antigens
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25. Draube A, Beyer M, Wolf J: Activation of autologous leukemia-specific T cells in acute myeloid leukemia: monocyte-derived dendritic cells cocultured with leukemic blasts compared with leukemia-derived dendritic cells. Eur J Haematol; 2008 Oct;81(4):281-8
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  • [Title] Activation of autologous leukemia-specific T cells in acute myeloid leukemia: monocyte-derived dendritic cells cocultured with leukemic blasts compared with leukemia-derived dendritic cells.
  • In acute myeloid leukemia (AML) blasts can be differentiated into dendritic cell (DC) like cells (AML-DC).
  • These cells have a mature DC-like phenotype, are strong stimulators in mixed leukocyte reactions and can be used to generate leukemia-specific cytotoxic T cells.
  • Thus, we investigated the ability to generate MoDC from peripheral blood of 17 AML patients in first remission and their functional integrity to stimulate leukemia-specific T cells by simple coculture with leukemic blasts.
  • Additionally, functional analysis demonstrated the ability of remission MoDC to activate autologous leukemia-specific T cells in 11 of 12 patients, whereas AML-DC led to a specific T cell activation in four of eight patients.
  • [MeSH-major] Dendritic Cells / immunology. Leukemia, Myeloid, Acute / immunology. Lymphocyte Activation / immunology. Monocytes / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18573171.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
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26. Bélien-Pallet V, Cabrol S, Fasola S, Petit A, Landman-Parker J, Auvrignon A, Leverger G: [Is there a risk of steroid-induced adrenal deficit after induction treatment of acute lymphoblastic leukemia?]. Arch Pediatr; 2010 Dec;17(12):1637-44
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  • [Title] [Is there a risk of steroid-induced adrenal deficit after induction treatment of acute lymphoblastic leukemia?].
  • [Transliterated title] Existe-t-il un risque de déficit corticotrope au décours du traitement d'induction d'une leucémie aiguë lymphoblastique ?
  • The occurrence of eight cases of adrenal deficit in children hospitalized for acute lymphoblastic leukemia (ALL) led us to conduct a prospective study from May 2006 to May 2007 to better characterize this corticoid-induced adrenal deficit.
  • The diagnosis of adrenal deficit was not more common for children who had received dexamethasone (13/19) or prednisone (14/21), or for those who had (19/29) or had not (8/11) experienced corticoid toxicity during induction.
  • The clinical signs suggesting adrenal deficit were identical in the two groups and none of the children presented an acute episode.
  • [MeSH-major] Adrenal Insufficiency / chemically induced. Adrenal Insufficiency / diagnosis. Dexamethasone / adverse effects. Glucocorticoids / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prednisone / adverse effects

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20943354.001).
  • [ISSN] 1769-664X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Hormones; 16960-16-0 / Cosyntropin; 53468-06-7 / adrenocorticotropin zinc; 7S5I7G3JQL / Dexamethasone; VB0R961HZT / Prednisone
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27. Nussenzveig RH, Cortes J, Sever M, Quintás-Cardama A, Ault P, Manshouri T, Bueso-Ramos C, Prchal JT, Kantarjian H, Verstovsek S: Imatinib mesylate therapy for polycythemia vera: final result of a phase II study initiated in 2001. Int J Hematol; 2009 Jul;90(1):58-63
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  • Patients with PV are at a risk of thrombosis, bleeding, and transformation to myelofibrosis or acute myeloid leukemia.

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  • (PMID = 19484334.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Other-IDs] NLM/ NIHMS672549; NLM/ PMC4378576
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28. Meyer C, Schneider B, Reichel M, Angermueller S, Strehl S, Schnittger S, Schoch C, Jansen MW, van Dongen JJ, Pieters R, Haas OA, Dingermann T, Klingebiel T, Marschalek R: Diagnostic tool for the identification of MLL rearrangements including unknown partner genes. Proc Natl Acad Sci U S A; 2005 Jan 11;102(2):449-54
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  • Approximately 50 different chromosomal translocations of the human MLL gene are currently known and associated with high-risk acute leukemia.
  • The large number of different MLL translocation partner genes makes a precise diagnosis a demanding task.
  • This method was applied to biopsy material derived from 40 leukemia patients known to carry MLL abnormalities.
  • Furthermore, the determined patient-specific fusion sequences are useful for minimal residual disease monitoring of MLL associated acute leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] GTPase-Activating Proteins. Histone-Lysine N-Methyltransferase. Humans. Membrane Glycoproteins / genetics. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein. Receptors, Interleukin-1 / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4568-73 [11930009.001]
  • [Cites] Oncogene. 2002 Oct 3;21(44):6729-39 [12360400.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):393-401 [12619163.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3095-100 [12626751.001]
  • [Cites] Leukemia. 2003 Mar;17(3):637-41 [12646957.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):214-9 [12696071.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Sep;38(1):8-12 [12874781.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2395-402 [12805060.001]
  • [Cites] Leukemia. 2004 May;18(5):895-908 [15042105.001]
  • [Cites] Genetics. 1988 Nov;120(3):621-3 [2852134.001]
  • [Cites] Nature. 1989 Nov 23;342(6248):453-6 [2531290.001]
  • [Cites] Nucleic Acids Res. 1992 Feb 11;20(3):595-600 [1371352.001]
  • [Cites] Br J Haematol. 1994 Feb;86(2):275-83 [8199015.001]
  • [Cites] Br J Haematol. 1995 Jun;90(2):308-20 [7794749.001]
  • [Cites] Genes Chromosomes Cancer. 1995 Jun;13(2):75-85 [7542910.001]
  • [Cites] Cancer Res. 1996 May 1;56(9):2171-7 [8616868.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:484-5 [9209433.001]
  • [Cites] Annu Rev Nutr. 1997;17:77-99 [9240920.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2456-64 [9310498.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11583-8 [9326653.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4532-8 [9373264.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4679-86 [9389682.001]
  • [Cites] Haematologica. 1998 Apr;83(4):350-7 [9592986.001]
  • [Cites] Leukemia. 1998 Jun;12(6):976-81 [9639429.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3357-62 [10416593.001]
  • [Cites] Oncogene. 1999 Aug 19;18(33):4663-71 [10467413.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2417-24 [15333468.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2145-50 [10681437.001]
  • [Cites] J Biol Chem. 2001 Jan 12;276(2):974-83 [11027684.001]
  • [Cites] Oncogene. 2001 May 24;20(23):2900-7 [11420702.001]
  • [Cites] Nat Immunol. 2001 Sep;2(9):835-41 [11526399.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Leukemia. 2002 Mar;16(3):344-51 [11896537.001]
  • [Cites] Gene. 2002 Jun 12;292(1-2):167-71 [12119110.001]
  • (PMID = 15626757.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GTPase-Activating Proteins; 0 / MLL protein, human; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / Receptors, Interleukin-1; 0 / SMAP1 protein, human; 0 / TIRAP protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC544299
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29. Buchwald M, Pietschmann K, Müller JP, Böhmer FD, Heinzel T, Krämer OH: Ubiquitin conjugase UBCH8 targets active FMS-like tyrosine kinase 3 for proteasomal degradation. Leukemia; 2010 Aug;24(8):1412-21
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  • Nonetheless, constitutively active mutant FLT3 (FLT3-ITD) causally contributes to transformation and is associated with poor prognosis of acute myeloid leukemia (AML) patients.
  • These results provide novel insights into antileukemic activities of HDACi and position UBCH8, which have been implicated primarily in processes in the nucleus, as a previously unrecognized important modulator of FLT3-ITD stability and leukemic cell survival.
  • [MeSH-minor] Blotting, Western. Cell Line. Cell Separation. Flow Cytometry. Histone Deacetylase Inhibitors / pharmacology. Humans. Hydrolysis. Immunoprecipitation. Mutation. Phosphorylation. Tyrosine / metabolism

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  • (PMID = 20508617.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 42HK56048U / Tyrosine; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / UBE2L6 protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
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30. Yan WH, Lin A, Chen BG, Luo WD, Dai MZ, Chen XJ, Xu HH, Li BL: Unfavourable clinical implications for HLA-G expression in acute myeloid leukaemia. J Cell Mol Med; 2008 Jun;12(3):889-98
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  • [Title] Unfavourable clinical implications for HLA-G expression in acute myeloid leukaemia.
  • In the current study, HLA-G expression was analysed in different types of patients: de novo acute myeloid leukaemia (AML, n = 54), B cell acute lymphoblastic leukaemia (B-ALL, n= 13), chronic myeloid leukaemia (CML, n= 9) and myelodysplastic syndrome (MDS, n= 11).
  • In AML, HLA-G-positive patients had a significant higher bone marrow leukaemic blast cell percentage when compared with that of HLA-G-negative patients (P < 0.01).
  • Total T-cell percentage was dramatically decreased in HLA-G-positive patients (P < 0.05).
  • Ex vivo cytotoxicity analysis revealed that HLA-G expression in AML leukaemic cells could directly inhibit NK cell cytolysis (P < 0.01).
  • [MeSH-major] HLA Antigens / immunology. Histocompatibility Antigens Class I / immunology. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18494931.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; EC 1.1.1.27 / L-Lactate Dehydrogenase; I223NX31W9 / Fluorescein-5-isothiocyanate
  • [Other-IDs] NLM/ PMC4401132
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31. Nurmio M, Keros V, Lähteenmäki P, Salmi T, Kallajoki M, Jahnukainen K: Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility. J Clin Endocrinol Metab; 2009 Jun;94(6):2119-22
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  • [Title] Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility.
  • CONTEXT: Isolation of spermatogonial stem cells before potentially sterilizing cancer therapy, followed by transplantation of these cells into the testis after such treatment, may be an effective approach to prevent infertility among prepubertal boys suffering from acute lymphoblastic leukemia (ALL).
  • A key clinical consideration in this context is the timing of biopsy, if collection of spermatogonia could be delayed from diagnosis to the later phase of leukemia treatment, better patient selection could be offered.
  • OBJECTIVE: The objective of the study was to examine the routine testicular biopsy material collected to detect testicular leukemia to evaluate if treatment for leukemia affects numbers and maturation of the spermatogonia during the prepubertal period.
  • OUTCOME MEASURE: Samples were stained immunohistochemically to evaluate the expression of the spermatogonial markers MAGE 4A, OCT4, CD9, and AP2gamma, and of the Sertoli cell marker WT-1.
  • No significant alteration in spermatogonial numbers was associated with testicular leukemia.
  • CONCLUSION: Treatment for childhood leukemia without high-dose cyclophosphamide seldom depletes the spermatogonial stem cell pool totally.
  • [MeSH-major] Cyclophosphamide / adverse effects. Fertility / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatogonia / pathology

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  • (PMID = 19318447.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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32. Murase T, Fujita A, Ueno H, Park JW, Yano T, Hoshikawa M, Takagi M, Kuramochi S: A case of age-related EBV-associated B-cell lymphoproliferative disorder metachronously showing two distinct morphologic appearances, one of a polymorphic disease resembling classical Hodgkin lymphoma, and the other of a large-cell lymphoma. Int J Hematol; 2009 Jan;89(1):80-5
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  • [Title] A case of age-related EBV-associated B-cell lymphoproliferative disorder metachronously showing two distinct morphologic appearances, one of a polymorphic disease resembling classical Hodgkin lymphoma, and the other of a large-cell lymphoma.
  • We report a case of age-related EBV-associated B-cell lymphoproliferative disorder (age-related EBV+ B-cell LPD) metachronously showing two distinct morphologic appearances: one of a polymorphic disease resembling classical Hodgkin lymphoma (CHL), and the other of a large-cell lymphoma.
  • Right axillary lymph node biopsy revealed mixed cellularity classical Hodgkin lymphoma (MCHL).
  • Biopsy of the right cervical mass revealed a diagnosis of diffuse large B-cell lymphoma.
  • Two years later, the patient developed acute myeloid leukemia (AML).
  • The biopsy again revealed diagnosis of MCHL.
  • Both HRS-like cells at the time of diagnosis of Hodgkin lymphoma and lymphoma cells at the time of diagnosis of non-Hodgkin lymphoma were positive for CD20 and EBV-encoded small RNAs.
  • This case was finally diagnosed as having age-related EBV+ B-cell LPD.
  • We report the case here as it underscores the difficulty in diagnosing age-related EBV+ B-cell LPDs and also suggests an important role of EBV in the pathogenesis of lymphoid neoplasms.
  • [MeSH-major] Lymphoma, B-Cell / pathology
  • [MeSH-minor] Aged. Herpesvirus 4, Human. Hodgkin Disease / pathology. Humans. Lymph Nodes / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Male

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  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5124-32 [17785567.001]
  • [Cites] J Clin Oncol. 1994 Feb;12(2):312-25 [8113838.001]
  • [Cites] Pathol Int. 2007 Oct;57(10):688-93 [17803658.001]
  • [Cites] Am J Surg Pathol. 2003 Jan;27(1):16-26 [12502924.001]
  • [Cites] Ann Oncol. 1991 Feb;2 Suppl 2:83-92 [2049324.001]
  • [Cites] Blood. 2001 Jan 15;97(2):496-501 [11154228.001]
  • [Cites] N Engl J Med. 1979 Mar 1;300(9):452-8 [366418.001]
  • [Cites] J Clin Oncol. 2002 Aug 15;20(16):3484-94 [12177110.001]
  • [Cites] Rinsho Ketsueki. 1986 Feb;27(2):252-6 [2425103.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2444-51 [15941916.001]
  • [Cites] Eur J Immunol. 2000 Feb;30(2):458-69 [10671201.001]
  • [Cites] Int J Cancer. 1997 May 16;71(4):510-6 [9178801.001]
  • [Cites] N Engl J Med. 1988 Jan 14;318(2):76-81 [3336397.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(3):487-97 [10653864.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):885-95 [1415907.001]
  • [Cites] J Clin Oncol. 2001 Apr 1;19(7):2026-32 [11310450.001]
  • [Cites] Arch Intern Med. 1983 Mar;143(3):445-50 [6338848.001]
  • (PMID = 19093168.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


33. Ivanoff J, Talme T, Sundqvist KG: The role of chemokines and extracellular matrix components in the migration of T lymphocytes into three-dimensional substrata. Immunology; 2005 Jan;114(1):53-62
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  • We examined the influence of chemokines and fibronectin on the infiltration properties of non-infiltrative (do not migrate into 3D substrata) and spontaneously infiltrative (migrate into 3D substrata) T-cell lines.
  • Infiltrative and non-infiltrative T-acute lymphocytic leukaemic cell lines exhibited no consistent differences with respect to the expression of various chemokine receptors or beta(1)-integrins.
  • Chemokines presented inside the collagen increased the depth of migration of infiltrative T-cell lines, but did not render non-infiltrative T-cell lines infiltrative, although they augmented the attachment of non-infiltrative T-cell lines to the upper surface of the collagen.
  • The presence of fibronectin inside the collagen did not render non-infiltrative T-cell lines infiltrative, but markedly augmented the migration of 'infiltrative' T-cell lines into collagen.
  • Both infiltrative and non-infiltrative T-cell lines showed migratory responses to chemokines in Boyden assays (migration detected on 2D substrata).
  • These results indicate that the process of T-cell infiltration/migration into 3D substrata depends on a tissue penetration mechanism distinguishable from migration on 2D substrata and that the basic capacity of T cells to infiltrate is independent of chemokines and ECM components applied as attractants.
  • [MeSH-minor] Cell Adhesion / immunology. Cells, Cultured. Collagen / metabolism. Humans. Leukemia, T-Cell / immunology. Receptors, Chemokine / metabolism. Tumor Cells, Cultured

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  • [Cites] Blood. 2003 Nov 1;102(9):3262-9 [12855577.001]
  • [Cites] J Cell Biol. 1982 Mar;92(3):747-52 [7085756.001]
  • [Cites] J Cell Biol. 1983 Apr;96(4):1089-96 [6833393.001]
  • [Cites] Int J Cancer. 1990 Aug 15;46(2):282-6 [2166712.001]
  • [Cites] Nature. 1990 Oct 18;347(6294):669-71 [1699135.001]
  • [Cites] Cell. 1991 May 31;65(5):859-73 [1710173.001]
  • [Cites] Immunol Today. 1992 Mar;13(3):106-12 [1622542.001]
  • [Cites] Nature. 1993 Jan 7;361(6407):79-82 [7678446.001]
  • [Cites] Science. 1993 Apr 16;260(5106):355-8 [7682337.001]
  • [Cites] J Immunol. 1995 May 1;154(9):4379-89 [7722295.001]
  • [Cites] FASEB J. 1995 Nov;9(14):1473-81 [7589989.001]
  • [Cites] J Immunol. 1996 Jan 1;156(1):160-7 [8598457.001]
  • [Cites] Cell Immunol. 1996 Feb 1;167(2):269-75 [8603436.001]
  • [Cites] J Immunol. 1996 May 15;156(10):3583-6 [8621890.001]
  • [Cites] Cancer Metastasis Rev. 1995 Dec;14(4):351-62 [8821095.001]
  • [Cites] Crit Rev Immunol. 1995;15(3-4):285-316 [8834453.001]
  • [Cites] J Immunol. 1997 Jan 1;158(1):76-84 [8977177.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15376-81 [8986819.001]
  • [Cites] J Exp Med. 1996 Sep 1;184(3):873-82 [9064347.001]
  • [Cites] J Exp Med. 1996 Sep 1;184(3):963-9 [9064356.001]
  • [Cites] J Leukoc Biol. 1997 Mar;61(3):246-57 [9060447.001]
  • [Cites] Biochem J. 1997 Feb 15;322 ( Pt 1):1-18 [9078236.001]
  • [Cites] J Immunol. 1997 Apr 1;158(7):3046-53 [9120256.001]
  • [Cites] J Exp Med. 1997 Jul 7;186(1):139-46 [9207008.001]
  • [Cites] J Cell Biol. 1997 Dec 1;139(5):1349-60 [9382879.001]
  • [Cites] J Exp Med. 1998 Jan 5;187(1):129-34 [9419219.001]
  • [Cites] Eur J Immunol. 1998 Aug;28(8):2331-43 [9710211.001]
  • [Cites] J Cell Biol. 1999 Feb 22;144(4):755-65 [10037796.001]
  • [Cites] Clin Exp Metastasis. 1999;17(8):695-711 [10919715.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9201-8 [10734056.001]
  • [Cites] EMBO J. 1997 Aug 1;16(15):4606-16 [9303305.001]
  • [Cites] J Immunol. 2000 Sep 15;165(6):3423-9 [10975862.001]
  • [Cites] Dev Immunol. 2000;7(2-4):67-75 [11097202.001]
  • [Cites] Nat Immunol. 2001 Jun;2(6):508-14 [11376337.001]
  • [Cites] Eur J Immunol. 2002 Feb;32(2):404-12 [11813159.001]
  • [Cites] Biochim Biophys Acta. 1993 Apr 16;1176(3):265-8 [8471628.001]
  • [Cites] Exp Cell Res. 1993 May;206(1):100-10 [8482352.001]
  • [Cites] J Exp Med. 1993 Jun 1;177(6):1821-6 [7684437.001]
  • [Cites] Science. 1993 Jul 2;261(5117):101-3 [8316840.001]
  • [Cites] Immunology. 1993 Dec;80(4):553-60 [8307606.001]
  • [Cites] J Cell Biol. 1994 Jun;125(5):1165-78 [7515069.001]
  • [Cites] Eur J Immunol. 1994 Jan;24(1):273-6 [8020566.001]
  • [Cites] Curr Opin Immunol. 1994 Jun;6(3):380-4 [7917105.001]
  • [Cites] J Cell Biol. 1994 Dec;127(5):1485-95 [7525609.001]
  • [Cites] Science. 1994 Nov 25;266(5189):1395-9 [7973732.001]
  • [Cites] J Immunol. 1995 Apr 15;154(8):3654-66 [7706709.001]
  • (PMID = 15606795.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Receptors, Chemokine; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ PMC1782061
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34. Matsuo Y, Takeishi S, Miyamoto T, Nonami A, Kikushige Y, Kunisaki Y, Kamezaki K, Tu L, Hisaeda H, Takenaka K, Harada N, Kamimura T, Ohno Y, Eto T, Teshima T, Gondo H, Harada M, Nagafuji K: Toxoplasmosis encephalitis following severe graft-vs.-host disease after allogeneic hematopoietic stem cell transplantation: 17 yr experience in Fukuoka BMT group. Eur J Haematol; 2007 Oct;79(4):317-21
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  • [Title] Toxoplasmosis encephalitis following severe graft-vs.-host disease after allogeneic hematopoietic stem cell transplantation: 17 yr experience in Fukuoka BMT group.
  • Toxoplasmosis is a rare but rapidly fatal complication that can occur following hematopoietic stem cell transplantation (HSCT).
  • Over a 17-yr period at our institutions, a definite diagnosis of toxoplasmosis was made in only two of 925 allogeneic HSCT recipients (0.22%) and none of 641 autologous HSCT recipients.
  • These two patients received a conventional conditioning regimen followed by transplantation from an HLA-matched donor; however, they developed severe graft-vs.-host disease, which required intensive immunosuppressive therapy.
  • Despite prophylactic treatment with trimethoprim/sulfamethoxazole, their immunosuppressive state, as indicated by a low CD4(+) cell count, might have resulted in toxoplasmosis encephalitis.
  • Rapid and non-invasive methods such as a polymerase chain reaction (PCR) test of their cerebrospinal fluid for Toxoplasma gondii and magnetic resonance imaging of the brain were useful for providing a definitive diagnosis and prompt therapy in these patients: one patient stabilized and survived after responding to treatment with pyrimethamine/sulfodiazine whereas the other died of bacterial infection.
  • In addition, retrospective PCR analyses of the frozen stored peripheral blood samples disclosed that detection of T. gondii preceded the onset of disease, indicating routine PCR testing of peripheral blood specimens may be an early diagnostic tool.
  • [MeSH-major] Encephalitis / etiology. Graft vs Host Disease / complications. Hematopoietic Stem Cell Transplantation. Toxoplasma. Toxoplasmosis, Cerebral / etiology
  • [MeSH-minor] Animals. Antimalarials / administration & dosage. Asian Continental Ancestry Group. Bacterial Infections / blood. Bacterial Infections / cerebrospinal fluid. Bacterial Infections / drug therapy. Bacterial Infections / etiology. Bacterial Infections / radiography. CD4 Lymphocyte Count. DNA, Protozoan / blood. DNA, Protozoan / cerebrospinal fluid. Fatal Outcome. Female. Humans. Japan. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / cerebrospinal fluid. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / parasitology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiography. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / cerebrospinal fluid. Leukemia, Myeloid, Acute / parasitology. Leukemia, Myeloid, Acute / radiography. Leukemia, Myeloid, Acute / therapy. Magnetic Resonance Imaging. Male. Middle Aged. Polymerase Chain Reaction. Remission Induction. Retrospective Studies. Severity of Illness Index. Transplantation Conditioning. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 17680814.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antimalarials; 0 / DNA, Protozoan
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35. Tabata R, Tabata C, Omori K, Nagai T: Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation. Int Arch Allergy Immunol; 2010;152(4):407-12
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  • BACKGROUND: Here we report 2 rare cases of acute myeloid leukemia (AML) complicated with hemolytic anemia limited to the myelodysplastic syndrome (MDS) stage, and disappearing in leukemic transformation.
  • In another case, a 68-year-old man was admitted to hospital when laboratory findings showed a white blood cell count of 24,800/microl with increased myeloblasts (62.5%), leading to the diagnosis of AML with multilineage dysplasia.
  • CONCLUSIONS: The simultaneous loss of autoimmunity and leukemic cell expansion observed in our cases may possibly suggest a common underlying mechanism.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Aged. Autoimmunity. Cell Count. Cell Proliferation. Cell Transformation, Neoplastic. Glucocorticoids / therapeutic use. Granulocyte Precursor Cells / pathology. Humans. Male. Methylprednisolone / therapeutic use. Reticulocytes / pathology


36. Bosch FJ, Badenhorst L, Le Roux JA, Louw VJ: Successful treatment of Chromobacterium violaceum sepsis in South Africa. J Med Microbiol; 2008 Oct;57(Pt 10):1293-5
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  • As far as could be ascertained, this infection has never been reported in a patient with leukaemia.
  • We describe what we believe to be the first such case of C. violaceum sepsis, in a 16-year-old female patient with acute biphenotypic leukaemia, which developed during the neutropenic phase after intensive chemotherapy.
  • [MeSH-minor] Adolescent. Antifungal Agents / pharmacology. Candidiasis / complications. Candidiasis / drug therapy. Female. Humans. Leukemia / complications. Neutropenia / complications. South Africa / epidemiology. Treatment Outcome

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  • (PMID = 18809561.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents
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37. Faber J, Krivtsov AV, Stubbs MC, Wright R, Davis TN, van den Heuvel-Eibrink M, Zwaan CM, Kung AL, Armstrong SA: HOXA9 is required for survival in human MLL-rearranged acute leukemias. Blood; 2009 Mar 12;113(11):2375-85
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  • [Title] HOXA9 is required for survival in human MLL-rearranged acute leukemias.
  • Leukemias that harbor translocations involving the mixed lineage leukemia gene (MLL) possess unique biologic characteristics and often have an unfavorable prognosis.
  • Gene expression analyses demonstrate a distinct profile for MLL-rearranged leukemias with consistent high-level expression of select Homeobox genes, including HOXA9.
  • Here, we investigated the effects of HOXA9 suppression in MLL-rearranged and MLL-germline leukemias using RNA interference.
  • Gene expression profiling after HOXA9 suppression demonstrated co-down-regulation of a program highly expressed in human MLL-AML and murine MLL-leukemia stem cells, including HOXA10, MEIS1, PBX3, and MEF2C.
  • We demonstrate that HOXA9 depletion in 17 human AML/ALL cell lines (7 MLL-rearranged, 10 MLL-germline) induces proliferation arrest and apoptosis specifically in MLL-rearranged cells (P = .007).
  • Moreover, mice transplanted with HOXA9-depleted t(4;11) SEMK2 cells revealed a significantly lower leukemia burden, thus identifying a role for HOXA9 in leukemia survival in vivo.
  • Our data indicate an important role for HOXA9 in human MLL-rearranged leukemias and suggest that targeting HOXA9 or downstream programs may be a novel therapeutic option.

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  • [Cites] Leukemia. 2002 Jul;16(7):1293-301 [12094253.001]
  • [Cites] Blood. 2002 Aug 1;100(3):862-8 [12130496.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1685-90 [12200682.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):161-71 [12620410.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):173-83 [12620411.001]
  • [Cites] Blood. 2003 Jul 1;102(1):262-8 [12637319.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] Genes Dev. 2003 Sep 15;17(18):2298-307 [12952893.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1823-8 [14615372.001]
  • [Cites] Nat Genet. 2004 Mar;36(3):257-63 [14770183.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3192-9 [15070702.001]
  • [Cites] Leukemia. 1988 Oct;2(10):672-6 [3172843.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] Blood. 1993 May 1;81(9):2386-93 [8481519.001]
  • [Cites] Blood. 1993 Aug 15;82(4):1080-5 [8353274.001]
  • [Cites] Blood. 1993 Dec 15;82(12):3705-11 [8260707.001]
  • [Cites] Blood. 1994 Apr 15;83(8):2274-84 [8161794.001]
  • [Cites] Blood. 1994 Jul 15;84(2):570-3 [8025282.001]
  • [Cites] Blood. 1994 Dec 1;84(11):3835-42 [7949140.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12223-7 [7527557.001]
  • [Cites] Genes Dev. 1995 Jul 15;9(14):1753-65 [7622039.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):154-8 [8563753.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):159-67 [8563754.001]
  • [Cites] Am J Hematol. 1996 Dec;53(4):264-6 [8948668.001]
  • [Cites] Blood. 1997 Mar 15;89(6):1922-30 [9058712.001]
  • [Cites] Blood. 1998 Jul 15;92(2):383-93 [9657735.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1222-30 [15479723.001]
  • [Cites] EMBO J. 2005 Jan 26;24(2):368-81 [15635450.001]
  • [Cites] Nat Biotechnol. 2005 Jun;23(6):709-17 [15908939.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8 [15941828.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2841-8 [15998836.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3988-94 [16091451.001]
  • [Cites] Exp Hematol. 2000 May;28(5):569-74 [10812247.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10984-9 [10995463.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):224-34 [11113197.001]
  • [Cites] EMBO J. 2001 Feb 1;20(3):350-61 [11157742.001]
  • [Cites] Oncogene. 2001 Feb 15;20(7):874-8 [11314021.001]
  • [Cites] Blood. 2001 Aug 1;98(3):885-7 [11468194.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5695-707 [11607819.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]
  • [Cites] Exp Hematol. 1995 Oct;23(11):1160-6 [7556525.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):149-53 [8563752.001]
  • [Cites] Blood. 2002 Jan 1;99(1):121-9 [11756161.001]
  • [Cites] Exp Hematol. 2002 Jan;30(1):49-57 [11823037.001]
  • [Cites] Leukemia. 2002 Feb;16(2):186-95 [11840284.001]
  • [Cites] Lancet. 2002 Jun 1;359(9321):1909-15 [12057554.001]
  • [Cites] Oncogene. 2002 Jun 20;21(27):4247-56 [12082612.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11367-74 [16357144.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Nat Methods. 2006 Sep;3(9):677-81 [16929311.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1929-35 [17008526.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]
  • [Cites] Leukemia. 2007 Apr;21(4):593-4 [17301807.001]
  • [Cites] Nat Cell Biol. 2007 Oct;9(10):1208-15 [17891136.001]
  • [Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]
  • [Cites] Cancer Cell. 2008 Nov 4;14(5):355-68 [18977325.001]
  • [CommentIn] Blood. 2009 Mar 12;113(11):2372-3 [19282462.001]
  • (PMID = 19056693.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / P01 CA66996
  • [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 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2656267
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38. Lengfelder E, Saussele S, Weisser A, Büchner T, Hehlmann R: Treatment concepts of acute promyelocytic leukemia. Crit Rev Oncol Hematol; 2005 Nov;56(2):261-74
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  • [Title] Treatment concepts of acute promyelocytic leukemia.
  • In the past, acute promyelocytic leukemia (APL) was associated with a high risk of early mortality resulting from severe coagulopathy, frequently inducing fatal cerebral hemorrhage.
  • With the introduction of the differentiating agent all-trans retinioc acid (ATRA) APL has changed to the best curable subtype of acute myeloid leukemia (AML).
  • PML/RARalpha, the molecular fusion transcript of the specific translocation t(15;17) represents not only the target for ATRA but also permits a precise diagnosis and provides a marker for the identification of minimal residual or recurrent disease (MRD).
  • Currently, arsenic compounds and transplantation procedures seem to be the most promising options in relapsed disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / therapy. Stem Cell Transplantation

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  • (PMID = 16236522.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 121
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39. Imataki O, Kamioka T, Fukuda T, Tanosaki R, Takaue Y: Cost and effectiveness of reduced-intensity and conventional allogeneic hematopoietic stem cell transplantation for acute myelogenous leukemia and myelodysplastic syndrome. Support Care Cancer; 2010 Dec;18(12):1565-9
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  • [Title] Cost and effectiveness of reduced-intensity and conventional allogeneic hematopoietic stem cell transplantation for acute myelogenous leukemia and myelodysplastic syndrome.
  • GOALS OF WORK: Allogeneic stem cell transplantation with a reduced-intensity regimen (RIST) has been evaluated mostly in terms of its clinical benefit, and the pharmacoeconomic aspects of this procedure remain unclear.
  • We compared the cost and effectiveness of RIST with those of stem cell transplantation using a conventional myeloablative regimen (CST).
  • PATIENTS AND METHODS: Fifty consecutive patients who underwent transplantation for myeloid malignancy were included.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / economics. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery


40. Verheyden S, Ferrone S, Mulder A, Claas FH, Schots R, De Moerloose B, Benoit Y, Demanet C: Role of the inhibitory KIR ligand HLA-Bw4 and HLA-C expression levels in the recognition of leukemic cells by Natural Killer cells. Cancer Immunol Immunother; 2009 Jun;58(6):855-65
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  • Transplantation of acute myeloid leukemia (AML) patients with grafts from related haploidentical donors has been shown to result in a potent graft-versus-leukemia effect.
  • This effect is mediated by NK cells because of the lack of activation of inhibitory killer cell immunoglobulin-like receptors (KIRs) which recognize HLA-Bw4 and HLA-C alleles.
  • Therefore in the present study, utilizing a large panel of human monoclonal antibodies we have measured the level of expression of HLA-A, -B and -C alleles on 20 B-chronic lymphoid leukemic (B-CLL) cell preparations, on 16 B-acute lymphoid leukemic (B-ALL) cell preparations and on 19 AML cell preparations.
  • The potential functional relevance of these abnormalities is suggested by the dose-dependent enhancement of NK cell activation caused by coating the HLA-HLA-Bw4 epitope with monoclonal antibodies on leukemic cells which express NK cell activating ligands.

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  • [Cites] Blood. 2004 Apr 15;103(8):3122-30 [15070694.001]
  • [Cites] Leukemia. 2008 Feb;22(2):249-57 [18046448.001]
  • [Cites] Immunol Today. 1990 Jul;11(7):237-44 [2201309.001]
  • [Cites] Science. 1993 May 21;260(5111):1121-4 [8493555.001]
  • [Cites] Cancer Res. 1993 Jul 15;53(14):3349-54 [7686817.001]
  • [Cites] J Exp Med. 1993 Aug 1;178(2):597-604 [8340759.001]
  • [Cites] J Immunol Methods. 1993 Nov 5;166(1):45-54 [8228287.001]
  • [Cites] J Exp Med. 1995 Mar 1;181(3):1133-44 [7532677.001]
  • [Cites] J Exp Med. 1995 Aug 1;182(2):605-9 [7629517.001]
  • [Cites] Hum Immunol. 1997 Aug-Sep;56(1-2):106-13 [9455499.001]
  • [Cites] Hum Immunol. 1998 Aug;59(8):524-8 [9712358.001]
  • [Cites] Tissue Antigens. 1998 Oct;52(4):393-6 [9820605.001]
  • [Cites] Eur J Cancer. 1998 Sep;34(10):1618-22 [9893639.001]
  • [Cites] Blood. 1999 Jul 1;94(1):333-9 [10381530.001]
  • [Cites] J Exp Med. 1999 Jul 19;190(2):205-15 [10432284.001]
  • [Cites] Blood. 2005 Mar 1;105(5):2066-73 [15536144.001]
  • [Cites] Leukemia. 2001 Jan;15(1):128-33 [11243380.001]
  • [Cites] Hum Immunol. 2002 Mar;63(3):200-10 [11872238.001]
  • [Cites] Science. 2002 Mar 15;295(5562):2097-100 [11896281.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3825-7 [12393440.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6178-86 [12414645.001]
  • [Cites] Br J Haematol. 2003 Mar;120(6):1000-8 [12648070.001]
  • [Cites] Leuk Res. 2003 Jul;27(7):643-8 [12681364.001]
  • [Cites] Hum Immunol. 2003 Oct;64(10):941-50 [14522091.001]
  • [Cites] Tissue Antigens. 2004 Mar;63(3):204-11 [14989709.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2860-1; author reply 2862 [15033884.001]
  • [Cites] Exp Hematol. 2005 Mar;33(3):344-52 [15730858.001]
  • [Cites] Curr Opin Immunol. 2005 Oct;17(5):553-9 [16085405.001]
  • [Cites] J Immunol. 2006 Nov 15;177(10):6904-10 [17082605.001]
  • [Cites] Cancer Sci. 2007 Jan;98(1):102-8 [17083564.001]
  • [Cites] Blood. 2007 Jul 1;110(1):433-40 [17371948.001]
  • [Cites] Transplantation. 2004 Oct 15;78(7):1081-5 [15480179.001]
  • (PMID = 18841361.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA138188; United States / NCI NIH HHS / CA / R01CA110249; United States / NCI NIH HHS / CA / R01 CA110249; United States / NCI NIH HHS / CA / P01 CA109688; United States / NCI NIH HHS / CA / R01CA113861; United States / NCI NIH HHS / CA / R01 CA113861
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / HLA-Bw4 antigen; 0 / HLA-C Antigens; 0 / Ligands; 0 / Receptors, KIR
  • [Other-IDs] NLM/ NIHMS395042; NLM/ PMC3426282
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41. Sabry W, Le Blanc R, Labbé AC, Sauvageau G, Couban S, Kiss T, Busque L, Cohen S, Lachance S, Roy DC, Roy J: Graft-versus-host disease prophylaxis with tacrolimus and mycophenolate mofetil in HLA-matched nonmyeloablative transplant recipients is associated with very low incidence of GVHD and nonrelapse mortality. Biol Blood Marrow Transplant; 2009 Aug;15(8):919-29
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  • [Title] Graft-versus-host disease prophylaxis with tacrolimus and mycophenolate mofetil in HLA-matched nonmyeloablative transplant recipients is associated with very low incidence of GVHD and nonrelapse mortality.
  • Incidence of grade II-IV acute graft-versus-host disease (aGVHD) in nonmyeloablative (NMA) transplant recipients remains high.
  • Most common diagnoses included MM (N = 62), non-Hodgkin lymphoma (NHL, N = 46), and acute leukemia (N = 10).
  • Following NMA transplant, disease-free survival (DFS) was highest in recipients with follicular NHL (79.8%: 95% CI: 57.6-91.2) and lowest in large cell NHLs (34.3%: 95% CI: 1.6-75.9).
  • [MeSH-major] Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation / adverse effects. Mycophenolic Acid / analogs & derivatives. Tacrolimus / administration & dosage

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  • (PMID = 19589481.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / Immunosuppressive Agents; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; WM0HAQ4WNM / Tacrolimus
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42. Yamaguchi T, Hashiguchi K, Katsuki S, Iwamoto W, Tsuruhara S, Terada S: Activation of the intrinsic and extrinsic pathways in high pressure-induced apoptosis of murine erythroleukemia cells. Cell Mol Biol Lett; 2008;13(1):49-57
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  • [MeSH-major] Apoptosis / physiology. Leukemia, Erythroblastic, Acute / pathology. Signal Transduction / physiology
  • [MeSH-minor] Animals. Caspase Inhibitors. Caspases / physiology. Cell Line, Tumor. Cell Separation. Flow Cytometry. Membrane Potentials / physiology. Mice. Mitochondrial Membranes / enzymology. Mitochondrial Membranes / pathology. Pressure

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  • (PMID = 17952376.001).
  • [ISSN] 1689-1392
  • [Journal-full-title] Cellular & molecular biology letters
  • [ISO-abbreviation] Cell. Mol. Biol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Caspase Inhibitors; EC 3.4.22.- / Caspases
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43. Ninomiya M, Abe A, Yokozawa T, Ozeki K, Yamamoto K, Ito M, Ito M, Kiyoi H, Emi N, Naoe T: Establishment of a myeloid leukemia cell line, TRL-01, with MLL-ENL fusion gene. Cancer Genet Cytogenet; 2006 Aug;169(1):1-11
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  • [Title] Establishment of a myeloid leukemia cell line, TRL-01, with MLL-ENL fusion gene.
  • We established a leukemia cell line derived from therapy-related acute myeloid leukemia with the t(11;19) by xenotransplantation into the NOD/SCID mouse with IL-2Rgamma(c)-/- (NOG mouse).
  • The cell line, TRL-01, could be serially transplanted from mouse to mouse and also grown in an adherence-dependent manner on a murine bone marrow stroma cell line, HESS-5.
  • TRL-01 had the same immunophenotype as the original leukemia cells: positive for CD13, CD33, CD11a, CD18, CD29, CD49d, CD49e, CD54, CD62L, and CD117, and negative for CD3, CD4, CD8, CD19, CD34, CD41a, CD41b, CD135, and myeloperoxidase.
  • These results suggest that TRL-01 is a useful cell line for studying not only the leukemia-related biology of MLL-ENL but also the intercellular association between leukemia and stroma.
  • [MeSH-major] Gene Fusion. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Amino Acid Sequence. Animals. Apoptosis. Base Sequence. Cell Line, Tumor. DNA Primers. DNA, Complementary. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Mice. Mice, Inbred NOD. Mice, SCID. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16875930.001).
  • [ISSN] 0165-4608
  • [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 / DNA Primers; 0 / DNA, Complementary; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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44. Imatinib: new indication. New indications, but not robust evidence. Prescrire Int; 2008 Jun;17(95):91-4
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  • (1) Imatinib, a tyrosine kinase inhibitor, was first marketed for the treatment of chronic myeloid leukaemia and some gastrointestinal stromal tumours.
  • Its indications have gradually expanded over the years. (2) There is no consensus treatment for adults with Philadelphia chromosome-positive acute lymphoblastic leukaemia.
  • In three non-comparative trials including patients with relapsed or refractory disease after chemotherapy, 50% of patients showed a survival time of at least 7 months.
  • In the absence of any direct comparisons, we do not know if this represents an improvement over the results obtained with the best palliative care. (3) The only potential cure for myelodysplastic syndromes is allogeneic haematopoietic stem cell transplantation but this is not always feasible.
  • [MeSH-major] Dermatofibrosarcoma / drug therapy. Hypereosinophilic Syndrome / drug therapy. Myelodysplastic Syndromes / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use

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  • (PMID = 18623899.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines
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45. Shalapour S, Zelmer A, Pfau M, Moderegger E, Costa-Blechschmidt C, van Landeghem FK, Taube T, Fichtner I, Bührer C, Henze G, Seeger K, Wellmann S: The thalidomide analogue, CC-4047, induces apoptosis signaling and growth arrest in childhood acute lymphoblastic leukemia cells in vitro and in vivo. Clin Cancer Res; 2006 Sep 15;12(18):5526-32
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  • [Title] The thalidomide analogue, CC-4047, induces apoptosis signaling and growth arrest in childhood acute lymphoblastic leukemia cells in vitro and in vivo.
  • PURPOSE: Thalidomide and its analogues have shown promise in the treatment of multiple myeloma but their therapeutic potential has not been evaluated in models of acute lymphoblastic leukemia (ALL).
  • EXPERIMENTAL DESIGN: We assessed the effects of the thalidomide analogue, CC-4047, on the growth and apoptosis signaling of human B cell precursor (BCP) ALL cell lines and freshly obtained childhood BCP-ALL cells grown with or without stromal cells.
  • RESULTS: CC-4047 reduced the proliferation of human BCP-ALL cell lines in vitro.
  • In contrast with the antileukemic effect of cytarabin, this was more pronounced when cell lines or freshly obtained childhood BCP-ALL cells were cocultured with stromal cells.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / analogs & derivatives

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  • (PMID = 17000689.001).
  • [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] 4Z8R6ORS6L / Thalidomide; D2UX06XLB5 / pomalidomide; EC 3.4.22.- / Caspase 3
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46. Saudemont A, Jouy N, Hetuin D, Quesnel B: NK cells that are activated by CXCL10 can kill dormant tumor cells that resist CTL-mediated lysis and can express B7-H1 that stimulates T cells. Blood; 2005 Mar 15;105(6):2428-35
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  • We previously showed in the DA1-3b/C3H mouse model of acute myeloid leukemia that dormant tumor cells resist cytotoxic T-lymphocyte (CTL)-mediated killing because they overexpress B7-H1.
  • Vaccinated mice developed a strong systemic immunity that led to the cure of established leukemia without persistence of dormant tumor cells.
  • [MeSH-major] Antigens, CD80 / immunology. Cancer Vaccines / immunology. Chemokines, CXC / immunology. Gene Expression Regulation, Leukemic / immunology. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / immunology. Membrane Glycoproteins / immunology. Peptides / immunology
  • [MeSH-minor] Animals. Antigens, CD274. Cell Line, Tumor. Cell Proliferation. Chemokine CXCL10. Female. Humans. Interferon-gamma / biosynthesis. Interferon-gamma / immunology. Lymphocyte Depletion. Mice. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / metabolism. Transduction, Genetic. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / immunology. Vaccination

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  • (PMID = 15536145.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD274; 0 / Antigens, CD80; 0 / Cancer Vaccines; 0 / Cd274 protein, mouse; 0 / Chemokine CXCL10; 0 / Chemokines, CXC; 0 / Cxcl10 protein, mouse; 0 / Membrane Glycoproteins; 0 / Peptides; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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47. Kanno S, Hiura T, Ohtake T, Koiwai K, Suzuki H, Ujibe M, Ishikawa M: Characterization of resistance to cytosine arabinoside (Ara-C) in NALM-6 human B leukemia cells. Clin Chim Acta; 2007 Feb;377(1-2):144-9
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  • [Title] Characterization of resistance to cytosine arabinoside (Ara-C) in NALM-6 human B leukemia cells.
  • BACKGROUND: Cytosine arabinoside (1-beta-D-arabinofuranosylcytosine;Ara-C) is the most important antimetabolite used for acute leukemia.
  • We established Ara-C (0.003-1 micromol/l)-resistant NALM-6 leukemia cells, and attempted the characterization of their resistance.
  • METHODS: The Ara-C-resistant cell lines were developed by stepwise increases in the drug.
  • [MeSH-major] Cytarabine / pharmacology. Drug Resistance, Neoplasm. Leukemia / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Cytidine Deaminase / metabolism. Cytoprotection / drug effects. Deoxycytidine Kinase / metabolism. Dipyridamole / pharmacology. Gene Expression / drug effects. Humans. RNA, Messenger / genetics. Thioinosine / analogs & derivatives. Thioinosine / pharmacology

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  • (PMID = 17097625.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger; 04079A1RDZ / Cytarabine; 38048-32-7 / 4-nitrobenzylthioinosine; 46S541971T / Thioinosine; 64ALC7F90C / Dipyridamole; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.5.4.5 / Cytidine Deaminase
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48. Onimaru Y, Tsukasaki K, Murata K, Imaizumi Y, Choi YL, Hasegawa H, Sugahara K, Yamada Y, Hayashi T, Nakashima M, Taguchi T, Mano H, Kamihira S, Tomonaga M: Autocrine and/or paracrine growth of aggressive ATLL cells caused by HGF and c-Met. Int J Oncol; 2008 Oct;33(4):697-703
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  • Adult T-cell leukemia/lymphoma (ATLL) is a neoplasia characterized by the massive invasion of various organs by tumor cells.
  • Previously, we found that expression of the gene for c-Met, a receptor tyrosine kinase for hepatocyte growth factor (HGF), was specific to the acute type among 41 patients with ATLL by microarray.
  • Then, we analyzed the growth of ATLL cells caused by HGF and c-Met. c-Met was expressed in 0/7 chronic ATLLs, 12/14 acute ATLLs, 1/1 IL-2-independent ATLL cell line and 1/7 IL-2-dependent ATLL cell lines as assessed by flow cytometry.
  • HGF induced the proliferation of primary cells from most acute cases examined as well as the c-Met-positive KK1 cell line in contrast to c-Met-negative cells.
  • HGF induced autophosphorylation of c-Met in c-Met-positive cells from an acute case and KK1 cells.
  • The plasma level of HGF was elevated in acute as compared to chronic cases.
  • The levels of HGF and/or IL-6 which induces the production of HGF by stromal cells, were elevated in the supernatant of short-term cultured cells from certain patients with acute or chronic disease.
  • Finally, infiltrated ATLL cells and adjacent stromal cells in liver were shown to be positive for c-Met/HGF and HGF, respectively, in acute cases.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Gene Expression Regulation, Neoplastic. Hepatocyte Growth Factor / metabolism. Leukemia-Lymphoma, Adult T-Cell / immunology. Proto-Oncogene Proteins c-met / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Membrane / metabolism. Cell Proliferation. Cytokines / metabolism. Humans. Interleukin-6 / metabolism. Models, Biological. Phosphorylation. Time Factors

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  • (PMID = 18813782.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-6; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
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49. Zuckerman T, Rowe JM: Hematopoietic stem cell transplantation for adults with acute lymphoblastic leukemia. Curr Opin Hematol; 2009 Nov;16(6):453-9
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  • [Title] Hematopoietic stem cell transplantation for adults with acute lymphoblastic leukemia.
  • PURPOSE OF REVIEW: The long-term survival for patients with adult acute lymphoblastic leukemia (ALL) has not significantly changed over the past two decades and, as opposed to pediatric ALL, it is less than 40% despite high initial complete remission rate.
  • The follow-up of minimal residual disease status, adopting protocols from childhood ALL to young adults and use of targeted therapy may improve long-term survival.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma


50. Neid T, Danz B, Eismann R, Bramsiepe I, Wohlrab J, Marsch WC, Fiedler E: [Sclerodermiform chronic graft-versus-host disease after allogenic peripheral blood stem-cell transplantation]. Dtsch Med Wochenschr; 2009 May;134(21):1106-9
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  • [Title] [Sclerodermiform chronic graft-versus-host disease after allogenic peripheral blood stem-cell transplantation].
  • Due to acute myelotic leukemia (AML), an allogenic peripheral blood stem-cell transplantation with subsequent immunosupression with mycophenolatmofetil (MMF) and ciclosporin A had been performed 8 years previously.
  • DIAGNOSIS, THERAPY AND COURSE: The histological pattern in conjunction with the anamnesis indicated a cutaneous chronic graft-versus-host disease (GvHD).
  • CONCLUSION: After stem-cell transplantation, early diagnosis of GvHD is especially important due to possible irreversible sclerodermatous changes and other organ manifestations.
  • [MeSH-major] Graft vs Host Disease / etiology. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / adverse effects. Scleroderma, Localized / etiology
  • [MeSH-minor] Anti-Infective Agents / therapeutic use. Cyclosporine / therapeutic use. Humans. Immunosuppressive Agents / therapeutic use. Laser-Doppler Flowmetry. Leg Ulcer / diagnosis. Leg Ulcer / etiology. Leg Ulcer / therapy. Male. Middle Aged. Mycophenolic Acid / analogs & derivatives. Mycophenolic Acid / therapeutic use. PUVA Therapy. Patient Compliance. Pentoxifylline / therapeutic use. Physical Therapy Modalities. Transplantation, Homologous. Vasodilator Agents / therapeutic use


51. Sidhom I, Shaaban K, Soliman S, Ezzat S, El-Anwar W, Hamdy N, Yassin D, Salem S, Hassanein H, Mansour MT: Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia. J Egypt Natl Canc Inst; 2008 Jun;20(2):111-20
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  • [Title] Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Cell-marker profiling has led to conflicting conclusions about its prognostic significance in T-ALL.
  • AIM: To investigate the prevalence of the expression of CD34, CD10 and myeloid associated antigens (CD13/ CD33) in childhood T-ALL and to relate their presence to initial clinical and biologic features and early response to therapy.
  • Immunophenotypic markers and minimal residual disease (MRD) were studied by five-color flow cytometry.
  • No significant association was encountered between CD34, CD10 or myeloid antigen positivity and the presenting clinical features as age, sex, TLC and CNS leukemia.
  • CD34 and CD13/CD33 expression was significantly associated with T-cell maturation stages (p<0.05).
  • CD34(+), CD13/CD33(+) and early T-cell stage had high MRD levels on day 15 that was statistically highly significant (p<0.01), but CD10(+) had statistically significant lower MRD level on day 15 (p=0.049).
  • CONCLUSIONS: CD34, CD10, CD13/CD33 expression, as well as T-cell maturation stages, may have prognostic significance in pediatric T-ALL as they have a significant impact on early clearance of leukemic cells detected by MRD day 15.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm, Residual / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Differentiation. Child. Child, Preschool. Egypt. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Neprilysin / metabolism. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 20029466.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 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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52. Craddock C, Nagra S, Peniket A, Brookes C, Buckley L, Nikolousis E, Duncan N, Tauro S, Yin J, Liakopoulou E, Kottaridis P, Snowden J, Milligan D, Cook G, Tholouli E, Littlewood T, Peggs K, Vyas P, Clark F, Cook M, Mackinnon S, Russell N: Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia. Haematologica; 2010 Jun;95(6):989-95
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  • [Title] Factors predicting long-term survival after T-cell depleted reduced intensity allogeneic stem cell transplantation for acute myeloid leukemia.
  • BACKGROUND: Reduced intensity conditioning regimens permit the delivery of a potentially curative graft-versus-leukemia effect in older patients with acute myeloid leukemia.
  • Although T-cell depletion is increasingly used to reduce the risk of graft-versus-host disease its impact on the graft-versus-leukemia effect and long-term outcome post-transplant is unknown.
  • DESIGN AND METHODS: We have characterized pre- and post-transplant factors determining overall survival in 168 patients with acute myeloid leukemia transplanted using an alemtuzumab based reduced intensity conditioning regimen with a median duration of follow-up of 37 months.
  • RESULTS: The 3-year overall survival for patients transplanted in CR1 or CR2/CR3 was 50% (95% CI, 38% to 62%) and 44% (95% CI, 31% to 56%), respectively compared to 15% (95% CI, 2% to 36%) for patients with relapsed/refractory disease.
  • Multivariate analysis demonstrated that both survival and disease relapse were influenced by status at transplant (P=0.008) and presentation cytogenetics (P=0.01).
  • CONCLUSIONS: Disease stage, presentation karyotype and post-transplant CsA exposure are important predictors of outcome in patients undergoing a T-cell depleted reduced intensity conditioning allograft for acute myeloid leukemia.
  • These data confirm the presence of a potent graft-versus-leukemia effect after a T-cell depleted reduced intensity conditioning allograft in acute myeloid leukemia and identify CsA exposure as a manipulable determinant of outcome in this setting.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. T-Lymphocytes. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / immunology. Graft vs Host Disease / mortality. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Predictive Value of Tests. Time Factors. Transplantation, Homologous. Treatment Outcome. Young Adult

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  • [Cites] Blood. 1998 Feb 1;91(3):756-63 [9446633.001]
  • [Cites] JAMA. 2009 Jun 10;301(22):2349-61 [19509382.001]
  • [Cites] Br J Haematol. 2000 Jan;108(1):99-104 [10651732.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3390-400 [11369628.001]
  • [Cites] Bone Marrow Transplant. 2001 Nov;28(10):909-15 [11753543.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1071-8 [11807015.001]
  • [Cites] Cytotherapy. 2001;3(3):197-201 [12171726.001]
  • [Cites] Bone Marrow Transplant. 2003 Jun;31(12):1089-95 [12796788.001]
  • [Cites] Blood. 2003 Jul 15;102(2):470-6 [12649133.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1548-56 [14576063.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Blood. 1991 Apr 1;77(7):1423-8 [2009366.001]
  • [Cites] Blood. 1997 Jun 15;89(12):4531-6 [9192777.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):444-53 [16344316.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Feb;11(2):108-14 [15682071.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5675-87 [16110027.001]
  • [Cites] Cancer. 2005 Nov 1;104(9):1931-8 [16178004.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9387-93 [16314618.001]
  • [Cites] Leukemia. 2006 Feb;20(2):322-8 [16307018.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2184-91 [16254140.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Apr;13(4):454-62 [17382251.001]
  • [Cites] Blood. 2007 Jul 1;110(1):409-17 [17374741.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1530-9 [17495133.001]
  • [Cites] J Clin Oncol. 2008 Feb 1;26(4):577-84 [18086801.001]
  • [Cites] Biol Blood Marrow Transplant. 2009 May;15(5):610-7 [19361753.001]
  • [CommentIn] Haematologica. 2010 Jun;95(6):860-3 [20513805.001]
  • [CommentIn] Haematologica. 2010 Jun;95(6):857-9 [20513804.001]
  • (PMID = 19951968.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ PMC2878799
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53. O'Brien MM, Lee-Kim Y, George TI, McClain KL, Twist CJ, Jeng M: Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer; 2008 Feb;50(2):381-3
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  • [Title] Precursor B-cell acute lymphoblastic leukemia presenting with hemophagocytic lymphohistiocytosis.
  • Hemophagocytic lymphohistiocytosis (HLH) is a hyperinflammatory syndrome which can be an inherited congenital disorder or can develop secondary to malignancy, infection, or autoimmune disease.
  • Secondary HLH due to malignancy occurs most commonly with T or NK-cell lymphoid neoplasms.
  • HLH with B-cell malignancies is less common and HLH has rarely been described in association with precursor B-cell acute lymphoblastic leukemia (B-ALL).
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


54. Jäger R, Gisslinger H, Passamonti F, Rumi E, Berg T, Gisslinger B, Pietra D, Harutyunyan A, Klampfl T, Olcaydu D, Cazzola M, Kralovics R: Deletions of the transcription factor Ikaros in myeloproliferative neoplasms. Leukemia; 2010 Jul;24(7):1290-8
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  • Transformation to acute leukemia is a major complication of myeloproliferative neoplasms (MPNs), however, the genetic changes leading to transformation remain largely unknown.
  • We screened nine patients with post-MPN leukemia for chromosomal aberrations using microarray karyotyping.
  • We further examined the frequency of IKZF1 deletions in a total of 29 post-MPN leukemia and 526 MPN patients without transformation and observed a strong association of IKZF1 deletions with post-MPN leukemia in two independent cohorts.
  • IKZF1 deletions were observed in both undifferentiated and differentiated myeloid cell types, indicating that IKZF1 loss does not cause differentiation arrest but rather renders progenitors susceptible to transformation, most likely through chromosomal instability.


55. Schmiegelow K, Forestier E, Kristinsson J, Söderhäll S, Vettenranta K, Weinshilboum R, Wesenberg F, Nordic Society of Paediatric Haematology and Oncology: Thiopurine methyltransferase activity is related to the risk of relapse of childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study. Leukemia; 2009 Mar;23(3):557-64
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  • [Title] Thiopurine methyltransferase activity is related to the risk of relapse of childhood acute lymphoblastic leukemia: results from the NOPHO ALL-92 study.
  • Of 601 children with acute lymphoblastic leukemia (ALL) who were treated by the NOPHO ALL-92 protocol, 117 had TPMT genotype determined, whereas for 484 patients only erythrocyte TPMT activity was available.

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  • [Cites] J Natl Cancer Inst. 1999 Dec 1;91(23):2001-8 [10580024.001]
  • [Cites] J Pediatr Hematol Oncol. 2008 Nov;30(11):831-49 [18989161.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2001 Jan;15(1):74-9 [11243403.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Feb;25(2):114-7 [12571461.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1332-9 [12663723.001]
  • [Cites] Leukemia. 2003 Jul;17(7):1344-8 [12835723.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2736-40 [12843002.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Clin Chim Acta. 1978 May 2;85(3):323-33 [657528.001]
  • [Cites] Haematol Blood Transfus. 1990;33:110-7 [2323622.001]
  • [Cites] Lancet. 1990 Jul 28;336(8709):225-9 [1973780.001]
  • [Cites] Eur J Clin Pharmacol. 1992;43(4):329-39 [1451710.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1993 Feb;15(1):80-6 [8447563.001]
  • [Cites] J Clin Oncol. 1995 Feb;13(2):345-51 [7531219.001]
  • [Cites] Biochemistry. 1997 Mar 4;36(9):2501-6 [9054555.001]
  • [Cites] Br J Clin Pharmacol. 1997 Nov;44(5):455-61 [9384462.001]
  • [Cites] Acta Paediatr. 1998 Jan;87(1):108-11 [9510461.001]
  • [Cites] Br J Haematol. 1998 Jul;102(2):439-43 [9695957.001]
  • [Cites] Lancet. 1998 Nov 28;352(9142):1731-8 [9848348.001]
  • [Cites] Blood. 1999 May 1;93(9):2817-23 [10216075.001]
  • [Cites] Lancet. 1999 Jul 3;354(9172):34-9 [10406363.001]
  • [Cites] Cancer. 1999 Sep 15;86(6):1080-6 [10491537.001]
  • [Cites] Blood. 1953 Nov;8(11):965-99 [13105700.001]
  • [Cites] JAMA. 2005 Mar 23;293(12):1485-9 [15784872.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1145-52 [15902295.001]
  • [Cites] Aliment Pharmacol Ther. 2005 Oct 1;22(7):605-11 [16181300.001]
  • [Cites] Blood. 2006 Jan 15;107(2):843-4 [16401827.001]
  • [Cites] Annu Rev Med. 2006;57:119-37 [16409140.001]
  • [Cites] Invest New Drugs. 2005 Dec;23(6):523-32 [16267626.001]
  • [Cites] Oncogene. 2006 Mar 13;25(11):1629-38 [16550163.001]
  • [Cites] Inflamm Bowel Dis. 2006 Apr;12(4):251-7 [16633046.001]
  • [Cites] Pharmacogenomics. 2006 Jul;7(5):783-92 [16886902.001]
  • [Cites] Lancet. 2006 Oct 14;368(9544):1339-48 [17046466.001]
  • [Cites] Expert Rev Mol Diagn. 2007 Jul;7(4):371-93 [17620046.001]
  • [Cites] Br J Clin Pharmacol. 1995 Apr;39(4):456-9 [7640156.001]
  • [Cites] Pediatr Blood Cancer. 2007 Sep;49(3):250-5 [16856155.001]
  • [Cites] Drug Metab Dispos. 2007 Sep;35(9):1452-4 [17553913.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):24-36 [18097462.001]
  • [Cites] Pediatr Hematol Oncol. 1996 Sep-Oct;13(5):433-41 [10897815.001]
  • (PMID = 18987654.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM028157; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NIGMS NIH HHS / GM / R01-GM28157; United States / NIGMS NIH HHS / GM / U01 GM61388
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Neoplasm Proteins; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase; FTK8U1GZNX / Thioguanine
  • [Other-IDs] NLM/ NIHMS546648; NLM/ PMC3898327
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56. Kanno S, Hiura T, Shouji A, Osanai Y, Ujibe M, Ishikawa M: Resistance to Ara-C up-regulates the activation of NF-kappaB, telomerase activity and Fas expression in NALM-6 cells. Biol Pharm Bull; 2007 Nov;30(11):2069-74
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  • Cytosine arabinoside (1-beta-D-arabinofuranosylcytosine; Ara-C) is the most important antimetabolite used to induce remission in acute leukemia, but cellular resistance to Ara-C reflects a poor prognosis in cancer chemotherapy.
  • The induction of apoptosis and reduction of cell viability by cytotoxic anti-Fas antibody was more susceptible in resistant cells than parental cells.
  • [MeSH-minor] Antigens, CD95 / metabolism. Apoptosis / drug effects. BH3 Interacting Domain Death Agonist Protein / metabolism. Cell Line, Tumor. Formazans / metabolism. Humans. Leukemia / enzymology. Leukemia / metabolism. Leukemia / pathology. Tetrazolium Salts / metabolism. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17978477.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antimetabolites, Antineoplastic; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Formazans; 0 / NF-kappa B; 0 / Tetrazolium Salts; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 04079A1RDZ / Cytarabine; 23305-68-2 / MTT formazan; EC 2.7.7.49 / Telomerase
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57. Davidsson J, Lilljebjörn H, Panagopoulos I, Fioretos T, Johansson B: BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias. Leukemia; 2008 Aug;22(8):1619-21
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  • [Title] BRAF mutations are very rare in B- and T-cell pediatric acute lymphoblastic leukemias.
  • [MeSH-major] B-Lymphocytes / immunology. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins B-raf / genetics. T-Lymphocytes / immunology

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  • [CommentOn] Leukemia. 2005 Feb;19(2):310-2 [15538400.001]
  • (PMID = 18273045.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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58. Mora JR, Knoll JH, Rogan PK, Getts RC, Wilson GS: Dendrimer FISH detection of single-copy intervals in acute promyelocytic leukemia. Mol Cell Probes; 2006 Apr;20(2):114-20
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  • [Title] Dendrimer FISH detection of single-copy intervals in acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (AML-M3) is characterized by a translocation between chromosomes 15 and 17 [t(15;17)].
  • The detection of t(15;17) at the single cell level, is commonly done by fluorescence in situ hybridization (FISH) using recombinant locus specific genomic probes greater than 14 kilobases kb in length.
  • [MeSH-major] Genome, Human. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. DNA Probes / chemistry. Dendrimers / chemistry. Humans. In Situ Hybridization, Fluorescence. Interphase. Metaphase

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  • (PMID = 16460913.001).
  • [ISSN] 0890-8508
  • [Journal-full-title] Molecular and cellular probes
  • [ISO-abbreviation] Mol. Cell. Probes
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM08359
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Probes; 0 / Dendrimers
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59. Uno S, Kinoshita Y, Azuma Y, Tsunenari T, Yoshimura Y, Iida S, Kikuchi Y, Yamada-Okabe H, Fukushima N: Antitumor activity of a monoclonal antibody against CD47 in xenograft models of human leukemia. Oncol Rep; 2007 May;17(5):1189-94
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  • [Title] Antitumor activity of a monoclonal antibody against CD47 in xenograft models of human leukemia.
  • To confirm whether the ligation of CD47 caused cell death in vivo, we examined the antitumor activity of F(ab')2 of mAb-MABL in two xenograft models: The acute lymphoblastic leukemia (CCRF-CEM) and the B-cell chronic lymphocytic leukemia (JOK-1) cell line.
  • Thus, monoclonal antibodies that cause cell death from the ligation of CD47 could be novel therapeutic agents for incurable leukemia after further optimization such as humanization or making single chain diabodies.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD47 / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Humans. Leukemia L1210. Male. Mice. Mice, SCID. Xenograft Model Antitumor Assays

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  • (PMID = 17390064.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD47
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60. Wang PY, Young F, Chen CY, Stevens BM, Neering SJ, Rossi RM, Bushnell T, Kuzin I, Heinrich D, Bottaro A, Jordan CT: The biologic properties of leukemias arising from BCR/ABL-mediated transformation vary as a function of developmental origin and activity of the p19ARF gene. Blood; 2008 Nov 15;112(10):4184-92
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  • [Title] The biologic properties of leukemias arising from BCR/ABL-mediated transformation vary as a function of developmental origin and activity of the p19ARF gene.
  • Recent reports have shown that upon expression of appropriate oncogenes, both stem cells and more differentiated progenitor populations can serve as leukemia-initiating cells.
  • However, no study has described how specific mutations influence the ability of differentiating cell subsets to serve as leukemia-initiating cells and if varying such cellular origins confers a functional difference.
  • We have examined the role of the tumor suppressor gene p19(ARF) in a murine model of acute lymphoblastic leukemia and found that loss of p19(ARF) changes the spectrum of cells capable of tumor initiation.
  • In a p19(ARF)-null genetic background expression of the BCR/ABL fusion protein renders functionally defined HSCs, common lymphoid progenitors (CLP), and precursor B-lymphocytes competent to generate leukemia stem cells.
  • Furthermore, we show that leukemias arising from p19(ARF)-null HSC versus pro-B cells differ biologically, including relative response to drug insult.

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  • [Cites] Blood. 2000 Feb 1;95(3):1007-13 [10648416.001]
  • [Cites] Genes Dev. 2008 Jun 1;22(11):1411-5 [18519632.001]
  • [Cites] Blood Cells Mol Dis. 2001 Jan-Feb;27(1):201-5 [11358380.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3925-30 [11389036.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9654-9 [11481442.001]
  • [Cites] Nature. 2001 Sep 6;413(6851):83-6 [11544530.001]
  • [Cites] Nature. 2001 Sep 6;413(6851):86-91 [11544531.001]
  • [Cites] Exp Hematol. 2003 Mar;31(3):204-10 [12644017.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2919-25 [15242869.001]
  • [Cites] Br J Haematol. 1990 Sep;76(1):39-44 [2223647.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2013-6 [7718873.001]
  • [Cites] Cell. 1996 Apr 5;85(1):27-37 [8620534.001]
  • [Cites] Cell. 1997 Nov 28;91(5):649-59 [9393858.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13194-9 [9789064.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Trends Cell Biol. 1999 Jun;9(6):233-8 [10354570.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):311-21 [15803157.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] Trends Immunol. 2005 Aug;26(8):426-33 [15979407.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93 [16618932.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Immunity. 2007 Jun;26(6):703-14 [17582343.001]
  • [Cites] Genes Dev. 2007 Sep 15;21(18):2283-7 [17761812.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2578-85 [17601986.001]
  • [Cites] Leuk Res. 2007 Dec;31(12):1625-32 [18246599.001]
  • [Cites] J Virol. 2000 Oct;74(20):9479-87 [11000217.001]
  • (PMID = 18755985.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA122206; United States / NCI NIH HHS / CA / R21 CA107355; United States / NCI NIH HHS / CA / R01-CA122206; United States / NCI NIH HHS / CA / R21-CA107355
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2581986
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61. Sato Y, Yokoyama A, Shibata K, Akimoto Y, Ogino S, Nodasaka Y, Kohgo T, Tamura K, Akasaka T, Uo M, Motomiya K, Jeyadevan B, Ishiguro M, Hatakeyama R, Watari F, Tohji K: Influence of length on cytotoxicity of multi-walled carbon nanotubes against human acute monocytic leukemia cell line THP-1 in vitro and subcutaneous tissue of rats in vivo. Mol Biosyst; 2005 Jul;1(2):176-82
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  • [Title] Influence of length on cytotoxicity of multi-walled carbon nanotubes against human acute monocytic leukemia cell line THP-1 in vitro and subcutaneous tissue of rats in vivo.
  • In this paper, we investigated the activation of the human acute monocytic leukemia cell line THP-1 in vitro and the response in subcutaneous tissue in vivo to CNTs of different lengths.
  • [MeSH-minor] Animals. Cell Line, Tumor. Culture Media / chemistry. Culture Media / pharmacology. Humans. Inflammation / etiology. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microscopy, Electron, Scanning. Microscopy, Electron, Transmission. Nanostructures / chemistry. Nanostructures / ultrastructure. Nanotechnology / methods. Rats. Rats, Wistar. Spectrophotometry, Infrared. Subcutaneous Tissue / pathology. Subcutaneous Tissue / ultrastructure. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16880981.001).
  • [ISSN] 1742-206X
  • [Journal-full-title] Molecular bioSystems
  • [ISO-abbreviation] Mol Biosyst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media; 0 / Nanotubes, Carbon; 0 / Tumor Necrosis Factor-alpha
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62. Lindblom A, Heyman M, Gustafsson I, Norbeck O, Kaldensjö T, Vernby A, Henter JI, Tolfvenstam T, Broliden K: Parvovirus B19 infection in children with acute lymphoblastic leukemia is associated with cytopenia resulting in prolonged interruptions of chemotherapy. Clin Infect Dis; 2008 Feb 15;46(4):528-36
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  • [Title] Parvovirus B19 infection in children with acute lymphoblastic leukemia is associated with cytopenia resulting in prolonged interruptions of chemotherapy.
  • We evaluated the complications of parvovirus B19 infection, including delays in the scheduled course of chemotherapy, in children with acute lymphoblastic leukemia (ALL).
  • Clinical and laboratory data were collected from the Nordic Childhood Leukemia Registry and from medical records.
  • Patients with viremia at diagnosis or during therapy for infection had lower viral loads (median viral load, 7 x 10(4) copies/mL) than did those who became viremic during maintenance therapy (median viral load, 2 x 10(8) copies/mL).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Pancytopenia / virology. Parvoviridae Infections / diagnosis. Parvoviridae Infections / pathology. Parvovirus B19, Human / isolation & purification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [CommentIn] Clin Infect Dis. 2008 Feb 15;46(4):537-9 [18194096.001]
  • (PMID = 18194100.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Viral
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63. Cornelissen JJ, van Putten WL, Verdonck LF, Theobald M, Jacky E, Daenen SM, van Marwijk Kooy M, Wijermans P, Schouten H, Huijgens PC, van der Lelie H, Fey M, Ferrant A, Maertens J, Gratwohl A, Lowenberg B: Results of a HOVON/SAKK donor versus no-donor analysis of myeloablative HLA-identical sibling stem cell transplantation in first remission acute myeloid leukemia in young and middle-aged adults: benefits for whom? Blood; 2007 May 1;109(9):3658-66
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  • [Title] Results of a HOVON/SAKK donor versus no-donor analysis of myeloablative HLA-identical sibling stem cell transplantation in first remission acute myeloid leukemia in young and middle-aged adults: benefits for whom?
  • The Dutch-Belgian Hemato-Oncology Cooperative Group and the Swiss Group for Clinical Cancer Research (HOVON-SAKK) collaborative study group evaluated outcome of patients (pts) with acute myeloid leukemia (AML) in first remission (CR1) entered in 3 consecutive studies according to a donor versus no-donor comparison.
  • Between 1987 and 2004, 2287 pts were entered in these studies of whom 1032 pts (45%) without FAB M3 or t(15;17) were in CR1 after 2 cycles of chemotherapy, received consolidation treatment, and were younger than 55 years of age and therefore eligible for allogeneic hematopoietic stem cell transplantation (allo-SCT).
  • Despite more treatment-related mortality (TRM) in the donor group (21% versus 4%, P < .001), disease-free survival (DFS) appeared significantly better in the donor group (48% +/- 3% versus 37% +/- 2% in the no-donor group, P < .001).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Living Donors. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Age Factors. Disease-Free Survival. Female. Follow-Up Studies. Histocompatibility Testing. Humans. Male. Meta-Analysis as Topic. Middle Aged. Recurrence. Retrospective Studies. Risk Factors. Survival Rate. Transplantation, Homologous


64. Mortier E, Quéméner A, Vusio P, Lorenzen I, Boublik Y, Grötzinger J, Plet A, Jacques Y: Soluble interleukin-15 receptor alpha (IL-15R alpha)-sushi as a selective and potent agonist of IL-15 action through IL-15R beta/gamma. Hyperagonist IL-15 x IL-15R alpha fusion proteins. J Biol Chem; 2006 Jan 20;281(3):1612-9
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  • In sharp contrast with this finding, we demonstrate in this report that a recombinant, soluble sushi domain of IL-15R alpha, which bears most of the binding affinity for IL-15, behaves as a potent IL-15 agonist by enhancing its binding and biological effects (proliferation and protection from apoptosis) through the IL-15R beta/gamma heterodimer, whereas it does not affect IL-15 binding and function of the tripartite IL-15R alpha/beta/gamma membrane receptor.
  • [MeSH-minor] Animals. CHO Cells. Cell Line, Tumor. Cricetinae. Dimerization. Humans. Interleukin Receptor Common gamma Subunit. Interleukin-2 Receptor beta Subunit. Kinetics. Leukemia, Erythroblastic, Acute. Models, Molecular. Protein Binding. Protein Structure, Secondary. Receptors, Interleukin-15. Transfection

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  • (PMID = 16284400.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL-15Ralpha-sushi domain-linker-IL-15 fusion protein; 0 / IL15RA protein, human; 0 / IL2RB protein, human; 0 / IL2RG protein, human; 0 / Interleukin Receptor Common gamma Subunit; 0 / Interleukin-15; 0 / Interleukin-2 Receptor beta Subunit; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-15; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins
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65. Dellett M, O'Hagan KA, Colyer HA, Mills KI: Identification of gene networks associated with acute myeloid leukemia by comparative molecular methylation and expression profiling. Biomark Cancer; 2010;2:43-55
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  • [Title] Identification of gene networks associated with acute myeloid leukemia by comparative molecular methylation and expression profiling.
  • Around 80% of acute myeloid leukemia (AML) patients achieve a complete remission, however many will relapse and ultimately die of their disease.

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  • (PMID = 24179384.001).
  • [Journal-full-title] Biomarkers in cancer
  • [ISO-abbreviation] Biomark Cancer
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3783331
  • [Keywords] NOTNLM ; AML / NPM / cytogenetics / methylation
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66. Mkrtchyan H, Glaser M, Gross M, Wedding U, Hoffken K, Liehr T, Karst C, Aroutiounian R: Multicolor-FISH applied to resolve complex chromosomal changes in a case of T-ALL (FAB L2). Cytogenet Genome Res; 2006;114(3-4):270-3
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  • We report on a patient with a clinically diagnosed acute lymphoblastic leukemia (ALL) with partial unrecorded complex translocation events especially involving chromosomes 5, 9 and 18.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16954665.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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67. 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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  • 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.
  • 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.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Mobilization / methods. Hematopoietic Stem Cell Transplantation / methods. Killer Cells, Natural / immunology. Killer Cells, Natural / transplantation
  • [MeSH-minor] Adult. Antigens, CD56 / immunology. Bone Marrow Cells / drug effects. Disease-Free Survival. Female. Graft vs Host Disease / immunology. HLA Antigens / immunology. Histocompatibility Testing. Humans. Male. Tissue Donors. Transplantation Conditioning / methods. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 19377516.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / HLA Antigens; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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68. Inukai T, Hirose K, Inaba T, Kurosawa H, Hama A, Inada H, Chin M, Nagatoshi Y, Ohtsuka Y, Oda M, Goto H, Endo M, Morimoto A, Imaizumi M, Kawamura N, Miyajima Y, Ohtake M, Miyaji R, Saito M, Tawa A, Yanai F, Goi K, Nakazawa S, Sugita K: Hypercalcemia in childhood acute lymphoblastic leukemia: frequent implication of parathyroid hormone-related peptide and E2A-HLF from translocation 17;19. Leukemia; 2007 Feb;21(2):288-96
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  • [Title] Hypercalcemia in childhood acute lymphoblastic leukemia: frequent implication of parathyroid hormone-related peptide and E2A-HLF from translocation 17;19.
  • To clarify the clinical characteristics, mechanisms of hypercalcemia, response to management for hypercalcemia, incidence of t(17;19) and final outcome of childhood acute lymphoblastic leukemia (ALL) accompanied by hypercalcemia, clinical data of 22 cases of childhood ALL accompanied by hypercalcemia (>12 mg/dl) reported in Japan from 1990 to 2005 were retrospectively analyzed.
  • Twenty patients had low white blood cell count (<20 x 10(9)/l), 15 showed hemoglobin> or =8 g/dl and 14 showed platelet count > or =100 x 10(9)/l.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 19. DNA-Binding Proteins / genetics. Hypercalcemia / complications. Hypercalcemia / genetics. Oncogene Proteins, Fusion / genetics. Parathyroid Hormone-Related Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic


69. Kreft A, Holtmann H, Schad A, Kirkpatrick CJ: Detection of residual leukemic blasts in adult patients with acute T-lymphoblastic leukemia using bone marrow trephine biopsies: comparison of fluorescent immunohistochemistry with conventional cytologic and flow-cytometric analysis. Pathol Res Pract; 2010 Aug 15;206(8):560-4
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  • [Title] Detection of residual leukemic blasts in adult patients with acute T-lymphoblastic leukemia using bone marrow trephine biopsies: comparison of fluorescent immunohistochemistry with conventional cytologic and flow-cytometric analysis.
  • Evaluation of remission in adult acute lymphoblastic leukemia (ALL) normally relies on cytologic evaluation and flow-cytometric analysis.
  • [MeSH-major] Bone Marrow / pathology. Flow Cytometry. Fluorescent Antibody Technique. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Biopsy. Cell Separation. Cytological Techniques. Female. Humans. Male. Middle Aged. Sensitivity and Specificity. Young Adult

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  • (PMID = 20413226.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
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70. Sood S, Das R, Trehan A, Ahluwalia J, Sachdeva MU, Varma N, Bansal D, Marwaha RK: Methylenetetrahydrofolate reductase gene polymorphisms: association with risk for pediatric acute lymphoblastic leukemia in north Indians. Leuk Lymphoma; 2010 May;51(5):928-32
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  • [Title] Methylenetetrahydrofolate reductase gene polymorphisms: association with risk for pediatric acute lymphoblastic leukemia in north Indians.
  • Genetic polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene have been associated with the development of acute leukemias and various malignancies.
  • We conducted a case-control study in 95 north Indian children with acute lymphoblastic leukemia (ALL) and 255 controls, to investigate the role of MTHFR C677T and A1298C polymorphisms as risk factors in the development of ALL.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Single Nucleotide / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Female. Genetic Predisposition to Disease. Genotype. Humans. India. Infant. Male. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Risk Factors

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  • (PMID = 20367562.001).
  • [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] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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71. Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia. Cancer Res; 2010 Oct 15;70(20):8097-107
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  • [Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.
  • Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.
  • Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.
  • NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.
  • NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.
  • Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.
  • [MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects


72. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.
  • It may also prove to have a useful role in both diagnosis and prognosis.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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73. Litzow MR, Tarima S, Pérez WS, Bolwell BJ, Cairo MS, Camitta BM, Cutler CS, de Lima M, Dipersio JF, Gale RP, Keating A, Lazarus HM, Luger S, Marks DI, Maziarz RT, McCarthy PL, Pasquini MC, Phillips GL, Rizzo JD, Sierra J, Tallman MS, Weisdorf DJ: Allogeneic transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia. Blood; 2010 Mar 4;115(9):1850-7
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  • [Title] Allogeneic transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia.
  • Therapy-related myelodysplastic syndromes (t-MDSs) and acute myeloid leukemia (t-AML) have a poor prognosis with conventional therapy.
  • Disease-free (DFS) and overall survival (OS) were 32% (95% CI, 29-36) and 37% (34-41) at 1 year and 21% (18-24) and 22% (19-26) at 5 years, respectively.


74. Hiramatsu H, Morishima T, Nakanishi H, Mizushima Y, Miyazaki M, Matsubara H, Kobayashi M, Nakahata T, Adachi S: Successful treatment of a patient with Klinefelter's syndrome complicated by mediastinal germ cell tumor and AML(M7). Bone Marrow Transplant; 2008 May;41(10):907-8
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  • [Title] Successful treatment of a patient with Klinefelter's syndrome complicated by mediastinal germ cell tumor and AML(M7).
  • [MeSH-major] Klinefelter Syndrome / complications. Klinefelter Syndrome / therapy. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / etiology. Mediastinal Neoplasms / etiology. Mediastinal Neoplasms / surgery. Teratoma / etiology. Teratoma / surgery
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cord Blood Stem Cell Transplantation. Humans. Male

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  • (PMID = 18223696.001).
  • [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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75. Fonseca C, Soiffer R, Ho V, Vanneman M, Jinushi M, Ritz J, Neuberg D, Stone R, DeAngelo D, Dranoff G: Protein disulfide isomerases are antibody targets during immune-mediated tumor destruction. Blood; 2009 Feb 19;113(8):1681-8
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  • Toward this end, we screened a murine renal cell carcinoma cDNA expression library with sera from mice vaccinated with irradiated tumor cells engineered to secrete granulocyte macrophage colony-stimulating factor (GM-CSF).
  • Multiple nonmutated, overexpressed proteins that function in tumor cell migration, protein/nucleic acid homeostasis, metabolism, and stress responses were detected.
  • High titer antibodies to human PDI were similarly induced in an acute myeloid leukemia patient who achieved a complete response after vaccination with irradiated, autologous GM-CSF-secreting tumor cells in the setting of nonmyeloablative allogeneic bone marrow transplantation.
  • Moreover, ERp5, a closely related disulfide isomerase involved in major histocompatibility complex (MHC) class I chain-related protein A (MICA) shedding, also evoked potent humoral reactions in diverse solid and hematologic malignancy patients who responded to GM-CSF-secreting tumor cell vaccines or antibody blockade of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4).

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  • [Cites] J Clin Oncol. 2003 Feb 15;21(4):624-30 [12586798.001]
  • [Cites] Nat Med. 2007 Sep;13(9):1050-9 [17704786.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4712-7 [12682289.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8874-9 [12847287.001]
  • [Cites] J Clin Oncol. 2003 Sep 1;21(17):3343-50 [12947071.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):11-22 [14708024.001]
  • [Cites] Br J Dermatol. 2004 Feb;150(2):252-8 [14996095.001]
  • [Cites] Biochim Biophys Acta. 2004 Jun 1;1699(1-2):35-44 [15158710.001]
  • [Cites] Cancer Res. 2000 May 1;60(9):2444-8 [10811122.001]
  • [Cites] FEBS Lett. 2000 Jun 16;475(2):89-92 [10858494.001]
  • [Cites] Cancer Res. 2000 Jun 15;60(12):3239-46 [10866317.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):162-71 [11196155.001]
  • [Cites] Arthritis Res. 2000;2(5):407-14 [11056675.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):880-3 [11221874.001]
  • [Cites] Annu Rev Immunol. 2001;19:225-52 [11244036.001]
  • [Cites] J Exp Med. 2001 Oct 1;194(7):893-902 [11581312.001]
  • [Cites] Trends Immunol. 2002 Jan;23(1):31-9 [11801452.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):796-800 [11830535.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6919-24 [11983866.001]
  • [Cites] J Cell Physiol. 2002 Nov;193(2):154-63 [12384992.001]
  • [Cites] Immunol Rev. 2002 Oct;188:9-21 [12445277.001]
  • [Cites] Lupus. 2004;13(6):463-8 [15303574.001]
  • [Cites] Nat Med. 2004 Sep;10(9):942-9 [15322536.001]
  • [Cites] Nature. 1990 Feb 1;343(6257):425-30 [1967820.001]
  • [Cites] Biochem Soc Symp. 1989;55:167-92 [2619767.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3539-43 [8097319.001]
  • [Cites] Autoimmunity. 1991;9(1):13-9 [1669843.001]
  • [Cites] Science. 1994 May 13;264(5161):961-5 [7513904.001]
  • [Cites] Int J Cancer. 1997 May 2;71(3):396-401 [9139875.001]
  • [Cites] Exp Hematol. 1997 Jul;25(7):601-7 [9216735.001]
  • [Cites] Immunity. 1997 Oct;7(4):445-50 [9354465.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10067-71 [9707601.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13141-6 [9789055.001]
  • [Cites] J Exp Med. 1998 Dec 21;188(12):2357-68 [9858522.001]
  • [Cites] Nat Med. 1999 Feb;5(2):221-5 [9930872.001]
  • [Cites] Oncogene. 1999 Feb 18;18(7):1435-46 [10050880.001]
  • [Cites] Biochem J. 1999 Apr 1;339 ( Pt 1):1-10 [10085220.001]
  • [Cites] J Exp Med. 1999 Aug 2;190(3):355-66 [10430624.001]
  • [Cites] Int J Cancer. 1999 Nov 12;83(4):456-64 [10508479.001]
  • [Cites] Immunity. 1999 Sep;11(3):263-70 [10514004.001]
  • [Cites] EMBO Rep. 2005 Jan;6(1):28-32 [15643448.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 3;102(18):6243-4 [15851655.001]
  • [Cites] Nature. 2005 Aug 25;436(7054):1186-90 [15995699.001]
  • [Cites] Curr Top Microbiol Immunol. 2006;298:121-38 [16329186.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18538-43 [16344461.001]
  • [Cites] J Clin Immunol. 2005 Nov;25(6):534-40 [16380817.001]
  • [Cites] Annu Rev Med. 2006;57:33-47 [16409135.001]
  • [Cites] Adv Immunol. 2006;90:297-339 [16730267.001]
  • [Cites] Adv Immunol. 2006;90:341-68 [16730268.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9190-5 [16754847.001]
  • [Cites] Immunity. 2006 Sep;25(3):429-40 [16973388.001]
  • [Cites] Immunity. 2006 Sep;25(3):417-28 [16973389.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1960-4 [17008531.001]
  • [Cites] Cancer Res. 2006 Oct 15;66(20):9895-902 [17047051.001]
  • [Cites] Endocr Relat Cancer. 2006 Dec;13 Suppl 1:S125-35 [17259553.001]
  • [Cites] Annu Rev Immunol. 2007;25:267-96 [17134371.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):745-7 [17429391.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6696-701 [17420453.001]
  • [Cites] J Clin Invest. 2007 May;117(5):1195-203 [17476349.001]
  • [Cites] Nature. 2007 May 24;447(7143):482-6 [17495932.001]
  • [Cites] J Clin Invest. 2007 Jul;117(7):1902-13 [17557120.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):108-13 [17692803.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2385-8 [17786234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3398-403 [12626761.001]
  • (PMID = 19008459.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Cancer Vaccines; 0 / Ctla4 protein, mouse; 0 / Histocompatibility Antigens Class I; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 5.3.4.1 / PDIA6 protein, human; EC 5.3.4.1 / Protein Disulfide-Isomerases
  • [Other-IDs] NLM/ PMC2647666
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76. Buck AK, Bommer M, Juweid ME, Glatting G, Stilgenbauer S, Mottaghy FM, Schulz M, Kull T, Bunjes D, Möller P, Döhner H, Reske SN: First demonstration of leukemia imaging with the proliferation marker 18F-fluorodeoxythymidine. J Nucl Med; 2008 Nov;49(11):1756-62
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  • [Title] First demonstration of leukemia imaging with the proliferation marker 18F-fluorodeoxythymidine.
  • Acute myeloid leukemia (AML) is a neoplasm of hematopoietic stem cells with partial or complete loss of the ability to differentiate but with preserved proliferation capacity.
  • The aim of our study was to evaluate if the in vivo proliferation marker 3'-deoxy-3'-18F-fluorothymidine (FLT) is suitable for visualizing leukemia manifestation sites and if 18F-FLT is a surrogate marker for disease activity.
  • 18F-FLT PET in 10 patients with benign pulmonary nodules and the absence of malignant or inflammatory disease served as controls.
  • Outside bone marrow, focal 18F-FLT uptake showed extramedullary manifestation sites of leukemia in 4 patients (meningeal disease, pericardial, abdominal, testicular, and lymph node), proven by other diagnostic procedures.
  • CONCLUSION: This pilot study indicated that PET using 18F-FLT is able to visualize extramedullary manifestation sites of AML and reflects disease activity.
  • [MeSH-major] Dideoxynucleosides. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / radionuclide imaging
  • [MeSH-minor] Adult. Aged. Bone Marrow / metabolism. Case-Control Studies. Cell Proliferation. Female. Humans. Male. Middle Aged. Positron-Emission Tomography. Tissue Distribution. Young Adult

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  • (PMID = 18927328.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dideoxynucleosides; PG53R0DWDQ / alovudine
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77. Sasaki H, Nishikata I, Shiraga T, Akamatsu E, Fukami T, Hidaka T, Kubuki Y, Okayama A, Hamada K, Okabe H, Murakami Y, Tsubouchi H, Morishita K: Overexpression of a cell adhesion molecule, TSLC1, as a possible molecular marker for acute-type adult T-cell leukemia. Blood; 2005 Feb 1;105(3):1204-13
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  • [Title] Overexpression of a cell adhesion molecule, TSLC1, as a possible molecular marker for acute-type adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) caused by human T-cell leukemia virus type 1 (HTLV-1) infection, occurs in 2% to 4% of the HTLV-1 carriers with a long latent period, suggesting that additional alterations participate in the development of ATL.
  • To characterize and identify novel markers of ATL, we examined the expression profiles of more than 12 000 genes in 8 cases of acute-type ATL using microarray.
  • TSLC1 is a cell adhesion molecule originally identified as a tumor suppressor in the lung but lacks its expression in normal or activated T cells.
  • We confirmed ectopic expression of the TSLC1 in all acute-type ATL cells and in 7 of 10 ATL- or HTLV-1-infected T-cell lines.
  • Introduction of TSLC1 into a human ATL cell line ED enhanced both self-aggregation and adhesion ability to vascular endothelial cells.
  • These results suggested that the ectopic expression of TSLC1 could provide a novel marker for acute-type ATL and may participate in tissue invasion, a characteristic feature of the malignant ATL cells.
  • [MeSH-major] Immunoglobulins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Membrane Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Cell Adhesion Molecules. Cell Line. Endothelium, Vascular / pathology. Female. Humans. Leukocyte Count. Male. Middle Aged. Tumor Suppressor Proteins

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  • (PMID = 15471956.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CADM1 protein, human; 0 / Cell Adhesion Molecules; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / Tumor Suppressor Proteins
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78. Chan L, Hardwick N, Darling D, Galea-Lauri J, Gäken J, Devereux S, Kemeny M, Mufti G, Farzaneh F: IL-2/B7.1 (CD80) fusagene transduction of AML blasts by a self-inactivating lentiviral vector stimulates T cell responses in vitro: a strategy to generate whole cell vaccines for AML. Mol Ther; 2005 Jan;11(1):120-31
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  • [Title] IL-2/B7.1 (CD80) fusagene transduction of AML blasts by a self-inactivating lentiviral vector stimulates T cell responses in vitro: a strategy to generate whole cell vaccines for AML.
  • However, poor rates of gene transfer and inefficient expression of multiple transgenes encoded by single vectors have hampered the development of such autologous tumor cell vaccines for clinical trials in acute myeloid leukemia (AML) patients.
  • [MeSH-major] Antigens, CD80 / metabolism. Cancer Vaccines / immunology. Interleukin-2 / metabolism. Lentivirus / genetics. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / metabolism. T-Lymphocytes / immunology
  • [MeSH-minor] Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Cell Proliferation. Cells, Cultured. Gene Expression Regulation, Neoplastic. Genetic Vectors / genetics. Humans. Lymphocyte Activation. Th1 Cells / immunology. Th1 Cells / metabolism. Transduction, Genetic

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  • (PMID = 15585413.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Cancer Vaccines; 0 / Interleukin-2
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79. Yang J, Zhou X, Wang B, Gao C, Zhang RD, Li B: [Severe hypercalcemia complicated in acute lymphoblastic leukemia (ALL) with E2A-HLF fusion gene: report of two cases and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2009 Sep;30(9):615-8
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  • [Title] [Severe hypercalcemia complicated in acute lymphoblastic leukemia (ALL) with E2A-HLF fusion gene: report of two cases and literature review].
  • OBJECTIVE: To improve the understanding of severe hypercalcemia complicated in acute lymphoblastic leukemia (ALL) with E2A-HLF fusion gene, and to explore the mechanism of pathogenesis and the relationship between the special gene translocation and severe hypercalcemia.
  • RESULTS: Two patients with E2A-HLF fusion gene, which is generated by t(17;19) (q22, p13) translocation, suffered relapse of leukemia three months after chemotherapy, and developed severe hypercalcemia.
  • In B cell lymphoblastic leukemia with E2A-HLF fusion gene, the fusion gene showed be closely monitored for evaluating the disease situation.
  • [MeSH-major] DNA-Binding Proteins / genetics. Hypercalcemia / etiology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 19954622.001).
  • [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] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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80. Harter C, Schulze B, Goldschmidt H, Benner A, Geiss HK, Hoppe-Tichy T, Ho AD, Egerer G: Piperacillin/tazobactam vs ceftazidime in the treatment of neutropenic fever in patients with acute leukemia or following autologous peripheral blood stem cell transplantation: a prospective randomized trial. Bone Marrow Transplant; 2006 Feb;37(4):373-9
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  • [Title] Piperacillin/tazobactam vs ceftazidime in the treatment of neutropenic fever in patients with acute leukemia or following autologous peripheral blood stem cell transplantation: a prospective randomized trial.
  • Piperacillin/tazobactam was compared with ceftazidime for the empirical treatment of febrile neutropenia in patients with acute leukemia or following autologous peripheral blood stem cell transplantation.
  • [MeSH-major] Ceftazidime / therapeutic use. Fever / drug therapy. Leukemia / complications. Neutropenia / complications. Penicillanic Acid / analogs & derivatives. Peripheral Blood Stem Cell Transplantation. Piperacillin / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Aged. Anti-Bacterial Agents / economics. Anti-Bacterial Agents / therapeutic use. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prospective Studies. Survival Rate. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 16400334.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 87-53-6 / Penicillanic Acid; 9M416Z9QNR / Ceftazidime; SE10G96M8W / tazobactam; X00B0D5O0E / Piperacillin
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81. Sato K, Nakaoka T, Yamashita N, Yagita H, Kawasaki H, Morimoto C, Baba M, Matsuyama T: TRAIL-transduced dendritic cells protect mice from acute graft-versus-host disease and leukemia relapse. J Immunol; 2005 Apr 1;174(7):4025-33
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  • [Title] TRAIL-transduced dendritic cells protect mice from acute graft-versus-host disease and leukemia relapse.
  • TRAIL preferentially induces apoptotic cell death in a wide variety of transformed cells, whereas it induces no apoptosis, but inhibits activation of Ag-specific T cells via blockade of cell cycle progression.
  • We report in this study the potential usefulness of TRAIL-transduced dendritic cells (DCs) for the treatment of lethal acute graft-vs-host disease (GVHD) and leukemia relapse.
  • In addition, treatment with genetically modified DCs expressing TRAIL of allogeneic BM transplants recipients with leukemia was effective for protection against acute GVHD and leukemia relapse.
  • Thus, gene transfer of TRAIL to DCs is a novel modality for the treatment of acute GVHD and leukemia relapse by selective targeting of pathogenic T cells and leukemic cells.
  • [MeSH-major] Genetic Therapy / methods. Graft vs Host Disease / therapy. Leukemia / therapy. Membrane Glycoproteins / therapeutic use. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Acute Disease. Animals. Apoptosis / drug effects. Apoptosis Regulatory Proteins. Bone Marrow Transplantation / adverse effects. CD4-Positive T-Lymphocytes / immunology. Dendritic Cells / metabolism. Humans. Mice. Mice, Inbred BALB C. Secondary Prevention. TNF-Related Apoptosis-Inducing Ligand. Transduction, Genetic

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  • (PMID = 15778360.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha
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82. Dong S, Kang S, Gu TL, Kardar S, Fu H, Lonial S, Khoury HJ, Khuri F, Chen J: 14-3-3 Integrates prosurvival signals mediated by the AKT and MAPK pathways in ZNF198-FGFR1-transformed hematopoietic cells. Blood; 2007 Jul 1;110(1):360-9
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  • Human 8p11 stem cell leukemia/lymphoma syndrome usually presents as a myeloproliferative disorder (MPD) that evolves to acute myeloid leukemia and/or lymphoma.
  • Moreover, purified recombinant transactivator of transcription (TAT)-conjugated R18 proteins effectively transduced into human leukemia cells and induced significant apoptosis in KG-1a cells expressing FGFR1OP2-FGFR1 fusion tyrosine kinase but not in control HL-60 and Jurkat T cells.
  • Disrupting 14-3-3-ligand association may represent an effective therapeutic strategy to treat 8p11 stem cell MPD.


83. Crespo M, Villamor N, Giné E, Muntañola A, Colomer D, Marafioti T, Jones M, Camós M, Campo E, Montserrat E, Bosch F: ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia. Clin Cancer Res; 2006 Feb 1;12(3 Pt 1):726-34
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  • [Title] ZAP-70 expression in normal pro/pre B cells, mature B cells, and in B-cell acute lymphoblastic leukemia.
  • PURPOSE: The ZAP-70 gene is normally expressed in T and natural killer cells, where it is required for the T-cell receptor (TCR) signaling.
  • More recently, it has been described that ZAP-70 contributes to the B-cell development at early stages of B-cell differentiation in mice.
  • The purpose was to investigate the presence of ZAP-70 in normal pro/pre B cells and mature B cells and in tumoral cells from B-acute lymphoblastic leukemias (B-ALL).
  • Among tumoral cells, ZAP-70 was expressed in 56% of B-ALLs with pro/pre B-cell phenotype and in 4 of 6 Burkitt/ALL lymphomas.
  • CONCLUSIONS: Among normal B-cell subsets, ZAP-70 was found expressed in normal pro/pre B cells but not in a significant proportion of normal B cells with mature phenotype.
  • The lack of ZAP-70 expression in normal mature B cells suggests that its expression in mature-derived neoplasms with different cellular origin, such as Burkitt's lymphoma and chronic lymphocytic leukemia, might be due to an aberrant phenomenon.
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA Mutational Analysis. Humans. Middle Aged. Phenotype. Phosphorylation. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 16467082.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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84. Guinn BA, Bullinger L, Thomas NS, Mills KI, Greiner J: SSX2IP expression in acute myeloid leukaemia: an association with mitotic spindle failure in t(8;21), and cell cycle in t(15;17) patients. Br J Haematol; 2008 Jan;140(2):250-1
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  • [Title] SSX2IP expression in acute myeloid leukaemia: an association with mitotic spindle failure in t(8;21), and cell cycle in t(15;17) patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / blood. Neoplasm Proteins / blood. Repressor Proteins / blood. Spindle Apparatus / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Cycle / genetics. Humans

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  • (PMID = 18028484.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Repressor Proteins; 164289-47-8 / synovial sarcoma X breakpoint proteins
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85. Cox CV, Diamanti P, Evely RS, Kearns PR, Blair A: Expression of CD133 on leukemia-initiating cells in childhood ALL. Blood; 2009 Apr 2;113(14):3287-96
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  • [Title] Expression of CD133 on leukemia-initiating cells in childhood ALL.
  • Optimization of therapy for childhood acute lymphoblastic leukemia (ALL) requires a greater understanding of the cells that proliferate to maintain this malignancy because a significant number of cases relapse, resulting from failure to eradicate the disease.
  • Moreover, these CD133(+)/CD19(-) cells could self-renew to engraft serial nonobese diabetic-severe combined immunodeficient recipients and differentiate in vivo to produce leukemias with similar immunophenotypes and karyotypes to the diagnostic samples.
  • Furthermore, these CD133(+)/CD19(-) ALL cells were more resistant to treatment with dexamethasone and vincristine, key components in childhood ALL therapy, than the bulk leukemia population.
  • These data suggest that leukemia-initiating cells in childhood B-ALL have a primitive CD133(+)/CD19(-) and CD38(-) phenotype.
  • [MeSH-major] Antigens, CD / metabolism. Glycoproteins / metabolism. Neoplastic Stem Cells / metabolism. Peptides / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Animals. Antigens, CD19 / metabolism. Antigens, CD38 / metabolism. Cell Proliferation. Child. Child, Preschool. Gene Rearrangement, T-Lymphocyte / physiology. Humans. Immunoglobulin Heavy Chains / genetics. Membrane Glycoproteins / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Phenotype. Transplantation, Heterologous. Tumor Cells, Cultured

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  • [CommentIn] Blood. 2009 Apr 30;113(18):4476-7; author reply 4477 [19407001.001]
  • (PMID = 19147788.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Glycoproteins; 0 / Immunoglobulin Heavy Chains; 0 / Membrane Glycoproteins; 0 / Peptides; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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86. Miyakura T, Yamamoto T, Kurashige Y, Nagai A, Iguchi T, Aota Y, Tsuboi R: Leukemia cutis originating in the extravasation site of i.v. gabexate mesilate infusion. J Dermatol; 2008 Jan;35(1):29-32
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  • [Title] Leukemia cutis originating in the extravasation site of i.v. gabexate mesilate infusion.
  • Leukemia cutis is a localized or disseminated skin infiltration by leukemic cells.
  • A 64-year-old man was diagnosed with acute myeloid leukemia (AML) complicated by disseminated intravascular coagulation.
  • Immunohistochemical staining for intercellular adhesion molecule-1 and platelet/endothelial cell adhesion molecule-1 showed strong expression of endothelial cells and leukemic cells.
  • We speculate that the gabexate mesilate might have played a role in the induction of leukemia cutis via adhesion molecules in our case.
  • [MeSH-major] Anticoagulants / adverse effects. Extravasation of Diagnostic and Therapeutic Materials / complications. Gabexate / adverse effects. Leukemia, Myeloid, Acute / etiology. Skin Neoplasms / etiology

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  • (PMID = 18181773.001).
  • [ISSN] 0385-2407
  • [Journal-full-title] The Journal of dermatology
  • [ISO-abbreviation] J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antigens, CD31; 126547-89-5 / Intercellular Adhesion Molecule-1; 4V7M9137X9 / Gabexate
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87. Walters DK, Mercher T, Gu TL, O'Hare T, Tyner JW, Loriaux M, Goss VL, Lee KA, Eide CA, Wong MJ, Stoffregen EP, McGreevey L, Nardone J, Moore SA, Crispino J, Boggon TJ, Heinrich MC, Deininger MW, Polakiewicz RD, Gilliland DG, Druker BJ: Activating alleles of JAK3 in acute megakaryoblastic leukemia. Cancer Cell; 2006 Jul;10(1):65-75
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  • [Title] Activating alleles of JAK3 in acute megakaryoblastic leukemia.
  • Tyrosine kinases are aberrantly activated in numerous malignancies, including acute myeloid leukemia (AML).
  • This allowed the identification of an activating mutation (A572V) in the JAK3 pseudokinase domain in the acute megakaryoblastic leukemia (AMKL) cell line CMK.
  • JAK3(A572V), JAK3(V722I), and JAK3(P132T) each transform Ba/F3 cells to factor-independent growth, and JAK3(A572V) confers features of megakaryoblastic leukemia in a murine model.

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  • (PMID = 16843266.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-04; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / JAK3 protein, human; 0 / Mutant Proteins; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 0 / RNA, Small Interfering; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Jak3 protein, mouse; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human
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88. Cauwelier B, Dastugue N, Cools J, Poppe B, Herens C, De Paepe A, Hagemeijer A, Speleman F: Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes. Leukemia; 2006 Jul;20(7):1238-44
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  • [Title] Molecular cytogenetic study of 126 unselected T-ALL cases reveals high incidence of TCRbeta locus rearrangements and putative new T-cell oncogenes.
  • Chromosomal aberrations of T-cell receptor (TCR) gene loci often involve the TCRalphadelta (14q11) locus and affect various known T-cell oncogenes.
  • Therefore, we initiated a screening of 126 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma cases and 19 T-ALL cell lines using FISH break-apart assays for the different TCR loci.
  • Some of these chromosome aberrations target new putative T-cell oncogenes at chromosome 11q24, 20p12 and 6q22.
  • Five patients and one cell line carried chromosomal rearrangements affecting both TCRbeta and TCRalphadelta loci.
  • In conclusion, this study presents the first inventory of chromosomal rearrangements of TCR loci in T-ALL, revealing an unexpected high number of cryptic chromosomal rearrangements of the TCRbeta locus and further broadening the spectrum of genes putatively implicated in T-cell oncogenesis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / genetics. Genes, T-Cell Receptor beta / genetics. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Genes, T-Cell Receptor alpha / genetics. Genes, T-Cell Receptor delta / genetics. Humans. In Situ Hybridization, Fluorescence. Incidence. Male. Middle Aged. Retrospective Studies. Translocation, Genetic

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  • (PMID = 16673021.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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89. Qian W, Liu J, Jin J, Ni W, Xu W: Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1. Leuk Res; 2007 Mar;31(3):329-39
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  • [Title] Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1.
  • Although recent data shows that arsenic trioxide (As2O3) is capable of inducing cell death via cell cycle arrest and apoptosis both in acute promyelocytic leukemia (APL) and in non-APL cells, the mechanisms of As2O3-mediated cell death are not fully understood.
  • In this study, we investigated the in vitro effects of As2O3 on cell growth inhibition and cell death in human T-lymphocytic leukemia and myelodysplastic syndrome (MDS) cell lines.
  • Autophagic cell death (programmed cell death type II) and apoptosis (programmed cell death type I) were activated together in leukemia cell lines after exposed to As2O3.
  • Furthermore, 3-methyladenine (an autophagy inhibitor) significantly reduced autophagic cell death and sequentially induced apoptosis.
  • Finally, leukemia cells treated with 4 microM As2O3 showed a considerable up-regulation of Beclin-1 (a Bcl-2-interacting protein) expression, which was independent of transcription of mRNA and required protein synthesis.
  • In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells.
  • These results may lead to a better understanding of the mechanism of action of As2O3, and provide a suggestion that As2O3 may be of therapeutic value for the treatment of patients with human T-lymphocytic leukemia and myelodysplastic syndrome.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Arsenicals / pharmacology. Leukemia, T-Cell / drug therapy. Membrane Proteins / metabolism. Myelodysplastic Syndromes / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Structure-Activity Relationship. Up-Regulation / drug effects

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  • (PMID = 16882451.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Oxides; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S7V92P67HO / arsenic trioxide
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90. Bornhauser BC, Bonapace L, Lindholm D, Martinez R, Cario G, Schrappe M, Niggli FK, Schäfer BW, Bourquin JP: Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway. Blood; 2007 Sep 15;110(6):2084-91
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  • [Title] Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway.
  • Incorporation of apoptosis-inducing agents into current therapeutic regimens is an attractive strategy to improve treatment for drug-resistant leukemia.
  • We tested the potential of arsenic trioxide (ATO) to restore the response to dexamethasone in glucocorticoid (GC)-resistant acute lymphoblastic leukemia (ALL).
  • Low-dose ATO markedly increased in vitro GC sensitivity of ALL cells from T-cell and precursor B-cell ALL patients with poor in vivo response to prednisone.
  • In GC-resistant cell lines, this effect was mediated, at least in part, by inhibition of Akt and affecting downstream Akt targets such as Bad, a proapoptotic Bcl-2 family member, and the X-linked inhibitor of apoptosis protein (XIAP).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / administration & dosage. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Glucocorticoids / pharmacology. Oxides / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Caspases. Cell Line, Tumor / drug effects. Cell Survival / drug effects. Drug Synergism. Humans. Neoplasm, Residual / diagnosis. Phosphorylation / drug effects. Prednisone / pharmacology. RNA, Small Interfering / pharmacology. Reactive Oxygen Species / metabolism. Remission Induction. Sirolimus / pharmacology. Transfection. X-Linked Inhibitor of Apoptosis Protein / metabolism. bcl-Associated Death Protein / metabolism


91. Bernaldez-Rios R, Ortega-Alvarez MC, Perez-Saldivar ML, Alatoma-Medina NE, Del Campo-Martinez Mde L, Rodriguez-Zepeda Mdel C, Montero-Ponce I, Franco-Ornelas S, Fernandez-Castillo G, Nuñez-Villegas NN, Taboada-Flores MA, Flores-Lujano J, Argüelles-Sanchez ME, Juarez-Ocaña S, Fajardo-Gutierrez A, Mejia-Arangure JM: The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City. J Pediatr Hematol Oncol; 2008 Mar;30(3):199-203
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  • [Title] The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City.
  • The objective of this population-based survey was to assess the peak age of incidence of B-cell precursor acute lymphoblastic leukemia (ALL) in children in Mexico City (MC).
  • All patients were classified according to their immunophenotype, and only B-cell precursor and T-lineage were analyzed.
  • The frequency of B-cell precursor ALL was 76.1%, whereas T lineage ALL showed a frequency of 23.6%.
  • B-cell precursor ALL was the major contributor to peak age; T lineage ALL showed a peak among 1 and 3 years of age.
  • We conclude that the age peak for children with ALL in MC is within the ranges reported for developed countries and that B-cell precursor ALL is the main contributor to these peak.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology


92. Wang L, Wang J, Blaser BW, Duchemin AM, Kusewitt DF, Liu T, Caligiuri MA, Briesewitz R: Pharmacologic inhibition of CDK4/6: mechanistic evidence for selective activity or acquired resistance in acute myeloid leukemia. Blood; 2007 Sep 15;110(6):2075-83
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  • [Title] Pharmacologic inhibition of CDK4/6: mechanistic evidence for selective activity or acquired resistance in acute myeloid leukemia.
  • Entry into the cell cycle is mediated by cyclin-dependent kinase 4/6 (CDK4/6) activation, followed by CDK2 activation.
  • We found that pharmacologic inhibition of the Flt3 internal tandem duplication (ITD), a mutated receptor tyrosine kinase commonly found in patients with acute myelogenous leukemia (AML), led to the down-regulation of cyclin D2 and D3 followed by retinoblastoma protein (pRb) dephosphorylation and G(1) cell-cycle arrest.
  • Indeed, single-agent PD0332991, a selective CDK4/6 inhibitor, caused sustained cell-cycle arrest in Flt3 ITD AML cell lines and prolonged survival in an in vivo model of Flt3 ITD AML.
  • PD0332991 caused an initial cell-cycle arrest in well-established Flt3 wild-type (wt) AML cell lines, but this was overcome by down-regulation of p27(Kip) and reactivation of CDK2.
  • In summary, the mechanism of cell-cycle arrest after treatment of Flt3 ITD AML with a Flt3 inhibitor involves down-regulation of cyclin D2 and D3.
  • [MeSH-major] Cyclin-Dependent Kinase 4 / antagonists & inhibitors. Cyclin-Dependent Kinase 6 / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Animals. Blotting, Western. Bone Marrow Cells / metabolism. Cell Proliferation. Cyclin D2. Cyclin D3. Cyclin-Dependent Kinase Inhibitor p27. Cyclins / metabolism. G1 Phase / drug effects. Humans. Immunoprecipitation. Indoles / pharmacology. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mice, SCID. Morpholines / pharmacology. Mutation. Phosphorylation. Piperazines / pharmacology. Pyridines / pharmacology. Pyrroles / pharmacology. Retinoblastoma Protein / metabolism. Signal Transduction. Tumor Cells, Cultured

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  • (PMID = 17537993.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-((5-fluoro-2-oxo-1,2-dihydro-3H-indol-3-ylidene)methyl)-N-(2-hydroxy-3-morpholin-4-ylpropyl)-2,4-dimethyl-1H-pyrrole-3-carboxamide; 0 / CCND2 protein, human; 0 / CCND3 protein, human; 0 / CDKN1B protein, human; 0 / Ccnd3 protein, mouse; 0 / Cyclin D2; 0 / Cyclin D3; 0 / Cyclins; 0 / Indoles; 0 / Intracellular Signaling Peptides and Proteins; 0 / Morpholines; 0 / Piperazines; 0 / Pyridines; 0 / Pyrroles; 0 / Retinoblastoma Protein; 0 / THRX 165724; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; G9ZF61LE7G / palbociclib
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93. Chan EM, Comer EM, Brown FC, Richkind KE, Holmes ML, Chong BH, Shiffman R, Zhang DE, Slovak ML, Willman CL, Noguchi CT, Li Y, Heiber DJ, Kwan L, Chan RJ, Vance GH, Ramsey HC, Hromas RA: AML1-FOG2 fusion protein in myelodysplasia. Blood; 2005 Jun 1;105(11):4523-6
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  • Core binding factor (CBF) participates in specification of the hematopoietic stem cell and functions as a critical regulator of hematopoiesis.
  • Translocation or point mutation of acute myeloid leukemia 1 (AML1)/RUNX1, which encodes the DNA-binding subunit of CBF, plays a central role in the pathogenesis of acute myeloid leukemia and myelodysplasia.

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  • (PMID = 15705784.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-FOG2 fusion protein, human; 0 / CCAAT-Binding Factor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Phosphoproteins; 0 / Repressor Proteins; 0 / Transcription Factors; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / C-terminal binding protein
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94. Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H: Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening. Leuk Lymphoma; 2007 May;48(5):978-86
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  • Biphenotypic acute leukemia (BAL) is a relatively rare subtype of acute leukemia characterized by the presence of both myeloid and lymphoid cell surface antigens.
  • Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in leukemia patients, especially in those with refractory disease.
  • Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of acute leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Leukemia / metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Cell Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic

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  • (PMID = 17487742.001).
  • [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 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
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95. Henrich S, Crossett B, Christopherson RI: Differentially expressed nuclear proteins in human CCRF-CEM, HL-60, MEC-1 and Raji cells correlate with cellular properties. Proteomics Clin Appl; 2007 Oct;1(10):1252-65
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  • The human cell lines CCRF-CEM (T-cell acute lymphocytic leukemia), HL-60 (acute myeloid leukemia), MEC-1 (B-cell chronic lymphocytic leukemia) and Raji (Burkitt's B-cell lymphoma) have been analysed for differences in their nuclear proteomes.
  • Using 2-D DIGE, 55 nuclear proteins have been identified that are differentially expressed (p<0.025) between the four cell lines, including proteins associated with transcription, proliferation, DNA repair and apoptosis.
  • Of these 55 proteins, 22 were over-expressed in just one cell line, and four were down-regulated in one cell line.
  • Proteins uniquely over-expressed between myeloid and lymphoid cell lines include those that may have use as markers for diagnosis, disease progression and B-cell maturation and differentiation.
  • Expression of various proliferation-associated nuclear proteins correlated with relative growth rates of the cell lines, giving these proteins potential diagnostic applications for distinction of chronic versus acute subtypes of haematological malignancies.
  • Identification of these differentially expressed nuclear proteins should facilitate elucidation of the molecular mechanisms underlying leukocyte differentiation and transformation to leukemias and lymphomas.
  • The nuclear expression profiles should enable classification of subtypes of leukemia, and identify potential nuclear protein targets for development of diagnostic and therapeutic strategies.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136623.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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96. Zhao L, Cannons JL, Anderson S, Kirby M, Xu L, Castilla LH, Schwartzberg PL, Bosselut R, Liu PP: CBFB-MYH11 hinders early T-cell development and induces massive cell death in the thymus. Blood; 2007 Apr 15;109(8):3432-40
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  • [Title] CBFB-MYH11 hinders early T-cell development and induces massive cell death in the thymus.
  • Recent studies suggest that the chromosome 16 inversion, associated with acute myeloid leukemia M4Eo, takes place in hematopoietic stem cells.
  • Here we studied T-cell development in mice expressing Cbfb-MYH11 and compared them with mice compound-heterozygous for a Cbfb null and a hypomorphic GFP knock-in allele (Cbfb(-/GFP)), which had severe Cbfb deficiency.
  • Our data suggest that Cbfb-MYH11 suppressed Cbfb in several stages of T-cell development and provide a mechanism for CBFB-MYH11 association with myeloid but not lymphoid leukemia.

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  • [Cites] Cancer Genet Cytogenet. 2005 Jan 15;156(2):175-8 [15642400.001]
  • [Cites] J Immunol. 1997 Dec 1;159(11):5318-28 [9548471.001]
  • [Cites] Annu Rev Immunol. 2005;23:601-49 [15771582.001]
  • [Cites] Blood. 2005 Jul 15;106(2):494-504 [15784726.001]
  • [Cites] Nat Rev Immunol. 2005 Jul;5(7):571-7 [15999096.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10205-19 [16287839.001]
  • [Cites] Cancer Cell. 2006 Jan;9(1):57-68 [16413472.001]
  • [Cites] Blood. 2007 Jan 1;109(1):11-21 [16940420.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2449-56 [12239155.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):1083-96 [12453416.001]
  • [Cites] Nat Genet. 2002 Dec;32(4):639-44 [12434156.001]
  • [Cites] Cell. 2002 Nov 27;111(5):621-33 [12464175.001]
  • [Cites] Blood Cells Mol Dis. 2003 Mar-Apr;30(2):164-9 [12732179.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7731-6 [12796513.001]
  • [Cites] Blood. 2004 Jan 15;103(2):562-70 [14504086.001]
  • [Cites] Oncogene. 2000 Jan 6;19(1):106-14 [10644985.001]
  • [Cites] EMBO J. 2000 Jun 15;19(12):3004-15 [10856244.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Cell. 2001 Mar 9;104(5):755-67 [11257229.001]
  • [Cites] Int Rev Immunol. 2001 Feb;20(1):45-64 [11342297.001]
  • [Cites] Immunity. 2001 Nov;15(5):763-74 [11728338.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11590-5 [9751710.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7432-43 [9819429.001]
  • [Cites] Development. 1999 Jun;126(11):2563-75 [10226014.001]
  • [Cites] Nat Struct Biol. 1999 Jul;6(7):620-3 [10404215.001]
  • [Cites] Nat Struct Biol. 1999 Jul;6(7):624-7 [10404216.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):144-6 [10508507.001]
  • [Cites] Immunity. 1999 Sep;11(3):281-8 [10514006.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15678-87 [14747476.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4924-9 [15044690.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4297-307 [15156186.001]
  • [Cites] Adv Immunol. 2004;84:201-38 [15246254.001]
  • [Cites] Cell. 1991 Nov 29;67(5):879-88 [1835668.001]
  • [Cites] Science. 1993 Feb 5;259(5096):822-5 [8430336.001]
  • [Cites] Virology. 1993 May;194(1):314-31 [8386878.001]
  • [Cites] Mol Cell Biol. 1993 Jun;13(6):3324-39 [8497254.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jul 15;90(14):6859-63 [8341710.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Cell. 1994 Jun 17;77(6):917-29 [8004678.001]
  • [Cites] EMBO J. 1994 Aug 1;13(15):3570-9 [8062832.001]
  • [Cites] Blood. 1995 Oct 15;86(8):2906-12 [7579382.001]
  • [Cites] Immunity. 1995 Oct;3(4):521-30 [7584142.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Cell. 1996 Nov 15;87(4):687-96 [8929537.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Cell. 1997 Nov 28;91(5):661-72 [9393859.001]
  • [Cites] J Immunol. 2005 Mar 15;174(6):3526-33 [15749889.001]
  • (PMID = 17185462.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096983; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Cbfb protein, mouse; 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
  • [Other-IDs] NLM/ PMC1852246
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97. Ramsingh G, Koboldt DC, Trissal M, Chiappinelli KB, Wylie T, Koul S, Chang LW, Nagarajan R, Fehniger TA, Goodfellow P, Magrini V, Wilson RK, Ding L, Ley TJ, Mardis ER, Link DC: Complete characterization of the microRNAome in a patient with acute myeloid leukemia. Blood; 2010 Dec 9;116(24):5316-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete characterization of the microRNAome in a patient with acute myeloid leukemia.
  • In this study, we applied next generation sequencing techniques to comprehensively assess miRNA expression, identify genetic variants of miRNA genes, and screen for alterations in miRNA binding sites in a patient with acute myeloid leukemia.
  • Sequencing of all known miRNA genes revealed several novel germline polymorphisms but no acquired mutations in the leukemia genome.