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1. Lapucci A, Lulli M, Amedei A, Papucci L, Witort E, Di Gesualdo F, Bertolini F, Brewer G, Nicolin A, Bevilacqua A, Schiavone N, Morello D, Donnini M, Capaccioli S: zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia. FASEB J; 2010 Jun;24(6):1852-65
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  • [Title] zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia.
  • The human antiapoptotic bcl-2 gene has been discovered in t(14;18) B-cell leukemias/lymphomas because of its overexpression caused at a transcriptional control level by the bcl-2/IgH fusion gene.
  • An increased Bcl-2 level observed in normal phytohemagglutinin (PHA)-activated T lymphocytes, acute lymphatic leukemia (ALL) T-cell lines, and T cells of patients with leukemia in comparison with normal non-PHA-activated T lymphocytes was concomitant with an increase in zeta-crystallin level.
  • The specific association of zeta-crystallin with the bcl-2 ARE was significantly enhanced in T cells of patients with ALL, which accounts for the higher stability of bcl-2 mRNA and suggests a possible contribution of zeta-crystallin to bcl-2 overexpression occurring in this leukemia.
  • [MeSH-major] 3' Untranslated Regions / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. zeta-Crystallins / metabolism
  • [MeSH-minor] Blotting, Western. Cytoplasm / drug effects. Cytoplasm / metabolism. Female. Gene Expression Regulation. Humans. Immunoprecipitation. Male. Middle Aged. Phytohemagglutinins. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. T-Lymphocytes / drug effects. T-Lymphocytes / pathology

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  • (PMID = 20103721.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443-16
  • [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 / 3' Untranslated Regions; 0 / Phytohemagglutinins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / zeta-Crystallins
  • [Other-IDs] NLM/ PMC2874474
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2. Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB: Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids. Cancer Cell Int; 2007 Nov 28;7:18
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  • By activating the glucocorticoid receptor (GR), GCs evoke apoptosis through transcriptional regulation of a complex, interactive gene network over a period of time preceding activation of the apoptotic enzymes.
  • Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
  • GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.
  • Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).
  • To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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  • (PMID = 18045478.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041407
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2228275
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3. Drakos E, Rassidakis GZ, Tsioli P, Lai R, Jones D, Medeiros LJ: Differential expression of WT1 gene product in non-Hodgkin lymphomas. Appl Immunohistochem Mol Morphol; 2005 Jun;13(2):132-7
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  • The tumor suppressor gene wt1 (Wilms tumor 1) encodes a zinc finger transcription factor reported to be expressed in many tumors, including mesotheliomas, carcinomas, and acute leukemias.
  • The authors assessed for WT1 expression in six lymphoma/leukemia cell lines using Western blot methods after subcellular fractionation.
  • The B-cell NHLs analyzed were 18 diffuse large B-cell lymphomas, 13 marginal zone B-cell lymphomas, 9 small lymphocytic lymphomas, (DLBCLs), 8 follicular lymphomas, 6 mantle cell lymphomas, 5 Burkitt lymphomas, 3 lymphoplasmacytic lymphomas, and 2 B-cell lymphoblastic lymphomas.
  • The T-cell NHLs analyzed were 43 anaplastic large cell lymphomas (ALCLs), 26 peripheral T-cell lymphomas unspecified, 13 angioimmunoblastic T-cell lymphomas, 6 cutaneous ALCLs, 6 cases of mycosis fungoides, 5 extranodal NK/T-cell lymphomas of nasal type, and 4 T-cell lymphoblastic lymphomas.
  • WT1 levels were higher in cytoplasmic extracts than in nuclear extracts of the Karpas 299 and SU-DHL-1 lymphoma cell lines but were higher in nuclear extracts than in the cytoplasmic extracts of the Jurkat, HH, U-937, and K562 leukemia cell lines.
  • In NHLs, WT1 was positive in 4 of 5 (80%) Burkitt lymphomas, 9 of 12 (75%) ALK-positive ALCLs, 3 of 6 (50%) lymphoblastic lymphomas (2 of 4 T-cell, 1 of 2 B-cell), 14 of 31 (45%) ALK-negative ALCLs, 6 of 18 (33%) DLBCLs, and 1 of 6 (17%) cutaneous ALCLs.
  • WT1 immunoreactivity was primarily cytoplasmic in all positive NHLs except T-cell lymphoblastic lymphoma.
  • In conclusion, WT1 protein is frequently detected in the cytoplasm of a subset of high-grade NHLs.

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  • (PMID = 15894924.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / WT1 Proteins
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4. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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5. Goldstein BD: Benzene as a cause of lymphoproliferative disorders. Chem Biol Interact; 2010 Mar 19;184(1-2):147-50
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  • There is a long standing issue concerning the strength of evidence relating benzene to lymphocytic neoplasms.
  • Because benzene is a known cause of human acute myelogenous leukemia there has been little reason for organizations such as the International Agency for Research on Cancer (IARC) or the US National Toxicology Program (NTP) to perform standard hazard identification reviews of benzene as a possible cause of other cancers such as lymphomas.
  • A broad range of genotoxic effects in the lymphocytes of benzene-exposed workers has been well documented, as has the role of chromosomal effects in carcinogenesis.
  • There is also increasing evidence of a close relationship between lymphoid tumors and the types of myeloid tumors known to be caused by benzene.
  • This includes the not infrequent finding of biphenotypic lineage as well as the formation of lymphoid as well as myeloid leukemias following chemotherapy.
  • Studies of the mechanism of benzene toxicity are consistent with a relatively non-specific mechanism capable of producing multiple chromosomal changes, and there is evidence that the early hematopoietic stem cell, which is believed to be targeted by benzene in causing myeloid cancers, is also the progenitor of lymphocytic cell types.
  • Furthermore, the classification of lymphomas has evolved so that non-Hodgkin lymphoma now includes such formerly distinct disorders as chronic lymphocytic leukemia and multiple myeloma, and there is less of a distinction between leukemia and non-leukemia forms of lymphoma.

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  • [Copyright] Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20035727.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] J64922108F / Benzene
  • [Number-of-references] 54
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6. Lucas DM, Edwards RB, Lozanski G, West DA, Shin JD, Vargo MA, Davis ME, Rozewski DM, Johnson AJ, Su BN, Goettl VM, Heerema NA, Lin TS, Lehman A, Zhang X, Jarjoura D, Newman DJ, Byrd JC, Kinghorn AD, Grever MR: The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo. Blood; 2009 May 7;113(19):4656-66
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  • [Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.
  • Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.
  • Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.
  • In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.
  • We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.
  • In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.
  • These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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  • (PMID = 19190247.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956
  • [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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol
  • [Other-IDs] NLM/ PMC2680369
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7. Kern W, Kohlmann A, Schoch C, Schnittger S, Haferlach T: Comparison of mRNA abundance quantified by gene expression profiling and percentage of positive cells using immunophenotyping for diagnostic antigens in acute and chronic leukemias. Cancer; 2006 Nov 15;107(10):2401-7
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  • [Title] Comparison of mRNA abundance quantified by gene expression profiling and percentage of positive cells using immunophenotyping for diagnostic antigens in acute and chronic leukemias.
  • BACKGROUND: Microarray analysis is considered a future diagnostic tool in leukemias.
  • Whereas data accumulate on specific gene expression patterns in biologically defined leukemia entities, data on the correlation between flow cytometrically determined protein expression, which are essential in the diagnostic setting today, and microarray results are limited.
  • METHODS: The results obtained by microarray analysis were compared using the Affymetrix GeneChip HG-U133 system in parallel with flow cytometric findings of 36 relevant targets in 814 patients with newly diagnosed acute and chronic leukemias as well as in normal bone marrow samples.
  • RESULTS: In a total of 21,581 individual comparisons between signal intensities obtained by microarray analysis and percentages of positive cell as determined by flow cytometry, coefficients of correlation in the range of 0.171 to 0.807 were obtained.
  • They are in favor of a future application of the microarray technology as a robust diagnostic tool in leukemias.
  • [MeSH-major] Antigens, Surface / analysis. Biomarkers, Tumor / analysis. Immunophenotyping. Leukemia / diagnosis. Microarray Analysis. Molecular Diagnostic Techniques / methods. RNA, Messenger / analysis
  • [MeSH-minor] Antigens, CD / analysis. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Flow Cytometry. Gene Expression Profiling. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17041886.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Surface; 0 / Biomarkers, Tumor; 0 / RNA, Messenger
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8. Grzybowska-Izydorczyk O, Smolewski P: [The role of the inhibitor of apoptosis protein (IAP) family in hematological malignancies]. Postepy Hig Med Dosw (Online); 2008 Feb 14;62:55-63
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  • The apoptotic mode of cell death is a major regulatory process in all complex organisms.
  • The low proliferative index and slow accumulation of malignant cells in chronic lymphocytic leukemia (CLL), the most frequent type of leukemia in Europe and North America, suggests that the disease is caused by a defect in apoptosis regulation.
  • Overexpression of several IAPs has been detected in various hematological malignancies, including acute leukemias, myelodysplastic syndrome (MDS), chronic myeloid leukemia (CML), and many types of lymphoid malignancies, such as chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL).
  • Many publications revealed significant correlation between a high level of IAPs, especially of XIAP and survivin, and tumor progression.
  • It seems that overexpression of XIAP in acute myeloid leukemia (AML) and survivin in acute lymphoblastic leukemia (ALL) and DLBCL could become a new unfavorable prognostic factor.

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  • (PMID = 18283236.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Inhibitor of Apoptosis Proteins
  • [Number-of-references] 67
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9. Robazzi TC, Barreto JH, Silva LR, Santiago MB, Mendonça N: Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil. J Pediatr Hematol Oncol; 2007 Sep;29(9):622-6
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  • [Title] Osteoarticular manifestations as initial presentation of acute leukemias in children and adolescents in Bahia, Brazil.
  • OBJECTIVE: This study was to determine the prevalence and characteristics of the osteoarticular manifestations on initial clinical presentation of acute leukemias (ALs) on childhood in the state of Bahia, Brazil.
  • RESULTS: Acute lymphocytic leukemia (ALL) was diagnosed in 313 (77.1%) patients and acute myeloid leukemia (AML), in 93 (22.9%) patients, including 241 males (59.4%) and 165 females (40.6%).
  • Prior referral to our center, the most frequent initial diagnosis was anemia (15.8%), leukemia (15.0%), amygdalitis (3.7%), and rheumatic fever (2.7%).
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Osteoarthritis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Brazil. Child. Child, Preschool. Female. Humans. Infant. Male

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  • (PMID = 17805037.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Title] [Effects of proteasome inhibitors on leukemias].
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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11. Belson M, Kingsley B, Holmes A: Risk factors for acute leukemia in children: a review. Environ Health Perspect; 2007 Jan;115(1):138-45
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  • [Title] Risk factors for acute leukemia in children: a review.
  • Although overall incidence is rare, leukemia is the most common type of childhood cancer.
  • Within this population, acute lymphocytic leukemia (ALL) occurs approximately five times more frequently than acute myelogenous leukemia (AML) and accounts for approximately 78% of all childhood leukemia diagnoses.
  • Epidemiologic studies of acute leukemias in children have examined possible risk factors, including genetic, infectious, and environmental, in an attempt to determine etiology.
  • Most environmental risk factors have been found to be weakly and inconsistently associated with either form of acute childhood leukemia.
  • Our review focuses on the demographics of childhood leukemia and the risk factors that have been associated with the development of childhood ALL or AML.
  • Knowledge of these particular risk factors can be used to support measures to reduce potentially harmful exposures and decrease the risk of disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Child. Communicable Diseases / complications. Environmental Exposure. Genetic Predisposition to Disease. Humans. Risk Factors

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  • (PMID = 17366834.001).
  • [ISSN] 0091-6765
  • [Journal-full-title] Environmental health perspectives
  • [ISO-abbreviation] Environ. Health Perspect.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 145
  • [Other-IDs] NLM/ PMC1817663
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12. Neviani P, Santhanam R, Oaks JJ, Eiring AM, Notari M, Blaser BW, Liu S, Trotta R, Muthusamy N, Gambacorti-Passerini C, Druker BJ, Cortes J, Marcucci G, Chen CS, Verrills NM, Roy DC, Caligiuri MA, Bloomfield CD, Byrd JC, Perrotti D: FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia. J Clin Invest; 2007 Sep;117(9):2408-21
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  • [Title] FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia.
  • Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute lymphocytic leukemia (ALL) are 2 fatal BCR/ABL-driven leukemias against which Abl kinase inhibitors fail to induce a long-term response.
  • We assessed the therapeutic potential of the PP2A activator FTY720 (2-amino-2-[2-(4-octylphenyl)ethyl]-1,3-propanediol hydrochloride), an immunomodulator in Phase III trials for patients with multiple sclerosis or undergoing organ transplantation, in CML-BC and Ph1 ALL patient cells and in in vitro and in vivo models of these BCR/ABL+ leukemias.
  • Our data indicate that FTY720 induces apoptosis and impairs clonogenicity of imatinib/dasatinib-sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph1 ALL(CD34+/CD19+) progenitors but not of normal CD34+ and CD34+/CD19+ bone marrow cells.
  • Altogether, these results highlight the therapeutic relevance of rescuing PP2A tumor suppressor activity in Ph1 leukemias and strongly support the introduction of the PP2A activator FTY720 in the treatment of CML-BC and Ph1 ALL patients.

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  • (PMID = 17717597.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / P30 CA016058
  • [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 / Piperazines; 0 / Propylene Glycols; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1950458
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13. Fasseu M, Aplan PD, Chopin M, Boissel N, Bories JC, Soulier J, von Boehmer H, Sigaux F, Regnault A: p16INK4A tumor suppressor gene expression and CD3epsilon deficiency but not pre-TCR deficiency inhibit TAL1-linked T-lineage leukemogenesis. Blood; 2007 Oct 1;110(7):2610-9
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  • Inactivation of the CDKN2 genes that encode the p16(INK4A) and p14(ARF) proteins occurs in the majority of human T-cell acute lymphoblastic leukemias (T-ALLs).
  • In TAL1xLMO1 mice, leukemia develops in 100% of mice at 5 months.
  • We report here that expression of P16(INK4A) in developing TAL1xLMO1 thymocytes blocks leukemogenesis in the majority of the mice, and the leukemias that eventually develop show P16(INK4A) loss of expression.
  • Events related to the T-cell receptor beta selection process are thought to be important for leukemic transformation.

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  • (PMID = 17507663.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CCND3 protein, human; 0 / CD3E protein, human; 0 / Ccnd3 protein, mouse; 0 / Cyclin D3; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclins; 0 / LIM Domain Proteins; 0 / Lmo1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell; 0 / Tal1 protein, mouse; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC1988920
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14. Svecová D, Pallová A, Chmurová N, Babal P: Paraneoplastic vasculitis associated with hairy cell leukemia. Prague Med Rep; 2008;109(1):83-7
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  • [Title] Paraneoplastic vasculitis associated with hairy cell leukemia.
  • Hairy cell leukemia (HCL) is a rare B-cell lymphoproliferative disease, accounting for about 2-3% of all leukemias in adults.
  • Vasculitis in lymphoproliferative disease is relatively uncommon and may predate the diagnosis of lymphoproliferative disease.
  • A 54-year old female with one month history of general symptoms and sudden onset of maculopapular exanthema on the skin, suffered from anemia, leukopenia and thrombocytopenia.
  • Examination of the skin biopsy revealed lymphocytic vasculitis.
  • Immunophenotyping of the skin biopsy revealed cell population with CD45RO, and small groups with CD20, partly DBA44 positivity.
  • The diagnosis of HCL was confirmed by flow cytometry of the bone marrow and of the peripheral blood cells that revealed pathological cell population with expression of CD11c, CD19, CD25, CD103.
  • The patient with acute vasculitis should be screened and monitored for possible lymphoproliferative diseases.
  • Skin manifestation of acute vasculitis accompanied with hairy cells may be the first manifestation of HCL.
  • [MeSH-major] Leukemia, Hairy Cell / complications. Paraneoplastic Syndromes / complications. Vasculitis / complications

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  • (PMID = 19097393.001).
  • [ISSN] 1214-6994
  • [Journal-full-title] Prague medical report
  • [ISO-abbreviation] Prague Med Rep
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Czech Republic
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15. Wiederschain D, Kawai H, Shilatifard A, Yuan ZM: Multiple mixed lineage leukemia (MLL) fusion proteins suppress p53-mediated response to DNA damage. J Biol Chem; 2005 Jul 1;280(26):24315-21
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  • [Title] Multiple mixed lineage leukemia (MLL) fusion proteins suppress p53-mediated response to DNA damage.
  • Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are often observed in acute leukemias of both myeloid and lymphocytic origin.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. DNA Primers / chemistry. Humans. Immunoprecipitation. Luciferases / metabolism. Models, Genetic. Myeloid-Lymphoid Leukemia Protein. Plasmids / metabolism. Protein Structure, Tertiary. RNA / chemistry. Radiation, Ionizing. Recombinant Fusion Proteins / chemistry. Retroviridae / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transcriptional Activation. Transfection. Translocation, Genetic

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  • (PMID = 15851483.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES11627; United States / NCI NIH HHS / CA / R01 CA85679-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MLL-AF10 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ELL fusion protein, human; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 63231-63-0 / RNA; EC 1.13.12.- / Luciferases
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16. Peffault de Latour R, Robin M, Bay JO: [Monoclonal antibodies for lymphomas and leukemias in 2005]. Bull Cancer; 2006 Jan;93(1):107-18
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  • [Title] [Monoclonal antibodies for lymphomas and leukemias in 2005].
  • Combined treatments resulted in an increase of global response and complete remission in non previously pre-treated patients with follicular lymphoma, diffuse large cell lymphoma and chronic lymphocytic leukemia.
  • The role of MAb in the treatment of myelodysplastic syndrome remains uncertain although the use of anti-CD33 in acute myeloid leukemias is promising.
  • The aim of this review is to present an updated overview of the most used MAb in the treatment of leukemias and lymphomas not involving bone marrow transplantation.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia / immunology. Leukemia / therapy. Lymphoma / immunology. Lymphoma / therapy

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  • (PMID = 16455513.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 157
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17. Kozlov I, Beason K, Yu C, Hughson M: CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity. Cancer Genet Cytogenet; 2005 Nov;163(1):62-7
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  • [Title] CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
  • Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL).
  • CD79a functions in and has a high degree of specificity for B-cell differentiation.
  • It has only recently begun to be reported in biphenotypic acute leukemias.
  • Cases of acute leukemia submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to leukemia and lymphoma panels.
  • Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-cell differentiation, represented the aberrant presence of a B-cell antigen in leukemias of distinct myeloid linage.
  • [MeSH-major] Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology

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  • [CommentIn] Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7 [17350472.001]
  • (PMID = 16271957.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
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18. Blum W, Phelps MA, Klisovic RB, Rozewski DM, Ni W, Albanese KA, Rovin B, Kefauver C, Devine SM, Lucas DM, Johnson A, Schaaf LJ, Byrd JC, Marcucci G, Grever MR: Phase I clinical and pharmacokinetic study of a novel schedule of flavopiridol in relapsed or refractory acute leukemias. Haematologica; 2010 Jul;95(7):1098-105
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  • [Title] Phase I clinical and pharmacokinetic study of a novel schedule of flavopiridol in relapsed or refractory acute leukemias.
  • BACKGROUND: A pharmacokinetically derived schedule of flavopiridol administered as a 30 min intravenous bolus followed by 4-hour continuous intravenous infusion (IVB/CIVI) is active in fludarabine-refractory chronic lymphocytic leukemia, but no studies examining the feasibility and maximum tolerated dose of this schedule have been reported in acute leukemia.
  • DESIGN AND METHODS: We conducted a phase I dose escalation trial of single-agent flavopiridol in adults with relapsed/refractory acute leukemias, utilizing a modification of the intravenous bolus/continuous intravenous infusion approach, intensifying treatment for administration on days 1, 2, and 3 of 21-day cycles.
  • RESULTS: Twenty-four adults with relapsed/refractory acute myeloid leukemia (n=19) or acute lymphoblastic leukemia (n=5) were enrolled.
  • One refractory acute myeloid leukemia patient had short-lived complete remission with incomplete count recovery.
  • CONCLUSIONS: Flavopiridol as a single agent given by intravenous bolus/continuous intravenous infusion causes marked, immediate cytoreduction in relapsed/refractory acute leukemias, but objective clinical responses were uncommon.
  • [MeSH-major] Flavonoids / administration & dosage. Leukemia / drug therapy. Piperidines / administration & dosage
  • [MeSH-minor] Acute Disease. Adult. Aged. Drug Administration Schedule. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Pharmacokinetics. Salvage Therapy / methods. Treatment Outcome. Young Adult

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  • (PMID = 20460644.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101231
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / U01 CA 76576; United States / NCI NIH HHS / CA / K23CA120708; United States / NCI NIH HHS / CA / U01 CA076576; United States / NCRR NIH HHS / RR / UL1 RR025755
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 45AD6X575G / alvocidib
  • [Other-IDs] NLM/ PMC2895033
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19. Taniguchi H, Fernández AF, Setién F, Ropero S, Ballestar E, Villanueva A, Yamamoto H, Imai K, Shinomura Y, Esteller M: Epigenetic inactivation of the circadian clock gene BMAL1 in hematologic malignancies. Cancer Res; 2009 Nov 1;69(21):8447-54
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  • Normal and malignant tissues often show asynchronies in cell proliferation and metabolic rhythms.
  • Herein, we show that the BMAL1 gene, a core component of the circadian clock, is transcriptionally silenced by promoter CpG island hypermethylation in hematologic malignancies, such as diffuse large B-cell lymphoma and acute lymphocytic and myeloid leukemias.
  • We also describe how BMAL1 reintroduction in hypermethylated leukemia/lymphoma cells causes growth inhibition in colony assays and nude mice, whereas BMAL1 depletion by RNA interference in unmethylated cells enhances tumor growth.
  • [MeSH-minor] Animals. Blotting, Western. CLOCK Proteins / metabolism. Cell Proliferation. Chromatin Immunoprecipitation. Circadian Rhythm. CpG Islands. DNA Methylation. Female. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Lymphocytes / metabolism. Lymphocytes / pathology. Mice. Mice, Nude. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 19861541.001).
  • [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 / ARNTL Transcription Factors; 0 / ARNTL protein, human; 0 / RNA, Messenger; EC 2.3.1.48 / CLOCK Proteins
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20. Winrow CJ, Pankratz DG, Vibat CR, Bowen TJ, Callahan MA, Warren AJ, Hilbush BS, Wynshaw-Boris A, Hasel KW, Weaver Z, Lockhart DJ, Barlow C: Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas. Hum Mol Genet; 2005 Sep 15;14(18):2671-84
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  • [Title] Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas.
  • Ataxia telangiectasia (A-T) is an autosomal recessive disease caused by loss of function of the serine/threonine protein kinase ATM (ataxia telangiectasia mutated).
  • A-T patients have a 250-700-fold increased risk of developing lymphomas and leukemias which are typically highly invasive and proliferative.
  • In addition, a subset of adult acute lymphoblastic leukemias and aggressive B-cell chronic lymphocytic leukemias that occur in the general population show loss of heterozygosity for ATM.
  • To define the specific role of ATM in lymphomagenesis, we studied T-cell lymphomas isolated from mice with mutations in ATM and/or p53 using cytogenetic analysis and mRNA transcriptional profiling.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell / genetics. Models, Biological. Protein-Serine-Threonine Kinases / genetics. Recombination, Genetic / genetics. Serine Endopeptidases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Ataxia Telangiectasia Mutated Proteins. Blotting, Northern. Cell Line, Tumor. Computational Biology. Cytogenetic Analysis. DNA Primers. Gene Expression Profiling. Granzymes. In Situ Hybridization, Fluorescence. Mice. Mice, Knockout. Microarray Analysis. Mutation / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16087685.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS039601-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Gzmb protein, mouse; EC 3.4.21.- / Gzmc protein, mouse; EC 3.4.21.- / Serine Endopeptidases
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26. Tigay JH: A comparison of acute lymphoblastic leukemia in Down syndrome and non-Down syndrome children: the role of trisomy 21. J Pediatr Oncol Nurs; 2009 Nov-Dec;26(6):362-8
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  • [Title] A comparison of acute lymphoblastic leukemia in Down syndrome and non-Down syndrome children: the role of trisomy 21.
  • Among the many aberrations caused by DS, including shortened stature and distorted facies, are several blood dyscrasias, including childhood leukemias-namely, acute myeloid leukemia (AML) and acute lymphoblastic, or lymphocytic, leukemia (ALL).
  • Other mutations are the gene fusion at TEL/AML1, and a new mutation found, which labels the Janus Kinase gene or JAK2 as on oncogenic precursor, which when associated with the B-cell precursor gene or BCP is highly leukomogenic.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


27. Ren SY, Xue F, Feng J, Skorski T: Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase. Exp Hematol; 2005 Oct;33(10):1222-8
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  • OBJECTIVE: BCR/ABL fusion tyrosine kinase is responsible for the initiation and maintenance of the Philadelphia chromosome-positive chronic myelogenous leukemia (CML) and a cohort of acute lymphocytic leukemias.
  • RESULTS: We show here that the SH3 domain of p85alpha (p85alpha-SH3) pulls down the p210BCR/ABL kinase from hematopoietic cell lysates.
  • [MeSH-minor] Amino Acid Substitution. Animals. Cell Line, Tumor. Fusion Proteins, bcr-abl. Hematopoietic Stem Cells / metabolism. Humans. Immunoprecipitation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Mice. Mutagenesis, Site-Directed. Point Mutation / genetics. Protein Binding

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  • (PMID = 16219545.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA83700
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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28. Su X, Della-Valle V, Delabesse E, Azgui Z, Berger R, Merle-Béral H, Bernard OA, Nguyen-Khac F: Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder. Haematologica; 2008 Jul;93(7):1081-5
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  • [Title] Transcriptional activation of the cardiac homeobox gene CSX1/NKX2-5 in a B-cell chronic lymphoproliferative disorder.
  • Study of T-cell acute lymphoblastic leukemia identified the related non-clustered homeobox transcription factors, TLX1 and TLX3, as frequently ectopically expressed as a result of chromosomal translocations.
  • We report the deregulation of a non-clustered homeobox gene in a new type of t(5;14)(q35;q11) translocation in a mature peripheral B-cell leukemia.
  • Our study establishes that deregulation of homeobox encoding genes is not restricted to acute leukemic proliferations, but is also observed in chronic malignant diseases.
  • [MeSH-major] B-Lymphocytes / metabolism. Gene Expression Regulation. Homeodomain Proteins / genetics. Lymphoproliferative Disorders / genetics. Lymphoproliferative Disorders / pathology. Transcription Factors / genetics. Transcriptional Activation
  • [MeSH-minor] Cell Proliferation. Chronic Disease. Cytogenetics. Female. Humans. Middle Aged. Models, Biological. Mutation. Sequence Analysis, DNA. Translocation, Genetic

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  • (PMID = 18492690.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NKX2-5 protein, human; 0 / Transcription Factors
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29. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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  • [Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
  • In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
  • The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
  • Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.
  • The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.
  • The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
  • It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.
  • These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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  • (PMID = 16403255.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20
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30. Cooper TM: Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag; 2007 Dec;3(6):1135-41
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  • [Title] Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.
  • T-cell malignancies have distinct biochemical, immunologic, and clinical features which set them apart from non-T-cell malignancies.
  • In the past, T-cell leukemia portended a worse prognosis than leukemia of B-cell origin.
  • Cure rates have improved with intensification of therapy and advanced understanding of the molecular genetics of T-cell malignancies.
  • Further advances in the treatment of T-cell leukemia will require the development of novel agents that can target specific malignancies without a significant increase in toxicity.
  • Nelarabine is water soluble and rapidly converted to ara-G, which is specifically cytotoxic to T-lymphocytes and T-lymphoblastoid cells.
  • Clinical and pharmacokinetic investigations have established that nelarabine is active as a single agent which has led to exploration of an expanded role in the treatment of T-cell hematologic malignances.

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  • (PMID = 18516261.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387290
  • [Keywords] NOTNLM ; 9-β-D-arabinofuranosylguanine / T-cell acute lymphoblastic leukemia / nelarabine
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31. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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32. Tang HR, Wang FC, Jiang YW, Fei X, Jiang Q, Xu WL, Lin J: [CD36 expression in leukemia cells checked with multi-parameter flow cytometry and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Feb;15(1):29-34
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  • [Title] [CD36 expression in leukemia cells checked with multi-parameter flow cytometry and its significance].
  • The aim of study was to investigate the expression of CD36 in leukemia cells and to explore its significance in diagnosis and differential diagnosis for leukemia in patients.
  • Blood samples from 133 cases of leukemias were analyzed by CD45/SSC double parameters and multi-color flow cytometry in order to determine the CD36 and other leukocyte differentiation antigens.
  • The results show that the CD36 positive rate was 21.8% (29/133) in 133 cases of leukemia, 41.9% (26/62) in 62 cases of AML (acute myeloid leukemia), and none of the 54 cases of lymphocytic leukemia was positive for this antigen.
  • In monocyte lineage involved leukemia (MLIL), the positive rate of CD36 (92.6%, 25/27) was significantly higher than that of CD14 (48.1%, 13/27)(P = 0.001).

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  • (PMID = 17490515.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD36; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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33. Casnici C, Volpe G, Lattuada D, Crotta K, Kuka M, Panuzzo C, Mastrotto C, Tonon G, Fazio VM, Saglio G, Marelli O: Out of frame peptides from BCR/ABL alternative splicing are immunogenic in HLA A2.1 transgenic mice. Cancer Lett; 2009 Apr 8;276(1):61-7
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  • New, potentially tumor-specific antigens have been described in Bcr/Abl positive leukemias.
  • These variants are expressed in chronic myelogenous leukemia and acute lymphocytic leukemia patients.
  • Peptides A and B, but not C, induced the production of specific antisera, while A and C induced the generation of specific cytotoxic T lymphocytes.
  • [MeSH-major] Alternative Splicing. Cancer Vaccines / immunology. Frameshift Mutation / immunology. Fusion Proteins, bcr-abl / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / immunology. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. HLA-A2 Antigen / genetics. Humans. Interferon-gamma / biosynthesis. Interferon-gamma / immunology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Peptides / genetics. Peptides / immunology. Proto-Oncogene Proteins c-bcr / genetics. Proto-Oncogene Proteins c-bcr / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 19062160.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / HLA-A2 Antigen; 0 / Peptides; 82115-62-6 / Interferon-gamma; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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34. Chiaretti S, Ritz J, Foa R: Genomic analysis in lymphoid leukemias. Rev Clin Exp Hematol; 2005 Jun;9(1):E3
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  • [Title] Genomic analysis in lymphoid leukemias.
  • Important biological insights have been revealed by this technique in several tumors: in acute lymphoblastic leukemia (ALL), these studies have allowed to identify specific patterns associated with known molecular abnormalities, as well as with phenotypic characteristics and with different prognostic features.
  • In chronic lymphocytic leukemia (CLL), this approach has helped to dissect that this disease is a single entity with distinct variants that are characterized by a diverse IgVH mutational status, that can be discriminated by a small set of genes, has allowed to define a similarity between this disease and memory B cells and has also led to hypothesize that CLL cells from IgVH unmutated patients may be continuously stimulated in vivo, thus showing a gene profile that is reminiscent of the B cell receptor.
  • In multiple myeloma (MM), gene expression profiles has provided insights into the disease and has offered the opportunity of stratifying patients according to the degree of aggressiveness of the disease.
  • [MeSH-major] Genomics / methods. Leukemia, Lymphoid / genetics

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  • (PMID = 16027105.001).
  • [ISSN] 1825-151X
  • [Journal-full-title] Reviews in clinical and experimental hematology
  • [ISO-abbreviation] Rev Clin Exp Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Number-of-references] 140
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35. Usvasalo A, Ninomiya S, Räty R, Hollmén J, Saarinen-Pihkala UM, Elonen E, Knuutila S: Focal 9p instability in hematologic neoplasias revealed by comparative genomic hybridization and single-nucleotide polymorphism microarray analyses. Genes Chromosomes Cancer; 2010 Apr;49(4):309-18
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  • Copy number losses in chromosome arm 9p are well-known aberrations in malignancies, including leukemias.
  • We have used microarray comparative genomic hybridization to study patients with acute lymphoblastic leukemia (ALL, n = 140), acute myeloid leukemia (n = 50), chronic lymphocytic leukemia (n = 20), and myelodysplastic syndromes (n = 37).
  • [MeSH-major] Chromosomal Instability. Chromosomes, Human, Pair 9. Leukemia / genetics. Myelodysplastic Syndromes / genetics. Oligonucleotide Array Sequence Analysis / methods


36. Malani AK, Gupta C, Rangineni R, Singh J, Ammar H: Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia. Acta Oncol; 2007;46(2):247-9
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  • [Title] Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.
  • T-cell large granular lymphocyte leukemia (T-LGL) also known as T-cell chronic lymphocytic leukemia is rare and comprises a small minority of all small lymphocytic leukemias.
  • The concomitant presentation of T-LGL with acute myeloid leukemia (AML) has not been previously reported.
  • We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of morphologic evaluation, immunophenotyping by flow cytometry, and T-cell gene rearrangement studies.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male

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  • (PMID = 17453377.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 17
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37. Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias. Leuk Res; 2005 Feb;29(2):179-83
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  • [Title] The expression of iASPP in acute leukemias.
  • To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).
  • There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).
  • The expression level of iASPP gene and its overexpression in M3 and M4EO were significantly lower than in other subtypes of AML.
  • However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.
  • The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 15607367.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53
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38. Ma W, Kantarjian H, Zhang K, Zhang X, Wang X, Chen C, Donahue AC, Zhang Z, Yeh CH, O'Brien S, Garcia-Manero G, Caporaso N, Landgren O, Albitar M: Significant association between polymorphism of the erythropoietin gene promoter and myelodysplastic syndrome. BMC Med Genet; 2010 Nov 16;11:163
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  • METHODS: We genotyped the EPO rS1617640 SNP in 189 patients with MDS, 257 with acute myeloid leukemia (AML), 106 with acute lymphoblastic leukemia, 97 with chronic lymphocytic leukemia, 353 with chronic myeloid leukemia, and 95 healthy controls.
  • RESULTS: The G/G genotype was significantly more common in MDS patients (47/187; 25.1%) than in controls (6/95; 6.3%) or in patients with other leukemias (101/813; 12.4%) (all P < 0.001).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Genotype. Humans. Leukemia, Lymphocytic, Chronic, B-Cell. Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Leukemia, Myeloid, Acute. Middle Aged. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Treatment Outcome. Young Adult


39. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Other-IDs] NLM/ PMC2791935
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40. Sait SN, Claydon MA, Conroy JM, Nowak NJ, Barcos M, Baer MR: Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):143-6
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  • [Title] Translocation (4;11)(p12;q23) with rearrangement of FRYL and MLL in therapy-related acute myeloid leukemia.
  • Reciprocal chromosomal translocations involving the MLL gene at chromosome region 11q23 are recurring cytogenetic abnormalities in both de novo and therapy-related acute myeloid leukemia (AML) and in acute lymphoblastic leukemia.
  • We report a t(4;11)(p12;q23) with rearrangement of MLL and FRYL (also known as AF4p12), a human homolog to the furry gene of Drosophila, in an adult patient with therapy-related AML after fludarabine and rituximab therapy for small lymphocytic lymphoma and radiation therapy for breast carcinoma.
  • Both of the previous patients had therapy-related leukemias after exposure to topoisomerase II inhibitors, whereas our patient had received cytotoxic therapy that did not include a topoisomerase II inhibitor.
  • Thus, t(4;11)(p12;q23) with MLL and FRYL involvement represents a new recurring 11q23 translocation, to date seen only in therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. DNA-Binding Proteins / genetics. Gene Rearrangement. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Middle Aged. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17854671.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; 4F4X42SYQ6 / Rituximab; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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41. Haferlach C, Rieder H, Lillington DM, Dastugue N, Hagemeijer A, Harbott J, Stilgenbauer S, Knuutila S, Johansson B, Fonatsch C: Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes. Genes Chromosomes Cancer; 2007 May;46(5):494-9
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  • [Title] Proposals for standardized protocols for cytogenetic analyses of acute leukemias, chronic lymphocytic leukemia, chronic myeloid leukemia, chronic myeloproliferative disorders, and myelodysplastic syndromes.
  • Therefore, laboratory techniques have to be optimized to provide reliable results for optimal patient care.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Diagnosis, Differential. Humans. Karyotyping


42. Zhu DX, Miao KR, Zhu YD, Zhu HY, Fan L, Liu P, Xu W, Li JY: [Detection of miRNA levels in leukemia patients by real-time quantitative PCR]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Jun;18(3):757-61
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  • [Title] [Detection of miRNA levels in leukemia patients by real-time quantitative PCR].
  • This study was purposed to establish a method for detecting miRNA expression by using fluorescent quantitative polymerase chain reaction (RQ-PCR), and to investigate the application value of this method in quantitative detection of miRNA.
  • Total RNA was extracted from the peripheral blood or bone marrow of 82 patients with chronic lymphocytic leukemia (CLL) and 70 patients with acute leukemias (AL).

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  • (PMID = 20561445.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MicroRNAs
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43. Taniguchi A, Nemoto Y, Yokoyama A, Kotani N, Imai S, Shuin T, Daibata M: Promoter methylation of the bone morphogenetic protein-6 gene in association with adult T-cell leukemia. Int J Cancer; 2008 Oct 15;123(8):1824-31
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  • [Title] Promoter methylation of the bone morphogenetic protein-6 gene in association with adult T-cell leukemia.
  • Bone morphogenetic proteins (BMP), belonging to the transforming growth factor-beta superfamily, are multifunctional regulators of cell proliferation, differentiation and apoptosis in various types of malignant cells.
  • In this study, we investigated BMP-6 promoter methylation in patients with various types of leukemias.
  • The BMP-6 methylation was found preferentially in adult T-cell leukemia (ATL) (49 of 60, 82%) compared with other types of leukemias studied including acute myeloid leukemia (3 of 67, 5%), acute lymphoblastic leukemia (6 of 38, 16%) and chronic lymphocytic leukemia (1 of 21, 5%).
  • Among subtypes of ATL, the BMP-6 gene was more frequently methylated in aggressive ATL forms of acute (96%) and lymphoma (94%) types than less malignant chronic ATL (44%) and smoldering ATL (20%).
  • These findings suggested that BMP-6 promoter methylation is likely to be a common epigenetic event at later stages of ATL and that the methylation profiles may be useful for the staging of ATL as well as for evaluation of the individual risk of developing the disease.
  • [MeSH-major] Bone Morphogenetic Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 18688853.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMP6 protein, human; 0 / Bone Morphogenetic Protein 6; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; 0 / Sulfites; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine; OJ9787WBLU / hydrogen sulfite
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44. Small D: Targeting FLT3 for the treatment of leukemia. Semin Hematol; 2008 Jul;45(3 Suppl 2):S17-21
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  • [Title] Targeting FLT3 for the treatment of leukemia.
  • FLT3 is a receptor tyrosine kinase with important roles in hematopoietic stem/progenitor cell survival and proliferation.
  • It is frequently overexpressed in acute leukemias and is frequently mutated in acute myeloid leukemia (AML).
  • Anti-FLT3 antibodies may also prove to be an excellent way of targeting FLT3 in AML and acute lymphocytic leukemia (ALL) by inhibiting signaling and through antibody-dependent cell-mediated cytotoxicity.

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  • (PMID = 18760705.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / R01 CA090668-01A1; United States / NCI NIH HHS / CA / CA090668-01A1; United States / NCI NIH HHS / CA / P01 CA070970-10A16432; United States / NCI NIH HHS / CA / CA070970-10A16432
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 34
  • [Other-IDs] NLM/ NIHMS69701; NLM/ PMC2597087
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45. Fischer S, Mann G, Konrad M, Metzler M, Ebetsberger G, Jones N, Nadel B, Bodamer O, Haas OA, Schmitt K, Panzer-Grümayer ER: Screening for leukemia- and clone-specific markers at birth in children with T-cell precursor ALL suggests a predominantly postnatal origin. Blood; 2007 Oct 15;110(8):3036-8
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  • [Title] Screening for leukemia- and clone-specific markers at birth in children with T-cell precursor ALL suggests a predominantly postnatal origin.
  • Childhood T-cell precursor acute lymphoblastic leukemia (TCP ALL) is an aggressive disease with a presumably short latency that differs in many biologic respects from B-cell precursor (BCP) ALL.
  • We therefore addressed the issue of in utero origin of this particular type of leukemia by tracing oncogenic mutations and clone-specific molecular markers back to birth.
  • These markers included various first- and second-hit genetic alterations (TCRD-LMO2 breakpoint regions, n = 2; TAL1 deletions, n = 3; Notch1 mutations, n = 1) and nononcogenic T-cell receptor rearrangements (n = 13) that were derived from leukemias of 16 children who were 1.5 to 11.2 years old at diagnosis of leukemia.
  • Despite highly sensitive polymerase chain reaction (PCR) approaches (1 cell with a specific marker among 100,000 normal cells), we identified the leukemic clone in the neonatal blood spots in only 1 young child.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Rearrangement, T-Lymphocyte / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17557895.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 135471-20-4 / TAL1 protein, human
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46. Aleskog A, Larsson R, Höglund M, Kristensen J, Nygren P, Lindhagen E: In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia. Anticancer Drugs; 2005 Mar;16(3):277-83
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  • [Title] In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia.
  • The aim of the study was to evaluate cellular drug resistance in B cell chronic lymphocytic leukemia (B-CLL) in vitro, and compare it with that in acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL).
  • In vitro drug resistance was analyzed by the fluorometric microculture cytotoxicity assay (FMCA) in all samples from patients with leukemia sent to our laboratory between 1992 and 2001.
  • For all drugs, there was a good agreement between the activity in vitro and the known clinical disease-specific activity.
  • The study also demonstrated an acquired cellular drug resistance in B-CLL, but not in the acute leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


47. Salerni BL, Bates DJ, Albershardt TC, Lowrey CH, Eastman A: Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed. Mol Cancer Ther; 2010 Apr;9(4):791-802
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  • [Title] Vinblastine induces acute, cell cycle phase-independent apoptosis in some leukemias and lymphomas and can induce acute apoptosis in others when Mcl-1 is suppressed.
  • Inhibition of the extracellular signal-regulated kinase by PD98059 dramatically accelerates vinblastine-mediated apoptosis in ML-1 leukemia with cells dying in 4 hours from all phases of the cell cycle.
  • Inhibition of protein synthesis by cycloheximide also markedly accelerated vinblastine-induced apoptosis, showing that the proteins required for this acute apoptosis are constitutively expressed.
  • We also investigated the response of 13 other leukemia and lymphoma cell lines and cells from seven chronic lymphocytic leukemia patients.
  • Four cell lines and all chronic lymphocytic leukemia cells were killed in 6 hours by vinblastine alone.
  • Two additional cell lines were sensitized to vinblastine by PD98059, which suppressed Mcl-1.
  • This acute apoptosis either alone or in combination with PD98059 required vinblastine-mediated activation of c-Jun-NH(2)-terminal kinase.
  • PD98059 did not suppress Mcl-1 in other cell lines whereas sorafenib did, but this did not sensitize the cells to vinblastine, suggesting that the acute apoptosis varies depending on which Bcl-2 protein mediates protection.
  • Most of the cell lines were sensitized to vinblastine by cycloheximide, suggesting that inhibition of a short-lived protein in addition to Mcl-1 can acutely sensitize cells.

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  • (PMID = 20371726.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009658-17; United States / NCI NIH HHS / CA / CA23108; United States / NCI NIH HHS / CA / CA009658-17; United States / NCI NIH HHS / CA / T32 CA009658; United States / NCI NIH HHS / CA / R01 CA050224; United States / NCI NIH HHS / CA / P30 CA023108-315657; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA023108-315657; United States / NCI NIH HHS / CA / CA050224-14; United States / NCI NIH HHS / CA / R01 CA050224-14; United States / NCI NIH HHS / CA / CA50224
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 5V9KLZ54CY / Vinblastine; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS184304; NLM/ PMC2852489
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48. Gebhart E: Genomic imbalances in human leukemia and lymphoma detected by comparative genomic hybridization (Review). Int J Oncol; 2005 Sep;27(3):593-606
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic imbalances in human leukemia and lymphoma detected by comparative genomic hybridization (Review).
  • Some of these alterations seem to play an important role in disease progression and specificity of the disease.
  • The patterns of genomic alterations found by CGH can characterize certain disease entities and differentiate them from others.
  • If the chromosomal segments affected in > 10% of the cases of each basic disease entity [acute myeloblastic leukemia (AML), acute lymphoblastic leukemia (ALL), chronic lymphocytic leukemia (CLL) and multiple myeloma (MM)] are compared, most of the frequently involved chromosomal regions differ from entity to entity in the leukemias.
  • With respect to their clinical significance, the presence of genomic imbalances is associated with disease progression and, therefore, poorer prognosis.
  • [MeSH-major] Chromosome Aberrations. Leukemia / genetics. Lymphoma / genetics. Nucleic Acid Hybridization / methods

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  • (PMID = 16077907.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 148
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49. Chang P, Kang M, Xiao A, Chang J, Feusner J, Buffler P, Wiemels J: FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia. BMC Cancer; 2010 Sep 27;10:513
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  • [Title] FLT3 mutation incidence and timing of origin in a population case series of pediatric leukemia.
  • BACKGROUND: Mutations in FLT3 result in activated tyrosine kinase activity, cell growth stimulation, and a poor prognosis among various subtypes of leukemia.
  • We evaluated the prevalence and timing of origin of FLT3 mutations in a population series of childhood leukemia patients from Northern California.
  • METHODS: We screened and sequenced FLT3 mutations (point mutations and internal tandem duplications, ITDs) among 517 childhood leukemia patients, and assessed whether these mutations occurred before or after birth using sensitive "backtracking" methods.
  • RESULTS: We determined a mutation prevalence of 9 of 73 acute myeloid leukemias (AMLs, 12%) and 9 of 441 acute lymphocytic leukemias (ALLs, 2%).

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  • (PMID = 20875128.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NIEHS NIH HHS / ES / P42ES0470; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / R01CA89032; United States / NIEHS NIH HHS / ES / R01ES09137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2955609
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50. Dunwell TL, Dickinson RE, Stankovic T, Dallol A, Weston V, Austen B, Catchpoole D, Maher ER, Latif F: Frequent epigenetic inactivation of the SLIT2 gene in chronic and acute lymphocytic leukemia. Epigenetics; 2009 May 16;4(4):265-9
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  • [Title] Frequent epigenetic inactivation of the SLIT2 gene in chronic and acute lymphocytic leukemia.
  • Recently a mouse model of T/natural killer acute lymphoblastic leukemia was used to assess global promoter methylation across the mouse genome using the restriction landmark genomic scanning technique.
  • We have previously demonstrated that SLIT2 is frequently inactivated in lung, breast, colorectal and glioma tumors by hypermethylation of a CpG island in its promoter region, whilst inactivating somatic mutations are rare.
  • In this report we determined the methylation status of the SLIT2 gene in leukemias (CLL and ALL).
  • SLIT2 was methylated in all ten leukemia cell lines analyzed (eight completely and two partially methylated).
  • Methylation results in leukemia cell lines and ALL and CLL primary samples were confirmed by direct sequencing of bisulfite modified DNA.
  • [MeSH-major] DNA Methylation. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Nerve Tissue Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Bone Marrow / metabolism. Cell Line, Tumor. CpG Islands / genetics. Humans

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  • (PMID = 19550140.001).
  • [ISSN] 1559-2308
  • [Journal-full-title] Epigenetics
  • [ISO-abbreviation] Epigenetics
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nerve Tissue Proteins; 0 / Slit homolog 2 protein
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51. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
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  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • Thirteen cases of TEL-AML1, 10 cases of rearrangement in the MLL gene, 4 cases of E2A-PBX1, 4 cases of E2A-HLF, 3 cases of BCR-ABL, 2 cases of TLS-ERG, 32 cases of HOX11 were detected by Multiplex PCR in B-lineage leukemias.
  • SIL-TAL1 had been found in 4 of 7 of T-lineage leukemias.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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52. Ross JA, Sinner PJ, Blair CK, Cerhan JR, Folsom AR: Hormone replacement therapy is not associated with an increased risk of leukemia (United States). Cancer Causes Control; 2005 Jun;16(5):483-8
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  • [Title] Hormone replacement therapy is not associated with an increased risk of leukemia (United States).
  • Since estrogen receptors are expressed on certain hematopoietic cells, it is possible that HRT use may also increase the risk of leukemia.
  • A total of 201 cases of leukemia were identified over 16 years of follow-up including 74 acute myeloid leukemias (AMLs) and 87 chronic lymphocytic leukemias (CLLs).
  • RESULTS: Compared to never users of HRT at study baseline, current [multivariate relative risk (RR), 1.09; 95% confidence interval (CI) 0.70-1.71)] and former users (RR=0.82, 95% CI=0.59-1.15) were at no increased risk of developing leukemia.
  • CONCLUSION: We conclude that HRT is unlikely to be an appreciable risk factor for leukemia.
  • [MeSH-major] Hormone Replacement Therapy. Leukemia / epidemiology

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  • (PMID = 15986103.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA39741
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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53. Krämer A, Neben K, Ho AD: Centrosome aberrations in hematological malignancies. Cell Biol Int; 2005 May;29(5):375-83
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  • Normally, the single centrosome of a G1 cell duplicates precisely once prior to mitosis in a process that is intimately linked to the cell division cycle via cyclin-dependent kinase (cdk) 2 activity that couples centrosome duplication to the onset of DNA replication at the G1/S transition.
  • In addition to solid neoplasias, centrosome aberrations have recently been described in several different hematological malignancies like acute myeloid leukemias, myelodysplastic syndromes, Hodgkin's as well as non-Hodgkin's lymphomas, chronic lymphocytic leukemias and multiple myelomas.
  • In analogy to many solid tumors a correlation between centrosome abnormalities on the one hand and karyotype aberrations as well as clinical aggressiveness on the other hand seems to exist in myeloid malignancies, chronic lymphocytic leukemias and at least some types of non-Hodgkin's lymphomas.
  • [MeSH-minor] Cell Cycle

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  • (PMID = 15996491.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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54. Nurzyńska-Flak J, Kowalczyk JR: [Incidence of childhood leukemia in the Lublin region of Poland in 1988-2000]. Wiad Lek; 2005;58(5-6):284-6
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  • [Title] [Incidence of childhood leukemia in the Lublin region of Poland in 1988-2000].
  • Purpose of the work was the analysis of the number and structure of leukemia in children living in the Lublin Region of Poland.
  • Among leukemias, according to the International Classification of Childhood Cancers, were counted: lymphoid leukemia, acute non-lymphocytic leukemia, chronic myeloid leukemia, other specified and unspecified leukemias.
  • Number of cases and incidence for the whole group as well as sex, age and descending (rural and urban) distribution of leukemias were calculated.
  • RESULTS: 244 cases of leukemia were reported (152 boys--62.3% and 92 girls--37.7%).
  • CONCLUSIONS: In the Lublin Region lower percentage of leukemia was observed compared to the values determined for the country.
  • Incidence of leukemia was falling, but the analysis in age-groups proved, that it was caused by the decreasing incidence in children under 5 year.
  • [MeSH-major] Leukemia / epidemiology

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  • (PMID = 16238118.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
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55. Smith MT, McHale CM, Wiemels JL, Zhang L, Wiencke JK, Zheng S, Gunn L, Skibola CF, Ma X, Buffler PA: Molecular biomarkers for the study of childhood leukemia. Toxicol Appl Pharmacol; 2005 Aug 07;206(2):237-45
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  • [Title] Molecular biomarkers for the study of childhood leukemia.
  • Various specific chromosome rearrangements, including t(8;21), t(15;17), and inv(16), are found in acute myeloid leukemia (AML) and in childhood acute lymphocytic leukemia (ALL), t(12;21) and t(1;19) are common.
  • These findings show that most childhood leukemias begin before birth and that maternal and perinatal exposures such as chemical and infectious agents are likely to be critical.
  • Indeed, we have reported that exposure to indoor pesticides during pregnancy and the first year of life raises leukemia risk, but that later exposures do not.
  • We have also examined aberrant gene methylation in different cytogenetic subgroups and have found striking differences between them, suggesting that epigenetic events are also important in the development of some forms of childhood leukemia.
  • Further, at least two studies now show that the inactivating NAD(P)H:quinone acceptor oxidoreductase (NQO1) C609T polymorphism is positively associated with leukemias arising in the first 1-2 years of life and polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene have been associated with adult and childhood ALL.
  • Thus, low folate intake and compounds that are detoxified by NQO1 may be important in elevating leukemia risk in children.
  • Finally, we are exploring the use of proteomics to subclassify leukemia, because cytogenetic analysis is costly and time-consuming.
  • Several proteins have been identified that may serve as useful biomarkers for rapidly identifying different forms of childhood leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15967214.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES0098137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 935E97BOY8 / Folic Acid; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
  • [Number-of-references] 55
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56. Bhatia S, Kaul D, Varma N: Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia. Mol Cell Biochem; 2010 Jul;340(1-2):97-106
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  • [Title] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.
  • Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).
  • Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.
  • Also down-regulation of c-myc gene was accompanied by decreased expressions of c-myc effector genes coding for hTERT, Bcl-2, and AATF.
  • Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.
  • Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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  • (PMID = 20549547.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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57. Kong Y, Yoshida S, Saito Y, Doi T, Nagatoshi Y, Fukata M, Saito N, Yang SM, Iwamoto C, Okamura J, Liu KY, Huang XJ, Lu DP, Shultz LD, Harada M, Ishikawa F: CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL. Leukemia; 2008 Jun;22(6):1207-13
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  • [Title] CD34+CD38+CD19+ as well as CD34+CD38-CD19+ cells are leukemia-initiating cells with self-renewal capacity in human B-precursor ALL.
  • In human acute myelogenous leukemia (AML), the leukemia stem cells (LSCs) have been phenotypically restricted within the CD34+CD38- fraction.
  • To understand the origin of malignant cells in primary human B-precursor acute lymphocytic leukemia (B-ALL), we established a novel in vivo xenotransplantation model.
  • The identification of CD34+CD38+CD19+ self-renewing B-ALL cells proposes a hierarchy of leukemia-initiating cells (LICs) distinct from that of AML.
  • [MeSH-major] Antigens, CD19 / metabolism. Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Hematopoietic Stem Cells / pathology. Neoplastic Stem Cells / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Animals. Animals, Newborn. Cell Differentiation. Cell Lineage. Child. Flow Cytometry. Graft Survival. Humans. Immunophenotyping. Infant. Mice. Mice, Inbred NOD. Mice, SCID. Transplantation, Heterologous. Tumor Cells, Cultured. Whole-Body Irradiation

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  • (PMID = 18418410.001).
  • [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 / Antigens, CD19; 0 / Antigens, CD34; EC 3.2.2.5 / Antigens, CD38
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58. Saxena A, Rai A, Raina V, Seth T, Mitra DK: Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells. Cancer Immunol Immunother; 2010 Jan;59(1):125-35
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  • [Title] Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells.
  • Expression of cell surface CD13 in acute B-cell leukemia (ALL-B) is often viewed, as an aberrant expression of a myeloid lineage marker.
  • Here, we attempted to study the stage specific expression of CD13 on ALL-B blasts and understand its role in leukemogenesis as pertaining to stage of B-cell ontogeny.
  • Among 68 cases of early B-cell ALL, 22 cases with distinct immunophenotype was identified as immature B-cell ALL.
  • This strongly indicates leukemogenesis at an early stage of B-cell development.
  • We also identified, the existence of a subpopulation of cells with remarkably similar phenotype in non-leukemic marrow from healthy subjects (expressing CD10, CD19, CD22, CD24, Tdt together with the co-expression of CD13).
  • By blocking their cell surface CD13 in leukemic blasts with monoclonal antibody we were able to inhibit their proliferation.
  • CD13 may thus be an important target for novel molecular therapy of early stage acute B-cell leukemia.
  • [MeSH-major] Antigens, CD13 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19562339.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13
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59. Kantarjian H, le Coutre P, Cortes J, Pinilla-Ibarz J, Nagler A, Hochhaus A, Kimura S, Ottmann O: Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance. Cancer; 2010 Jun 1;116(11):2665-72
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  • [Title] Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.
  • BACKGROUND: : INNO-406, a dual v-abl Abelson murine leukemia viral oncogene homolog (Abl)/v-yes-1 Yamaguchi sarcoma viral-related oncogene homolog (Lyn) tyrosine kinase inhibitor (TKI), has demonstrated specific Lyn kinase inhibitory activity with no or limited activity against other sarcoma (Src) family member kinases.
  • In the current study, the authors evaluated the use of INNO-406 in patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) after imatinib resistance or intolerance.
  • Cohorts of at least 3 patients were treated at each dose level until the maximum tolerated dose (MTD) was reached.

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  • [Copyright] (c) 2010 American Cancer Society.
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  • (PMID = 20310049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632-070007; United States / NCI NIH HHS / CA / CA100632-070007; United States / NCI NIH HHS / CA / P01CA049639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA049639
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS189694; NLM/ PMC2876208
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60. Clark BR, Ferketich AK, Fisher JL, Ruymann FB, Harris RE, Wilkins JR 3rd: Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio. Pediatr Blood Cancer; 2007 Nov;49(6):797-802
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  • [Title] Evidence of population mixing based on the geographical distribution of childhood leukemia in Ohio.
  • BACKGROUND: This ecologic study examined the geographic distribution of childhood leukemias in Ohio, 1996-2000, among children aged 0-19 for evidence that population mixing may be a factor.
  • RESULTS: Of the 585 cases, 73.3% were acute lymphocytic leukemia (ALL), 16.6% acute myelogenous leukemia (AML), 3.2% acute monocytic leukemia (AMoL), and 2.6% chronic myelogenous leukemia (CML).
  • Rates for total leukemia burden were significantly below national levels for all races (P = 0.00001), likely due to poor ascertainment of cases.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Population Density. Population Dynamics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Rural Population. Urban Population


61. Fenaux P: Inhibitors of DNA methylation: beyond myelodysplastic syndromes. Nat Clin Pract Oncol; 2005 Dec;2 Suppl 1:S36-44
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  • DNA methyltransferase (DNMT) inhibitors, azacitidine (Vidaza, Pharmion, Boulder, CO, USA) and decitabine (Dacogen; SuperGen Inc, Dublin, CA, USA, and MGI Pharma Inc, Bloomington, MN, USA), have had a significant impact on the treatment paradigm of myelodysplastic syndromes (MDSs), previously managed mainly by supportive care and hematopoietic-stem-cell transplantation.
  • The positive clinical experience seen in MDS to date coupled with the persistent challenges faced in the treatment of other hematologic malignancies has served as the impetus for further exploration of the therapeutic value of DNMT inhibitors beyond MDS.
  • In that respect, the majority of data for these agents are in the setting of acute myelogenous leukemia (AML).
  • Some use has also been described in chronic myelogenous leukemia and acute lymphocytic leukemia.
  • Further studies are needed to clarify the appropriate dose and the number and duration of cycles in the treatment of leukemias, and to identify ideal candidates for therapy, explore the role of DNMT inhibitors in combination with other agents, especially histone deacetylase inhibitors, delineate differences between the commercially available agents, and establish the long-term safety of these agents.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia / drug therapy. Leukemia / genetics

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  • (PMID = 16341239.001).
  • [ISSN] 1743-4254
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Number-of-references] 73
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62. Wang X, Yuling H, Yanping J, Xinti T, Yaofang Y, Feng Y, Ruijin X, Li W, Lang C, Jingyi L, Zhiqing T, Jingping O, Bing X, Li Q, Chang AE, Sun Z, Youxin J, Jinquan T: CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells. J Immunol; 2007 Sep 1;179(5):2880-8
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  • [Title] CCL19 and CXCL13 synergistically regulate interaction between B cell acute lymphocytic leukemia CD23+CD5+ B Cells and CD8+ T cells.
  • In a previous study, we have reported that ligation of CCL19-CCR7 and CXCL13-CXCR5 activates paternally expressed gene 10 (PEG10), resulting in an enhancement of apoptotic resistance in B-cell acute lymphocytic leukemia (B-ALL) CD23+CD5+ B cells.
  • Here, we report that B-ALL CD23+CD5+ B cells produce IL-10 at high level, which can be further elevated by costimulation with CCL19 and CXCL13.
  • CCL19/CXCL13-activated B-ALL CD23+CD5+ B cells, in turn, increase IL-10 expression in syngeneic CD8+ T cells in a B cell-derived IL-10-dependent manner and requiring a cell-cell contact.
  • Moreover, using a short hairpin RNA to knockdown PEG10, we provide direct evidence that increased expression of PEG10 in B-ALL CD23+CD5+ B cells is involved in malignant B-T cell interaction, contributing to the up-regulation of IL-10 expression, as well as to the impairment of cytotoxicity of syngeneic CD8+ T cells.
  • [MeSH-major] B-Lymphocytes / immunology. Burkitt Lymphoma / immunology. CD8-Positive T-Lymphocytes / immunology. Chemokine CCL19 / physiology. Chemokine CXCL13 / physiology. Immunologic Surveillance / immunology

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  • [ErratumIn] J Immunol. 2007 Nov 15;179(10):7184
  • (PMID = 17709502.001).
  • [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 / Antigens, CD5; 0 / CXCL13 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / PEG10 protein, human; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Receptors, IgE; 130068-27-8 / Interleukin-10
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63. Kara IO, Sahin B, Gunesacar R: Levels of serum and cerebrospinal fluid soluble CD27 in the diagnosis of leptomeningeal involvement of hematolymphoid malignancies. Adv Ther; 2007 Jul-Aug;24(4):741-7
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  • Reportedly, soluble CD27 (sCD27) is a sensitive and specific marker for leptomeningeal involvement (LI) of CD27-expressing lymphoproliferations, such as B-cell non-Hodgkin's lymphoma and chronic B-lymphocytic leukemia.
  • On morphologic analysis of cerebrospinal fluid (CSF), one third of patients suspected of LI have false negatives, so a diagnostic marker for LI in B-cell non-Hodgkin's lymphoma or B-lymphocytic leukemia would be extremely valuable. sCD27 was detected in the serum and CSF samples from 35 selected patients in whom 18 cases of acute lymphoblastic leukemia (ALL) (3 with LI), 7 of non-Hodgkin's lymphoma, and 5 of acute myelogenous leukemia (3 with LI) were submitted for (immuno)morphologic detection of malignant cells and intrathecal therapy, along with samples from 5 control patients (2 submitted for epidural hemorrhage, 3 for lumbar disc protrusion).
  • The cutoff value was 350 U/mL.
  • Serum and CSF-sCD27 concentrations above the cutoff value were not detected.
  • [MeSH-minor] Biomarkers, Tumor / blood. Biomarkers, Tumor / cerebrospinal fluid. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / cerebrospinal fluid. Leukemia, Myeloid, Acute / pathology. Lymphoma, Non-Hodgkin / blood. Lymphoma, Non-Hodgkin / cerebrospinal fluid. Lymphoma, Non-Hodgkin / pathology. Meninges / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / cerebrospinal fluid. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Predictive Value of Tests

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  • (PMID = 17901023.001).
  • [ISSN] 0741-238X
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Biomarkers, Tumor
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64. Volinia S, Galasso M, Costinean S, Tagliavini L, Gamberoni G, Drusco A, Marchesini J, Mascellani N, Sana ME, Abu Jarour R, Desponts C, Teitell M, Baffa R, Aqeilan R, Iorio MV, Taccioli C, Garzon R, Di Leva G, Fabbri M, Catozzi M, Previati M, Ambs S, Palumbo T, Garofalo M, Veronese A, Bottoni A, Gasparini P, Harris CC, Visone R, Pekarsky Y, de la Chapelle A, Bloomston M, Dillhoff M, Rassenti LZ, Kipps TJ, Huebner K, Pichiorri F, Lenze D, Cairo S, Buendia MA, Pineau P, Dejean A, Zanesi N, Rossi S, Calin GA, Liu CG, Palatini J, Negrini M, Vecchione A, Rosenberg A, Croce CM: Reprogramming of miRNA networks in cancer and leukemia. Genome Res; 2010 May;20(5):589-99
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  • [Title] Reprogramming of miRNA networks in cancer and leukemia.
  • We also built, for the first time, specialized miRNA networks for solid tumors and leukemias.
  • Other miRNAs, such as hsa-miR-30 and hsa-miR-204, were found to be physically altered at the DNA copy number level as well.
  • Finally, we experimentally validated the miRNA network with acute lymphocytic leukemia originated in Mir155 transgenic mice.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia. MicroRNAs / genetics. Neoplasms
  • [MeSH-minor] Adenocarcinoma / metabolism. Animals. Cell Line, Tumor. Gene Dosage. Humans. Lung / metabolism. Lung Neoplasms / metabolism. Mice. Oligonucleotide Array Sequence Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


65. Vallera DA, Oh S, Chen H, Shu Y, Frankel AE: Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases. Mol Cancer Ther; 2010 Jun;9(6):1872-83
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  • [Title] Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases.
  • The aims were to reduce toxin immunogenicity using mutagenesis, measure the ability of mutated drug to elicit antitoxin antibody responses, and show that mutated drug was effective against systemic B-cell lymphoma in vivo.
  • Site-specific mutagenesis was used to mutate amino acids in seven key epitopic toxin regions that dictate B-cell generation of neutralizing antitoxin antibodies.
  • Finally, a powerful genetically altered luciferase xenograft model was used that could be imaged in real time to determine the effect on systemic malignant human B-cell lymphoma, Raji-luc.
  • Patient B-lineage acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia, and B lymphoma were high in CD22 and CD19 expression.

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  • (PMID = 20530709.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108637; United States / NCI NIH HHS / CA / R01 CA082154; United States / NCI NIH HHS / CA / CA036725-25; United States / NCI NIH HHS / CA / CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725; United States / NCI NIH HHS / CA / R01-CA36725; United States / NCI NIH HHS / CA / R01-CA082154; United States / NCI NIH HHS / CA / R01 CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725-25
  • [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 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Virulence Factors; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
  • [Other-IDs] NLM/ NIHMS198461; NLM/ PMC2884080
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66. Dubowy R, Graham M, Hakami N, Kletzel M, Mahoney D, Newman E, Ravindranath Y, Camitta B: Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study. J Pediatr Hematol Oncol; 2008 May;30(5):353-7
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  • [Title] Sequential oral hydroxyurea and intravenous cytosine arabinoside in refractory childhood acute leukemia: a pediatric oncology group phase 1 study.
  • At concentrations >0.1 mM, hydroxyurea (HU) enhances the accumulation of cytosine arabinoside (ara-C) in leukemia cells in vitro.
  • This study of children with refractory acute leukemia was designed to take advantage of this biochemical modulation.
  • Thirty-three children [26 acute lymphocytic leukemia (ALL), 7 acute nonlymphocytic leukemia] were treated; 29 received at least 1 full course.
  • There were 6 complete responses (5 ALL), 5 partial responses (3 ALL), and 19 patients with no response or progressive disease.
  • There was no dosage effect for response with 2 complete responses occurring at the lowest ara-C level.
  • Twenty of twenty-six patients achieved a peak serum HU level >0.5 mM by 2 hours after the HU dose.
  • The mean level at 2 hours was 0.57 mM (range: 0.21 to 0.99 mM).
  • This combination of HU and ara-C is tolerable and has efficacy in refractory leukemias.
  • Responses at the lowest ara-C dose level suggests synergism.
  • [MeSH-major] Cytarabine / toxicity. Hydroxyurea / toxicity. Leukemia / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Humans. Infection / epidemiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / mortality. Liver / drug effects. Liver / pathology. Skin / drug effects. Skin / pathology. Survival Analysis

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  • (PMID = 18458568.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098413; United States / NCI NIH HHS / CA / U10 CA098543
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS721202; NLM/ PMC4601800
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67. Grüllich C, Friske V, Finke J: Ex vivo detection of primary leukemia cells resistant to granule cytotoxin-induced cell death: a rapid isolation method to study granzyme-B-mediated cell death. Ann Hematol; 2008 Sep;87(9):701-8
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  • [Title] Ex vivo detection of primary leukemia cells resistant to granule cytotoxin-induced cell death: a rapid isolation method to study granzyme-B-mediated cell death.
  • Cytotoxic T lymphocytes and natural killer cells (CTL/NK) induce cell death in leukemia cells by the granzyme B (grB)-dependent granule cytotoxin (GC) pathway.
  • Resistance to GC may be involved in immune evasion of leukemia cells.
  • We developed a rapid method for the isolation of GC to investigate GC-mediated cell death in primary leukemia cells.
  • We isolated GC containing grB, grB complexes and PFN by detergent free hypotonic lysis of the human NK cell leukemia line YT.
  • The human leukemia cell lines KG-1, U937, K562 (myeloid leukemia), Jurkat, Daudi, and BV173 (lymphoblastic leukemia) treated with GC internalized grB and underwent cell death.
  • In primary leukemia cells analyzed ex vivo, we found GC-resistant leukemia cells in three out of seven patients with acute myeloid leukemia and one out of six patients with acute lymphoblastic leukemia.
  • We conclude that our method is fast (approximately 1 h) and yields active GC that induce grB-dependent cell death.
  • Furthermore, resistance to GC can be observed in acute leukemias and may be an important mechanism contributing to leukemia cell immune evasion.
  • [MeSH-major] Cell Death / drug effects. Cytotoxins / toxicity. Granzymes / toxicity. Leukemia / pathology
  • [MeSH-minor] Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. K562 Cells / drug effects. K562 Cells / pathology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myeloid, Acute / pathology. Perforin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. T-Lymphocytes, Cytotoxic / immunology. U937 Cells / drug effects. U937 Cells / pathology

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  • (PMID = 18437383.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cytotoxins; 126465-35-8 / Perforin; EC 3.4.21.- / Granzymes
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68. Kusy S, Gerby B, Goardon N, Gault N, Ferri F, Gérard D, Armstrong F, Ballerini P, Cayuela JM, Baruchel A, Pflumio F, Roméo PH: NKX3.1 is a direct TAL1 target gene that mediates proliferation of TAL1-expressing human T cell acute lymphoblastic leukemia. J Exp Med; 2010 Sep 27;207(10):2141-56
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  • [Title] NKX3.1 is a direct TAL1 target gene that mediates proliferation of TAL1-expressing human T cell acute lymphoblastic leukemia.
  • TAL1 (also known as SCL) is expressed in >40% of human T cell acute lymphoblastic leukemias (T-ALLs).
  • TAL1 encodes a basic helix-loop-helix transcription factor that can interfere with the transcriptional activity of E2A and HEB during T cell leukemogenesis; however, the oncogenic pathways directly activated by TAL1 are not characterized.
  • In this study, we show that, in human TAL1-expressing T-ALL cell lines, TAL1 directly activates NKX3.1, a tumor suppressor gene required for prostate stem cell maintenance.
  • In human T-ALL cell lines, NKX3.1 gene activation is mediated by a TAL1-LMO-Ldb1 complex that is recruited by GATA-3 bound to an NKX3.1 gene promoter regulatory sequence.
  • Finally, TAL1 or NKX3.1 knockdown abrogates the ability of human T-ALL cells to efficiently induce leukemia development in mice.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / genetics. Homeodomain Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cell Line, Tumor. Cell Proliferation. DNA-Binding Proteins / metabolism. GATA3 Transcription Factor / metabolism. Gene Knockdown Techniques. Genes, Tumor Suppressor. Humans. LIM Domain Proteins. Male. Metalloproteins / metabolism. Mice. Neoplasm Transplantation. Prostate / metabolism. Prostate / pathology. Protein Binding. Stem Cells / physiology

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  • (PMID = 20855495.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / GATA3 Transcription Factor; 0 / GATA3 protein, human; 0 / Homeodomain Proteins; 0 / LDB1 protein, human; 0 / LIM Domain Proteins; 0 / LMO1 protein, human; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / NKX3-1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
  • [Other-IDs] NLM/ PMC2947082
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69. Tasca S, Carli E, Caldin M, Menegazzo L, Furlanello T, Gallego LS: Hematologic abnormalities and flow cytometric immunophenotyping results in dogs with hematopoietic neoplasia: 210 cases (2002-2006). Vet Clin Pathol; 2009 Mar;38(1):2-12
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  • RESULTS: Based on cell morphology and phenotype, cases were classified as: acute lymphoblastic leukemia (ALL, n=51), acute myeloid leukemia (AML, n=33), chronic lymphocytic leukemia (CLL, n=61), and leukemic high-grade lymphoma (L-HGL, n=65).
  • Most cases of ALL (47/51) and L-HGL (41/65) had a B-cell phenotype, while most cases of CLL (54/61) had a T-cell phenotype, with a high prevalence of the large granular lymphocyte subtype (49/61).
  • Neutropenia was seen in 64-78% of acute leukemias (AML and ALL) in contrast to no cases of CLL and 11% of L-HGL.
  • Thrombocytopenia was seen in 88-90% of acute leukemias in contrast to 15% of CLL and 40% of L-HGL.
  • Thrombocytopenia was more prevalent (71% vs 22%) and significantly more severe in T-cell vs B-cell L-HGL.

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  • (PMID = 19171020.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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70. StatBite: Estimated new cases for the four major leukemias, 2008. J Natl Cancer Inst; 2009 Mar 18;101(6):371
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  • [Title] StatBite: Estimated new cases for the four major leukemias, 2008.
  • [MeSH-major] Leukemia / epidemiology
  • [MeSH-minor] Humans. Incidence. Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Research Support as Topic / trends. United States / epidemiology

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  • (PMID = 19276455.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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71. Gluzman D, Imamura N, Sklyarenko L, Nadgornaya V, Zavelevich M, Machilo V: Patterns of hematological malignancies in Chernobyl clean-up workers (1996-2005). Exp Oncol; 2006 Mar;28(1):60-3
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  • AIM: The question as to whether the incidence of leukemias and malignant lymphomas among the Chernobyl clean-up workers increased in 20 years after the catastrophe is still a point of much controversy.
  • RESULTS: Various types of oncohematological diseases developing 10-20 years after Chernobyl accident were registered in a group of clean-up workers under study including myelodysplastic syndromes (MDS), acute leukemias (ALL and AML), chronic myelogenous leukemia (CML) and other chronic myeloproliferative diseases, chronic lymphocytic leukemia (B-CLL) and other chronic lymphoproliferative diseases of B and T cell origin.
  • Among 34 AML cases, leukemia was preceded by MDS in seven patients.
  • The relative contribution of CML to the total number of clean-up workers with leukemia was higher than the corresponding percentage value in general population examined at the same period (9.17 vs. 6.59%).
  • CONCLUSION: The verified diagnosis of tumors of hematopoietic and lymphoid tissue according to modern classification (EGIL, WHO) could be the prerequisite for further molecular genetic and analytical epidemiology study of leukemias that may be related to Chernobyl NPP accident consequences.
  • [MeSH-minor] Antigens, CD / analysis. Bone Marrow Cells / pathology. Humans. Immunohistochemistry. Leukemia / epidemiology. Ukraine / epidemiology

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  • (PMID = 16614710.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Radioactive Fallout
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72. Kotani A, Ha D, Schotte D, den Boer ML, Armstrong SA, Lodish HF: A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells. Cell Cycle; 2010 Mar 15;9(6):1037-42
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  • [Title] A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells.
  • MLL-AF4 acute lymphocytic leukemia has a poor prognosis, and the mechanisms by which these leukemias develop are not understood despite intensive research based on well-known concepts and methods.

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  • (PMID = 20237425.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK068348-05; United States / NIDDK NIH HHS / DK / DK068348-06A1; United States / NIDDK NIH HHS / DK / R56 DK068348-06A1; United States / NIDDK NIH HHS / DK / R01 DK068348-05; United States / NIDDK NIH HHS / DK / R56 DK068348; United States / NIDDK NIH HHS / DK / R01 DK068348
  • [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 / Glucocorticoids; 0 / MIRN128 microRNA, human; 0 / MIRN221 microRNA, human; 0 / MicroRNAs
  • [Other-IDs] NLM/ NIHMS277523; NLM/ PMC3096720
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73. Bourette RP, Grasset MF, Mouchiroud G: E2a/Pbx1 oncogene inhibits terminal differentiation but not myeloid potential of pro-T cells. Oncogene; 2007 Jan 11;26(2):234-47
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  • E2a/Pbx1 is a fusion oncoprotein resulting from the t(1;19) translocation found in human pre-B acute lymphocytic leukemia and in a small number of acute T-lymphoid and myeloid leukemias.
  • To address this question, we introduced the receptor of the macrophage-colony-stimulating factor (M-CSF-R) in pro-T cells immortalized by a conditional, estradiol-dependent, E2a/Pbx1-protein, and continuously proliferating in response to stem cell factor and interleukin-7.
  • We asked whether M-CSF-R would be functional in an early T progenitor cell and influence the fate of E2a/Pbx1-immortalized cells.
  • This demonstrated that M-CSF-R is functional for proliferation and differentiation signaling in a T-lymphoid progenitor cell, which, in addition, unveiled myeloid potential of pro-T progenitors.
  • [MeSH-major] Cell Differentiation. Cell Lineage. Cell Transformation, Neoplastic. Homeodomain Proteins / physiology. Oncogene Proteins, Fusion / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Proliferation. Estradiol / pharmacology. Female. Flow Cytometry. Genes, fms / genetics. Genes, fms / physiology. Green Fluorescent Proteins / metabolism. Interleukin-7 / pharmacology. Lymphocytes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Myeloid Cells / metabolism. Phagocytosis. Receptor, Macrophage Colony-Stimulating Factor / genetics. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Stem Cell Factor / pharmacology. Stem Cells / metabolism. Stem Cells / pathology

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  • (PMID = 16819510.001).
  • [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 / Homeodomain Proteins; 0 / Interleukin-7; 0 / Oncogene Proteins, Fusion; 0 / Stem Cell Factor; 0 / enhanced green fluorescent protein; 146150-85-8 / E2A-Pbx1 fusion protein; 147336-22-9 / Green Fluorescent Proteins; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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74. Bloomfield CD, Mrózek K, Caligiuri MA: Cancer and leukemia group B leukemia correlative science committee: major accomplishments and future directions. Clin Cancer Res; 2006 Jun 1;12(11 Pt 2):3564s-71s
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  • [Title] Cancer and leukemia group B leukemia correlative science committee: major accomplishments and future directions.
  • The Cancer and Leukemia Group B (CALGB) Leukemia Correlative Science Committee (LCSC) has a remarkable history of outstanding productivity and has been at the cutting edge of correlative science for adult leukemia for almost 25 years.
  • Its work, initially focused on the use of immunophenotyping for diagnosis and prognosis of acute lymphoblastic leukemia and acute myeloid leukemia, has, for the last 15 years, focused on the clinical use of cytogenetic and molecular genetic markers in acute myeloid leukemia and acute lymphoblastic leukemia as well as in chronic lymphocytic leukemia.
  • Numerous CALGB LCSC studies have had a major effect on the way we currently diagnose, predict outcome, select appropriate treatment, document complete remission, and monitor residual disease in adults with acute leukemia.
  • In part as a result of the work of the CALGB LCSC, we are increasingly moving toward molecularly targeted therapy in acute and chronic leukemias.
  • In this report, we briefly review those contributions from the CALGB LCSC that have had, or are likely to have in the future, a major effect on how we currently manage leukemia and outline directions of ongoing and future research conducted by the CALGB LCSC.
  • [MeSH-major] Cytogenetics / trends. Leukemia / genetics. Molecular Biology / trends. Societies, Medical / trends

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  • (PMID = 16740786.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 80
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75. Erdag G, Meck JM, Meloni-Ehrig A, Matyakhina L, Donohue T, Srinivasan R, Mowrey P, Kelly J, Smith A, Childs R: Long-term persistence of nonpathogenic clonal chromosome abnormalities in donor hematopoietic cells after allogeneic stem cell transplantation. Cancer Genet Cytogenet; 2009 Apr 15;190(2):125-30
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  • [Title] Long-term persistence of nonpathogenic clonal chromosome abnormalities in donor hematopoietic cells after allogeneic stem cell transplantation.
  • We describe the cases of two unrelated patients who exhibited multiple chromosomal abnormalities in donor cells after allogeneic peripheral blood stem cell transplantation (PBSCT).
  • The patients were diagnosed with chronic myeloid leukemia and chronic lymphocytic leukemia, respectively, and both underwent nonmyeloablative conditioning with cyclophosphamide and fludarabine followed by PBSCT from their HLA-matched opposite-sex siblings.
  • In contrast, only rare reports of chromosome abnormalities in donor cells exist, all of which have been associated with post-bone marrow transplant myelodysplastic syndrome or acute leukemias.
  • [MeSH-major] Chromosome Aberrations. Hematopoietic Stem Cell Transplantation
  • [MeSH-minor] Aged. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Male. Middle Aged

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  • (PMID = 19380032.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 HL999999
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS129478; NLM/ PMC2764294
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76. Belov L, Huang P, Chrisp JS, Mulligan SP, Christopherson RI: Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells. J Immunol Methods; 2005 Oct 20;305(1):10-9
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  • We have developed a microarray (DotScan) that enables rapid immunophenotyping and classification of leukaemias and lymphomas by measuring the capture of cells by immobilized dots of 82 CD antibodies [Belov, L., de la Vega, O., dos Remedios, C.G., Mulligan, S.P., 2001.
  • Immunophenotyping of leukemia using a cluster of differentiation antibody microarray. Cancer Res.
  • Identification of repertoires of surface antigens on leukemias using an antibody microarray.
  • After blocking the remaining nitrocellulose surface, individual arrays were incubated with each of 7 cell types from a human leukaemia cell panel consisting of three cell lines, CCRF-CEM (a T-cell acute lymphocytic leukaemia), MEC-1 (derived from B-cell chronic lymphocytic leukaemia) and HL-60 (a promyelocytic leukaemia), and four leukaemias from patients: a T-cell prolymphocytic leukaemia, a B-cell chronic lymphocytic leukaemia, and two acute myeloid leukaemias.
  • The data obtained show the unique expression profiles of the 7 cell types in the leukaemia cell panel obtained with the DotScan microarray, and the differential capture patterns for these 7 cell types screened against the 498 antibodies in the HLDA8 microarray constructed for this study.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, CD / analysis. Leukemia / classification. Protein Array Analysis / methods
  • [MeSH-minor] Cell Line, Tumor. Collodion / chemistry. Flow Cytometry. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / immunology. Leukemia, Myeloid / classification. Leukemia, Myeloid / immunology. Leukemia, T-Cell / classification. Leukemia, T-Cell / immunology

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  • (PMID = 16125720.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 9004-70-0 / Collodion
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77. Ostrowska H, Hempel D, Holub M, Sokolowski J, Kloczko J: Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias. Clin Biochem; 2008 Nov;41(16-17):1377-83
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  • [Title] Assessment of circulating proteasome chymotrypsin-like activity in plasma of patients with acute and chronic leukemias.
  • OBJECTIVE: We evaluated whether the proteasomal chymotrypsin-like (ChT-L) activity is increased in plasma of patients with acute lymphoblastic (ALL), acute myeloblastic (AML) and chronic lymphocytic (CLL) leukemias.
  • CONCLUSIONS: Plasma proteasome ChT-L activity can be a useful bio-marker for patients with acute leukemia at the blast stage.
  • [MeSH-major] Chymotrypsin / blood. Leukemia / blood. Proteasome Endopeptidase Complex / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Female. Humans. Hydrolysis / drug effects. L-Lactate Dehydrogenase / blood. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Male. Middle Aged. Oligopeptides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Proteasome Inhibitors. Protein Subunits / metabolism. Sodium Dodecyl Sulfate / pharmacology

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  • (PMID = 18773885.001).
  • [ISSN] 1873-2933
  • [Journal-full-title] Clinical biochemistry
  • [ISO-abbreviation] Clin. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Proteasome Inhibitors; 0 / Protein Subunits; 134381-21-8 / epoxomicin; 368GB5141J / Sodium Dodecyl Sulfate; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.4.21.1 / Chymotrypsin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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78. Figueroa ME, Reimers M, Thompson RF, Ye K, Li Y, Selzer RR, Fridriksson J, Paietta E, Wiernik P, Green RD, Greally JM, Melnick A: An integrative genomic and epigenomic approach for the study of transcriptional regulation. PLoS One; 2008 Mar 26;3(3):e1882
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  • The molecular heterogeneity of acute leukemias and other tumors constitutes a major obstacle towards understanding disease pathogenesis and developing new targeted-therapies.
  • We predicted that integration of different genome-wide epigenetic regulatory marks along with gene expression levels would provide greater power in capturing biological differences between leukemia subtypes.
  • Gene expression, cytosine methylation and histone H3 lysine 9 (H3K9) acetylation were measured using high-density oligonucleotide microarrays in primary human acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) specimens.
  • We found that DNA methylation and H3K9 acetylation distinguished these leukemias of distinct cell lineage, as expected, but that an integrative analysis combining the information from each platform revealed hundreds of additional differentially expressed genes that were missed by gene expression arrays alone.

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  • (PMID = 18365023.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104348; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / GM007288
  • [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 Primers; 0 / Histones
  • [Other-IDs] NLM/ PMC2266992
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79. Manola KN, Sambani C, Karakasis D, Kalliakosta G, Harhalakis N, Papaioannou M: Leukemias associated with Turner syndrome: report of three cases and review of the literature. Leuk Res; 2008 Mar;32(3):481-6
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  • [Title] Leukemias associated with Turner syndrome: report of three cases and review of the literature.
  • Cases of leukemia associated with Turner syndrome (TS) are rare.
  • Here we report three TS patients with leukemia including one case of T-large granular lymphocyte leukemia (T-LGL), one rare case of coexistence of chronic lymphocytic leukemia (CLL) and idiopathic myelofibrosis (IMF) and one case of a patient with AML-M2 who received autologous stem cell transplantation (SCT).
  • T-LGL and coexistence of CLL and IMF associated with TS are reported for the first time while the last case represents the first report of SCT in a leukemia patient with TS.
  • Our cases and the limited data of previously reported leukemia patients with TS suggest that TS is not associated with a specific type of leukemia and that presentation, clinical course and response to treatment are similar to that of the non-TS leukemia patients.
  • Interestingly, in the mosaic TS patients, the abnormal clones were restricted to the monosomic 45,X cells, indicating that the leukemic clones possibly originate from the monosomic cell line.
  • Even in cases with no additional chromosome abnormalities, the ratio of X/XX cells in bone marrow cells was significantly increased compared to that in constitutional karyotype, indicating that monosomic cells possibly provide a survival advantage for leukemia cells or that reduced programmed cell death may be responsible for the expansion of the monosomic cells.
  • [MeSH-major] Leukemia / complications. Turner Syndrome / complications
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Large Granular Lymphocytic / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Myeloid, Acute / complications. Middle Aged. Monosomy. Treatment Outcome

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  • (PMID = 17669490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
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80. Kiss F, Buslig J, Szegedi I, Scholtz B, Kappelmayer J, Kiss C: Early relapse after rituximab chemoimmunotherapy. Pediatr Blood Cancer; 2008 Feb;50(2):372-5
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  • In relapsed/refractory childhood acute lymphoblastic leukemia (ALL) of the B-cell lineage rituximab, a monoclonal anti-CD20 antibody was used successfully in some cases.
  • We report on a 15-year-old female with relapsed CD20-positive B-cell progenitor ALL treated with rituximab because of positive minimal residual disease signals after chemotherapy, as checked by flow cytometry and real time quantitative-PCR.
  • The patient died with fulminant aspergillosis before hematopoietic stem cell transplantation could be performed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Flow Cytometry. Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Humans. Neoplasm, Residual / pathology. Recurrence. Rituximab

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17973316.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
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81. Hatakeyama N, Tamura Y, Sahara H, Suzuki N, Suzuki K, Hori T, Mizue N, Torigoe T, Tsutsumi H, Sato N: Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells. Exp Hematol; 2006 Feb;34(2):197-207
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  • [Title] Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells.
  • OBJECTIVE: Several studies have demonstrated that dendritic cells (DCs) pulsed with tumor lysate or apoptotic tumor cells can elicit effective T-cell responses.
  • We applied this approach to induce HLA class I- and class II-restricted T-cell responses directed against autologous acute lymphocytic leukemia (B-ALL) cell line NH-1.
  • METHODS: Autologous T cells were stimulated by apoptotic tumor cell-loaded DCs generated from a patient with ALL.
  • The stimulated and expanded T cells were isolated into CD8(+) T-cell line and CD4(+) T-cell line, and each of them was examined as to their functions.
  • RESULTS: Both CD8(+) and CD4(+) T-cell lines demonstrated cytotoxicity against NH-1 in an major histocompatibility complex-dependent manner.
  • Finally, we established two independent CD4(+) T-cell clones restricted to HLA-DR.
  • The CD4(+) T-cell line responded strongly to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) but not to autologous normal cells.
  • Furthermore, the T-cell clones also responded to allogeneic EBV-LCLs and B-ALL cell lines in the context of the HLA-DRB1( *)04051 molecule.
  • Interestingly, 293T and COS-7 cells, which had been transfected with the HLA-DRB1( *)04051, were also recognized by T-cell clones.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Fusion. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Apoptosis / immunology. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. Epitopes / immunology. Epstein-Barr Virus Nuclear Antigens / immunology. Female. HLA-DR Antigens / classification. HLA-DR Antigens / immunology. Histocompatibility Antigens Class II / immunology. Histocompatibility Antigens Class II / pharmacology. Humans. Infant. Lymphocyte Activation

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  • (PMID = 16459188.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Epitopes; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / HLA-DR Antigens; 0 / Histocompatibility Antigens Class II
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82. Howard RA, Gilbert ES, Chen BE, Hall P, Storm H, Pukkala E, Langmark F, Kaijser M, Andersson M, Joensuu H, Fossa SD, Travis LB: Leukemia following breast cancer: an international population-based study of 376,825 women. Breast Cancer Res Treat; 2007 Nov;105(3):359-68
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  • [Title] Leukemia following breast cancer: an international population-based study of 376,825 women.
  • PURPOSE: To quantify long-term temporal trends in the excess absolute risk (EAR) of secondary leukemia among breast cancer (BC) survivors, using multivariate analyses to evaluate the effects of subtype, age at BC diagnosis, attained age, and calendar year.
  • RESULTS: A total of 687 non-chronic lymphocytic leukemias (EAR = 9.05; 95% confidence interval (CI) = 7.5-10.7) was reported.
  • Significantly elevated risks were observed for the first time for chronic myeloid leukemia (CML) (EAR = 2.06; 95% CI = 1.3-2.9) and acute lymphoblastic leukemia (ALL) (EAR = 0.62; 95% CI = 0.2-1.1), in addition to acute myeloid leukemia (AML) (EAR = 5.00; 95% CI = 3.9-6.2).
  • Excesses of CML, ALL, AML and all leukemias combined persisted over 25 years after BC diagnosis.
  • For all leukemias, EAR decreased with increasing calendar year (P = 0.04) of BC diagnosis.
  • Risk for all leukemia and AML by calendar year of BC diagnosis depended on age at diagnosis.
  • For women diagnosed with BC after 1985, the 10-year cumulative risk of leukemia for those diagnosed before and after age 50 was small, 0.10% and 0.14%, respectively.
  • CONCLUSIONS: Although secondary leukemia is a rare event, BC survivors experience statistically significant excesses for at least 25 years after diagnosis, including CML and ALL.
  • Decreasing leukemia risks in recent calendar years likely reflect changes in treatment.
  • [MeSH-major] Breast Neoplasms / complications. Breast Neoplasms / epidemiology. Leukemia / complications. Leukemia / epidemiology. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukemia, Radiation-Induced / complications. Leukemia, Radiation-Induced / diagnosis. Leukemia, Radiation-Induced / epidemiology. Middle Aged. Risk Factors

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  • (PMID = 17221155.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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83. Terzakis JA, Santagada E, Hernandez A, Taskin M: Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias. Ultrastruct Pathol; 2005 Jan-Feb;29(1):19-28
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  • [Title] Scanning electron microscopy of peripheral blood smears: comparison of normal blood with some common leukemias.
  • Peripheral blood smears prepared routinely from nonneoplastic and leukemia cases were studied using the scanning electron microscope (SEM).
  • The peripheral blood glass slide is examined directly in the SEM following application of a thin carbon coat.
  • Certain cell features are measured as well with the use of the measuring software resident in the SEM.
  • The problem of cell constituent loss and overall shrinkage in the routinely processed and sectioned material is noted.
  • The monoblast resembles the normal monocyte but both cell size and nuclear size are greater; the moderately reticulated nuclear chromatin distinguishes the monoblast.
  • The neoplastic lymphoid cell shows coarse clumping of nuclear chromatin and in some instances coarse chromatin anastomoses to distinguish it from the normal lymphocyte.
  • Lymphoid cells of acute lymphoblastic leukemia are 33% larger than those of chronic lymphocytic leukemia and normal lymphocytes.
  • A candidate for such a cell is recognized morphologically as well.
  • [MeSH-major] Blood Cells / pathology. Blood Cells / ultrastructure. Cytodiagnosis. Leukemia / diagnosis. Microscopy, Electron, Scanning
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Size. Female. Flow Cytometry. Humans. Male. Middle Aged. Reproducibility of Results

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  • (PMID = 15931777.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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84. Josef K, Heidi M, Robert P, Pavel K, Marek T: Expression of CD66 in non-Hodgkin lymphomas and multiple myeloma. Eur J Haematol; 2010 Dec;85(6):496-501
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  • PATIENTS AND METHODS: Bone marrow samples from 260 patients were examined for the expression of CD66 on tumor cells in 104 B-chronic lymphocytic leukemias (B-CLL), 28 mantle cell lymphomas (MCL), 22 follicular lymphomas (FCL), 15 marginal zone lymphomas (MZL), 12 lymphoplasmacytic lymphomas (LPL), 13 diffuse large B cell lymphomas (DLBCL), 4 T-non-Hodgkin lymphomas (T-NHL), 3 B-NHL not otherwise specified (B-NHL NOS), 3 B acute lymphoblastic leukemias (B-ALL), and in 56 multiple myelomas (MM) by flow cytometry.
  • [MeSH-major] Antigens, CD / biosynthesis. Bone Marrow / metabolism. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation, Neoplastic. Lymphoma, Non-Hodgkin / metabolism. Multiple Myeloma / metabolism

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • [CommentIn] Eur J Haematol. 2011 Dec;87(6):554-5 [21883478.001]
  • (PMID = 20887387.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CD66 antigens; 0 / Cell Adhesion Molecules
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85. Wang ZY, Chen QS: [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Apr;13(2):169-73
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  • [Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].
  • One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.
  • Four kinds of immunotherapy for acute leukemia are under investigation:.
  • (1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.
  • Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.
  • (2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.
  • (4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.
  • In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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  • (PMID = 15854271.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines
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86. Staratschek-Jox A, Classen S, Gaarz A, Debey-Pascher S, Schultze JL: Blood-based transcriptomics: leukemias and beyond. Expert Rev Mol Diagn; 2009 Apr;9(3):271-80
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  • [Title] Blood-based transcriptomics: leukemias and beyond.
  • In 1999, Golub et al. proposed for the first time microarray-based transcriptional profiling to be used as a new technology for the differential diagnosis of acute myeloid leukemias and acute lymphocytic leukemias.
  • This very preliminary study sparked great enthusiasm beyond the leukemias.
  • Here we highlight the advances in the field of blood transcriptomics during the last 10 years and also critically discuss the issues that need to be resolved before blood transcriptomics will become part of daily diagnostics in the leukemias, as well as in other diseases showing involvement of peripheral blood.
  • [MeSH-major] Blood. Gene Expression Profiling / methods. Leukemia / diagnosis. Leukemia / genetics. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 19379085.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 57
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87. Lin TL, Wang QH, Brown P, Peacock C, Merchant AA, Brennan S, Jones E, McGovern K, Watkins DN, Sakamoto KM, Matsui W: Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926. PLoS One; 2010 Dec 28;5(12):e15262
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  • [Title] Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926.
  • Recent data suggests that Hh signaling plays a role in normal B-cell development, and we hypothesized that Hh signaling may be important in precursor B-cell acute lymphocytic leukemia (B-ALL).
  • We found that the expression of Hh pathway components was common in human B-ALL cell lines and clinical samples.

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  • (PMID = 21203400.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / R01 CA127574; United States / NCI NIH HHS / CA / R01CA127574; United States / NCI NIH HHS / CA / R01 CA127574-05; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NHLBI NIH HHS / HL / T32 HL086345; United States / NCI NIH HHS / CA / P01CA15396
  • [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 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / IPI-926; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Veratrum Alkaloids; EC 1.2.1.3 / Aldehyde Dehydrogenase; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ PMC3011010
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88. Zeng Z, Samudio IJ, Munsell M, An J, Huang Z, Estey E, Andreeff M, Konopleva M: Inhibition of CXCR4 with the novel RCP168 peptide overcomes stroma-mediated chemoresistance in chronic and acute leukemias. Mol Cancer Ther; 2006 Dec;5(12):3113-21
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  • [Title] Inhibition of CXCR4 with the novel RCP168 peptide overcomes stroma-mediated chemoresistance in chronic and acute leukemias.
  • Using peptide-based CXCR4 inhibitors derived from the chemokine viral macrophage inflammatory protein II, we tested the hypothesis that the inhibition of CXCR4 increases sensitivity to chemotherapy by interfering with stromal/leukemia cell interactions.
  • Results showed that the polypeptide RCP168 had the strongest antagonistic effect on the SDF-1alpha- or stromal cell-induced chemotaxis of leukemic cells.
  • Finally, RCP168 significantly enhanced chemotherapy-induced apoptosis in stroma-cocultured Jurkat, primary chronic lymphocytic leukemia, and in a subset of acute myelogenous leukemia cells harboring Flt3 mutation.
  • Our data therefore suggest that the SDF-1alpha/CXCR4 interaction contributes to the resistance of leukemia cells to chemotherapy-induced apoptosis.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Peptides / pharmacology. Pyridines / pharmacology. Receptors, CXCR4 / antagonists & inhibitors

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  • (PMID = 17172414.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / CA55164
  • [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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / N-(1,4,8,11- tetraazacyclotetradecanyl-1,4-phenylenebis(methylene))-2-(aminomethyl)- pyridine; 0 / Peptides; 0 / Pyridines; 0 / Receptors, CXCR4; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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89. Mai YJ, Qiu LG, Li ZJ, Yu Z, Li CH, Wang YF, Wang GR, Li Q: [The expression of beta-catenin and its significance in leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2007 Aug;28(8):541-4
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  • [Title] [The expression of beta-catenin and its significance in leukemia cells].
  • OBJECTIVE: To investigate the expression of beta-catenin in patients with leukemia and explore its significance in leukemias.
  • METHODS: RT-PCR was used to detect the expression of beta-catenin in bone marrow mononuclear cells (BMMNCs) from patients with leukemia.
  • RESULTS: Expression of beta-catenin was statistically higher in acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) samples than in normal donors (P = 0.001 and 0.016 respectively) and chronic phase chronic myeloid leukemia (CML) patients (P = 0.001 and P = 0.008 respectively), while there was no statistic difference between AML and ALL patients (P = 0.58).
  • Immunocytochemical analysis revealed that BMMNCs from normal donors expressed beta-catenin on the plasma membrane and cytoplasma, while those from acute leukemia expressed beta-catenin to varying degrees in the nucleus as well.
  • The expression of beta-catenin gene statistically showed the highest level in M5 (n = 15) and the lowest level in M3 (n = 18).
  • No clinical features, such as, age, initial WBC count, therapy response rate, blast cell numbers or cytogenetic risk was found to be correlated with the expression of beta-catenin excepting for CD34+ positive rate (P = 0.004) in AML.
  • CONCLUSION: As a key mediator of Wnt signal transduction way, overexpression of beta-catenin in leukemia cells indicates that it might be aberrantly activated in acute leukemia, accelerated or blastic phase of CML.
  • [MeSH-major] Leukemia / metabolism. beta Catenin / metabolism

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  • (PMID = 18078131.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / beta Catenin
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90. Garcia-Manero G, Yang H, Bueso-Ramos C, Ferrajoli A, Cortes J, Wierda WG, Faderl S, Koller C, Morris G, Rosner G, Loboda A, Fantin VR, Randolph SS, Hardwick JS, Reilly JF, Chen C, Ricker JL, Secrist JP, Richon VM, Frankel SR, Kantarjian HM: Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes. Blood; 2008 Feb 1;111(3):1060-6
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  • [Title] Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes.
  • Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in leukemia.
  • Patients with relapsed or refractory leukemias or myelodysplastic syndromes (MDS) and untreated patients who were not candidates for chemotherapy were eligible.
  • Of 41 patients, 31 had acute myeloid leukemia (AML), 4 chronic lymphocytic leukemia, 3 MDS, 2 acute lymphoblastic leukemia, and 1 chronic myelocytic leukemia.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors. Hydroxamic Acids / therapeutic use. Leukemia / drug therapy. Leukemia / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology