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1. Gaidzik VI, Schlenk RF, Moschny S, Becker A, Bullinger L, Corbacioglu A, Krauter J, Schlegelberger B, Ganser A, Döhner H, Döhner K, German-Austrian AML Study Group: Prognostic impact of WT1 mutations in cytogenetically normal acute myeloid leukemia: a study of the German-Austrian AML Study Group. Blood; 2009 May 7;113(19):4505-11
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  • [Title] Prognostic impact of WT1 mutations in cytogenetically normal acute myeloid leukemia: a study of the German-Austrian AML Study Group.
  • To evaluate the incidence and clinical impact of WT1 gene mutations in younger adult patients with cytogenetically normal acute myeloid leukemia (CN-AML), sequencing of the complete coding region was performed in diagnostic samples from 617 patients who were treated on 3 German-Austrian AML Study Group protocols.
  • In conclusion, in our large cohort of younger adults with CN-AML, WT1 mutation as a single molecular marker did not impact on outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation / genetics. WT1 Proteins / genetics

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  • (PMID = 19221039.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / WT1 Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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2. Walter K, Cockerill PN, Barlow R, Clarke D, Hoogenkamp M, Follows GA, Richards SJ, Cullen MJ, Bonifer C, Tagoh H: Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5. Oncogene; 2010 May 20;29(20):2927-37
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  • [Title] Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5.
  • Co-expression of lymphoid and myeloid molecules is a well-known feature of acute myeloblastic leukemia (AML) with t(8;21).
  • These cells consistently express the B-cell-specific transcription factor PAX5, and the B-cell-specific cell surface protein CD19.
  • We show that CD19 chromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation.
  • Our results also show a positive correlation between PAX5 and CD19 expression in t(8;21)-positive AML cells and demonstrate that PAX5 binds to the promoter and enhancer of CD19 gene and remodels chromatin structure at the promoter.
  • This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role of a progenitor-specific chromatin configuration in myeloid leukemia.
  • [MeSH-major] Antigens, CD19 / genetics. B-Cell-Specific Activator Protein / genetics. Chromatin / chemistry. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 20208555.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Chromatin; 0 / PAX5 protein, human
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3. Ferrara F, Palmieri S, Pedata M, Viola A, Izzo T, Criscuolo C, Mele G: Autologous stem cell transplantation for elderly patients with acute myeloid leukaemia conditioned with continuous infusion idarubicin and busulphan. Hematol Oncol; 2009 Mar;27(1):40-5
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  • [Title] Autologous stem cell transplantation for elderly patients with acute myeloid leukaemia conditioned with continuous infusion idarubicin and busulphan.
  • Different studies have suggested the potential utility of autologous stem cell transplantation (ASCT) in acute myeloid leukaemia (AML) of the elderly with encouraging results in selected patients.
  • One possibility to ameliorate therapeutic results could rely on the adoption of conditioning regimens specifically designed for AML.
  • We report therapeutic results from a series of 40 AML patients older than 60 years (median age 67 years) autografted in first complete remission (CR), after conditioning with continuous infusion (c.i.) high dose idarubicin and busulphan.
  • After a median follow-up of 25 months, median disease free and overall survival (OS) for the whole patient population were 13 and 22 months, respectively.
  • Three patients died while in CR from causes unrelated to AML.
  • Our data confirm the feasibility of a conditioning regimen based on high-dose idarubicin plus busulphan in older selected AML patients and suggest clinical improvement in patients with normal cytogenetics.
  • [MeSH-major] Busulfan / therapeutic use. Idarubicin / therapeutic use. Leukemia, Myeloid, Acute / surgery
  • [MeSH-minor] Aged. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Stem Cell Transplantation / methods. Survival Analysis. Transplantation, Autologous

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  • [Copyright] Copyright 2009 John Wiley & Sons, Ltd.
  • (PMID = 19206083.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; G1LN9045DK / Busulfan; ZRP63D75JW / Idarubicin
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4. Taussig DC, Pearce DJ, Simpson C, Rohatiner AZ, Lister TA, Kelly G, Luongo JL, Danet-Desnoyers GA, Bonnet D: Hematopoietic stem cells express multiple myeloid markers: implications for the origin and targeted therapy of acute myeloid leukemia. Blood; 2005 Dec 15;106(13):4086-92
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  • [Title] Hematopoietic stem cells express multiple myeloid markers: implications for the origin and targeted therapy of acute myeloid leukemia.
  • However, recent work suggests that genes associated with the myeloid lineage are transcribed in mouse HSCs.
  • Here, we explore whether myeloid genes are actually translated in human HSCs.
  • We show that CD33, CD13, and CD123, well-established myeloid markers, are expressed on human long-term repopulating cells from cord blood and bone marrow.
  • In addition, we demonstrate that nonobese diabetic/severe combined immunodeficiency (NOD/SCID) leukemia-initiating cells (SL-ICs) are restricted to the CD33+ fraction in 11 of 12 acute myeloid leukemia (AML) samples studied, indicating that leukemic stem cells (LSCs) express this antigen.
  • Furthermore, based on the phenotypic similarity of HSCs and LSCs, our data provide support for the hypothesis that AML derives from an HSC.
  • Our findings also provide a challenge to contemporary attempts to improve the outcome of AML using myeloid antigen-targeted therapies, given the potential for HSC killing.


5. Aref S, El Sherbiny M, Goda T, Fouda M, Al Askalany H, Abdalla D: Soluble VEGF/sFLt1 ratio is an independent predictor of AML patient out come. Hematology; 2005 Apr;10(2):131-4
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  • [Title] Soluble VEGF/sFLt1 ratio is an independent predictor of AML patient out come.
  • In the present work, we tested the differential prognostic relevance of soluble vascular endothelial growth factor (VEGF), their receptors 1 (Flt-1), 2 (KDR), and the ratio between sVEGF/sFlt-1 in 43 patients with acute myeloid leukemia (AML).
  • Soluble VEGF, sFLT-1 and sKDR concentration levels were significantly higher in AML patients at diagnosis when compared to the levels in normal controls. sVEGF, sFlt1 and the sVEGF/sFlt1 ratio were significantly higher in non responders when compared to responders (P < 0.001 for all).
  • sVEGF, the sVEGF/sFlt1 ratio but not sFlt1 and sKDR levels were significantly elevated in those who did not survive, when compared to survivors. sVEGF, sFlt1 levels were significantly correlated to WBC counts (R = 0.93, P = 0.000, R = 0.56, P = 0.000, respectively); bone marrow blast cell counts (R = 0.92, P = 0.000; R = 56, P = 0.000, respectively); peripheral blood blast cell counts (R = 0.91, P = 0.000; R = 0.52, P = 0.000, respectively); sKDR was only correlated to peripheral blood blast cell counts(R=0.37,P=0.014).
  • Cox regression analysis results with sVEGF, sFlt1, sKDR, sVEGF/sFlt1 ratio suggest that the most important predictor for AML outcome is the sVEGF/sFlt1 ratio.
  • In conclusion, sVEGF/sVEGF ratio is independent predictor of AML patient out come, and its significance should be assessed when considering antiangiogenic therapy.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid, Acute / blood. Neovascularization, Pathologic / blood. Proteins / analysis. Vascular Endothelial Growth Factor A / blood

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  • (PMID = 16019458.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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6. Ehlers S, Herbst C, Zimmermann M, Scharn N, Germeshausen M, von Neuhoff N, Zwaan CM, Reinhardt K, Hollink IH, Klusmann JH, Lehrnbecher T, Roettgers S, Stary J, Dworzak M, Welte K, Creutzig U, Reinhardt D: Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse. J Clin Oncol; 2010 May 20;28(15):2591-7
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  • [Title] Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse.
  • PURPOSE: This prospective, multicenter Acute Myeloid Leukemia Berlin-Frankfurt-Muenster (AML-BFM) 98 study randomly tested the ability of granulocyte colony-stimulating factor (G-CSF) to reduce infectious complications and to improve outcomes in children and adolescents with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Of 154 SR patients in the AML-BFM 98 cohort, 50 patients were tested for G-CSF receptor (G-CSFR) RNA isoform I and IV expression, G-CSFR cell surface expression, and acquired mutations in the G-CSFR gene.
  • RESULTS: In patients randomly assigned to receive G-CSF after induction, 16 patients overexpressing the G-CSFR isoform IV showed an increased 5-year cumulative incidence of relapse (50% +/- 13%) compared with 14 patients with low-level isoform IV expression (14% +/- 10%; log-rank P = .04).
  • The level of G-CSFR isoform IV had no significant effect in patients not receiving G-CSF (P = .19).
  • Multivariate analyses of the G-CSF-treated subgroup, including the parameters G-CSFR isoform IV overexpression, sex, and favorable cytogenetics as covariables, revealed the prognostic relevance of G-CSFR isoform IV overexpression for 5-year event-free survival (P = .031) and the 5-year cumulative incidence of relapse (P = .049).
  • CONCLUSION: Our results demonstrate that children and adolescents with AMLs that overexpress the differentiation-defective G-CSFR isoform IV respond to G-CSF administration after induction, but with a significantly higher incidence of relapse.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Receptors, Granulocyte Colony-Stimulating Factor / biosynthesis


7. Manvelyan M, Kempf P, Weise A, Mrasek K, Heller A, Lier A, Höffken K, Fricke HJ, Sayer HG, Liehr T, Mkrtchyan H: Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics. Int J Mol Med; 2009 Sep;24(3):335-41
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  • [Title] Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics.
  • The impact of chromosome architecture in the formation of chromosome aberrations is a recent finding of interphase directed molecular cytogenetic studies.
  • Thus, disease specific chromosomal translocations could be due to tissue specific genomic organization.
  • In this study, BM of three secondary acute myelogenous leukemia (AML) cases with trisomy 8 and otherwise normal karyotype were evaluated.
  • Bone marrow cells of one AML and one ALL (acute lymphoblastic leukemia) case, peripheral blood lymphocytes and human sperm, all of them with normal karyotype, served as controls.
  • Interestingly, in myeloid bone marrow cells chromosomes 8 (di- and trisomic) and 21 tended to co-localize with their homologue chromosome(s), rather than to be separated.
  • Thus, the co-localization of chromosomes 8 and 21 might promote a translocation providing a selective advantage of t(8;21) cells in AML-M2.
  • [MeSH-major] Bone Marrow Cells / metabolism. Chromosomes, Human, Pair 21 / metabolism. Chromosomes, Human, Pair 8 / metabolism. Cytogenetic Analysis / methods. Myeloid Cells / metabolism
  • [MeSH-minor] Adult. Aged, 80 and over. Cell Nucleus / metabolism. Humans. In Situ Hybridization. Interphase. Male. Middle Aged

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  • (PMID = 19639225.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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8. Kiyoi H, Naoe T: FLT3 mutations in acute myeloid leukemia. Methods Mol Med; 2006;125:189-97
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  • [Title] FLT3 mutations in acute myeloid leukemia.
  • The prevalence of an internal tandem duplication (ITD) of the juxtamembrane domain-coding sequence and a missense mutation of D835 within the kinase domain of the FLT3 gene is 15-35% and 5-10% of adults with acute myeloid leukemia (AML), respectively.
  • Several large-scale studies in well-documented patients published to date have demonstrated that FLT3 mutations are strongly associated with a poor prognosis and a high leukemia cell count in patients with AML, suggesting that FLT3 mutations are involved in disease progression.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adult. DNA Mutational Analysis / methods. Gene Duplication. Humans. Mutation, Missense. Point Mutation. Sequence Deletion

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  • (PMID = 16502586.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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9. Robazzi TC, Silva LR, Mendonça N, Barreto JH: Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents. Acta Gastroenterol Latinoam; 2008 Jun;38(2):126-32
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  • [Title] Gastrointestinal manifestations as initial presentation of acute leukemias in children and adolescents.
  • OBJECTIVE: this study aimed to determine the prevalence and characteristics of gastrointestinal manifestations on initial clinical presentation of acute leukemias (AL) in childhood.
  • RESULTS: acute lymphoid leukemia (ALL) was diagnosed in 273 (77.1%) patients and acute non-lymphocytic leukemia (AML) in 81 (22.9%).
  • The most common presenting features were: abdominal pain (19.5% in ALL and 11.8% in AML), nausea and vomiting (14.9 in ALL and 14% in AML), abdominal distention (18.5 in ALL and 8.6% in AML; p 0.024), constipation (5% in ALL and 6.5% in AML), diarrhea (3.6% in ALL and 11.8% in AML; p 0.03%), and gastrointestinal bleeding (7.9% in ALL and 9.7% in AML).
  • An association is well-defined between abdominal symptoms like nausea, vomiting and pain and use of this therapy but this association did not occurred clearly in this study.
  • CONCLUSIONS: gastrointestinal symptoms are not very well-documented as initial manifestation of leukemia in children and should be considered on the differential diagnosis of gastrointestinal symptoms of unknown etiology in children.
  • [MeSH-major] Gastrointestinal Diseases / etiology. Leukemia, Myeloid, Acute / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 18697407.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Argentina
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10. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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11. Wieser R, Scheideler M, Hackl H, Engelmann M, Schneckenleithner C, Hiden K, Papak C, Trajanoski Z, Sill H, Fonatsch C: microRNAs in acute myeloid leukemia: expression patterns, correlations with genetic and clinical parameters, and prognostic significance. Genes Chromosomes Cancer; 2010 Mar;49(3):193-203
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  • [Title] microRNAs in acute myeloid leukemia: expression patterns, correlations with genetic and clinical parameters, and prognostic significance.
  • Acute myeloid leukemia (AML) is a malignant disease of hematopoietic cells whose emergence, course, and prognosis is affected by specific recurrent genetic alterations like chromosome aberrations and point mutations, as well as by changes in the expression of certain genes.
  • In the past 2 years, microRNAs (miRNAs)--a novel class of small RNA molecules involved in posttranscriptional gene regulation--have also been shown to be aberrantly expressed in AML.
  • Furthermore, specific miRNA expression patterns were found to be associated with certain genetic and cytogenetic alterations in this disease, and two studies identified miRNAs whose expression levels were predictive of survival.
  • This review summarizes published reports on the expression patterns of miRNAs in AML, and discusses possible reasons for the differences in their results.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. MicroRNAs / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hematopoietic Stem Cells / pathology. Hematopoietic Stem Cells / physiology. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. Survival Analysis. Transcription, Genetic

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  • (PMID = 20013895.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19795; Austria / Austrian Science Fund FWF / / P 20920; Austria / Austrian Science Fund FWF / / P 21401
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm
  • [Number-of-references] 72
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12. Mohamed WS, Samra MA, Fawzy MA: Presence of simian virus 40 DNA sequences in egyptian patients with lymphoproliferative disorders. Int J Health Sci (Qassim); 2007 Jan;1(1):11-6
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  • Several studies have detected SV40 DNA sequences in tumor tissues obtained from non-Hodgkin's lymphoma patients.
  • These cases consisted of 158 non-Hodgkin's lymphoma (NHL), 54 Hodgkin's disease(HD), 26 acute lymphocytic leukemia (ALL), 13 acute myeloid leukemia (AML), 8 chronic lymphoblastic leukemia (CLL), 7 chronic myeloid leukemia (CML), in addition to 34 subjects of control group.
  • RESULTS: Our results have shown that SV40 DNA sequences were found in 53.8% of non-Hodgkin lymphoma patients, 29.6% of Hodgkin's disease patients, and 40.7% of different types of leukemia cases.
  • Regarding the different histological types of non-Hodgkin's lymphoma, SV40 DNA sequences were detected frequently in diffuse large B-cell lymphoma and in follicular lymphoma.
  • CONCLUSIONS: The present study suggests that SV40 DNA virus is significantly associated with non-Hodgkin's lymphoma and might have a role in the development of these hematological malignancies.

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  • [Cites] J Virol. 2004 May;78(9):4917-20 [15078974.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):405-26 [10688861.001]
  • [Cites] Cancer Invest. 2006 Apr-May;24(3):223-8 [16809147.001]
  • [Cites] Science. 1972 Apr 14;176(4031):173-5 [4335386.001]
  • [Cites] Int J Cancer. 1998 Dec 9;78(6):669-74 [9833757.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7606-8 [14633675.001]
  • [Cites] Semin Cancer Biol. 2001 Feb;11(1):5-13 [11243894.001]
  • [Cites] Lancet. 2003 Jan 4;361(9351):88-9 [12517514.001]
  • [Cites] Chest. 1999 Dec;116(6 Suppl):470S-473S [10619511.001]
  • [Cites] Cancer Lett. 2001 Jan 10;162(1):57-64 [11121863.001]
  • [Cites] J Virol Methods. 1999 Oct;82(2):137-44 [10894630.001]
  • [Cites] Oncogene. 2002 Feb 14;21(8):1141-9 [11850833.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1):2-17 [11836664.001]
  • [Cites] J Natl Cancer Inst. 2003 Jul 2;95(13):1001-3 [12837836.001]
  • [Cites] Lancet. 2002 Mar 9;359(9309):851-2 [11897287.001]
  • [Cites] Cancer Invest. 2005;23(6):529-36 [16203661.001]
  • (PMID = 21475447.001).
  • [ISSN] 1658-3639
  • [Journal-full-title] International journal of health sciences
  • [ISO-abbreviation] Int J Health Sci (Qassim)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Other-IDs] NLM/ PMC3068659
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13. Willemze AJ, Geskus RB, Noordijk EM, Kal HB, Egeler RM, Vossen JM: HLA-identical haematopoietic stem cell transplantation for acute leukaemia in children: less relapse with higher biologically effective dose of TBI. Bone Marrow Transplant; 2007 Aug;40(4):319-27
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  • [Title] HLA-identical haematopoietic stem cell transplantation for acute leukaemia in children: less relapse with higher biologically effective dose of TBI.
  • To examine relapse, survival and transplant-related complications in relationship to disease- and pre-treatment-related characteristics, we evaluated 132 children, who consecutively received an allogeneic HLA-identical SCT for acute leukaemia in our centre: ALL in first remission (n=24), ALL in second remission (n=53) and AML in first remission (n=55).
  • The incidence of acute GVHD was 17%; 6% was grades II-IV.
  • AML patients with acute GVHD got no relapse (P=0.02); this was not the case in ALL patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Whole-Body Irradiation / methods
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Dose-Response Relationship, Radiation. Female. Graft Survival. Graft vs Host Disease. Humans. Infant. Kaplan-Meier Estimate. Male. Recurrence. Retrospective Studies. Transplantation Conditioning / methods. Transplantation, Homologous

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  • (PMID = 17572715.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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14. Ge Y, LaFiura KM, Dombkowski AA, Chen Q, Payton SG, Buck SA, Salagrama S, Diakiw AE, Matherly LH, Taub JW: The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy. Leukemia; 2008 Mar;22(3):521-9
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  • [Title] The role of the proto-oncogene ETS2 in acute megakaryocytic leukemia biology and therapy.
  • Acute myeloid leukemia (AML) in Down syndrome (DS) children has several unique features including a predominance of the acute megakaryocytic leukemia (AMkL) phenotype, higher event-free survivals compared to non-DS children using cytosine arabinoside (ara-C)/anthracycline-based protocols and a uniform presence of somatic mutations in the X-linked transcription factor gene, GATA1.
  • ETS2 transcripts measured by real-time RT-PCR were 1.8- and 4.1-fold, respectively, higher in DS and non-DS megakaryoblasts than those in non-DS myeloblasts.
  • In a doxycycline-inducible erythroleukemia cell line, K562pTet-on/ETS2, induction of ETS2 resulted in an erythroid to megakaryocytic phenotypic switch independent of GATA1 levels.
  • Microarray analysis of doxycycline-induced and doxycycline-uninduced cells revealed an upregulation by ETS2 of cytokines (for example, interleukin 1 and CSF2) and transcription factors (for example, TAL1), which are key regulators of megakaryocytic differentiation.
  • These results suggest that ETS2 expression is linked to the biology of AMkL in both DS and non-DS children, and that ETS2 acts by regulating expression of hematopoietic lineage and transcription factor genes involved in erythropoiesis and megakaryopoiesis, and in chemotherapy sensitivities.

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  • [Cites] Oncogene. 1998 Dec 3;17(22):2883-8 [9879994.001]
  • [Cites] Bioinformatics. 2006 May 1;22(9):1111-21 [16522673.001]
  • [Cites] Leukemia. 2000 May;14(5):786-91 [10803507.001]
  • [Cites] Leukemia. 2000 May;14(5):943-4 [10803530.001]
  • [Cites] J Biol Chem. 2001 Mar 23;276(12):8713-9 [11106643.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Mar-Apr;23(3):175-8 [11305722.001]
  • [Cites] Blood. 2002 Jan 1;99(1):245-51 [11756178.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):148-52 [12172547.001]
  • [Cites] J Immunol. 2002 Nov 1;169(9):4873-81 [12391198.001]
  • [Cites] Nature. 2003 Jan 30;421(6922):547-51 [12540851.001]
  • [Cites] Cancer Invest. 2003;21(1):105-36 [12643014.001]
  • [Cites] Lancet. 2003 May 10;361(9369):1617-20 [12747884.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4298-300 [12560215.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4333-41 [12576332.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4301-4 [12586620.001]
  • [Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3415-22 [12885836.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2960-8 [12816863.001]
  • [Cites] Exp Hematol. 2004 Jan;32(1):11-24 [14725896.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2480-9 [14656875.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4255-62 [15156181.001]
  • [Cites] J Biol Response Mod. 1986 Jun;5(3):250-62 [2425057.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5958-62 [2527368.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7833-7 [2813360.001]
  • [Cites] Genes Dev. 1990 Mar;4(3):401-9 [2186967.001]
  • [Cites] Blood. 1991 Apr 15;77(8):1627-52 [1826616.001]
  • [Cites] Br J Haematol. 1991 Aug;78(4):480-7 [1911339.001]
  • [Cites] Blood. 1992 Nov 1;80(9):2210-4 [1384797.001]
  • [Cites] Mol Cell Biol. 1993 Jan;13(1):668-76 [8417360.001]
  • [Cites] Leuk Res. 1994 Mar;18(3):163-71 [8139285.001]
  • [Cites] Nature. 1995 May 25;375(6529):318-22 [7753195.001]
  • [Cites] Cell. 1995 Jun 2;81(5):695-704 [7774011.001]
  • [Cites] Science. 1995 Jun 23;268(5218):1766-9 [7792603.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] N Engl J Med. 1996 May 30;334(22):1428-34 [8618581.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3248-9 [8874232.001]
  • [Cites] Mol Cell Biol. 1996 Dec;16(12):6851-8 [8943340.001]
  • [Cites] Prostate. 1997 Feb 15;30(3):145-53 [9122038.001]
  • [Cites] Blood. 1997 Aug 1;90(3):1291-9 [9242564.001]
  • [Cites] Blood. 1998 Jan 15;91(2):608-15 [9427716.001]
  • [Cites] Cancer Res. 1998 Feb 1;58(3):562-9 [9458106.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 2;97(3):226-31 [15687366.001]
  • [Cites] Br J Haematol. 2005 Mar;128(6):797-804 [15755283.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1355-60 [15920490.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7596-602 [16140924.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1570-81 [16249385.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3339-44 [16492768.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1393-400 [10438727.001]
  • (PMID = 18094719.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / R01 CA92308; United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NIEHS NIH HHS / ES / P30 ES006639; United States / NCI NIH HHS / CA / T32 CA009531; United States / NCI NIH HHS / CA / R01 CA120772
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ETS2 protein, human; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Protein c-ets-2; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS505525; NLM/ PMC3809919
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15. Zatkova A, Fonatsch C, Sperr WR, Valent P: A patient with de novo AML M1 and t(16;21) with karyotype evolution. Leuk Res; 2007 Sep;31(9):1319-21
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  • [Title] A patient with de novo AML M1 and t(16;21) with karyotype evolution.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17126398.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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16. Gassas A, Ishaqi MK, Afzal S, Finkelstein-Shechter T, Dupuis A, Doyle J: A comparison of the outcomes of children with acute myelogenous leukemia in either first or second complete remission (CR1 vs CR2) following allogeneic hematopoietic stem cell transplantation at a single transplant center. Bone Marrow Transplant; 2008 Jun;41(11):941-5
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  • [Title] A comparison of the outcomes of children with acute myelogenous leukemia in either first or second complete remission (CR1 vs CR2) following allogeneic hematopoietic stem cell transplantation at a single transplant center.
  • We reviewed 70 consecutive children with AML who received hematopoietic stem cell transplantation (HSCT) in our institution between 1994 and 2005.
  • Expectedly, there was a significant increase in acute GVHD incidence in CR2 patients (40 vs 25% for grades I-II and 30 vs 10% for grades III-IV; P=0.02) and a significant increase in transplant-related mortality (38 vs 11%; P=0.01).
  • Although the difference between 3-year EFS for CR1 and CR2 was not statistically significant, there was a significantly superior 3-year overall survival for CR1 patients (74 vs 51%; P=0.05).
  • Children with relapsed AML who achieve and maintain remission until HSCT, have a reasonable survival, but the outcome of children receiving HSCT in CR1 remains superior.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Hospitals, Pediatric. Humans. Infant. Male. Remission Induction. Retrospective Studies. Transplantation Conditioning. Transplantation, Homologous


17. Christiansen DH, Andersen MK, Desta F, Pedersen-Bjergaard J: Mutations of genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal transduction pathway in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2005 Dec;19(12):2232-40
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  • [Title] Mutations of genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal transduction pathway in therapy-related myelodysplasia and acute myeloid leukemia.
  • Mutations of the FLT3, c-KIT, c-FMS, KRAS, NRAS, BRAF and CEBPA genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal-transduction pathway are frequent in acute myeloid leukemia (AML).
  • We examined 140 patients with therapy-related myelodysplasia or AML (t-MDS/t-AML) for point mutations of these seven genes.
  • All but one patient with a FLT3 mutation presented with t-AML (P=0.0002).
  • RAS mutations were associated with AML1 point mutations (P=0.046) and with progression from t-MDS to t-AML (P=0.008).
  • Noteworthy, all three patients with BRAF mutations presented as t-AML of M5 subtype with t(9;11)(p22;q23) and MLL-rearrangement (P=0.01).
  • In t-AML RAS/BRAF mutations were significantly associated with a very short survival (P=0.017).
  • Half of the patients with a mutation in the RTK/RAS-BRAF signal-transduction pathway (denoted 'class-I' mutations) simultaneously disclosed mutation of a hematopoietic transcription factor (denoted 'class-II' mutations) (P=0.046) suggesting their cooperation in leukemogenesis.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Point Mutation. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. CCAAT-Enhancer-Binding Protein-alpha / genetics. Child. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins B-raf / genetics. Receptor, Macrophage Colony-Stimulating Factor / genetics. Signal Transduction. fms-Like Tyrosine Kinase 3. ras Proteins / genetics


18. Pogoda JM, Katz J, McKean-Cowdin R, Nichols PW, Ross RK, Preston-Martin S: Prescription drug use and risk of acute myeloid leukemia by French-American-British subtype: results from a Los Angeles County case-control study. Int J Cancer; 2005 Apr 20;114(4):634-8
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  • [Title] Prescription drug use and risk of acute myeloid leukemia by French-American-British subtype: results from a Los Angeles County case-control study.
  • Chemotherapy is a well-established risk factor for acute myeloid leukemia (AML) but little is known about other prescription drugs and AML risk.
  • Prescription nonsteroidal anti-inflammatory drug (NSAID) use for at least 4 weeks in the 2 to 10 years before diagnosis was associated with decreased risk (odds ratio = 0.5, 95% confidence interval=0.3, 1.0; p=0.04) with dose-response most evident for FAB subtype M2 (OR = 0.6, CI: 0.1, 2.9 for duration < or =6 months; OR = 0.2, CI: 0.0, 1.6 for >6 months).
  • For subtype M4, ORs increased with increasing duration of benzodiazepine use in the 2 to 10 years before diagnosis (OR = 1.5, CI: 0.3, 9.0 for < or =6 months vs. OR = 5.0, CI: 0.6, 42.8 for >6 months).
  • These results suggest that prescription drugs other than chemotherapy may have FAB subtype-specific effects on AML risk.
  • [MeSH-major] Drug Prescriptions. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / etiology
  • [MeSH-minor] Adult. Aged. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Benzodiazepines / adverse effects. Case-Control Studies. Dose-Response Relationship, Drug. Drug Therapy. Female. Humans. Los Angeles. Male. Middle Aged. Odds Ratio. Risk. Risk Factors. Time Factors

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  • (PMID = 15609330.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 5 P30 ES07048-06; United States / NCI NIH HHS / CA / CA17054; United States / NCI NIH HHS / CN / N01-CN-25403
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 12794-10-4 / Benzodiazepines
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19. Ford CD, Asch J, Konopa K, Petersen FB: CR with lenalidomide in del(5)(q13q33) AML relapsing after allogeneic hematopoietic SCT. Bone Marrow Transplant; 2010 Feb;45(2):403-4
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  • [Title] CR with lenalidomide in del(5)(q13q33) AML relapsing after allogeneic hematopoietic SCT.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Thalidomide / analogs & derivatives
  • [MeSH-minor] Aged. Chromosome Deletion. Chromosomes, Human, Pair 5. Female. Graft vs Host Disease / drug therapy. Humans. Recurrence

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  • (PMID = 19597424.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
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20. Kim SR, Kim HJ, Kim SH: [Clinical utility of fluorescence in-situ hybridization profile test in detecting genetic aberrations in acute leukemia]. Korean J Lab Med; 2009 Oct;29(5):371-8
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  • [Title] [Clinical utility of fluorescence in-situ hybridization profile test in detecting genetic aberrations in acute leukemia].
  • BACKGROUND: Cytogenetic abnormalities are one of the most reliable prognostic factors in acute leukemia.
  • The objective of this study was to investigate the utility of FISH profile analyses in the initial diagnosis of acute leukemia.
  • METHODS: Two hundred and forty one de novo acute leukemia patients diagnosed from January, 2002 to November, 2007 were included.
  • For acute lymphoblastic leukemia profile test, FISH probes for BCR/ABL, TEL/AML1, MLL gene rearrangement and CDKN2A deletion were used.
  • For acute myeloid leukemia profile test, probes for AML1/ETO, MLL and CBFbeta gene rearrangement were used.
  • RESULTS: ALL FISH profile tests revealed additional genetic aberrations not detected by chromosome analysis in 48.6% (67/138) of cases, including those with normal karyotypes or no mitotic cells (37%, 51/138).
  • AML FISH profile tests revealed additional genetic abnormalities in 7.8% (8/103) of cases.
  • CONCLUSIONS: FISH analysis as a profile test detected additional genetic aberrations in a significant proportion of acute leukemia, and was effective especially in detecting cryptic translocations, submicroscopic deletions and complex karyotypes.
  • Our study supports the need to incorporate FISH profile test at initial work up in acute leukemia.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor beta Subunit / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Female. Humans. Infant. Infant, Newborn. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Proto-Oncogene Proteins c-bcr / genetics

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  • (PMID = 19893343.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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21. Miesner M, Haferlach C, Bacher U, Weiss T, Macijewski K, Kohlmann A, Klein HU, Dugas M, Kern W, Schnittger S, Haferlach T: Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC). Blood; 2010 Oct 14;116(15):2742-51
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  • [Title] Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC).
  • The World Health Organization classification of acute myeloid leukemia (AML) is hierarchically structured and integrates genetics, data on patients' history, and multilineage dysplasia (MLD).
  • The category "AML with myelodysplastic syndrome (MDS)-related changes" (AML-MRC) is separated from "AML not otherwise specified" (AML-NOS) by presence of MLD, MDS-related cytogenetics, or history of MDS or MDS/myeloproliferative neoplasm (MPN).
  • We analyzed 408 adult patients categorized as AML-MRC or AML-NOS.
  • Three-year event-free survival (EFS; median, 13.8 vs 16.0 months) and 3-year overall survival (OS; 45.8% vs 53.9%) did not differ significantly between patients with MLD versus without.
  • Patients with MLD as sole AML-MRC criterion (AML-MLD-sole; n = 90) had less frequently FLT3 internal tandem duplication (P = .032) and lower median age than AML-NOS (n = 232).
  • Contrarily, patients with AML-NOS combined with AML-MLD-sole (n = 323) had better 3-year EFS (16.9 vs 10.7 months; P = .005) and 3-year OS (55.8% vs 32.5%; P = .001) than patients with history of MDS or MDS/MPN or MDS-related cytogenetics (n = 85).
  • Gene expression analysis showed distinct clusters for AML-MLD-sole combined with AML-NOS versus AML with MDS-related cytogenetics or MDS history.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cohort Studies. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Myeloproliferative Disorders / complications. Myeloproliferative Disorders / genetics. Prognosis. Retrospective Studies. Risk Factors. Survival Analysis. Young Adult


22. Kufner S, Zitzelsberger H, Kroell T, Pelka-Fleischer R, Salem A, de Valle F, Schweiger C, Nuessler V, Schmid C, Kolb HJ, Schmetzer HM: Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions. Scand J Immunol; 2005 Jul;62(1):86-98
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  • [Title] Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions.
  • Functional dendritic cells (DC) are professional antigen-presenting cells (APC) and can be generated in vitro from healthy as well as from leukaemic cells from acute myeloid leukemia (AML) patients giving rise to APC of leukaemic origin-presenting leukaemic antigens.
  • We describe the generation and characterization of DC from different mononuclear cell (MNC) fractions from 50 AML patients under different serum-free culture conditions, determine the optimal culture conditions and compare the results with that from 23 healthy donors.
  • In parallel cultures, we compared DC harvests after 7- or 14-day culture, with total or adherent MNC or T-cell depleted MNC or peripheral blood (PB) or bone marrow-MNC (BM-MNC), thawn or fresh MNC, in Xvivo or CellGro serum-free media, +/-10% autologous plasma or +/-FL.
  • In detail, we could show that AML-DC harvests were higher after 10-14 days culture (healthy DC: 7 days); total or adherent PB or BM-MNC fractions yield comparable DC counts, however, from magnetic cell sorting (MACS)-depleted MNC fractions or thawn MNC lower DC counts can be generated.
  • Optimal harvest of vital and mature DC from AML samples was obtained with a granulocyte/macrophage-colony stimulating factor, interleukin-4, FL and tumour necrosis factor-alpha-containing serum-free Xvivo medium after 10-14 days of culture (36/26% DC; 38/64% vital DC; 46/51% mature DC were generated from AML/healthy MNC samples).
  • Surface marker profiles (e.g. costimulatory antigen expressing) of DC obtained from AML samples were comparable with that of healthy DC.
  • The leukaemic derivation of AML-DC was demonstrated by the persistence of the clonal cytogenetic aberration in the DC or by coexpression of leukaemic antigens on DC.
  • Autologous T-cell activation of leukaemia-derived DC was demonstrated in cases with AML.
  • We demonstrate that the generation of leukaemia-derived DC is feasable in AML under serum-free culture conditions giving rise to DC with comparable characteristics as healthy DC and offering an anti-leukaemia-directed immunotherapeutical vaccination strategy in AML.
  • [MeSH-major] Bone Marrow Cells / immunology. Cell Culture Techniques. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Middle Aged. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology. Vaccination / methods

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  • (PMID = 16091128.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Culture Media, Serum-Free; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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23. da Costa Ramos FJ, Cartaxo Muniz MT, Silva VC, Araújo M, Leite EP, Freitas EM, Zanrosso CW, Hatagima A, de Mello MP, Yunes JA, Marques-Salles Tde J, Santos N, Brandalise SR, Pombo-De-Oliveira MS: Association between the MTHFR A1298C polymorphism and increased risk of acute myeloid leukemia in Brazilian children. Leuk Lymphoma; 2006 Oct;47(10):2070-5
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  • [Title] Association between the MTHFR A1298C polymorphism and increased risk of acute myeloid leukemia in Brazilian children.
  • The presence of polymorphisms that reduce the activity of MTHFR has been linked to the multifactor process of development of acute leukemia.
  • A case control study was conducted on Brazilian children in different regions of the country with the aim of investigating the role of MTHFR C677T and A1298C polymorphisms as risk factors in the development of acute myeloid leukemia (AML).
  • We used the polymerase chain reaction restriction fragment length polymorphism method to genotyping 182 AML and 315 healthy individuals.
  • The genotype 677 CT was associated with decreased risk [odds ratio (OR), 0.37; confidence interval (CI) 95%, 0.14 - 0.92], whereas 1298 AC genotype was linked with an increased risk [OR, 2.90; CI 95%, 1.26 - 6.71] of developing AML in non-white children.
  • Further epidemiological study is needed to unravel the complex multiple gene-environment interactions in the role of the AML leukemogenesis.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentIn] Leuk Lymphoma. 2006 Oct;47(10):2002-3 [17071465.001]
  • (PMID = 17071478.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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24. Kittang AO, Hatfield K, Sand K, Reikvam H, Bruserud Ø: The chemokine network in acute myelogenous leukemia: molecular mechanisms involved in leukemogenesis and therapeutic implications. Curr Top Microbiol Immunol; 2010;341:149-72
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  • [Title] The chemokine network in acute myelogenous leukemia: molecular mechanisms involved in leukemogenesis and therapeutic implications.
  • Acute myelogenous leukemia (AML) is a bone marrow disease in which the leukemic cells show constitutive release of a wide range of CCL and CXCL chemokines and express several chemokine receptors.
  • The AML cell release of various chemokines is often correlated and three release clusters have been identified: CCL2-4/CXCL1/8, CCL5/CXCL9-11, and CCL13/17/22/24/CXCL5.
  • Based on their overall constitutive release profile, patients can be classified into distinct subsets that differ in their T cell chemotaxis towards the leukemic cells.
  • The release profile is modified by hypoxia, differentiation status, pharmacological interventions, and T cell cytokine responses.
  • The best investigated single chemokine in AML is CXCL12 that binds to CXCR4.
  • CXCL12/CXCR4 is important in leukemogenesis through regulation of AML cell migration, and CXCR4 expression is an adverse prognostic factor for patient survival after chemotherapy.
  • Even though AML cells usually release high levels of several chemokines, there is no general increase of serum chemokine levels in these patients and the levels are also influenced by patient age, disease status, chemotherapy regimen, and complicating infections.
  • However, serum CXCL8 levels seem to partly reflect the leukemic cell burden in AML.
  • [MeSH-major] Chemokine CXCL12 / immunology. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Receptors, CXCR4 / immunology
  • [MeSH-minor] Cell Movement. Chemotaxis, Leukocyte. Humans. T-Lymphocytes / physiology


25. Fritsch S, Buske C, Wörmann B, Wedding U, Hiddemann W, Spiekermann K: [Therapy of acute myeloid leukemia (AML) for medically non-fit patients]. Med Klin (Munich); 2007 Apr 15;102(4):324-9
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  • [Title] [Therapy of acute myeloid leukemia (AML) for medically non-fit patients].
  • [Transliterated title] Die Therapie der akuten myeloischen Leukämie (AML) bei ''medically non-fit'' Patienten.
  • Acute myeloid leukemia (AML) has an increasing incidence with higher age, which is about 15 per 100,000 for patients > 65 years.
  • Many older AML patients show functional restrictions and have a high comorbidity status, so that they do not seem to be qualified for a curatively intended chemotherapy.
  • Decisive for the low cure rate of older AML patients are both patient-dependent and disease-dependent reasons such as secondary or therapy-related leukemia or adverse cytogenetics with complex chromosomal abnormalities, which are poor prognostic factors and are responsible for the low probability to achieve long-lasting complete remissions.
  • Prognostic scores are developed for identifying "medically non-fit" patients as objectively as possible.
  • In the future, these patients should not only be offered best supportive care but also well-tolerable concepts of therapy, which are feasible on an ambulatory basis.
  • [MeSH-major] Health Status. Leukemia, Myeloid, Acute / drug therapy


26. Sahu GR, Mishra R, Nagpal JK, Das BR: Notice of retraction. Alteration of p73 in acute myelogenous leukemia. Am J Hematol; 2008 Aug;83(8):691
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  • [Title] Notice of retraction. Alteration of p73 in acute myelogenous leukemia.

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  • [RetractionOf] Sahu GR, Mishra R, Nagpal JK, Das BR. Am J Hematol. 2005 May;79(1):1-7 [15849769.001]
  • (PMID = 18615454.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Retraction of Publication
  • [Publication-country] United States
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27. Shankar DB, Li J, Tapang P, Owen McCall J, Pease LJ, Dai Y, Wei RQ, Albert DH, Bouska JJ, Osterling DJ, Guo J, Marcotte PA, Johnson EF, Soni N, Hartandi K, Michaelides MR, Davidsen SK, Priceman SJ, Chang JC, Rhodes K, Shah N, Moore TB, Sakamoto KM, Glaser KB: ABT-869, a multitargeted receptor tyrosine kinase inhibitor: inhibition of FLT3 phosphorylation and signaling in acute myeloid leukemia. Blood; 2007 Apr 15;109(8):3400-8
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  • [Title] ABT-869, a multitargeted receptor tyrosine kinase inhibitor: inhibition of FLT3 phosphorylation and signaling in acute myeloid leukemia.
  • In 15% to 30% of patients with acute myeloid leukemia (AML), aberrant proliferation is a consequence of a juxtamembrane mutation in the FLT3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [FLT3-ITD]), causing constitutive kinase activity.
  • In normal human blood spiked with AML cells, ABT-869 inhibited phosphorylation of FLT3 (IC(50) approximately 100 nM), STAT5, and ERK, and decreased Pim-1 expression.
  • In methylcellulose-based colony-forming assays, ABT-869 had no significant effect up to 1000 nM on normal hematopoietic progenitor cells, whereas in AML patient samples harboring both FLT3-ITD and wt-FLT3, ABT-869 inhibited colony formation (IC(50) = 100 and 1000 nM, respectively).
  • ABT-869 is under clinical development for AML.

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  • [Cites] Leukemia. 2003 Jan;17(1):120-4 [12529668.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7241-6 [14612519.001]
  • [Cites] Expert Opin Investig Drugs. 2003 Dec;12(12):1951-62 [14640939.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5465-76 [14654525.001]
  • [Cites] Blood. 2004 Jan 1;103(1):267-74 [12969963.001]
  • [Cites] Br J Haematol. 2004 Feb;124(4):481-4 [14984498.001]
  • [Cites] Blood. 2004 May 15;103(10):3669-76 [14726387.001]
  • [Cites] Leuk Res. 2004 Jul;28(7):679-89 [15158089.001]
  • [Cites] Expert Opin Ther Targets. 2004 Jun;8(3):221-39 [15161429.001]
  • [Cites] Curr Pharm Des. 2004;10(16):1867-83 [15180525.001]
  • [Cites] J Biol Chem. 1995 Jul 7;270(27):15979-83 [7608156.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Dec 17;325(3):683-90 [15541343.001]
  • [Cites] Blood. 2005 Jan 1;105(1):335-40 [15345593.001]
  • [Cites] Blood. 2005 Jan 1;105(1):54-60 [15345597.001]
  • [Cites] Leuk Lymphoma. 2005 Feb;46(2):247-55 [15621809.001]
  • [Cites] Blood. 2005 Feb 1;105(3):986-93 [15459012.001]
  • [Cites] Int J Biochem Cell Biol. 2005 Jun;37(6):1168-72 [15778081.001]
  • [Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] Mol Cancer Ther. 2006 Apr;5(4):995-1006 [16648571.001]
  • [Cites] Stem Cells. 2006 May;24(5):1174-84 [16410383.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2617-9 [11895805.001]
  • [Cites] Hematol J. 2002;3(3):157-63 [12111653.001]
  • [Cites] Exp Hematol. 2002 Jul;30(7):767-73 [12135675.001]
  • [Cites] Blood. 2003 May 1;101(9):3597-605 [12531805.001]
  • (PMID = 17209055.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NCI NIH HHS / CA / R21 CA108545; United States / NHLBI NIH HHS / HL / HL 75826; United States / NCI NIH HHS / CA / CA 108545; United States / NHLBI NIH HHS / HL / R01 HL083077
  • [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 / Indazoles; 0 / Ki-67 Antigen; 0 / N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / STAT5 Transcription Factor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC1852258
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28. Olesen LH, Nyvold CG, Aggerholm A, Nørgaard JM, Guldberg P, Hokland P: Delineation and molecular characterization of acute myeloid leukemia patients with coduplication of FLT3 and MLL. Eur J Haematol; 2005 Sep;75(3):185-92
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  • [Title] Delineation and molecular characterization of acute myeloid leukemia patients with coduplication of FLT3 and MLL.
  • Partial tandem (PTD) and internal tandem duplications (ITD) of the MLL or FLT3 genes respectively, have been demonstrated in acute myeloid leukemia (AML).
  • We have therefore attempted to determine the presence and its consequence in AML and with the further aim of characterizing such patients with respect to other genetic aberrations and to prototype variables in this disease.
  • The four co-duplicated cases (2%) did not differ with respect to sex, age, FAB-type, or immunophenotype, promoter methylation of p15, E-cadherin (CDH1), Estrogen receptor, MDR1, expression of apoptosis-related or multidrug resistance-related genes, though a trend toward decreased gene expression of MDR1 was observed.
  • The extensive molecular characterization of FLT3/MLL coduplicated patients presented here indicates that, even though they do not differ molecularly from the groups of patients with single ITDs, their prognosis and overall survival is universally poor.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Duplication. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogenes / genetics. Receptor Protein-Tyrosine Kinases / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Base Sequence. DNA Methylation. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Mutation. Myeloid-Lymphoid Leukemia Protein. Promoter Regions, Genetic. fms-Like Tyrosine Kinase 3

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  • (PMID = 16104873.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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29. An LL, Ma XT, Yang YH, Lin YM, Song YH, Wu KF: Marked reduction of LL-37/hCAP-18, an antimicrobial peptide, in patients with acute myeloid leukemia. Int J Hematol; 2005 Jan;81(1):45-7
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  • [Title] Marked reduction of LL-37/hCAP-18, an antimicrobial peptide, in patients with acute myeloid leukemia.
  • We detected LL-37/hCAP-18 expression in the peripheral blood smears of 50 healthy donors and 143 patients with various hematological diseases.
  • Compared with that in the healthy donors, expression of the protein in the neutrophils was significantly lower in patients with acute myeloid leukemia (AML), especially those with infection, but no significant difference was detected in messenger RNA level.
  • We did not detect increased LL-37/hCAP-18 protein expression in U937 cells treated with lipopolysaccharide or Staphylococcus aureus Cowan strain.
  • Furthermore, LL-37/hCAP-18 protein production was not restored in differentiated myeloid cell lines NB4 or HL-60 induced by all-trans retinoic acid.
  • LL-37/hCAP-18 has been shown to play a role in host defense, and its deficiency in AML may be one of the explanations for susceptibility to infection among these patients.
  • [MeSH-major] Antimicrobial Cationic Peptides / metabolism. Leukemia, Myeloid / metabolism. Neutrophils / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. HL-60 Cells. Humans. Male. Middle Aged. U937 Cells

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  • [Cites] Blood. 1994 Jul 1;84(1):294-302 [7517212.001]
  • [Cites] Leuk Res. 2003 Oct;27(10):947-50 [12860015.001]
  • [Cites] N Engl J Med. 2002 Oct 10;347(15):1151-60 [12374875.001]
  • [Cites] Respir Res. 2000;1(3):141-50 [11667978.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3086-93 [11049988.001]
  • [Cites] J Leukoc Biol. 1998 Dec;64(6):845-52 [9850169.001]
  • [Cites] Cell Mol Life Sci. 2003 Apr;60(4):711-20 [12785718.001]
  • [Cites] J Biol Chem. 1997 Jun 13;272(24):15258-63 [9182550.001]
  • [Cites] Blood. 1997 Jan 1;89(1):166-75 [8978289.001]
  • [Cites] Leuk Res. 2002 Dec;26(12):1097-103 [12443882.001]
  • (PMID = 15717688.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimicrobial Cationic Peptides; 143108-26-3 / CAP18 lipopolysaccharide-binding protein
  •  go-up   go-down


30. Liesveld JL, Bechelli J, Rosell K, Lu C, Bridger G, Phillips G 2nd, Abboud CN: Effects of AMD3100 on transmigration and survival of acute myelogenous leukemia cells. Leuk Res; 2007 Nov;31(11):1553-63
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  • [Title] Effects of AMD3100 on transmigration and survival of acute myelogenous leukemia cells.
  • Acute myelogenous leukaemia (AML) blasts transmigrate in response to SDF-1alpha.
  • AMD3100, a novel bicyclam molecule which inhibits stromal-derived factor (SDF)-1alpha/CXCR4 interactions, inhibited the transmigration of AML blasts and inhibited outgrowth of leukemia colony forming units.
  • AMD3100 did not abrogate stroma-mediated protection from cytarabine-mediated apoptosis, except in the case of one promyelocytic leukemic sample tested, and it did not influence adhesion of blasts to endothelial monolayers.
  • When AML blasts were pretreated with AMD3100, the positive effects of SDF-1alpha on NOD/SCID engraftment were diminished.
  • This work confirms that AML is influenced by the SDF-1alpha/CXCR4 axis and demonstrates that disruption of this axis by the bicyclam AMD3100 can influence AML microenvironmental interactions.

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  • [Cites] J Leukoc Biol. 2004 Jul;76(1):185-94 [15075362.001]
  • [Cites] Blood. 2004 Jul 15;104(2):550-7 [15054042.001]
  • [Cites] Nat Med. 2004 Aug;10(8):858-64 [15235597.001]
  • [Cites] Leuk Lymphoma. 2004 Aug;45(8):1501-10 [15370200.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2111-7 [7528857.001]
  • [Cites] Leukemia. 1996 Jun;10(6):1041-7 [8667639.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9448-53 [9689100.001]
  • [Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]
  • [Cites] Blood. 1999 May 15;93(10):3379-90 [10233890.001]
  • [Cites] Circulation. 2004 Nov 23;110(21):3300-5 [15533866.001]
  • [Cites] Leuk Res. 2005 Feb;29(2):185-96 [15607368.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3117-26 [15618475.001]
  • [Cites] J Exp Med. 2005 Apr 18;201(8):1307-18 [15837815.001]
  • [Cites] Stem Cells. 2005 Aug;23(7):879-94 [15888687.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1867-74 [15890685.001]
  • [Cites] Hematology. 2005 Dec;10(6):483-94 [16321813.001]
  • [Cites] Blood. 2001 Feb 1;97(3):799-804 [11157500.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2942-9 [15070669.001]
  • [Cites] Stem Cells. 2004;22(2):188-201 [14990858.001]
  • [Cites] Blood Cells Mol Dis. 2004 Jan-Feb;32(1):52-7 [14757413.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):50-6 [11242036.001]
  • [Cites] Exp Hematol. 2001 Mar;29(3):345-55 [11274763.001]
  • [Cites] J Hematother Stem Cell Res. 2001 Feb;10(1):81-93 [11276362.001]
  • [Cites] Exp Hematol. 2001 Apr;29(4):448-57 [11301185.001]
  • [Cites] Blood. 2001 May 15;97(10):3283-91 [11342460.001]
  • [Cites] Ann N Y Acad Sci. 2001 Jun;938:26-34; discussion 34-5 [11458515.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1289-97 [11520773.001]
  • [Cites] Exp Hematol. 2001 Dec;29(12):1439-47 [11750103.001]
  • [Cites] Leukemia. 2002 Apr;16(4):650-7 [11960346.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1713-24 [12200686.001]
  • [Cites] FEBS Lett. 2002 Sep 11;527(1-3):255-62 [12220670.001]
  • [Cites] Exp Hematol. 2002 Sep;30(9):973-81 [12225788.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2778-86 [12351385.001]
  • [Cites] Leukemia. 2002 Oct;16(10):1992-2003 [12357350.001]
  • [Cites] J Immunol. 2003 Jan 1;170(1):421-9 [12496427.001]
  • [Cites] J Clin Invest. 2003 Jan;111(2):187-96 [12531874.001]
  • [Cites] Glia. 2003 Apr 15;42(2):139-48 [12655598.001]
  • [Cites] Nat Rev Drug Discov. 2003 Jul;2(7):581-7 [12815382.001]
  • [Cites] Leukemia. 2003 Jul;17(7):1294-300 [12835717.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2728-30 [12855591.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3136-46 [12869505.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13513-8 [14595012.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2900-7 [15070661.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1095-102 [15020611.001]
  • [Cites] Blood. 2004 Apr 15;103(8):2981-9 [15070674.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2817-24 [15087398.001]
  • (PMID = 17403536.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112835-02; United States / NCI NIH HHS / CA / R21 CA112835; United States / NCI NIH HHS / CA / R21 CA112835-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Chemokine CXCL12; 0 / Culture Media; 0 / Heterocyclic Compounds; 155148-31-5 / JM 3100
  • [Other-IDs] NLM/ NIHMS34260; NLM/ PMC2133372
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31. Rosenberg PS, Zeidler C, Bolyard AA, Alter BP, Bonilla MA, Boxer LA, Dror Y, Kinsey S, Link DC, Newburger PE, Shimamura A, Welte K, Dale DC: Stable long-term risk of leukaemia in patients with severe congenital neutropenia maintained on G-CSF therapy. Br J Haematol; 2010 Jul;150(2):196-9
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  • [Title] Stable long-term risk of leukaemia in patients with severe congenital neutropenia maintained on G-CSF therapy.
  • In severe congenital neutropenia (SCN), long-term therapy with granulocyte colony-stimulating factor (G-CSF) has reduced mortality from sepsis, revealing an underlying predisposition to myelodysplastic syndrome and acute myeloid leukaemia (MDS/AML).
  • We have reported the early pattern of evolution to MDS/AML, but the long-term risk remains uncertain.
  • We updated a prospective study of 374 SCN patients on long-term G-CSF enrolled in the Severe Chronic Neutropenia International Registry.
  • Long-term, the annual risk of MDS/AML attained a plateau (2.3%/year after 10 years).
  • This risk now appears similar to, rather than higher than, the risk of AML in Fanconi anaemia and dyskeratosis congenita.

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  • [Cites] Blood. 2009 Jun 25;113(26):6549-57 [19282459.001]
  • [Cites] Blood. 2003 Feb 1;101(3):822-6 [12393424.001]
  • [Cites] Blood Rev. 2003 Dec;17(4):209-16 [14556775.001]
  • [Cites] Blood. 1993 May 15;81(10):2496-502 [8490166.001]
  • [Cites] Blood. 2000 Jul 15;96(2):429-36 [10887102.001]
  • [Cites] Haematologica. 2005 Jan;90(1):45-53 [15642668.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4628-35 [16497969.001]
  • [Cites] N Engl J Med. 2009 Jan 1;360(1):3-5 [19118300.001]
  • [Cites] Biometrics. 1995 Sep;51(3):874-87 [7548706.001]
  • (PMID = 20456363.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL079582; United States / NIAID NIH HHS / AI / R24 AI049393; United States / Intramural NIH HHS / / Z99 CA999999; United States / NIAID NIH HHS / AI / 2R24AI049393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS216450; NLM/ PMC2906693
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32. Nishioka C, Ikezoe T, Yang J, Takeuchi S, Koeffler HP, Yokoyama A: MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells. Leuk Res; 2008 Sep;32(9):1382-92
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  • [Title] MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells.
  • This study explored the effect of MS-275, a novel histone deacetylase inhibitor (HDACI), against a variety of human leukemia cells with defined genetic alterations.
  • MS-275 profoundly induced growth arrest of acute myelogenous leukemia (AML) MOLM13 and biphenotypic leukemia MV4-11 cells, which possess internal tandem duplication mutation in the fms-like tyrosine kinase 3 (FLT3) gene (FLT3-ITD), with IC50s less than 1 microM, as measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay on day two of culture.
  • Moreover, we found that further inhibition of MEK/ERK signaling potentiated the action of MS-275 in leukemia cells.
  • Taken together, MS-275 may be useful for treatment of individuals with leukemia possessing activating mutation of FLT3 gene.
  • [MeSH-major] Benzamides / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Pyridines / pharmacology. Signal Transduction / drug effects. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Acetylation. Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Female. Flow Cytometry. Genotype. Histone Deacetylase 1. Histone Deacetylases / metabolism. Humans. Immunoprecipitation. MAP Kinase Kinase 1 / metabolism. Male. Middle Aged. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. STAT5 Transcription Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 18394702.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 0 / STAT5 Transcription Factor; 1ZNY4FKK9H / entinostat; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
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33. Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama J, Orfao A, European Working Group of Clinical Cell Analysis (EWGCCA): Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias. Cytometry B Clin Cytom; 2006 Jan;70(1):1-9
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  • [Title] Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias.
  • BACKGROUND: Multiparametric flow cytometry has become an indispensable but complex tool for the diagnosis of acute leukemias.
  • To address whether or not residual normal lymphocytes, usually present within leukemic samples, can serve as internal quality control for fluorescence intensity, 116 leukemic and 35 normal samples were analyzed.
  • METHODS: Eight laboratories participated in the study and recruited a total of 151 individuals including 29 patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), 77 with acute myeloid leukemia (AML), 10 with T-cell precursor acute lymphoblastic leukemia (T-ALL), and 35 normal bone marrow donors.
  • RESULTS: Normal lymphocytes within leukemic samples do not show substantial differences compared to lymphocytes from normal controls with respect to expression of CD19, CD22, CD7, and CD3.
  • CONCLUSION: Residual normal lymphocytes can serve as internal quality control for studies addressing fluorescence intensity in the setting of immunophenotyping of acute leukemias.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia. Lymphocytes / cytology. Lymphocytes / metabolism
  • [MeSH-minor] Acute Disease. Case-Control Studies. Fluorescence. Humans. Quality Control. Reference Standards

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16278833.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Monma F, Nishii K, Shiga J, Sugahara H, Lorenzo F 5th, Watanabe Y, Kawakami K, Hosokai N, Yamamori S, Katayama N, Shiku H: Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients. Leuk Res; 2007 Apr;31(4):471-6
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  • [Title] Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients.
  • The cytogenetic findings in acute myeloid leukemia (AML) are a powerful prognostic indicator.
  • Among these abnormalities, the World Health Organization has classified inv(16)(p13q22), which is closely associated with the M4E classification in the French-American-British system, as indicating a good-risk AML.
  • However, this chromosomal abnormality can often be difficult to detect.
  • In this study, we used RT-PCR and FISH analysis to examine 224 Japanese adult de novo AML patients for the presence of the CBFB/MYH11 fusion transcript at the time of diagnosis.
  • The CBFB/MYH11 fusion gene was detected in 17 patients (7.6%): eight patients had the inv(16) chromosome and in all of them it was M4E; nine patients did not have abnormalities in chromosome 16.
  • AML with the CBFB/MYH11 fusion gene but without inv(16) was found in M2, M4, and M5, but not in M4E patients.
  • These results indicate that even if eosinophilia is not found, molecular screening for CBFB/MYH11 fusion gene should be performed in all AML patients at the time of diagnosis to help guide disease management.
  • [MeSH-major] Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16. Humans. In Situ Hybridization, Fluorescence. Incidence. Japan. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction


35. Cucuianu A: Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia. Med Hypotheses; 2005;65(1):107-13
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  • [Title] Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia.
  • Despite the common clinical, hematological and prognostic features that define acute myeloid leukemia (AML) there is considerable heterogeneity among individual cases, suggesting different pathogenic pathways.
  • Based on a simple theoretical model, according to the vital characteristics of the leukemic clone (proliferative rate and resistance to apoptosis), I propose a classification of AML into two broad categories: (a) high leukemic clone vitality (HLV) AML or "dominant type" AML, corresponding roughly to the World Health Organization (WHO) classification group of entities "AML with recurrent cytogenetic abnormalities" and (b) low leukemic clone vitality (LLV) or "opportunistic type" AML corresponding to the WHO groups "AML with multilineage dysplasia" and "alkylating agent-related AML".
  • HLV-AML leukemic clones are characterized by rate-limiting genomic mutations capable of conferring proliferation/survival advantage over a normal hematopoietic environment while in LLV-AML, the leukemic clones are not particularly proliferative or apoptosis-resistant, but are nevertheless selected against an impaired, previously damaged hematopoietic environment.
  • Such a pathogenesis-oriented classification might have therapeutic and prognostic implications, providing a theoretical basis for a further adaptation of the current standard treatment strategies to the individual characteristics of the AML patients.
  • [MeSH-major] Clone Cells. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology
  • [MeSH-minor] Apoptosis. Cell Lineage. Cell Proliferation. Cytogenetic Analysis. Humans. Kinetics. Models, Biological. Mutation. Prognosis. Selection, Genetic. Survival Analysis. World Health Organization

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  • (PMID = 15893127.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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36. Li Y, Li XY, Wang L, Tian Z, Rao Q, Jia HR, Wang HJ, Wang M, Mi YC: [Biological characteristics of Wt1 gene in relation to Ph(+) leukemia cell line K562]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Jun;18(3):564-9
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  • [Title] [Biological characteristics of Wt1 gene in relation to Ph(+) leukemia cell line K562].
  • Wt1 is a dual-function gene involved in hematopoiesis, leukemogenesis and prognosis for leukemia.
  • This gene is highly expressed in acute myeloid leukemia (AML) and the progression of chronic myelogenous leukemia (CML).
  • It was reported elsewhere that high level of wt1 expression indicated worse prognosis for leukemia.
  • This study was aimed to investigate the expression and localization of wt1 mRNA and WT1 protein, and explore the effects of wt1 inhibitor, curcumin, on K562 cell proliferation, cell cycle and its possible mechanisms.
  • MTT method was used to detect cell proliferation; flow cytometry was used to analyze the alteration of cell cycle, and the immunofluorescence and Western blot technology were performed to observe the subcellular localization of WT1 protein.
  • The curcumin and imatinib (Glevec) both inhibit the cell proliferation resulting in the G(2)/M and G(0)/G(1) phase arrest respectively.
  • It is concluded that the alteration of wt1 gene affects the biological characteristics of Ph(+) K562 cells, such as cell proliferation, cell cycle and so on.
  • Gene wt1 is expected to be further studied as a new therapy target in Ph(+) leukemias.

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  • (PMID = 20561402.001).
  • [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 / RNA, Messenger; 0 / WT1 Proteins; IT942ZTH98 / Curcumin
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37. Flotho C, Claus R, Batz C, Schneider M, Sandrock I, Ihde S, Plass C, Niemeyer CM, Lübbert M: The DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells. Leukemia; 2009 Jun;23(6):1019-28
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  • [Title] The DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells.
  • The three DNA methyltransferase (DNMT)-inhibiting cytosine nucleoside analogues, azacitidine, decitabine and zebularine, which are currently studied as nonintensive therapy for myelodysplastic syndromes and acute myeloid leukemia (AML), differ in structure and metabolism, suggesting that they may have differential molecular activity.
  • We investigated cellular and molecular effects of the three substances relative to cytarabine in Kasumi-1 AML blasts.
  • Under in vitro conditions mimicking those used in clinical trials, the DNMT inhibitors inhibited proliferation and triggered apoptosis but did not induce myeloid differentiation.
  • The DNMT inhibitors showed no interference with cell-cycle progression whereas cytarabine treatment resulted in an S-phase arrest.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytidine / analogs & derivatives. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Apoptosis. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Differentiation. Cell Line, Tumor. Cell Proliferation. DNA Methylation. Enzyme Inhibitors / pharmacology. Gene Expression Profiling. Humans

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  • (PMID = 19194470.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 5CSZ8459RP / Cytidine; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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38. Kasner MT, Laury A, Kasner SE, Carroll M, Luger SM: Increased cerebral blood flow after leukapheresis for acute myelogenous leukemia. Am J Hematol; 2007 Dec;82(12):1110-2
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  • [Title] Increased cerebral blood flow after leukapheresis for acute myelogenous leukemia.
  • Leukapheresis is often considered in the management of acute myelogenous leukemia (AML) with hyperleukocytosis and its sequelae, including myocardial infarction, pulmonary complications, and stroke.
  • We present a woman with AML and a history of meningioma encasing her left internal carotid artery.
  • As her white blood cell continued to rise despite initiation of hydroxyurea therapy, she underwent leukapheresis emergently.
  • This is the first documentation that leukapheresis, in combination with hydroxyurea, improves cerebral hemodynamics in a patient with AML.
  • [MeSH-major] Blood Flow Velocity / physiology. Cerebrovascular Circulation / physiology. Leukemia, Myeloid, Acute / therapy


39. Borthakur G, Kantarjian H, Wang X, Plunkett WK Jr, Gandhi VV, Faderl S, Garcia-Manero G, Ravandi F, Pierce S, Estey EH: Treatment of core-binding-factor in acute myelogenous leukemia with fludarabine, cytarabine, and granulocyte colony-stimulating factor results in improved event-free survival. Cancer; 2008 Dec 1;113(11):3181-5
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  • [Title] Treatment of core-binding-factor in acute myelogenous leukemia with fludarabine, cytarabine, and granulocyte colony-stimulating factor results in improved event-free survival.
  • BACKGROUND: Acute myelogenous leukemia (AML) associated with core-binding-factor (CBF) abnormalities is the type of leukemia most responsive to cytarabine (ara-C) therapy and is of relative favorable prognosis.
  • METHODS: We analyzed the event-free survival of patients with newly diagnosed CBF AML treated with fludarabine and ara-C (FA) (N = 45) or with FA and GCSF (FLAG) (N = 22) and compared results to patients treated with regimens consisting of idarubicin and ara-C with or without GCSF (IA/IAG) (N = 47).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Cytarabine / therapeutic use. Disease-Free Survival. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Multivariate Analysis. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

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  • [Copyright] (c) 2008 American Cancer Society
  • [Cites] Blood. 2001 Dec 15;98(13):3575-83 [11739159.001]
  • [Cites] Br J Haematol. 2006 Oct;135(2):165-73 [16939487.001]
  • [Cites] Blood. 2003 Jul 15;102(2):462-9 [12649129.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2746-55 [12842988.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1087-94 [15020610.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3741-50 [15289486.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Cancer Res. 1987 Jun 1;47(11):3005-11 [3471322.001]
  • [Cites] Cancer Res. 1988 Jan 15;48(2):329-34 [3335008.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1825-31 [1391946.001]
  • [Cites] J Clin Oncol. 1993 Jan;11(1):116-24 [8418222.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Leukemia. 1998 Sep;12(9):1482-9 [9737700.001]
  • [Cites] Clin Cancer Res. 1995 Feb;1(2):169-78 [9815970.001]
  • [Cites] Leuk Res. 2006 Jun;30(6):657-8 [16386301.001]
  • [Cites] Blood. 2006 Jul 1;108(1):63-73 [16522815.001]
  • [Cites] Blood. 2002 May 15;99(10):3517-23 [11986202.001]
  • (PMID = 18932257.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; ZRP63D75JW / Idarubicin; FLAG protocol
  • [Other-IDs] NLM/ NIHMS595625; NLM/ PMC4126078
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40. Harousseau JL, Lancet JE, Reiffers J, Lowenberg B, Thomas X, Huguet F, Fenaux P, Zhang S, Rackoff W, De Porre P, Stone R, Farnesyltransferase Inhibition Global Human Trials (FIGHT) Acute Myeloid Leukemia Study Group: A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib in patients with refractory or relapsed acute myeloid leukemia. Blood; 2007 Jun 15;109(12):5151-6
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  • [Title] A phase 2 study of the oral farnesyltransferase inhibitor tipifarnib in patients with refractory or relapsed acute myeloid leukemia.
  • This phase 2 study evaluated the efficacy and safety of the oral farnesyltransferase inhibitor tipifarnib in adults with refractory or relapsed acute myeloid leukemia (AML).
  • Single-agent treatment with tipifarnib induced durable CR/CRp, which was associated with prolonged survival, in some patients with refractory or relapsed AML.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Quinolones / administration & dosage. Salvage Therapy / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Blast Crisis / pathology. Blast Crisis / prevention & control. Bone Marrow Cells / pathology. Farnesyltranstransferase / antagonists & inhibitors. Female. Humans. Male. Middle Aged. Remission Induction / methods. Survival Rate. Treatment Outcome

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  • (PMID = 17351110.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.1.29 / Farnesyltranstransferase
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41. Wykrzykowska JJ, Carrozza J, Laham RJ: Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting. J Invasive Cardiol; 2006 Aug;18(8):E217-20
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  • [Title] Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting.
  • Of the type-A dissections in the International Registry of Aortic Dissections (IRAD), 27% were caused by coronary interventions.
  • [MeSH-major] Aneurysm, Dissecting / therapy. Aortic Aneurysm / therapy. Coronary Aneurysm / therapy. Coronary Disease / therapy. Stents

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  • (PMID = 16877790.001).
  • [ISSN] 1557-2501
  • [Journal-full-title] The Journal of invasive cardiology
  • [ISO-abbreviation] J Invasive Cardiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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42. Jacobs P, Wood L: Clonogenic growth patterns correlate with chemotherapy response in acute myeloid leukaemia. Hematology; 2005 Aug;10(4):321-6
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  • [Title] Clonogenic growth patterns correlate with chemotherapy response in acute myeloid leukaemia.
  • Cytosine arabinoside and anthracycline-containing regimens induce remission in upwards of 60% of previously untreated patients with adult acute myeloid leukaemia (AML).
  • Reliable methods for uniformly recognising these two subgroups at presentation do not exist and therefore a further attempt has been made to relate in vitro toxicity, using a clonogenic assay, to clinical outcome.
  • In 10 normal controls and 12 chemotherapy naïve cases, mononuclear cells harvested by density gradient separation were re-suspended at a concentration of 2 x 10(5)/ml and quadruplicates of 250 microl per well cultured in methycellulose containing foetal calf serum and phytohaemagglutinin stimulated leucocyte conditioned medium.
  • Cell kill was determined for cytosine arabinoside, daunorubicin and etoposide either singly or in combination using both a pulsed and continuous exposure.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Myeloid, Acute / metabolism. Neoplastic Stem Cells / metabolism. Tumor Stem Cell Assay
  • [MeSH-minor] Adolescent. Adult. Cell Survival / drug effects. Cytarabine / therapeutic use. Female. Humans. Male. Middle Aged. Myeloid Progenitor Cells / metabolism. Myeloid Progenitor Cells / pathology. Pilot Projects. Predictive Value of Tests. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 16085545.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine
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43. Wandroo F, Stableforth P, Hasan Y: Aspergillus brain abscess in a patient with acute myeloid leukaemia successfully treated with voriconazole. Clin Lab Haematol; 2006 Apr;28(2):130-3
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  • [Title] Aspergillus brain abscess in a patient with acute myeloid leukaemia successfully treated with voriconazole.
  • [MeSH-major] Aspergillosis / drug therapy. Aspergillus fumigatus. Brain Abscess / drug therapy. Central Nervous System Fungal Infections / drug therapy. Leukemia, Erythroblastic, Acute / drug therapy. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 16630219.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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44. Sarafnejad A, Khosravi F, Alimoghadam K, Dianat S, Ansaripour B, Moradi B, Dorkhosh S, Amirzargar A: HLA class II allele and haplotype frequencies in iranian patients with acute myelogenous leukemia and control group. Iran J Allergy Asthma Immunol; 2006 Sep;5(3):115-9
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  • [Title] HLA class II allele and haplotype frequencies in iranian patients with acute myelogenous leukemia and control group.
  • We have analyzed HLA class II alleles and haplotypes in 60 Iranian patients with acute myelogenous leukemia (AML) and 180 unrelated normal subjects.
  • Significant positive association with the disease was found for HLA-DRB1*11 allele (35% vs. 24.7%, p=0.033).
  • It is suggested that HLA-DRB1*11 allele plays as a presumptive predisposing factor while the HLA-DRB4 and -DQB1*0303 alleles are suggested as protective genetic factors against acute myelogenous leukemia.
  • Larger studies are needed to confirm and establish the role of these associations with acute myelogenous leukemia.
  • [MeSH-major] HLA-DQ Antigens / genetics. HLA-DR Antigens / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Case-Control Studies. Gene Frequency. Genetic Predisposition to Disease. HLA-DQ alpha-Chains. HLA-DQ beta-Chains. Haplotypes. Humans. Iran / epidemiology

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  • (PMID = 17237562.001).
  • [ISSN] 1735-1502
  • [Journal-full-title] Iranian journal of allergy, asthma, and immunology
  • [ISO-abbreviation] Iran J Allergy Asthma Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / HLA-DQ Antigens; 0 / HLA-DQ alpha-Chains; 0 / HLA-DQ beta-Chains; 0 / HLA-DQA1 antigen; 0 / HLA-DQB1 antigen; 0 / HLA-DR Antigens
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45. Wergeland L, Sjøholt G, Haaland I, Hovland R, Bruserud Ø, Gjertsen BT: Pre-apoptotic response to therapeutic DNA damage involves protein modulation of Mcl-1, Hdm2 and Flt3 in acute myeloid leukemia cells. Mol Cancer; 2007;6:33
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  • [Title] Pre-apoptotic response to therapeutic DNA damage involves protein modulation of Mcl-1, Hdm2 and Flt3 in acute myeloid leukemia cells.
  • BACKGROUND: Acute myeloid leukemia (AML) cells are characterized by non-mutated TP53, high levels of Hdm2, and frequent mutation of the Flt3 receptor tyrosine kinase.
  • The juxtamembrane mutation of FLT3 is the strongest independent marker for disease relapse and is associated with elevated Bcl-2 protein and p53 hyper-phosphorylation in AML.
  • DNA damage forms the basic mechanism of cancer cell eradication in current therapy of AML.
  • RESULTS: Within one hour after exposure to ionizing radiation (IR), the AML cells (NB4, MV4-11, HL-60, primary AML cells) showed an increase in Flt3 protein independent of mRNA levels, while the Hdm2 protein decreased.
  • Daunorubicin (DNR) induced continuing down regulation of Hdm2 and Mcl-1 in both cell lines followed by apoptosis.
  • Cell death induction was associated with persistent attenuation of Mcl-1 and Hdm2.
  • These observations suggest that defining the pathway(s) modulating Flt3, Hdm2 and Mcl-1 may propose new strategies to optimize therapy for the relapse prone FLT3 mutated AML patients.
  • [MeSH-major] Apoptosis. DNA Damage. Daunorubicin / pharmacology. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-mdm2 / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Adult. Aged. Female. HL-60 Cells. Humans. Male. Middle Aged. Myeloid Cell Leukemia Sequence 1 Protein. Radiation, Ionizing. Tumor Suppressor Protein p53 / metabolism

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  • [Cites] Blood. 1993 Nov 1;82(9):2617-23 [8219216.001]
  • [Cites] Acta Oncol. 1992;31(1):53-8 [1586506.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jul 1;29(4):813-9 [8040028.001]
  • [Cites] Leukemia. 1994 Oct;8(10):1673-81 [7523798.001]
  • [Cites] J Cell Sci. 1994 Dec;107 ( Pt 12):3363-77 [7706392.001]
  • [Cites] Cell. 1995 Aug 11;82(3):405-14 [7634330.001]
  • [Cites] Blood. 1998 Feb 1;91(3):991-1000 [9446661.001]
  • [Cites] J Biol Chem. 1999 Jan 15;274(3):1677-82 [9880547.001]
  • [Cites] Br J Haematol. 1999 Oct;107(1):69-79 [10520026.001]
  • [Cites] Curr Cancer Drug Targets. 2005 Feb;5(1):9-20 [15720185.001]
  • [Cites] Leukemia. 2005 Jun;19(6):930-5 [15815726.001]
  • [Cites] Drug Resist Updat. 2005 Feb-Apr;8(1-2):5-14 [15939338.001]
  • [Cites] Oncogene. 2005 Jun 16;24(26):4271-80 [15824741.001]
  • [Cites] J Biol Chem. 2005 Jul 1;280(26):24315-21 [15851483.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):444-53 [16344316.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2184-91 [16254140.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):3985-92 [16818696.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]
  • [Cites] Leukemia. 2006 Dec;20(12):2130-6 [17066094.001]
  • [Cites] Mol Cell Biol. 2007 Jan;27(1):111-9 [17060450.001]
  • [Cites] Nat Cell Biol. 2007 Mar;9(3):331-8 [17293853.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2589-96 [17105820.001]
  • [Cites] J Hematother Stem Cell Res. 1999 Aug;8(4):431-41 [10634181.001]
  • [Cites] J Biol Chem. 2000 Mar 24;275(12):8945-51 [10722742.001]
  • [Cites] J Hematother Stem Cell Res. 2000 Dec;9(6):923-32 [11177606.001]
  • [Cites] Blood. 2001 Aug 15;98(4):913-24 [11493433.001]
  • [Cites] Leuk Res. 2002 Feb;26(2):207-14 [11755471.001]
  • [Cites] Lancet Oncol. 2001 Jun;2(6):366-70 [11905753.001]
  • [Cites] Hum Mutat. 2002 Jun;19(6):607-14 [12007217.001]
  • [Cites] Leukemia. 2003 Jan;17(1):120-4 [12529668.001]
  • [Cites] Genes Dev. 2003 Jun 15;17(12):1475-86 [12783855.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8247-52 [12821780.001]
  • [Cites] Radiat Res. 2003 Aug;160(2):224-31 [12859234.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12009-14 [14507994.001]
  • [Cites] EMBO J. 2004 Apr 7;23(7):1547-56 [15029243.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Jun;50(3):197-222 [15182826.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Br J Haematol. 1992 Feb;80(2):178-83 [1550773.001]
  • [Cites] Cancer Res. 1994 Jan 1;54(1):220-5 [8261442.001]
  • (PMID = 17498302.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ PMC1876473
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46. Bullinger L, Valk PJ: Gene expression profiling in acute myeloid leukemia. J Clin Oncol; 2005 Sep 10;23(26):6296-305
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  • [Title] Gene expression profiling in acute myeloid leukemia.
  • Over the last decades, significant advances have been made in the knowledge and treatment of acute myeloid leukemia (AML).
  • The WHO has recognized this new information by incorporating into its classification morphologic, immunophenotypic, genetic, and clinical features in an attempt to define biologically and clinically relevant entities.
  • Nevertheless, well-defined cytogenetic subgroups exhibit considerable heterogeneity, and in many AML subtypes the pathogenic event is still not known.
  • A classification system based on the underlying molecular pathogenetic abnormalities would be ideal, but such detailed knowledge is not yet available.
  • Novel approaches in genomics, such as surveying the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities to further refine the studies on AML.
  • Today, gene expression profiling in AML is becoming well established and has already been proven to be valuable in diagnosing different cytogenetic subtypes, discovering novel AML subclasses, and predicting clinical outcome.
  • Recently, gene expression profiling studies in AML showed a remarkable level of concordance in findings, which may ultimately lead to an increasingly refined molecular taxonomy.
  • While many challenges remain to be overcome, a combination of gene expression profiling with other microarray-based applications, high-throughput mutational analyses and proteomic approaches will not only significantly contribute to the classification and therapeutic decision making of AML, but also give important insights into the true pathobiologic nature of this type of leukemia.
  • [MeSH-major] Gene Expression Profiling. Genetic Predisposition to Disease / epidemiology. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16155012.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 74
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47. Maurillo L, Buccisano F, Del Principe MI, Del Poeta G, Spagnoli A, Panetta P, Ammatuna E, Neri B, Ottaviani L, Sarlo C, Venditti D, Quaresima M, Cerretti R, Rizzo M, de Fabritiis P, Lo Coco F, Arcese W, Amadori S, Venditti A: Toward optimization of postremission therapy for residual disease-positive patients with acute myeloid leukemia. J Clin Oncol; 2008 Oct 20;26(30):4944-51
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  • [Title] Toward optimization of postremission therapy for residual disease-positive patients with acute myeloid leukemia.
  • PURPOSE: Despite the identification of several baseline prognostic indicators, the outcome of patients with acute myeloid leukemia (AML) is generally heterogeneous.
  • The effects of autologous (AuSCT) or allogeneic stem-cell transplantation (SCT) are still under evaluation.
  • Minimal residual disease (MRD) states may be essential for assigning patients to therapy-dependent risk categories.
  • PATIENTS AND METHODS: By multiparametric flow cytometry, we assessed the levels of MRD in 142 patients with AML who achieved complete remission after intensive chemotherapy.
  • RESULTS: A level of 3.5 x 10(-4) residual leukemia cells (RLCs) after consolidation therapy was established to identify MRD-negative and MRD-positive cases, with 5-year relapse-free survival (RFS) rates of 60% and 16%, respectively (P < .0001) and overall survival (OS) rates of 62% and 23%, respectively (P = .0001).
  • CONCLUSION: A threshold of 3.5 x 10(-4) RLCs postconsolidation is critical for predicting disease outcome.
  • In the MRD-positive group, AuSCT does not improve prognosis and SCT represents the primary option.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adult. Aged. Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Neoplasm, Residual. Prognosis. Remission Induction. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 18606980.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide
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48. Kojima M, Nakamura N, Murayama K, Igarashi T, Matsumoto M, Matsuda H, Masawa N, Miura I, Morita Y: Reactive lymphoid hyperplasia with giant follicles associated with a posttherapeutic state of hematological malignancies. A report of eight cases. Tumori; 2010 Jan-Feb;96(1):143-8
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  • RESULTS: Six patients had a history of malignant lymphoma (diffuse large B-cell lymphoma [DLBCL] = 4, marginal zone B-cell lymphoma = 2), and two had acute myeloid leukemia (AML).
  • Six patients initially presented with lymphadenopathy of the head and neck area and the remaining one presented with swelling of the tonsil.
  • Histologically, all eight lesions were characterized by numerous enlarged, bizarre-shaped coalescing lymphoid follicles with follicular lysis.
  • Immunohistochemical and flow cytometry study demonstrated the reactive nature of the B cells in all eight lesions.
  • There was no development of B-cell lymphoma or recurrence of B-cell lymphoma in any of the three lesions demonstrating IgH rearrangement.
  • There were no human herpes virus type-8+ or human immunodeficiency virus type-1+ cells in any of the eight lesions.
  • ISH demonstrated Epstein-Barr virus (EBV)-encoded small RNA (EBER)+ cells in only two lesions.
  • PCR analyses demonstrated that there was no Toxoplasma gondii DNA in any of the eight lesions.
  • It is important for pathologists and clinicians to be aware of this type of lesion in diagnostic practice.
  • [MeSH-major] B-Lymphocytes / immunology. Castleman Disease / etiology. Hematologic Neoplasms / complications. Hematologic Neoplasms / therapy. Pseudolymphoma / etiology
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Flow Cytometry. Humans. Immunoglobulin Heavy Chains / analysis. Immunohistochemistry. In Situ Hybridization. Karyotyping. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / therapy. Lymphoma, B-Cell, Marginal Zone / complications. Lymphoma, B-Cell, Marginal Zone / therapy. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / therapy. Male. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 20437872.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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49. Dombret H, Raffoux E, Gardin C: Acute myeloid leukemia in the elderly. Semin Oncol; 2008 Aug;35(4):430-8
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  • [Title] Acute myeloid leukemia in the elderly.
  • The incidence of acute myeloid leukemia (AML) is increasing with age.
  • Reduced-intensity conditioning stem cell transplantation or other various immunological approaches represent another way of investigation.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Drug Resistance, Neoplasm. Humans. Middle Aged. Prognosis. Stem Cell Transplantation

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  • (PMID = 18692693.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 80
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50. Oliver L, Mahé B, Gréé R, Vallette FM, Juin P: HA14-1, a small molecule inhibitor of Bcl-2, bypasses chemoresistance in leukaemia cells. Leuk Res; 2007 Jun;31(6):859-63
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  • [Title] HA14-1, a small molecule inhibitor of Bcl-2, bypasses chemoresistance in leukaemia cells.
  • We analyzed the biological activity of HA14-1, a small organic compound inhibitor of Bcl-2, against established leukaemia cell lines and blasts from acute myeloid leukaemia (AML) patients.
  • HA14-1 had a potent killing activity against the leukaemia cell line that expressed endogenous or ectopic Bcl-2.
  • This activity was mostly caspase-independent and was not altered by the expression of a multidrug-resistant phenotype.
  • Moreover, HA14-1 efficiently induced cell death in a broad spectrum of AML blasts but not in normal peripheral blood lymphocytes.
  • Thus, single-agent regimens using Bcl-2 inhibitors such as HA14-1 may be advantageous in overcoming some forms of chemoresistance in AML.
  • [MeSH-major] Benzopyrans / pharmacology. Blast Crisis / metabolism. Drug Resistance, Neoplasm / drug effects. Enzyme Inhibitors / pharmacology. Leukemia, Myeloid, Acute / metabolism. Nitriles / pharmacology. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • [MeSH-minor] Caspases / metabolism. Cell Death / drug effects. HL-60 Cells. Humans. Lymphocytes / metabolism. Lymphocytes / pathology

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  • (PMID = 17224180.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzopyrans; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; EC 3.4.22.- / Caspases
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51. Nielsen J, Boysen A: Clozapine treatment associated with increased risk of acute myeloid leukemia (AML). Schizophr Res; 2010 Nov;123(2-3):270-2
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  • [Title] Clozapine treatment associated with increased risk of acute myeloid leukemia (AML).
  • [MeSH-major] Antipsychotic Agents / adverse effects. Clozapine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Schizophrenia / drug therapy


52. Xu W, Li JY, Liu Q, Zhu Y, Pan JL, Qiu HR, Xue YQ: Multiplex fluorescence in situ hybridization in identifying chromosome involvement of complex karyotypes in de novo myelodysplastic syndromes and acute myeloid leukemia. Int J Lab Hematol; 2010 Feb;32(1 Pt 1):e86-95
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  • [Title] Multiplex fluorescence in situ hybridization in identifying chromosome involvement of complex karyotypes in de novo myelodysplastic syndromes and acute myeloid leukemia.
  • Complex chromosomal aberrations (CCA) can be detected in a substantial proportion of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), which are associated with very poor prognosis.
  • In this study, M-FISH was used in 16 patients with de novo MDS and 22 with AML with CCA detected by R-banding CC, and revealed 206 aberrations involved all 24 chromosomes, including 73 numerical chromosomal abnormalities and 133 structural abnormalities.
  • There were some abnormalities that have not been previously described, including two complex t(8;21) and seven unbalanced translocations.
  • Our findings confirmed that M-FISH was a powerful molecular cytogenetic tool to characterize complex karyotypes in MDS and AML.
  • [MeSH-major] Chromosomes, Human / genetics. In Situ Hybridization, Fluorescence / methods. Karyotyping / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


53. Wang YL, Wang T, Xu F, Gang Y, Wang J: [Analysis of Flt-3 expression and Flt-3/ITD mutation in acute myeloid leukemia cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):446-9
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  • [Title] [Analysis of Flt-3 expression and Flt-3/ITD mutation in acute myeloid leukemia cells].
  • This study was aimed to explore the relationship between Flt-3 expression, Flt-3/ITD mutation in acute leukemia (AL) cell line and pathogenesis of AL, especially AML.
  • The Flt-3 expression and Flt-3/ITD mutation were detected by RT-PCR and sequencing method in 82 leukemia cell lines including 20 AML, 57 ALL and 5 CML cell lines.
  • The results indicated that positive results of Flt-3 expression were obtained in 48 out of 77 AL cell line, the positive rate was 62%; 12 cell lines were positive in 20 AML cell lines, the positive rate was 60%; 33 cell lines was positive in 57 ALL cell lines, the positive rate was 58%; 3 cell lines were positive in 5 CML cell lines, the positive rate was 60%.
  • There was abnormal gene product in 1 AMOL cell line out of 12 AML cell lines with Flt-3 positive expression (positive rate 8.3%).
  • The positive rate of Flt-3 expression in undifferentiated cell line was prominently higher than that in mature B cell ALL (P < 0.05).
  • It is concluded that the Flt-3 expression is different in various leukemia cells.
  • Flt-3/ITD duplication was found in one AML cell line.
  • The detection of Flt-3 gene and Flt-3/ITD mutation may contribute to the diagnosis of ALL, especially to AML.

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  • (PMID = 16800917.001).
  • [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] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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54. Hołowiecki J, Grosicki S, Kyrcz-Krzemien S, Skotnicki AB, Piatkowska-Jakubas B, Warzocha K, Seferynska I, Zdziarska B: Daunorubicin, cytarabine and fludarabine (DAF) for remission induction in relapsed or refractory acute myeloid leukemia. Evaluation of safety, tolerance and early outcome--Polish Adult Leukemia Group (PALG) pilot study. Ann Hematol; 2008 May;87(5):361-7
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  • [Title] Daunorubicin, cytarabine and fludarabine (DAF) for remission induction in relapsed or refractory acute myeloid leukemia. Evaluation of safety, tolerance and early outcome--Polish Adult Leukemia Group (PALG) pilot study.
  • Based on these findings and encouraging results of the addition of cladribine to standard daunorubicin+Ara-C induction regimen (DAC) in acute myeloid leukemia (AML), the Polish Adult Leukemia Group (PALG) conducted a pilot study on the administration of cytarabine, daunorubicin, and fludarabine (DAF) as a reinduction treatment of AML to assess tolerance, toxicity, and early outcome.
  • Thirty-four AML patients with median age 39, 24% relapsed and 76% refractory, were included into the study between September 2003 and August 2004.
  • Liver, kidney, or circulatory failure, diarrhea, or polyneuropathy were not observed.
  • The probability of leukemia-free survival (LFS) for 1 year was 38% (95% CI 22-54%).
  • Summarizing, DAF regimen used as the induction therapy in relapsed/refractory AML was well tolerated with acceptable toxicity and early efficacy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Poland. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives


55. Moreau-Gachelin F: Multi-stage Friend murine erythroleukemia: molecular insights into oncogenic cooperation. Retrovirology; 2008;5:99
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  • The Friend virus SFFV (Spleen Focus Forming Virus) provokes an acute erythroblastosis in susceptible strains of mice that progresses to overt erythroleukemia by a multi-step process.
  • For virologists, the Friend virus-induced disease has provided deep insights into the host mechanisms influencing susceptibility to retroviral infection and viremia.
  • For cell biologists and oncologists, this leukemia has been a powerful experimental model to identify critical oncogenes involved in a multi-stage process, to understand the contribution of host genes to cancer development, and to investigate the mechanisms leading to cell growth autonomy.
  • The Friend model of leukemia progression recapitulates the two phases of human acute myeloid leukemia (AML).
  • Coupling of insights from studies on the Friend erythroleukemia with knowledge on AML might allow a better understanding of the molecular mechanisms involved in the evolution of leukemia in mice and men.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Erythroblastic, Acute / virology. Oncogenes. Spleen Focus-Forming Viruses / pathogenicity
  • [MeSH-minor] Animals. Animals, Newborn. Cell Differentiation. Cell Proliferation. Humans. Leukemia, Myeloid, Acute / pathology. Male. Mice

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  • [Cites] Crit Rev Oncol Hematol. 2005 Apr;54(1):63-75 [15780908.001]
  • [Cites] J Virol. 2005 May;79(10):6560-4 [15858043.001]
  • [Cites] J Virol. 2004 Sep;78(18):9592-8 [15331691.001]
  • [Cites] Science. 1967 Jan 27;155(3761):461-2 [6015694.001]
  • [Cites] Science. 1967 May 12;156(3776):832-3 [4960553.001]
  • [Cites] Proc Soc Exp Biol Med. 1968 Jul;128(3):844-9 [5668141.001]
  • [Cites] J Natl Cancer Inst. 1970 Jul;45(1):163-9 [5449211.001]
  • [Cites] J Virol. 1985 Jul;55(1):184-92 [4009793.001]
  • [Cites] Science. 1985 Jun 28;228(4707):1549-52 [2990034.001]
  • [Cites] Nature. 1988 Jan 21;331(6153):277-80 [2827041.001]
  • [Cites] J Virol. 1988 Jun;62(6):2158-63 [2835516.001]
  • [Cites] Oncogene. 1988 Aug;3(2):179-85 [2842714.001]
  • [Cites] Nature. 1989 Jun 8;339(6224):446-51 [2725678.001]
  • [Cites] Cell. 1989 Sep 8;58(5):877-85 [2776214.001]
  • [Cites] J Virol. 1989 Nov;63(11):4958-61 [2552176.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7957-60 [2554298.001]
  • [Cites] Curr Top Microbiol Immunol. 1989;148:1-42 [2684547.001]
  • [Cites] Oncogene. 1989 Dec;4(12):1449-56 [2594367.001]
  • [Cites] J Virol. 1990 Mar;64(3):1057-62 [2154592.001]
  • [Cites] Nature. 1990 Feb 22;343(6260):762-4 [2154701.001]
  • [Cites] Cell. 1990 Apr 6;61(1):113-24 [2180582.001]
  • [Cites] Annu Rev Immunol. 1990;8:477-99 [2188671.001]
  • [Cites] Mol Cell Biol. 1990 Jul;10(7):3307-13 [1694008.001]
  • [Cites] EMBO J. 1990 Jul;9(7):2107-16 [2162763.001]
  • [Cites] J Virol. 1991 Jan;65(1):464-7 [1985210.001]
  • [Cites] Nature. 1991 Jan 17;349(6306):257-60 [1987478.001]
  • [Cites] Mol Cell Biol. 1991 Jun;11(6):3043-51 [1710023.001]
  • [Cites] Genes Dev. 1991 Jun;5(6):908-18 [2044959.001]
  • [Cites] EMBO J. 1991 Sep;10(9):2451-9 [1714377.001]
  • [Cites] Cell. 1991 Sep 6;66(5):831-4 [1889087.001]
  • [Cites] Cell. 1991 Dec 20;67(6):1089-102 [1662116.001]
  • [Cites] Oncogene. 1991 Dec;6(12):2197-201 [1766668.001]
  • [Cites] Mol Cell Biol. 1992 Jul;12(7):2949-57 [1320192.001]
  • [Cites] Mol Cell Biol. 1992 Jul;12(7):2967-75 [1620109.001]
  • [Cites] Mol Cell Biol. 1993 Mar;13(3):1456-63 [8441390.001]
  • [Cites] Nat Genet. 1993 Jun;4(2):124-9 [8348149.001]
  • [Cites] Blood. 1994 Jun 1;83(11):3160-9 [8193352.001]
  • [Cites] J Virol. 1995 Mar;69(3):1714-19 [7853508.001]
  • [Cites] EMBO J. 1995 Feb 1;14(3):473-83 [7532131.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9623-7 [7568185.001]
  • [Cites] Nat Genet. 1996 Mar;12(3):312-4 [8589724.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2453-63 [8628313.001]
  • [Cites] Nature. 1996 Aug 29;382(6594):826-9 [8752279.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5647-58 [8896458.001]
  • [Cites] Br J Haematol. 1997 Feb;96(2):374-6 [9029028.001]
  • [Cites] Immunity. 1997 Apr;6(4):437-47 [9133423.001]
  • [Cites] EMBO J. 1997 Sep 15;16(18):5639-53 [9312023.001]
  • [Cites] J Virol. 1998 Feb;72(2):919-25 [9444983.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1172-80 [9488432.001]
  • [Cites] Oncogene. 1998 Jun 11;16(23):2989-95 [9662331.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4456-68 [9687512.001]
  • [Cites] Leuk Lymphoma. 1998 Sep;31(1-2):231-6 [9720733.001]
  • [Cites] EMBO J. 1998 Nov 2;17(21):6250-62 [9799234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13236-41 [16141339.001]
  • [Cites] EMBO J. 2005 Nov 2;24(21):3712-23 [16222338.001]
  • [Cites] Cancer Cell. 2005 Dec;8(6):467-78 [16338660.001]
  • [Cites] Blood. 2006 Jan 1;107(1):73-8 [16174761.001]
  • [Cites] Oncogene. 2006 Apr 20;25(17):2433-43 [16314834.001]
  • [Cites] J Virol. 2006 Jun;80(12):5678-85 [16731906.001]
  • [Cites] Leuk Res. 2006 Sep;30(9):1141-9 [16527351.001]
  • [Cites] J Biol Chem. 2007 Mar 2;282(9):6316-23 [17218319.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Retrovirology. 2007;4:18 [17362524.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9 [15650049.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(4):1215-27 [15684376.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(7):2832-45 [15767686.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1590-600 [15914556.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1519-24 [15914558.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3007-14 [17132716.001]
  • [Cites] J Virol. 2008 Jan;82(1):419-27 [17959667.001]
  • [Cites] Vaccine. 2008 Jun 6;26(24):2981-96 [18255203.001]
  • [Cites] Science. 2008 Sep 5;321(5894):1343-6 [18772436.001]
  • [Cites] J Virol. 2008 Nov;82(22):10998-1008 [18786991.001]
  • [Cites] Br J Haematol. 1999 Jun;105(4):894-900 [10554798.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] Blood. 2000 Apr 15;95(8):2543-51 [10753833.001]
  • [Cites] Science. 2000 May 26;288(5470):1439-41 [10827957.001]
  • [Cites] J Virol. 2000 Sep;74(18):8444-51 [10954544.001]
  • [Cites] Oncogene. 2000 Oct 19;19(44):5106-10 [11042699.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):12295-9 [11027299.001]
  • [Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]
  • [Cites] Oncogene. 2001 May 24;20(23):2946-55 [11420707.001]
  • [Cites] J Virol. 2001 Sep;75(17):7893-903 [11483734.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • [Cites] Oncogene. 2001 Sep 6;20(39):5484-92 [11571646.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2372-81 [11588033.001]
  • [Cites] Immunity. 2002 Feb;16(2):285-96 [11869688.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):502-13 [12094236.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] Mol Cell. 2003 Sep;12(3):591-601 [14527406.001]
  • [Cites] Blood Rev. 2003 Dec;17(4):241-8 [14556779.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6363-9 [14559825.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43755-63 [12930840.001]
  • [Cites] Nat Med. 2003 Nov;9(11):1398-403 [14528301.001]
  • [Cites] Nature. 2004 Feb 26;427(6977):848-53 [14985764.001]
  • [Cites] J Virol. 2004 May;78(9):4573-81 [15078939.001]
  • [Cites] J Exp Med. 1971 Jun 1;133(6):1234-41 [4325133.001]
  • [Cites] Nat New Biol. 1971 Dec 22;234(51):230-3 [5288817.001]
  • [Cites] Int J Cancer. 1975 Mar 15;15(3):467-82 [1140862.001]
  • [Cites] Nature. 1975 Jul 24;256(5515):320-2 [1143333.001]
  • [Cites] J Natl Cancer Inst. 1975 Aug;55(2):443-6 [1159825.001]
  • [Cites] Annu Rev Biochem. 1978;47:419-48 [354501.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Jan;76(1):425-9 [284359.001]
  • [Cites] J Exp Med. 1979 Jul 1;150(1):10-9 [286744.001]
  • [Cites] Leuk Res. 1979;3(3):117-29 [381791.001]
  • [Cites] Curr Top Microbiol Immunol. 1979;86:67-122 [227645.001]
  • [Cites] J Virol. 1980 Sep;35(3):844-53 [7420541.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Mar;78(3):1703-7 [6940184.001]
  • [Cites] J Virol. 1982 Jul;43(1):223-33 [6955527.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Aug;80(15):4704-8 [6308644.001]
  • [Cites] Blood Cells. 1981;7(1):133-44 [7187746.001]
  • [Cites] J Virol. 1984 Jun;50(3):759-65 [6328005.001]
  • [Cites] J Virol. 1985 Jan;53(1):292-5 [2981349.001]
  • [Cites] Nature. 1985 Apr 18-24;314(6012):633-6 [3990796.001]
  • [Cites] Mol Cell Biol. 1999 Jan;19(1):121-35 [9858537.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] Genes Dev. 1999 Jun 1;13(11):1398-411 [10364157.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8705-10 [10411939.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):159-65 [10508511.001]
  • [Cites] Br J Haematol. 2005 Jan;128(1):18-34 [15606546.001]
  • [Cites] Mol Cell. 2004 Dec 22;16(6):849-59 [15610729.001]
  • [Cites] Stem Cells. 2005;23(1):16-43 [15625120.001]
  • [Cites] J Exp Med. 2005 Jan 17;201(2):221-31 [15657291.001]
  • [Cites] J Exp Med. 2005 May 2;201(9):1487-502 [15867096.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Blood. 2004 May 15;103(10):3615-23 [14739214.001]
  • [Cites] Blood. 2004 Jul 1;104(1):51-7 [14996702.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10774-9 [15249685.001]
  • (PMID = 18983647.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 132
  • [Other-IDs] NLM/ PMC2585586
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56. Tong XM, Yao HP, Qian WB, Zhu LF, Fu ZH, Huang ZL, Jin J: The biological characteristics of dendritic cells derived in vitro from myelogeneous leukemia cells and healthy donor cells. Int J Lab Hematol; 2008 Oct;30(5):372-81
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  • [Title] The biological characteristics of dendritic cells derived in vitro from myelogeneous leukemia cells and healthy donor cells.
  • Successful adoptive immunotherapy for leukemia depends on the generation of T cells that can specifically react with malignant cells.
  • Dendritic cells (DCs) are important antigen-presenting cells in the development of antileukemia T-cell responses.
  • Mononuclear cells (MNC) were isolated from peripheral blood or bone marrow of patients with chronic myelogenous leukemia (CML), and acute myelogenous leukemia (AML).
  • Fluorescence in situ hybridization demonstrated the presence of fusion gene in the nuclei of representative CML or AML-M3 samples, indicating that the cells were leukemic in origin.
  • IL-12 levels were significantly higher in AML-DCs and CML-DCs prestimulated with phorbol 12-myristate 13-acetate than in the corresponding leukemic cells, but were lower than that of healthy donors.
  • These cells were potent stimulators of lymphocyte proliferation in specific in vitro assays for DC function.
  • However, the stimulatory abilities of allogeneic T cells in a mixed lymphocyte reaction were impaired compared with those of mature DCs derived from healthy donors, although T-cell stimulatory effects were significantly increased in these differentiated leukemia-DCs.
  • These results suggest that functional DCs may be derived from leukemic (AML, CML) blasts in a significant number of patients and may be capable of inducing leukemia-specific immune responses with potentially clinically beneficial effects.
  • [MeSH-major] Cell Differentiation / immunology. Dendritic Cells / immunology. Leukemia, Myeloid / immunology
  • [MeSH-minor] Cells, Cultured. Flow Cytometry. Humans. In Vitro Techniques. Lymphocyte Culture Test, Mixed

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  • (PMID = 18205840.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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57. Nguyen LA, Pandolfi PP, Aikawa Y, Tagata Y, Ohki M, Kitabayashi I: Physical and functional link of the leukemia-associated factors AML1 and PML. Blood; 2005 Jan 1;105(1):292-300
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  • [Title] Physical and functional link of the leukemia-associated factors AML1 and PML.
  • The AML1-CBFbeta transcription factor complex is the most frequent target of specific chromosome translocations in acute myeloid leukemia (AML).
  • The promyelocytic leukemia (PML) gene is also frequently involved in AML-associated translocation.
  • Overexpression of PML I stimulates myeloid cells to differentiate.
  • These results suggest that PML I could act as a mediator for AML1 and its coactivator p300/CBP to assemble into functional complexes and, consequently, activate AML1-dependent transcription and myeloid cell differentiation.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Leukemia / metabolism. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Amino Acid Sequence. Animals. Binding Sites. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Nucleus / metabolism. Core Binding Factor Alpha 2 Subunit. E1A-Associated p300 Protein. Gene Expression Regulation, Neoplastic. Granulocyte Colony-Stimulating Factor / pharmacology. Humans. Mice. Molecular Sequence Data. Myeloid Cells / cytology. Myeloid Cells / drug effects. Protein Binding. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein Structure, Tertiary. Sequence Alignment. Signal Transduction. Trans-Activators / metabolism. Tumor Suppressor Proteins

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  • (PMID = 15331439.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Ep300 protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 143220-95-5 / PML protein, human; EC 2.3.1.48 / E1A-Associated p300 Protein
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58. Jiang SH, Shi WY, Liu H, Song GQ, Sun GX, Lu W, Liu DF: [Cytogenetic and clinical study of myeloid leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Oct;24(5):571-3
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  • [Title] [Cytogenetic and clinical study of myeloid leukemia].
  • OBJECTIVE: To explore the clinical cytogenetic features and prognosis of myeloid leukemia patients.
  • RESULTS: Among 420 patients with acute myeloid leukemia (AML), 223 cases were found to exhibit clonal chromosome abnormalities, accounted for 53.1%.
  • Out of 158 patients with chronic myeloid leukemia (CML), 96.8% (153/158) were found to exhibit clonal chromosome abnormalities.
  • T(9;22) was specifically associated with CML and some cases of M0, M1 and M2.
  • In these myeloid leukemia cases, there were 18 cases (AML 13 cases, CML 15 cases) without clonal chromosome abnormalities, accounted for 3.1% (18/578) and this phenomenon agreed with the diagnose of clinical signs, marrow morphology and immunology incompletely.
  • CONCLUSION: Karyotype analysis was not only helpful to the diagnose and differential diagnose of myeloid leukemia, but also an important standard of the remission, relapse and therapeutic effect of myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • (PMID = 17922430.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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59. Hsiao PC, Liu MC, Chen LM, Tsai CY, Wang YT, Chen J, Hsu LS: Promoter methylation of p16 and EDNRB gene in leukemia patients in Taiwan. Chin J Physiol; 2008 Feb 29;51(1):27-31
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  • [Title] Promoter methylation of p16 and EDNRB gene in leukemia patients in Taiwan.
  • In this study, we have identified the methylation frequency of p16 and endothelin receptor type B (EDNRB) of 26 leukemia patients and 8 randomly selected normal blood donors in Taiwan.
  • Promoter methylation of p16 was detected in 85% of acute lymphocytic leukemia (ALL), 83% in acute myeloid leukemia (AML) whereas no methylation was detected in chronic myeloid leukemia (CML) in blast crisis.
  • Hypermethylation of EDNRB was observed in 92% of ALL, 75% AML and 100% in CML in blast crisis.
  • Taken together, aberrant methylation of p16 and EDNRB was highly prevalent in leukemia patients in Taiwan.
  • [MeSH-major] DNA Methylation. Genes, p16. Leukemia / genetics. Receptor, Endothelin B / genetics

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  • (PMID = 18551992.001).
  • [ISSN] 0304-4920
  • [Journal-full-title] The Chinese journal of physiology
  • [ISO-abbreviation] Chin J Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Receptor, Endothelin B
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60. Rubnitz JE, Razzouk BI, Lensing S, Pounds S, Pui CH, Ribeiro RC: Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia. Cancer; 2007 Jan 1;109(1):157-63
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  • [Title] Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia.
  • BACKGROUND: Outcome after recurrence of childhood acute myeloid leukemia (AML) is poor.
  • We performed this study to identify prognostic factors for recurrence and for survival after recurrence of AML.
  • METHODS: The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo AML who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied.
  • Multivariable analysis indicated that male sex (P = .005), autologous stem cell transplant before recurrence (P = .097), each additional month from diagnosis to recurrence (P = .041), and stem cell transplant after recurrence (P < .001) were associated with a better survival after recurrence, whereas M5 or M7 morphology (P = .001) were significantly predictive of a lower survival estimate after recurrence.
  • CONCLUSIONS: Survival after recurrence was poor in children with AML.
  • Novel therapies are urgently needed to prevent or to treat recurring AML.
  • [MeSH-major] Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Multivariate Analysis. Prognosis. Recurrence. Sex Factors. Stem Cell Transplantation. Survival Rate. Time Factors. Transplantation, Autologous

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17133407.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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61. Dick JE: Acute myeloid leukemia stem cells. Ann N Y Acad Sci; 2005 Jun;1044:1-5
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  • [Title] Acute myeloid leukemia stem cells.
  • The concept that only a subpopulation of rare cancer stem cells (CSCs) is responsible for maintenance of the neoplasm emerged nearly 50 years ago; however, conclusive proof for the existence of a CSC was obtained only relatively recently.
  • The evidence for the existence of CSCs was first derived from the study of human acute myeloid leukemia (AML), largely because of the availability of quantitative stem cell assays for the leukemic stem cell (LSC).
  • These studies showed that only rare cells within the leukemic clone had the capacity to initiate AML growth after transplant into NOD/SCID mice, establishing the hierarchical organization of AML.
  • These findings have important implications for our understanding of the leukemogenic process as well as the design of more effective therapies to eliminate AML based on eradication of the LSCs.
  • [MeSH-major] Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Animals. Humans. Neoplastic Stem Cells / classification. Neoplastic Stem Cells / pathology. Neoplastic Stem Cells / transplantation


62. Fan LP, Shen JZ, Ye BG, Lin FA, Fu HY, Zhou HR, Shen SF, Yu AF: [Detection of p16 gene methylation status in adult patients with acute leukemia by using n-MSP]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):258-61
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  • [Title] [Detection of p16 gene methylation status in adult patients with acute leukemia by using n-MSP].
  • The study was aimed to explore the relationship between patterns of methylation or deletion and the development of acute leukemia, and further to clarify the possible mechanism in the development of adult acute leukemia.
  • Nested methylation-specific polymerase chain reaction (n-MSP) was adopted to analyze p16 gene methylation or deletion patterns in 82 adult acute leukemia patients with different subtypes and stages.
  • The results indicated that rate of p16 gene methylation was 39.0% in 82 adult acute leukemia patients, among them, 41.4% in acute myelogenous leukemia (AML) and 33.3% in acute lymphoblastic leukemia (ALL).
  • It were found that 36.6% of de novo AL patients and 54.5% of relapsed AL patients developed the hypermethylation of p16 gene.
  • Out of the 82 patients, 6 seemed to have deletion of p16 gene, including 1 AML (1.7%) and 5 ALL (20.8%).
  • It is concluded that methylation of p16 gene may play a more important role than homozygous deletion of p16 gene in the leukemogenesis and progression of adult acute leukemia.

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  • (PMID = 17493327.001).
  • [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 / DNA, Neoplasm
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63. Minderman H, Zhou Y, O'Loughlin KL, Baer MR: Bortezomib activity and in vitro interactions with anthracyclines and cytarabine in acute myeloid leukemia cells are independent of multidrug resistance mechanisms and p53 status. Cancer Chemother Pharmacol; 2007 Jul;60(2):245-55
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  • [Title] Bortezomib activity and in vitro interactions with anthracyclines and cytarabine in acute myeloid leukemia cells are independent of multidrug resistance mechanisms and p53 status.
  • PURPOSE: The proteasome inhibitor bortezomib may be effective in combination with cytarabine and anthracyclines in the treatment of acute myeloid leukemia (AML) by virtue of targeting aberrantly activated NF-kappaB in AML stem cells.
  • We tested whether bortezomib cytotoxicity is affected by multidrug resistance (MDR) proteins expressed in AML cells.
  • We also tested whether bortezomib interactions with cytarabine and anthracyclines are affected by p53, because proteasome inhibition stabilizes p53 and may thus cause cell cycle arrest.
  • EXPERIMENTAL DESIGN: Bortezomib sensitivity of cell lines overexpressing P-glycoprotein, multidrug resistance protein-1, breast cancer resistance protein and lung resistance protein was studied in the presence and absence of established modulators of these transport proteins.
  • Drug interactions during simultaneous and sequential exposure to bortezomib and anthracyclines or cytarabine in diverse ratios were evaluated by isobologram and combination index analyses in AML cell lines with wild type and inactive p53 and were correlated with cell cycle perturbations induced by bortezomib.
  • Interactions between bortezomib and anthracylines and cytarabine changed from antagonistic to additive or synergistic with increasing drug activity levels and were not affected by p53 status.
  • CONCLUSIONS: MDR proteins and p53 do not affect bortezomib cytotoxicity or in vitro interactions with anthracyclines or cytarabine, but these interactions are concentration-dependent, and this concentration-dependency should be considered in the design of combination regimens.
  • [MeSH-major] Anthracyclines / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Boronic Acids / pharmacology. Cytarabine / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Protease Inhibitors / pharmacology. Pyrazines / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Bortezomib. Cell Cycle / drug effects. Cell Survival / drug effects. Drug Interactions. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm / physiology. Drug Screening Assays, Antitumor. HL-60 Cells / drug effects. HL-60 Cells / metabolism. HL-60 Cells / pathology. Humans. Inhibitory Concentration 50. Multidrug Resistance-Associated Proteins / metabolism

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  • (PMID = 17096161.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Boronic Acids; 0 / Multidrug Resistance-Associated Proteins; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / Tumor Suppressor Protein p53; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib
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64. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
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  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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65. Sollars VE, Pequignot E, Rothstein JL, Buchberg AM: Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes. Mamm Genome; 2006 Aug;17(8):808-21
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  • [Title] Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes.
  • The myeloid progenitor cell compartment (MPC) exhibits pronounced expansion in human myeloid leukemias.
  • It is becoming more apparent that progression of myelodysplastic syndromes and myeloproliferative diseases to acute myelogenous leukemia is the result of defects in progenitor cell maturation.
  • The MPC of bone marrow was analyzed in mice using a cell culture assay for measuring the relative frequency of proliferative myeloid progenitors.
  • The SWR/J and FVB/J strains show consistently low frequencies of myeloid progenitors, while the DBA/2J and SJL/J inbred strains show consistently high frequencies of myeloid progenitors within the bone marrow compartment.
  • Given the importance of this cell compartment in leukemia progression and the soon to be released genomic sequence of 15 mouse strains, these differences may provide a valuable tool for research into leukemia.
  • [MeSH-major] Cell Proliferation. Genetic Predisposition to Disease. Leukemia / genetics. Myeloid Progenitor Cells / metabolism
  • [MeSH-minor] Animals. Bone Marrow / growth & development. Cell Size. Chromosomes, Mammalian. Cytokines / metabolism. Flow Cytometry. Linkage Disequilibrium. Male. Mice. Mice, Inbred Strains. Stem Cells

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  • [Cites] Blood. 2002 Jan 15;99(2):561-6 [11781239.001]
  • [Cites] Cancer Res. 1989 Jan 1;49(1):149-53 [2783241.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2343-50 [14630819.001]
  • [Cites] Annu Rev Immunol. 1990;8:303-33 [1693082.001]
  • [Cites] PLoS Biol. 2004 Dec;2(12):e393 [15534693.001]
  • [Cites] FASEB J. 1999 Apr;13(6):707-13 [10094931.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1274-81 [11222370.001]
  • [Cites] J Virol. 1981 Aug;39(2):632-40 [6268848.001]
  • [Cites] Blood. 1995 May 1;85(9):2331-6 [7727767.001]
  • [Cites] Blood. 1999 May 15;93(10):3294-301 [10233881.001]
  • [Cites] Blood. 2002 Jun 1;99(11):3947-54 [12010793.001]
  • [Cites] Exp Hematol. 2000 Apr;28(4):442-50 [10781902.001]
  • [Cites] Exp Hematol. 1999 May;27(5):928-35 [10340409.001]
  • [Cites] J Exp Med. 1996 Mar 1;183(3):1141-50 [8642256.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2003 Jan 1;23(1):117-22 [12524234.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Br J Haematol. 1997 Jun;97(4):920-6 [9217198.001]
  • [Cites] J Exp Med. 1997 Aug 18;186(4):529-36 [9254651.001]
  • [Cites] Cell. 1983 Dec;35(3 Pt 2):639-45 [6652681.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1543-50 [9057635.001]
  • [Cites] Science. 2001 Jun 8;292(5523):1915-8 [11397946.001]
  • [Cites] Physiol Genomics. 2002 Dec 3;11(3):185-93 [12419856.001]
  • [Cites] Nat Rev Genet. 2006 Jan;7(1):21-33 [16369569.001]
  • [Cites] Mamm Genome. 2003 Jan;14(1):81-5 [12532271.001]
  • [Cites] J Virol. 1984 Sep;51(3):586-94 [6088784.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1720-3 [7691233.001]
  • [Cites] J Virol. 1988 Mar;62(3):839-46 [2828679.001]
  • [Cites] Cancer Res. 1994 Jan 15;54(2):399-402 [8275475.001]
  • [Cites] Nat Genet. 1999 Nov;23(3):348-53 [10610183.001]
  • [Cites] J Mol Cell Immunol. 1987;3(1):29-36 [3509920.001]
  • [Cites] Blood. 2003 Jul 1;102(1):94-101 [12623852.001]
  • [Cites] Blood. 1997 Apr 15;89(8):2736-44 [9108391.001]
  • [Cites] J Virol. 1982 May;42(2):379-88 [6283161.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2446-8 [10733521.001]
  • [Cites] Cell Struct Funct. 2002 Apr;27(2):81-9 [12207049.001]
  • [Cites] Stem Cells. 2002;20(5):460-9 [12351816.001]
  • [Cites] Blood. 1991 Aug 15;78(4):961-6 [1714329.001]
  • [Cites] Blood. 2000 Apr 1;95(7):2449-51 [10733522.001]
  • [Cites] J Exp Med. 2005 Mar 21;201(6):881-90 [15781580.001]
  • (PMID = 16897342.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA09678
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
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66. Qadir M, O'Loughlin KL, Fricke SM, Williamson NA, Greco WR, Minderman H, Baer MR: Cyclosporin A is a broad-spectrum multidrug resistance modulator. Clin Cancer Res; 2005 Mar 15;11(6):2320-6
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  • PURPOSE: Overexpression of the multidrug resistance proteins P-glycoprotein (Pgp), multidrug resistance protein (MRP-1), breast cancer resistance protein (BCRP), and lung resistance protein (LRP) is associated with treatment failure in acute myeloid leukemia (AML) and other malignancies.
  • The Pgp modulator cyclosporin A has shown clinical efficacy in AML, whereas its analogue PSC-833 has not.
  • EXPERIMENTAL DESIGN: We studied the effects of cyclosporin A and PSC-833 on in vitro drug retention and cytotoxicity in resistant cell lines overexpressing Pgp, MRP-1, and BCRP and on nuclear-cytoplasmic drug distribution and cytotoxicity in cells overexpressing LRP.
  • Moreover, cyclosporin A enhanced nuclear distribution of doxorubicin in 8226/MR20 cells, which also express LRP, and increased doxorubicin cytotoxicity 12-fold without an effect on cellular doxorubicin content, consistent with expression of wild-type BCRP, which does not efflux doxorubicin.
  • Cyclosporin A also enhanced nuclear doxorubicin distribution in a second cell line with LRP overexpression, HT1080/DR4.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Antibiotics, Antineoplastic / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Nucleus / metabolism. Cells, Cultured. Cytoplasm / metabolism. Doxorubicin / metabolism. HL-60 Cells / drug effects. HL-60 Cells / metabolism. Humans. Kidney / drug effects. Kidney / metabolism. Mitoxantrone / metabolism. Neoplasm Proteins / metabolism. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 15788683.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 16056; United States / NCI NIH HHS / CA / R21 CA 98457; United States / NCI NIH HHS / CA / T32 CA 09072-28
  • [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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 80168379AG / Doxorubicin; 83HN0GTJ6D / Cyclosporine; BZ114NVM5P / Mitoxantrone
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67. Pedersen-Bjergaard J, Andersen MT, Andersen MK: Genetic pathways in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2007;:392-7
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  • [Title] Genetic pathways in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia.
  • In therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML), at least eight alternative genetic pathways have been defined based on characteristic recurrent chromosome abnormalities.
  • Patients presenting as t-MDS and patients presenting as overt t-AML cluster differently in these pathways.
  • Three types of gene mutations are observed in MDS and AML:.
  • (1) Activating mutations of genes in the tyrosine kinase-RAS/BRAF signal transduction pathway, leading to increased cell proliferation (Class I mutations);.
  • (2) Inactivating mutations of genes encoding hematopoietic transcription factors, resulting in disturbed cell differentiation (Class II mutations); and (3) Inactivating mutations of the tumor suppressor gene p53.
  • At least 14 different genes have been identified as mutated in t-MDS and t-AML, clustering differently and characteristically in the eight genetic pathways.
  • Class I and Class II mutations are significantly associated, indicating their cooperation in leukemogenesis The chromosome aberrations and gene mutations detected in the therapy-related and in the de novo subsets of MDS and AML are identical, although the frequencies with which they are observed may differ.
  • Hence, therapy-related and de novo MDS and AML are identical diseases and should be subclassified and treated similarly.


68. Isoyama K, Oda M, Kato K, Nagamura-Inoue T, Kai S, Kigasawa H, Kobayashi R, Mimaya J, Inoue M, Kikuchi A, Kato S, Japan Cord Blood Bank Network: Long-term outcome of cord blood transplantation from unrelated donors as an initial transplantation procedure for children with AML in Japan. Bone Marrow Transplant; 2010 Jan;45(1):69-77
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  • [Title] Long-term outcome of cord blood transplantation from unrelated donors as an initial transplantation procedure for children with AML in Japan.
  • To assess the outcome of unrelated umbilical cord blood transplantation (UCBT), 141 children with AML who underwent UCBT (39 in first CR (CR1), 33 in CR2, 4 in CR3 and 65 at more advanced stages (not in CR)) were analyzed in a retrospective multicenter study in Japan.
  • Short-term MTX was used for prophylaxis of acute GVHD in 80 cases (57%).
  • The cumulative incidences of neutrophil recovery, platelet recovery and acute GVHD (grades 2-4) were 78.7, 62.4 and 40.1%, respectively, and the 100-day transplantation-related mortality (TRM) was 10.8%.
  • Multivariate analysis showed that an infused CD34(+) cell dose of 1.35 x 10(5) cells per kg or more was associated with favorable neutrophil and platelet recovery, and that short-term MTX was associated with a lower 100-day TRM.
  • The 6-year relapse rate was 38.8% and was associated with disease status.
  • Six-year overall survival was 45.8% (70.4+/-8.3% in CR1, 59.3+/-11.3% in CR2, 75.5+/-21% in CR3 and 20.6+/-6.2% for children with non-CR).
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery
  • [MeSH-minor] Adolescent. Antigens, CD34 / metabolism. Child. Child, Preschool. Female. Graft Survival. Graft vs Host Disease / prevention & control. Humans. Infant. Japan / epidemiology. Leukocyte Count. Male. Neoplasm Recurrence, Local. Neutrophils. Platelet Count. Retrospective Studies. Tissue Donors. Transplantation Conditioning / methods. Treatment Outcome

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  • (PMID = 19430503.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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69. Lim AY, Gaffney K, Scott DG: Methotrexate-induced pancytopenia: serious and under-reported? Our experience of 25 cases in 5 years. Rheumatology (Oxford); 2005 Aug;44(8):1051-5
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  • Pancytopenia was defined as white blood cell count (WBC) <3.5 x 10(9)/l, haemoglobin (Hb) <11 g/dl and platelet count <130 x 10(9)/l.
  • There were seven deaths (28% mortality), five from sepsis and two from acute myeloid leukaemia.

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  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):361-2; author reply 363-4 [16332953.001]
  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):362-3; author reply 363-4 [16332952.001]
  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):361; author reply 363-4 [16332954.001]
  • (PMID = 15901903.001).
  • [ISSN] 1462-0324
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; YL5FZ2Y5U1 / Methotrexate
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70. Tsimberidou AM, Giles FJ, Estey E, O'Brien S, Keating MJ, Kantarjian HM: The role of gemtuzumab ozogamicin in acute leukaemia therapy. Br J Haematol; 2006 Feb;132(4):398-409
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  • [Title] The role of gemtuzumab ozogamicin in acute leukaemia therapy.
  • Gemtuzumab ozogamicin (GO) is an immunoconjugate that binds to CD33 on the surface of acute myeloid leukaemia (AML) blasts and, after internalisation, releases a cytotoxic drug, calicheamicin.
  • GO is approved by the US Food and Drug Administration for the treatment of CD33-positive AML at first relapse in patients 60 years and older who are not candidates for other cytotoxic therapy.
  • GO therapy at 9 mg/m(2) is complicated with hepatic veno-occlusive disease in 5-10% of patients, particularly prior to or following stem cell transplantation.
  • GO is probably most active in acute promyelocytic leukaemia (APL).
  • Case reports suggest that GO also has activity in CD33-positive acute lymphoblastic leukaemia.
  • In conclusion, single agent GO can induce responses in patients with CD33-positive AML in first recurrence.
  • Ongoing clinical trials may better define the role of GO combinations, particularly in untreated AML.
  • [MeSH-major] Aminoglycosides / administration & dosage. Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / administration & dosage. Antibodies, Monoclonal / therapeutic use. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance. Enediynes. Humans. Protein Binding. Randomized Controlled Trials as Topic. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16412015.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 82
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71. Burger JA, Velev NS, Jabbour EJ, Wierda WG, Ravandi F, Cortes JE, Kantarjian H, Nieto YL, Shpall EJ, Jorgensen JL: Failure is not fatal: long-term remission in refractory acute myeloid leukemia (AML) after graft failure of cord blood stem cells. Leukemia; 2010 Mar;24(3):666-8
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  • [Title] Failure is not fatal: long-term remission in refractory acute myeloid leukemia (AML) after graft failure of cord blood stem cells.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy


72. Yin WJ, Yang PD, Huang YZ, Li XP, Gong LZ: [Influences of bone marrow mesenchymal stem cells in patients with acute myeloid leukemia and non-leukemia on HL-60 cells -- a comparison study]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):545-50
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  • [Title] [Influences of bone marrow mesenchymal stem cells in patients with acute myeloid leukemia and non-leukemia on HL-60 cells -- a comparison study].
  • This study was aimed to compare the influences of bone marrow mesenchymal stem cells (BMMSCs) from patients with acute myeloid leukemia (AML), AML patients with complete remission (CR) and non-leukemia patients on HL-60 cells.
  • The HL-60 cells were divided into three groups: group of co-cultivation with BMMSCs of AML patients, group of co-cultivation with BMMSCs of AML patients with CR and group of co-cultivation with BMMSCs of non-leukemia patients.
  • The count of HL-60 cells, the CD11b and survivin expression of HL-60 cells, the cell cycle distribution of the HL-60 cells in 3 groups were compared by flow cytometry, the morphology and differentiation rate of HL-60 cells in 3 groups were observed and compared by microscopy.
  • The results showed that there were no differences in HL-60 cell count at five and seven days, in HL-60 distribution at the G(0)/G(1) phase, in survivin and CD 11b expressions in 3 groups.

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  • (PMID = 19549361.001).
  • [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] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
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73. Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E: Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia. Pediatr Blood Cancer; 2006 Feb;46(2):266
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  • [Title] Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
  • [MeSH-major] Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage. Leukemia, Myeloid, Acute / complications


74. Sallmyr A, Fan J, Datta K, Kim KT, Grosu D, Shapiro P, Small D, Rassool F: Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML. Blood; 2008 Mar 15;111(6):3173-82
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  • [Title] Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML.
  • Activating mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor occur in approximately 30% of acute myeloid leukemia (AML) patients and, at least for internal tandem duplication (ITD) mutations, are associated with poor prognosis.
  • We find that FLT3/ITD mutations start a cycle of genomic instability whereby increased reactive oxygen species (ROS) production leads to increased DNA double-strand breaks (DSBs) and repair errors that may explain aggressive AML in FLT3/ITD patients.
  • Cell lines transfected with FLT3/ITD and FLT3/ITD-positive AML cell lines and primary cells demonstrate increased ROS.
  • Our study suggests that the aggressiveness of the disease and poor prognosis of AML patients with FLT3/ITD mutations could be the result of increased genomic instability that is driven by higher endogenous ROS, increased DNA damage, and decreased end-joining fidelity.
  • [MeSH-major] Base Pair Mismatch / genetics. DNA Damage / genetics. Gene Duplication. Leukemia, Erythroblastic, Acute / metabolism. Reactive Oxygen Species / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Cell Line. Gene Expression Regulation, Neoplastic. Humans. Prognosis. STAT5 Transcription Factor / metabolism. Signal Transduction. rac1 GTP-Binding Protein / metabolism

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  • (PMID = 18192505.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668
  • [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 / Reactive Oxygen Species; 0 / STAT5 Transcription Factor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / rac1 GTP-Binding Protein
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75. Hollink IH, Zwaan CM, Zimmermann M, Arentsen-Peters TC, Pieters R, Cloos J, Kaspers GJ, de Graaf SS, Harbott J, Creutzig U, Reinhardt D, van den Heuvel-Eibrink MM, Thiede C: Favorable prognostic impact of NPM1 gene mutations in childhood acute myeloid leukemia, with emphasis on cytogenetically normal AML. Leukemia; 2009 Feb;23(2):262-70
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  • [Title] Favorable prognostic impact of NPM1 gene mutations in childhood acute myeloid leukemia, with emphasis on cytogenetically normal AML.
  • Nucleophosmin (NPM1) mutations occur frequently in adult cytogenetically normal acute myeloid leukemia (CN-AML) and confer favorable outcome.
  • We investigated the frequency and prognostic significance of NPM1 mutations in childhood AML (n=298), specifically focusing on the CN-AML subgroup (n=100).
  • Mutations were found in 8.4%, and clustered significantly in the CN-AML subgroup (22%).
  • No mutations were found in patients below the age of 3 years; in CN-AML, there was an increasing incidence above this age.
  • In the overall group, NPM1 mutations conferred an independent favorable prognostic impact on event-free survival (5-year pEFS 66 vs 39%; P=0.02), which did not translate into a significantly better overall survival (5-year pOS 68 vs 56%; P=0.30).
  • In the CN-AML cohort, NPM1 mutations were an independent prognostic factor on pEFS (80 vs 39%; P=0.01), and pOS (85 vs 60%; P=0.06), which was not influenced by FLT3/ITD.
  • However, in NPM1 wild-type CN-AML, FLT3/ITD-positive patients had a significantly worse outcome (pEFS 48 vs 18%; P<0.001).
  • We conclude that NPM1 mutations confer a favorable prognosis in childhood AML and in CN-AML in particular.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics


76. Fleĭshman EV, Sokova OI, Kirichenko OP, Konstantinova LN, Metel'kova NF, Popa AV, Shneĭder MM: [Complex karyotype abnormalities in pediatric acute myeloid leukemia]. Vestn Ross Akad Med Nauk; 2008;(5):3-7
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  • [Title] [Complex karyotype abnormalities in pediatric acute myeloid leukemia].
  • A majority of the data on the prognostic significance of distinct chromosome changes and combinations of them in pediatric acute myeloid leukemia (AML) has been derived from adult studies, with not numerous published data in pediatric patients.
  • We investigated characteristic features of complex karyotype in newly diagnosed pediatric AML de novo.
  • Cell clones with complex karyotype were found in 35 of 254 (13.8%) patients at the age from 0 to 15 years studied prior to therapy.
  • In 2nd subgroup karyotypes were not so considerably changed and no adverse risk markers were detected as distinct from 1st subgroup.
  • New data were obtained for complex karyotype differences of adult and pediatric AML.
  • Similar data were not published earlier.
  • Complex karyotype is considered to be characteristic of older AML patients and in the majority of the patients the karyotype contains markers of adverse risk.
  • Possibly, worse outcome in older AML patients is connected with the markers but not with multiple chromosome changes.
  • New data of frequency and the peculiarities of complex karyotype in pediatric AML are important for understanding of AML pathogenesis and for development a more effective AML treatment.

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  • (PMID = 18589906.001).
  • [ISSN] 0869-6047
  • [Journal-full-title] Vestnik Rossiiskoi akademii meditsinskikh nauk
  • [ISO-abbreviation] Vestn. Akad. Med. Nauk SSSR
  • [Language] RUS
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] Russia (Federation)
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77. Kamel AM, El-Sharkawy N, Yassin D, Shaaban K, Hussein H, Sidhom I, Abo El-Naga S, Ameen M, El-Hattab O, Aly El-Din NH: P-gp expression and Rh 123 efflux assay have no impact on survival in Egyptian pediatric acute lymphoblastic leukemia patients. J Egypt Natl Canc Inst; 2005 Sep;17(3):165-72
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  • [Title] P-gp expression and Rh 123 efflux assay have no impact on survival in Egyptian pediatric acute lymphoblastic leukemia patients.
  • PURPOSE: In a previous work we have studied MDR status in terms of P-glycoprotein (P-gp) expression and Rhodamine 123 efflux assay in Egyptian acute leukemia patients.
  • We have reported results comparable to the literature as regards ANLL both in pediatric and adult cases.
  • MATERIAL AND METHODS: A total of 108 cases were studied including 80 ALL and 28 ANLL.
  • ANLL cases included 18 male and 10 female with an age range of 6m to 18 yrs and a median of 8 yrs.
  • MDR expression and function were correlated to age, Hb, TLC, CD34 expression, immunophenotype and DNA index in ALL, FAB subtypes in ANLL as well as to CR, DFS and EFS in ALL.
  • In ANLL P-gp expression was encountered in 47.6% of cases, while positive Rh123 efflux assay was encountered in 75% of cases.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Rhodamine 123

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  • (PMID = 16799654.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123
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78. Majeti R, Chao MP, Alizadeh AA, Pang WW, Jaiswal S, Gibbs KD Jr, van Rooijen N, Weissman IL: CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells. Cell; 2009 Jul 23;138(2):286-99
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  • [Title] CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells.
  • Acute myeloid leukemia (AML) is organized as a cellular hierarchy initiated and maintained by a subset of self-renewing leukemia stem cells (LSC).
  • We hypothesized that increased CD47 expression on human AML LSC contributes to pathogenesis by inhibiting their phagocytosis through the interaction of CD47 with an inhibitory receptor on phagocytes.
  • We found that CD47 was more highly expressed on AML LSC than their normal counterparts, and that increased CD47 expression predicted worse overall survival in three independent cohorts of adult AML patients.
  • Furthermore, blocking monoclonal antibodies directed against CD47 preferentially enabled phagocytosis of AML LSC and inhibited their engraftment in vivo.
  • Finally, treatment of human AML LSC-engrafted mice with anti-CD47 antibody depleted AML and targeted AML LSC.
  • In summary, increased CD47 expression is an independent, poor prognostic factor that can be targeted on human AML stem cells with blocking monoclonal antibodies capable of enabling phagocytosis of LSC.
  • [MeSH-major] Antigens, CD47 / immunology. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Phagocytosis


79. Ustun C: Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia. J Laparoendosc Adv Surg Tech A; 2007 Apr;17(2):213-5
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  • [Title] Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia.
  • The management of acute myelogenous leukemia is often complicated by infections due to neutropenia, but the appendix is not a common site of infection in adult patients with acute myelogenous leukemia.
  • The diagnosis of acute appendicitis may be delayed or even missed because of the lack of characteristic signs and symptoms associated with acute appendicitis in neutropenic patients.
  • The case presented here is of a 33-year-old Hispanic man with acute myelogenous leukemia who developed severe diffuse acute abdominal pain with positive signs of rebound tenderness, fever, and hypotension ten days after receiving reinduction chemotherapy.
  • The patient was at his nadir, with a white blood cell count of 0.2 x 10(9)/L, platelet count of 20 x 10(9)/L, and hemoglobin of 7 g/dL.
  • A computed tomography scan of the abdomen was suspicious for acute appendicitis.
  • [MeSH-major] Appendicitis / surgery. Leukemia, Myeloid, Acute / complications

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  • (PMID = 17484650.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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80. Kracmarova A, Cermak J, Brdicka R, Bruchova H: High expression of ERCC1, FLT1, NME4 and PCNA associated with poor prognosis and advanced stages in myelodysplastic syndrome. Leuk Lymphoma; 2008 Jul;49(7):1297-305
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  • Myelodysplastic syndrome (MDS) represents a good model for research of prognostic/progression markers due to frequent transformation into acute myeloid leukemia (AML).
  • We analysed expression profiles of 26 MDS and 6 AML patients using cDNA arrays comprising 588 gene probes.
  • Furthermore, PCNA expression was correlated with peripheral blood blast percentage (r = 0.71, p < 0.05), while the other genes showed non-significant correlation.
  • Our findings demonstrate the progressive up-regulation of the genes along the sequence of 5q-syndrome/RCMD/RAEB/de novo AML, suggesting their association with disease progression.
  • [MeSH-major] DNA-Binding Proteins / genetics. Endonucleases / genetics. Gene Expression Profiling. Myelodysplastic Syndromes / diagnosis. NM23 Nucleoside Diphosphate Kinases / genetics. Proliferating Cell Nuclear Antigen / genetics. Vascular Endothelial Growth Factor Receptor-1 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Disease Progression. Female. Gene Expression. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Nucleoside Diphosphate Kinase D. Oligonucleotide Array Sequence Analysis. Prognosis


81. Pedersen M, Rönnstrand L, Sun J: The c-Kit/D816V mutation eliminates the differences in signal transduction and biological responses between two isoforms of c-Kit. Cell Signal; 2009 Mar;21(3):413-8
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  • Activating mutations of codon 816 of the Kit gene have been implicated in malignant cell growth of acute myeloid leukemia (AML), systemic mastocytosis and germ cell tumors.
  • Wild-type c-Kit is a tyrosine kinase receptor that requires its ligand, stem cell factor (SCF), for activation.
  • In this study we analysed the signal transduction downstream of the oncogenic c-Kit mutant D816V in an isoform specific context, using the hematopoietic cell line Ba/F3 stably transfected with the different versions of isoform and mutant receptor.
  • In addition, both isoforms of c-Kit/D816V induced SCF-independent cell survival and proliferation equally well.
  • This is in contrast to wild-type c-Kit, where c-Kit/GNNK- induced better cell survival and stronger proliferation than c-Kit/GNNK+, and both required stimulation with SCF.
  • [MeSH-minor] Alternative Splicing / genetics. Amino Acids / genetics. Animals. Cell Line. Cell Proliferation / drug effects. Cell Survival / genetics. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / genetics. Mice. Protein Isoforms / genetics. Stem Cell Factor / metabolism. Stem Cell Factor / pharmacology. Transfection

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  • (PMID = 19049823.001).
  • [ISSN] 1873-3913
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Protein Isoforms; 0 / Stem Cell Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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82. Matuszewski L, Persigehl T, Wall A, Meier N, Bieker R, Kooijman H, Tombach B, Mesters R, Berdel WE, Heindel W, Bremer C: Assessment of bone marrow angiogenesis in patients with acute myeloid leukemia by using contrast-enhanced MR imaging with clinically approved iron oxides: initial experience. Radiology; 2007 Jan;242(1):217-24
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  • [Title] Assessment of bone marrow angiogenesis in patients with acute myeloid leukemia by using contrast-enhanced MR imaging with clinically approved iron oxides: initial experience.
  • PURPOSE: To prospectively assess bone marrow (BM) angiogenesis in patients with acute myeloid leukemia (AML) by using iron oxide-enhanced magnetic resonance (MR) imaging.
  • Eleven patients (seven women, four men; mean age, 53 years+/-4.40 [standard deviation]) with an initial diagnosis of AML were enrolled in the study and underwent T2*-weighted two-echo echo-planar MR imaging of the pelvis before and after intravenous injection of a clinically approved iron oxide blood-pool contrast agent.
  • RESULTS: DeltaR2* maps showed prominent areas of highly vascularized BM in the patients with AML, whereas the control subjects had moderately vascularized BM with homogeneous vessel distribution.
  • Quantitative analysis revealed VVF values to be significantly higher in patients with AML than in control subjects: The mean VVF in the pelvis was 9.18%+/-1.54 for patients versus 3.91%+/-0.61 for control subjects (P=.010).
  • In accordance with MR results, MVD (P=.009) and VEGF expression (P=.017) were significantly elevated in the AML group compared with values in the control group.
  • CONCLUSION: Iron oxide-enhanced MR imaging enables assessment of BM angiogenesis in patients with AML.
  • [MeSH-major] Bone Marrow Neoplasms / blood supply. Bone Marrow Neoplasms / diagnosis. Ferric Compounds. Image Enhancement / methods. Leukemia, Myeloid, Acute / diagnosis. Magnetic Resonance Imaging / methods. Neovascularization, Pathologic / diagnosis


83. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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84. Luo J, Qi C, Xu W, Kamel-Reid S, Brandwein J, Chang H: Cytoplasmic expression of nucleophosmin accurately predicts mutation in the nucleophosmin gene in patients with acute myeloid leukemia and normal karyotype. Am J Clin Pathol; 2010 Jan;133(1):34-40
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  • [Title] Cytoplasmic expression of nucleophosmin accurately predicts mutation in the nucleophosmin gene in patients with acute myeloid leukemia and normal karyotype.
  • Mutations in the nucleophosmin (NPM1) exon 12 resulting in delocalization of NPM1 into the cytoplasm occur in 50% to 60% of acute myeloid leukemia cases with a normal karyotype (AML-NK).
  • As recent studies suggest such patients have a favorable prognosis and there are discordant reports of the immunohistochemical detection of cytoplasmic NPM1 (NPMc+) for predicting NPM1 gene mutations, we correlated the immunohistochemical detection of NPMc+, NPM1 gene mutations, and prognosis in 57 cases of AML-NK.
  • There was a favorable survival outcome in AML-NK cases that were NPM1 mutated and FLT3-ITD nonmutated.
  • Our data confirm that cytoplasmic NPM1 immunoreactivity predicts NPM1 mutations and warrants inclusion in the routine diagnostic and prognostic workup of AML.
  • [MeSH-major] Cytoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. DNA Mutational Analysis. DNA, Neoplasm / analysis. Disease-Free Survival. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 20023256.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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85. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • Patients who failed to achieve complete remission with AML-directed therapy could often be induced with a regimen of prednisone, vincristine, and L-asparaginase.
  • Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
  • We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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  • [Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]
  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]
  • [Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]
  • [Cites] Br J Haematol. 2004 Jun;125(6):814-5 [15180872.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Blood. 1985 Nov;66(5):1115-23 [3931724.001]
  • [Cites] Blood. 1990 Jan 1;75(1):198-202 [2294988.001]
  • [Cites] Leukemia. 1990 Feb;4(2):121-6 [2137547.001]
  • [Cites] N Engl J Med. 1991 Mar 21;324(12):800-8 [1997852.001]
  • [Cites] Blood. 1991 Sep 1;78(5):1327-37 [1878594.001]
  • [Cites] J Clin Oncol. 1992 Sep;10(9):1419-29 [1517785.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]
  • [Cites] Leukemia. 1996 Aug;10(8):1283-7 [8709632.001]
  • [Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]
  • [Cites] Blood. 1997 Jul 1;90(1):28-35 [9207434.001]
  • [Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]
  • [Cites] Leukemia. 1998 Dec;12(12):2038 [9844938.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3768-73 [9850020.001]
  • [Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Bioinformatics. 2006 Aug 15;22(16):1979-87 [16777905.001]
  • [Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]
  • [CommentIn] Blood. 2009 May 21;113(21):5036 [19470432.001]
  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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86. Basecke J, Podleschny M, Becker A, Seiffert E, Schwiers I, Schwiers R, Haase D, Glass B, Schmitz N, Trumper L, Griesinger F: Therapy-associated genetic aberrations in patients treated for non-Hodgkin lymphoma. Br J Haematol; 2008 Apr;141(1):52-9
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  • [Title] Therapy-associated genetic aberrations in patients treated for non-Hodgkin lymphoma.
  • Therapy-associated myelodysplastic syndromes and acute myeloid leukaemia (t-AML/MDS) following high dose chemotherapy are significant problems, with a cumulative incidence of 20% or more in myeloablative treatment regimen.
  • Retrospective findings indicated that t-AML/MDS associated genetic aberrations can be observed directly after exposure to chemotherapy and can precede t-AML by several months.
  • To determine the incidence of post-therapeutic aberrations and their predictive value, we prospectively investigated 316 samples of 95 patients with non-Hodgkin lymphoma (NHL) who were treated with intermediate and high dose chemotherapy (Arm A and B of the megaCHOEP (cyclophosphamide, doxorubicin, etoposide, vincristine, prednisolone) trial of the German High Grade NHL study group).
  • None of these patients developed a t-AML/MDS during a 3-year clinical follow up period.
  • We concluded that the high incidence of genetic aberrations reflected a dose-dependent, transient therapy-induced genetic damage which is not predictive of a t-AML/MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosome Aberrations / drug effects. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Follow-Up Studies. Humans. Leukemia, Myeloid, Acute / chemically induced. Middle Aged. Prednisolone / therapeutic use. Prognosis. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic. Vincristine / therapeutic use


87. Yao YY, Zhu Q, Zou LF, Dou HJ, Chen YM, Tang Y, Hu JP: [Clinical study on fludarabine combined with cytarabine regimen in the treatment of patients with refractory and relapsed acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):774-6
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  • [Title] [Clinical study on fludarabine combined with cytarabine regimen in the treatment of patients with refractory and relapsed acute myeloid leukemia].
  • The aim of study was to evaluate the clinical efficacy and toxicity of fludarabine combined with cytarabine (FA) regimen in the treatment of patients with refractory and/or relapsed acute myeloid leukemia (AML).
  • Nineteen cases with refractory/relapsed AML were treated with FA regimen in which fludarabine phosphate 25 mg/(m(2) x d), d1-5; cytarabine (Ara-C) 2 g/(m(2) x d), d1-5.
  • Nonhematologic complications consisted of gastrointestinal side effects, mucositis, liver toxicity, which were mild to moderate and could be alleviated with supportive therapy.
  • In conclusion, FA regimen is an effective regimen for treatment of refractory and relapsed AML.

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  • (PMID = 19549406.001).
  • [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] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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88. Sritana N, Auewarakul CU: KIT and FLT3 receptor tyrosine kinase mutations in acute myeloid leukemia with favorable cytogenetics: two novel mutations and selective occurrence in leukemia subtypes and age groups. Exp Mol Pathol; 2008 Dec;85(3):227-31
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  • [Title] KIT and FLT3 receptor tyrosine kinase mutations in acute myeloid leukemia with favorable cytogenetics: two novel mutations and selective occurrence in leukemia subtypes and age groups.
  • Mutations of the receptor tyrosine kinase (RTK) are frequently reported in acute myeloid leukemia (AML) with a normal karyotype.
  • In this study, Southeast Asian AML patients with a favorable karyotype including t(8;21)/AML-ETO, inv(16)(CBF beta/SMMHC), and t(15;17)/PML-RAR alpha were genotyped for KIT and FLT3 RTK mutations by PCR and sequencing.
  • KIT-mutated patients were older than FLT3-mutated patients and demonstrated a high expression of myeloid antigens and CD56 lymphoid antigen.
  • KIT and FLT3 mutations preferentially exist in distinct clinical and genetic AML subtypes, reflecting unique leukemogenetic mechanisms.
  • Targeting therapy with specific RTK inhibitors should provide benefits for a subgroup of AML patients with favorable chromosomes who also carry selective types of RTK mutations.
  • [MeSH-major] Cytogenetic Analysis. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18977345.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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89. Cammenga J, Horn S, Bergholz U, Sommer G, Besmer P, Fiedler W, Stocking C: Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate. Blood; 2005 Dec 1;106(12):3958-61
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  • [Title] Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate.
  • Multiple genetic alterations are required to induce acute myelogenous leukemia (AML).
  • Mutations in the extracellular domain of the KIT receptor are almost exclusively found in patients with AML carrying translocations or inversions affecting members of the core binding factor (CBF) gene family and correlate with a high risk of relapse.
  • Our data show that the addition of kinase inhibitors to conventional chemotherapy might be a new therapeutic option for CBF-AML expressing mutant KIT.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology. Stem Cell Factor / genetics

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  • (PMID = 16081693.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factors; 0 / Piperazines; 0 / Pyrimidines; 0 / Stem Cell Factor; 8A1O1M485B / Imatinib Mesylate
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90. Zhang Y, He Q, Huang XJ, Jiang H, Yang SM, Lu J, Qing YZ, Shi Y, Dang H, Qiu JY, Lu DP: [Cytogenetic study on eosinophilia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):454-7
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  • The aim of study was to investigate the importance of chromosome aberration in differential diagnosis of eosinophilia and the chromosomal aberrations involved in patients with clonal eosinophilia.
  • Combining clinical, hematological and cytogenetical data, the 5 patients were diagnosed as acute myeloid leukemia with eosinophilia, chronic eosinophilic leukemia, 8p11 myeloproliferative syndrome, chronic myeloid leukemia in acute phase and acute myeloid leukemia-M(4Eo) respectively.
  • In conclusion, cytogenetical detection is very important in differential diagnosis of clonal eosinophilic disorders and chronic eosinophilic leukemia, which is suggested to be done routinely in clinic.

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  • (PMID = 17605843.001).
  • [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
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91. Yanada M, Matsuo K, Suzuki T, Kiyoi H, Naoe T: Prognostic significance of FLT3 internal tandem duplication and tyrosine kinase domain mutations for acute myeloid leukemia: a meta-analysis. Leukemia; 2005 Aug;19(8):1345-9
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  • [Title] Prognostic significance of FLT3 internal tandem duplication and tyrosine kinase domain mutations for acute myeloid leukemia: a meta-analysis.
  • Two distinct forms of fms-like tyrosine kinase (FLT3) gene aberrations, internal tandem duplication (ITD) and tyrosine kinase domain (TKD) mutations, have been recognized in a substantial proportion of patients with acute myeloid leukemia (AML).
  • The summary hazard ratios for disease-free survival (DFS) were 1.88 (95% confidence interval (CI) 1.58-2.23; P<0.001) for FLT3 mutations, 1.86 (95% CI: 1.52-2.29; P<0.001) for ITD, and 1.90 (95% CI: 1.40-2.60; P<0.001) for TKD mutation.
  • Neither white blood cell count at diagnosis nor cytogenetic risk category was a significant source of heterogeneity.
  • These findings indicate that FLT3 mutations have an adverse effect on the outcome for AML, and that the negative impact of TKD mutation seems comparable to that of ITD with regard to DFS.
  • Although it should be borne in mind that this meta-analysis was based on data abstracted from observational studies, these results may justify the risk-adapted therapeutic strategies for AML according to the FLT3 status.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences
  • [MeSH-minor] Acute Disease. Disease-Free Survival. Humans. Prognosis. Proportional Hazards Models. Survival Rate. fms-Like Tyrosine Kinase 3

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  • [Copyright] Leukemia (2005) 19, 1345-1349.
  • (PMID = 15959528.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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92. Benzene 2009-Health effects and mechanisms of bone marrow toxicity: implications for t-AML and the mode of action framework. Proceedings of a meeting. September 7-12, 2009. Munich, Germany. Chem Biol Interact; 2010 Mar 19;184(1-2):1-312
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  • [Title] Benzene 2009-Health effects and mechanisms of bone marrow toxicity: implications for t-AML and the mode of action framework. Proceedings of a meeting. September 7-12, 2009. Munich, Germany.
  • [MeSH-major] Benzene / poisoning. Benzene / toxicity. Bone Marrow / drug effects. Bone Marrow Diseases / chemically induced. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 20414963.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] Ireland
  • [Chemical-registry-number] J64922108F / Benzene
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93. Takahashi T, Tsukuda H, Kimura H, Yoshimoto M, Tsujisaki M: Extramedullary relapse of AML with t(9;11)(p22;q23) associated with clonal evolution from trisomy 8 into tetrasomy 8. Intern Med; 2010;49(5):447-51
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  • [Title] Extramedullary relapse of AML with t(9;11)(p22;q23) associated with clonal evolution from trisomy 8 into tetrasomy 8.
  • This report describes a patient with extramedullary relapse of acute myeloid leukemia (AML) without involving bone marrow.
  • A 57-year-old man was diagnosed as having acute monoblastic leukemia with t(9;11)(p22;q23) and trisomy 8.
  • Bone marrow or meningeal relapse was not observed.
  • To our knowledge, this is the first case report of clonal evolution associated with the development of myeloid sarcoma as a relapse in AML.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / genetics. Trisomy / genetics

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  • (PMID = 20190481.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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94. Yoneda K, Morii T, Nieda M, Tsukaguchi N, Amano I, Tanaka H, Yagi H, Narita N, Kimura H: The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy. Leuk Res; 2005 Feb;29(2):147-52
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  • [Title] The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy.
  • In this study, we assessed the Valpha24+ NKT cell numbers in peripheral blood (PB) from 30 healthy donors and 70 patients with haematopoietic malignancy including chronic myelogenous leukemia (CML), malignant lymphoma (ML), acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • Here, we demonstrated that PB Valpha24+ NKT cell numbers were significantly decreased in all the patients with haematopoietic malignancy in comparison with that in healthy donors (P < 0.005).
  • In particular CD4- CD8- Valpha24+ NKT cell numbers were more significantly decreased in the patients with haematopoietic malignancy (P < 0.0001).
  • [MeSH-major] Hematologic Neoplasms / blood. Killer Cells, Natural / cytology. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Antigens, CD8 / biosynthesis. Flow Cytometry. Humans. Lymphocyte Count. Lymphocytes / cytology. Lymphocytes / immunology. Survival Analysis

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  • (PMID = 15607362.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Receptors, Antigen, T-Cell, alpha-beta
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95. Müller AM, Duque J, Shizuru JA, Lübbert M: Complementing mutations in core binding factor leukemias: from mouse models to clinical applications. Oncogene; 2008 Oct 2;27(44):5759-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complementing mutations in core binding factor leukemias: from mouse models to clinical applications.
  • A great proportion of acute myeloid leukemias (AMLs) display cytogenetic abnormalities including chromosomal aberrations and/or submicroscopic mutations.
  • These abnormalities significantly influence the prognosis of the disease.
  • Core binding factor (CBF) leukemias denote AMLs with chromosomal aberrations disrupting one of the CBF transcription factor genes; the most common examples are translocation t(8;21) and inversion inv(16), which result in the generation of the AML1-ETO and CBFbeta-MYH11 fusion proteins, respectively.
  • However, in murine models, these alterations alone do not suffice to generate full-blown leukemia, but rather, complementary events are required.
  • In fact, a substantial proportion of primary CBF leukemias display additional activating mutations, mostly of the receptor tyrosine kinase (RTK) c-KIT.
  • Here, we present a concise review on complementing mutations in CBF leukemias including pathophysiology, mouse models, and clinical implications.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / diagnosis. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Genetic Complementation Test. Mice. Prognosis

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  • (PMID = 18604246.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 118
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96. Zhang KH, Tian HY, Gao X, Lei WW, Hu Y, Wang DM, Pan XC, Yu ML, Xu GJ, Zhao FK, Song JG: Ferritin heavy chain-mediated iron homeostasis and subsequent increased reactive oxygen species production are essential for epithelial-mesenchymal transition. Cancer Res; 2009 Jul 1;69(13):5340-8
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  • To obtain a broad view of the molecules involved in EMT, we carried out a comparative proteomic analysis of transforming growth factor-beta1 (TGF-beta1)-induced EMT in AML-12 murine hepatocytes.
  • [MeSH-major] Apoferritins / physiology. Cell Differentiation / physiology. Epithelial Cells / cytology. Hepatocytes / cytology. Iron / metabolism. Mesoderm / cytology. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Adenocarcinoma / pathology. Animals. Cell Line, Tumor. Cell Movement / physiology. Esophageal Neoplasms / pathology. Homeostasis. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Mice. Neoplasms / pathology. Proteome. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta1 / genetics. Transforming Growth Factor beta1 / pharmacology. Transforming Growth Factor beta1 / physiology

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  • (PMID = 19531652.001).
  • [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 / Proteome; 0 / Reactive Oxygen Species; 0 / Transforming Growth Factor beta1; 9013-31-4 / Apoferritins; E1UOL152H7 / Iron
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97. Mi YC, Xue YP, Yu WJ, Liu SH, Zhao YZ, Meng QX, Bian SG, Wang JX: [Effectiveness analysis of HA based triple-drug regimen as induction chemotherapy in the treatment of acute myeloid leukemia and its relationship with karyotype]. Zhonghua Xue Ye Xue Za Zhi; 2005 Dec;26(12):705-9
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  • [Title] [Effectiveness analysis of HA based triple-drug regimen as induction chemotherapy in the treatment of acute myeloid leukemia and its relationship with karyotype].
  • OBJECTIVE: To analyze the complete remission (CR) rate, disease free survival (DFS) and overall survival (OS) of de novo acute myeloid leukemia (AML) patients treated with HA based three drugs induction chemotherapy and to explore the impact of cytogenetic abnormalities on the prognosis.
  • METHODS: Two hundred and forty-three untreated de novo AML patients were treated with HA based three drugs induction therapy.
  • Cytogenetics is the important prognostic factor for AML patients and SWOG karyotype subtyping criteria is more appropriate than that of MRC, the differences among the three groups being statistically significant.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Cytarabine / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Harringtonines / administration & dosage. Humans. Karyotyping. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies. Treatment Outcome

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  • (PMID = 16620570.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine
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98. Bayona C, Lassaletta A, Pérez A, Sevilla J, Albi G, Villa JR, Madero L: [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia]. An Pediatr (Barc); 2007 Sep;67(3):278-9
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  • [Title] [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia].
  • [Transliterated title] Hemoptisis fatal secundaria a aspergilosis pulmonar invasiva en una paciente con leucemia mieloblástica aguda.
  • [MeSH-major] Aspergillosis / complications. Hemoptysis / etiology. Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / complications

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  • (PMID = 17785168.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
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99. Chen HC, Hu WX, Liu QX, Li WK, Chen FZ, Rao ZZ, Liu XF, Luo YP, Cao YF: Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility. Eur J Cancer Prev; 2008 Jun;17(3):251-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility.
  • The genetic polymorphisms of biotransformation phase I enzymes, cytochrome P450 (CYP1A1 and CYP2D6), and phase II enzymes, glutathione S-transferase (GSTM1 and GSTT1), were analyzed in 204 healthy persons and 348 leukemia patients, who suffered from also acute lymphoblastic leukemia (ALL), acute nonlymphoblastic leukemia (ANLL) chronic myelogenous leukemia (CML), from the Han ethnic group in Changsha City of Hunan Province of China.
  • Our results showed that the frequencies of polymorphisms of CYP1A1, CYP2D6 and GSTT1 among the groups including acute lymphoblastic leukemia, ANLL, chronic myelogenous leukemia and healthy control have no significant differences.
  • The variation of GSTM1-null genotype alone correlated with the development of ANLL.
  • The combined genotypes of GSTM1-null with GSTT1-null, or GSTM1-null with CYP1A1 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant and CYP2D6 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant, CYP2D6 heterozygous mutant and GSTT1-null were found in individuals with high risk of ANLL.
  • All these findings suggest that GSTM1-null genotype alone or in coordination with the relevant genotypes of other metabolic enzymes might be susceptibility factors in the etiology of ANLL.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Glutathione Transferase / genetics. Leukemia / genetics. Polymorphism, Single Nucleotide
  • [MeSH-minor] Case-Control Studies. DNA Mutational Analysis. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Risk Factors

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  • (PMID = 18414197.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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100. Bashey A, Liu L, Ihasz A, Medina B, Corringham S, Keese K, Carrier E, Castro JE, Holman P, Lane TA, Hassidim K, Ball ED: Non-anthracycline based remission induction therapy for newly diagnosed patients with acute myeloid leukemia aged 60 or older. Leuk Res; 2006 Apr;30(4):503-6
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  • [Title] Non-anthracycline based remission induction therapy for newly diagnosed patients with acute myeloid leukemia aged 60 or older.
  • We assessed remission rates and toxicity in 24 consecutive elderly (age>or=60) patients with untreated Acute myeloid leukemia (AML) who received the anthracycline-free combination of fludarabine, cytosine arabinoside and G-CSF (FLAG) as initial induction chemotherapy at our center.
  • Fifteen patients proceeded to consolidation therapy and seven patients received a stem cell transplant (six autologous, one allogeneic).
  • Primary induction with FLAG in elderly AML patients achieves a high remission rate without prohibitive mucosal or cardiac toxicity and may thus be considered as an alternative to standard anthracycline-based regimens in this setting.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Cytarabine / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Middle Aged. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 16303178.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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