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Items 1 to 100 of about 10706
1. Ma L, Zhong MH, Feng DR, Long H, Shen J, Ma YG, Huang SZ: [FMS-like tyrosine kinase 3 gene mutation in acute myeloid leukemia detected by denaturing PAGE and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1386-9
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  • [Title] [FMS-like tyrosine kinase 3 gene mutation in acute myeloid leukemia detected by denaturing PAGE and its clinical significance].
  • The aim of this study was to analyze the frequency of flt3 length mutation (flt3-LM) in de novo acute myeloid leukemia patients and the relationship between flt3-LM and chromosome alterations, FAB subgroups, as well as efficiency of therapy.
  • Genomic DNA was amplified by PCR; 2% agarose gel or 8% denaturing PAGE were used to detect the length mutation of flt3 gene in 99 de novo acute myeloid leukemia patients; karyotyping in 72 AML patients was performed by G banding technique.
  • The flt3-LM was not detected in M(0) (only one patient was available), but flt3-LM occurrence in AML subtypes was as follow: in M(2) (9/30), M(3) (6/27), M(4) (4/14), M(5) (7/19), M(6) (3/8) respectively. flt3-LM in patients with normal karyotypes (39.13%) was more prevalent as compared with patients of abnormal karyotype (24.49%), but there was no statistical difference (p > 0.05).
  • The flt3 mutation represents a common genetic abnormality in AML patients, and the flt3-LM is associated with lower CR rate.

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  • (PMID = 21176335.001).
  • [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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2. 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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3. Rowe JM: Why is clinical progress in acute myelogenous leukemia so slow? Best Pract Res Clin Haematol; 2008 Mar;21(1):1-3
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  • [Title] Why is clinical progress in acute myelogenous leukemia so slow?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Disease-Free Survival. Drug Design. Drug Resistance, Neoplasm. Humans. Remission Induction

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  • (PMID = 18342806.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Introductory Journal Article
  • [Publication-country] England
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4. Frassoni F, Gualandi F, Podestà M, Raiola AM, Ibatici A, Piaggio G, Sessarego M, Sessarego N, Gobbi M, Sacchi N, Labopin M, Bacigalupo A: Direct intrabone transplant of unrelated cord-blood cells in acute leukaemia: a phase I/II study. Lancet Oncol; 2008 Sep;9(9):831-9
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  • [Title] Direct intrabone transplant of unrelated cord-blood cells in acute leukaemia: a phase I/II study.
  • The aim of this phase I/II study was to establish the safety and efficacy of a new administration route (intrabone) for cord-blood cells, measured by the donor-derived neutrophil and platelet engraftment.
  • METHODS: Adult patients with acute leukaemia, for whom an unrelated stem-cell transplantation was indicated and no suitable unrelated human leucocyte antigen (HLA)-matched donor had been identified, were included in the study and underwent a cord-blood transplant in San Martino Hospital, Genoa, Italy.
  • Eight patients were in first complete remission, ten in second complete remission, and 14 had advanced-stage, refractory disease.
  • Median transplanted cell dose was 2.6 x 10(7)/kg (range 1.4-4.2).
  • Secondary endpoints included the incidence of acute graft-versus-host disease, relapse, and overall survival.
  • FINDINGS: Between March 31, 2006, and Jan 25, 2008, 32 consecutive patients with acute myeloid leukaemia (n=20) or acute lymphoblastic leukaemia (n=12) underwent a cord-blood transplant (median age 36 years [range 18-66]).
  • Four patients with advanced-stage disease died within 12 days of the procedure.
  • No patient developed grade III-IV acute graft-versus-host disease.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


5. Zhou J, Khng J, Jasinghe VJ, Bi C, Neo CH, Pan M, Poon LF, Xie Z, Yu H, Yeoh AE, Lu Y, Glaser KB, Albert DH, Davidsen SK, Chen CS: In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor. Leuk Res; 2008 Jul;32(7):1091-100
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  • [Title] In vivo activity of ABT-869, a multi-target kinase inhibitor, against acute myeloid leukemia with wild-type FLT3 receptor.
  • We investigated the in vivo anti-leukemic effect of ABT-869 against AML with wild-type FLT3 using RFP transfected HL60 cells with in vivo imaging technology on both the subcutaneous and systemic leukemia xenograft models.
  • ABT-869 also reduced the leukemia burden and prolonged survival.
  • Our study supports the rationale for clinically testing an anti-angiogenesis agent in AML with wild-type FLT3.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Indazoles / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Phenylurea Compounds / therapeutic use. Protein Kinase Inhibitors / therapeutic use. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 18160102.001).
  • [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 / Antineoplastic Agents; 0 / Indazoles; 0 / N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N1-(2-fluoro-5-methylphenyl)urea; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 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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6. Sreekanth P, Narayana K, Shridhar NB, Bhat A: Toxicity studies of Calycopteris floribunda Lam. in calf, rabbit and rat. J Ethnopharmacol; 2006 Sep 19;107(2):229-33
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  • [Title] Toxicity studies of Calycopteris floribunda Lam. in calf, rabbit and rat.
  • The toxicological evaluation of the plant Calycopteris floribunda Lam. was done in calf, rabbit and rat.
  • Necropsy of calves revealed the congestion of liver, lung and petechiae on epicardium.
  • [MeSH-major] Combretaceae / toxicity. Liver / drug effects. Lung / drug effects. Pericardium / drug effects
  • [MeSH-minor] Alanine Transaminase / blood. Animals. Blood Glucose / analysis. Blood Urea Nitrogen. Cattle. Cholesterol / blood. Creatinine / blood. Male. Plant Extracts / isolation & purification. Plant Extracts / toxicity. Plant Leaves / chemistry. Plant Leaves / toxicity. Rabbits. Rats. Species Specificity. Toxicity Tests, Acute

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  • (PMID = 16677787.001).
  • [ISSN] 0378-8741
  • [Journal-full-title] Journal of ethnopharmacology
  • [ISO-abbreviation] J Ethnopharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Plant Extracts; 97C5T2UQ7J / Cholesterol; AYI8EX34EU / Creatinine; EC 2.6.1.2 / Alanine Transaminase
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7. Falini B, Bolli N, Liso A, Martelli MP, Mannucci R, Pileri S, Nicoletti I: Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1: molecular basis and clinical implications. Leukemia; 2009 Oct;23(10):1731-43
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  • [Title] Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1: molecular basis and clinical implications.
  • Mutations of NPM1 gene leading to aberrant cytoplasmic dislocation of nucleophosmin (NPMc+) occurs in about one third of acute myeloid leukaemia (AML) patients that exhibit distinctive biological and clinical features.
  • We discuss the latest advances in the molecular basis of nucleophosmin traffic under physiological conditions, describe the molecular abnormalities underlying altered transport of nucleophosmin in NPM1-mutated AML and present evidences supporting the view that cytoplasmic nucleophosmin is a critical event for leukaemogenesis.
  • We then outline how a highly specific immunohistochemical assay can be exploited to diagnose NPM1-mutated AML and myeloid sarcoma in paraffin-embedded samples by looking at aberrant nucleophosmin accumulation in cytoplasm of leukaemic cells.
  • Moreover, use of immunohistochemistry as surrogate for molecular analysis can serve as first-line screening in AML and should facilitate implementation of the 2008 World Health Organization classification of myeloid neoplasms that now incorporates AML with mutated NPM1 (synonym: NPMc+ AML) as a new provisional entity.
  • Finally, we discuss the future therapeutic perspectives aimed at reversing the altered nucleophosmin transport in AML with mutated NPM1.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation / genetics. Nuclear Proteins / genetics. Nuclear Proteins / metabolism

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  • (PMID = 19516275.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Number-of-references] 126
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8. Gupta S, Almyroudis NG, Battiwalla M, Bambach BJ, McCarthy PL, Proefrock AD, Ball D, Paplham P, Varma A, Kwon-Chung J, Segal BH: Successful treatment of disseminated fusariosis with posaconazole during neutropenia and subsequent allogeneic hematopoietic stem cell transplantation. Transpl Infect Dis; 2007 Jun;9(2):156-60
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  • [Title] Successful treatment of disseminated fusariosis with posaconazole during neutropenia and subsequent allogeneic hematopoietic stem cell transplantation.
  • We report the case of a 16-year-old girl with acute myelogenous leukemia with disseminated fusariosis, who responded to salvage posaconazole therapy.
  • She subsequently received additional cytotoxic chemotherapy and allogeneic hematopoietic stem cell transplantation with posaconazole continued as secondary prophylaxis.
  • Despite intensive immunosuppressive therapy for graft-versus-host disease, no recrudescence of infection occurred.
  • [MeSH-major] Antifungal Agents / therapeutic use. Fusarium / isolation & purification. Hematopoietic Stem Cell Transplantation. Mycoses / drug therapy. Neutropenia / complications. Triazoles / therapeutic use
  • [MeSH-minor] Adolescent. Female. Humans. Leukemia, Myeloid, Acute / complications

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  • (PMID = 17462004.001).
  • [ISSN] 1398-2273
  • [Journal-full-title] Transplant infectious disease : an official journal of the Transplantation Society
  • [ISO-abbreviation] Transpl Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
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9. Barata I: The laryngeal mask airway: prehospital and emergency department use. Emerg Med Clin North Am; 2008 Nov;26(4):1069-83, xi
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  • The LMA now has a well-established role in airway management.
  • There are several different types of LMAs to accommodate many different patient needs.
  • The LMA has become one of the most important and versatile tools in the management of patients with difficult airways.

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  • (PMID = 19059101.001).
  • [ISSN] 1558-0539
  • [Journal-full-title] Emergency medicine clinics of North America
  • [ISO-abbreviation] Emerg. Med. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Wu J, Li J, Zhu Z, Li J, Huang G, Tang Y, Gao X: Protective effects of echinocystic acid isolated from Gleditsia sinensis Lam. against acute myocardial ischemia. Fitoterapia; 2010 Jan;81(1):8-10
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  • [Title] Protective effects of echinocystic acid isolated from Gleditsia sinensis Lam. against acute myocardial ischemia.
  • Echinocystic acid (EA), a pentacyclic triterpene, was isolated and identified from the fruits of Gleditsia sinensis Lam.
  • The protective effects of EA were evaluated in rat models with acute myocardial ischemia induced by isoproterenol and vasopressin.

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  • (PMID = 19573579.001).
  • [ISSN] 1873-6971
  • [Journal-full-title] Fitoterapia
  • [ISO-abbreviation] Fitoterapia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adrenergic beta-Agonists; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vasoconstrictor Agents; 11000-17-2 / Vasopressins; 6SMK8R7TGJ / Oleanolic Acid; L4DUW10YOF / echinocystic acid; L628TT009W / Isoproterenol
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11. Yadav KS, Sawant KK: Formulation optimization of etoposide loaded PLGA nanoparticles by double factorial design and their evaluation. Curr Drug Deliv; 2010 Jan;7(1):51-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Etoposide is one of the most commonly used drugs in chemotherapy of acute lymphocytic leukemia and acute myelogenous leukaemia.

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  • (PMID = 20044908.001).
  • [ISSN] 1875-5704
  • [Journal-full-title] Current drug delivery
  • [ISO-abbreviation] Curr Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; 6PLQ3CP4P3 / Etoposide
  • [Number-of-references] 28
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12. Ito E: [The role of GATA1 mutation in acute megakaryocytic leukemia]. Rinsho Ketsueki; 2006 Nov;47(11):1415-22
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  • [Title] [The role of GATA1 mutation in acute megakaryocytic leukemia].
  • [MeSH-major] GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation

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  • (PMID = 17176883.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human
  • [Number-of-references] 53
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13. Jurek AM, Maldonado G, Spector LG, Ross JA: Periconceptional maternal vitamin supplementation and childhood leukaemia: an uncertainty analysis. J Epidemiol Community Health; 2009 Feb;63(2):168-72
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  • [Title] Periconceptional maternal vitamin supplementation and childhood leukaemia: an uncertainty analysis.
  • BACKGROUND: Recent studies in childhood cancer suggest that maternal vitamin supplementation may reduce the risk of leukaemia, neuroblastoma and certain types of childhood brain tumours.
  • For example, a previous study found a significantly reduced risk of acute lymphoblastic leukaemia (ALL) but not acute myeloid leukaemia (AML) in children with Down syndrome whose mothers reported any vitamin supplement use prior to knowledge of pregnancy (ALL OR adjusted for confounders 0.51, 95% confidence limits (CL): 0.30, 0.89; AML OR adjusted for confounders 0.92, 95% CL 0.48, 1.76).
  • Epidemiologists are encouraged to quantitatively adjust for systematic error in study results, but often do not.

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  • [CommentIn] J Epidemiol Community Health. 2009 Feb;63(2):91 [19141660.001]
  • (PMID = 18977808.001).
  • [ISSN] 1470-2738
  • [Journal-full-title] Journal of epidemiology and community health
  • [ISO-abbreviation] J Epidemiol Community Health
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075169; United States / NCI NIH HHS / CA / R01 CA75169
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Vitamins
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14. Cashen AF, Schiller GJ, O'Donnell MR, DiPersio JF: Multicenter, phase II study of decitabine for the first-line treatment of older patients with acute myeloid leukemia. J Clin Oncol; 2010 Feb 1;28(4):556-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multicenter, phase II study of decitabine for the first-line treatment of older patients with acute myeloid leukemia.
  • PURPOSE: Older patients with acute myeloid leukemia (AML) have limited treatment options because of the lack of effectiveness and the toxicity of available therapies.
  • We investigated the efficacy and toxicity of the hypomethylating agent decitabine as initial therapy in older patients with AML.
  • PATIENTS AND METHODS: In this multicenter, phase II study, patients older than 60 years who had AML (ie, > 20% bone marrow blasts) and no prior therapy for AML were treated with decitabine 20 mg/m(2) intravenously for 5 consecutive days of a 4-week cycle.
  • Patients continued to receive decitabine until disease progression or an unacceptable adverse event occurred.
  • CONCLUSION: Decitabine given in a low-dose, 5-day regimen has activity as upfront therapy in older patients with AML, and it has acceptable toxicity and 30-day mortality.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Neoplasm Recurrence, Local / drug therapy


15. Wang J, Ouyang J, Zhou R, Chen B, Yang Y: Autologous hematopoietic stem cell transplantation for acute myeloid leukemia in first complete remission: a meta-analysis of randomized trials. Acta Haematol; 2010;124(2):61-71
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  • [Title] Autologous hematopoietic stem cell transplantation for acute myeloid leukemia in first complete remission: a meta-analysis of randomized trials.
  • BACKGROUND: For those patients who are not candidates for allogeneic stem cell transplantation (SCT) or who do not have an HLA-matched donor, it is unclear whether consolidation therapy with autologous SCT results in a survival benefit compared with further intensive post-remission non-myeloablative chemotherapy or no further therapy.
  • METHODS: A meta-analysis evaluating autologous SCT versus further chemotherapy or no treatment for acute myeloid leukemia (AML) in first complete remission (CR1) was completed.
  • For adults, AML in CR1 compared with non-SCT, lower relapse and higher transplantation-related mortality were associated with autologous SCT, a significant disease-free survival benefit of autologous SCT was documented, and there was no difference in overall survival when studies were pooled.
  • For pediatric AML in CR1, there were no differences in relapse, transplantation-related mortality, disease-free survival and overall survival.
  • CONCLUSION: Our results support the conclusion that autologous SCT should not be considered as the first-line post-remission therapy for AML patients in CR1.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / mortality. Hematopoietic Stem Cell Transplantation / statistics & numerical data. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy


16. Pagel JM, Appelbaum FR, Eary JF, Rajendran J, Fisher DR, Gooley T, Ruffner K, Nemecek E, Sickle E, Durack L, Carreras J, Horowitz MM, Press OW, Gopal AK, Martin PJ, Bernstein ID, Matthews DC: 131I-anti-CD45 antibody plus busulfan and cyclophosphamide before allogeneic hematopoietic cell transplantation for treatment of acute myeloid leukemia in first remission. Blood; 2006 Mar 1;107(5):2184-91
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  • [Title] 131I-anti-CD45 antibody plus busulfan and cyclophosphamide before allogeneic hematopoietic cell transplantation for treatment of acute myeloid leukemia in first remission.
  • In an attempt to improve outcomes for patients with acute myeloid leukemia (AML) after allogeneic hematopoietic cell transplantation (HCT), we conducted a phase 1/2 study in which targeted irradiation delivered by 131I-anti-CD45 antibody was combined with targeted busulfan (BU; area-under-curve, 600-900 ng/mL) and cyclophosphamide (CY; 120 mg/kg).
  • Forty-six patients were treated with 102 to 298 mCi (3774-11 026 MBq) 131I, delivering an estimated 5.3 to 19 (mean, 11.3) Gy to marrow, 17-72 (mean, 29.7) Gy to spleen, and 3.5 Gy (n = 4) to 5.25 Gy (n = 42) to the liver.
  • The estimated 3-year nonrelapse mortality and disease-free survival (DFS) were 21% and 61%, respectively.
  • These results were compared with those from 509 similar International Bone Marrow Transplant Registry patients who underwent transplantation using BU/CY alone.

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  • (PMID = 16254140.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NCRR NIH HHS / RR / M01RR-00037; United States / NCI NIH HHS / CA / CA44991; United States / NCI NIH HHS / CA / K08CA95448; United States / NCI NIH HHS / CA / CA76930
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Iodine Isotopes; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan
  • [Other-IDs] NLM/ PMC1895719
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17. Gentles AJ, Plevritis SK, Majeti R, Alizadeh AA: Association of a leukemic stem cell gene expression signature with clinical outcomes in acute myeloid leukemia. JAMA; 2010 Dec 22;304(24):2706-15
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  • [Title] Association of a leukemic stem cell gene expression signature with clinical outcomes in acute myeloid leukemia.
  • The strongest support for this cancer stem cell model comes from transplantation assays in immunodeficient mice, which indicate that human acute myeloid leukemia (AML) is driven by self-renewing leukemic stem cells (LSCs).
  • OBJECTIVE: To identify an LSC gene expression signature and test its association with clinical outcomes in AML.
  • DESIGN, SETTING, AND PATIENTS: Retrospective study of global gene expression (microarray) profiles of LSC-enriched subpopulations from primary AML and normal patient samples, which were obtained at a US medical center between April 2005 and July 2007, and validation data sets of global transcriptional profiles of AML tumors from 4 independent cohorts (n = 1047).
  • MAIN OUTCOME MEASURES: Identification of genes discriminating LSC-enriched populations from other subpopulations in AML tumors; and association of LSC-specific genes with overall, event-free, and relapse-free survival and with therapeutic response.
  • RESULTS: Expression levels of 52 genes distinguished LSC-enriched populations from other subpopulations in cell-sorted AML samples.
  • An LSC score summarizing expression of these genes in bulk primary AML tumor samples was associated with clinical outcomes in the 4 independent patient cohorts.
  • For the largest cohort of patients with normal karyotypes (n = 163), the LSC score was significantly associated with overall survival as a continuous variable (hazard ratio [HR], 1.15; 95% confidence interval [CI], 1.08-1.22; log-likelihood P <.001).
  • The absolute risk of death by 3 years was 57% (95% CI, 43%-67%) for the low LSC score group compared with 78% (95% CI, 66%-86%) for the high LSC score group (HR, 1.9 [95% CI, 1.3-2.7]; log-rank P = .002).
  • In another cohort with available data on event-free survival for 70 patients with normal karyotypes, the risk of an event by 3 years was 48% (95% CI, 27%-63%) in the low LSC score group vs 81% (95% CI, 60%-91%) in the high LSC score group (HR, 2.4 [95% CI, 1.3-4.5]; log-rank P = .006).
  • In multivariate Cox regression including age, mutations in FLT3 and NPM1, and cytogenetic abnormalities, the HRs for LSC score in the 3 cohorts with data on all variables were 1.07 (95% CI, 1.01-1.13; P = .02), 1.10 (95% CI, 1.03-1.17; P = .005), and 1.17 (95% CI, 1.05-1.30; P = .005).
  • CONCLUSION: High expression of an LSC gene signature is independently associated with adverse outcomes in patients with AML.

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  • (PMID = 21177505.001).
  • [ISSN] 1538-3598
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA149145; United States / NCI NIH HHS / CA / U56 CA112973; United States / NCI NIH HHS / CA / 1U54CA149145; United States / NCI NIH HHS / CA / U56-CA112973
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS606664; NLM/ PMC4089862
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18. Liu QX, Chen HC, Liu XF, Cao YF, Zhang J, Liu J: [Study on the relationship between polymorphisms of Cyp1A1, GSTM1, GSTT1 genes and the susceptibility to acute leukemia in the general population of Hunan province]. Zhonghua Liu Xing Bing Xue Za Zhi; 2005 Dec;26(12):975-9
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  • [Title] [Study on the relationship between polymorphisms of Cyp1A1, GSTM1, GSTT1 genes and the susceptibility to acute leukemia in the general population of Hunan province].
  • OBJECTIVE: Based on the distribution of genetic polymorphisms regarding phase I metabolic enzyme cytochrome P450 1A1 (CYP1A1) and phase II metabolic enzymes glutathione S-transferase GSTM1 and GSTT1 genotypes in acute leukemia patients and health controls among general population of Hunan in China, this study was to explore the relationship between these gene polymorphisms and the susceptibility to acute leukemia.
  • METHODS: Using case-control methodology, we studied 204 healthy controls and 232 patients with acute leukemia, of which 112 patients were suffering acute lymphoblastic leukemia (ALL) and 120 with acute non-lymphoblastic leukemia (ANLL).
  • RESULTS: The variation frequencies of CYP1A1 gene (Msp I polymorphisms, site 3801T-C variation) in ALL and ANLL groups were 74.1% and 70.8% respectively which were higher than 63.3% appeared in the healthy controls.
  • However, the differences between patients (ALL or ANLL) and healthy controls were not statistically significant (P > 0.05 for both).
  • The null genotype of GSTM1 (GSTM1 -/-) in ALL group was 60.7%, which was not significantly different from the controls (55.4%).
  • However, GSTM1 -/- genotype in ANLL group was 68.3%, significantly different from the controls (P < 0.05).
  • The null genotypes among GSTT1 (GSTT1 -/-) in ALL, ANLL and control group were 50.9%, 55.0% and 49.0% but their differences were not statistically significant (P > 0.05).
  • The incidences of GSTM1 -/- and GSTT1 -/- combined genotype in ALL, ANLL and control group were 33.0%, 40.0% and 27.5%, of which the difference between ANLL group and control group was statistically significant (P < 0.05) and CYP1A1 gene heterozygous mutation type or homozygous mutation type combined with GSTM1 -/- and GSTT1 -/- increased the risk of ANLL (OR value 1.890, 95% CI: 1.084-3.295).
  • CONCLUSION: These results indicated that both the variation of CYP1A1 gene or GSTT1 -/- genotype alone might not be associated with the susceptibility of acute leukemia while GSTM1 -/- genotype alone or combined with GSTT1 -/- or the 3801 T-C variation of CYP1A1 gene were correlated with ANLL.
  • These findings suggest that GSTM1 - / - genotype alone or in combination with other defective genotypes might serve as risk factors to the etiology of ANLL.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16676594.001).
  • [ISSN] 0254-6450
  • [Journal-full-title] Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi
  • [ISO-abbreviation] Zhonghua Liu Xing Bing Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; 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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19. Cai D, Wang Y, Ottmann OG, Barth PJ, Neubauer A, Burchert A: FLT3-ITD-, but not BCR/ABL-transformed cells require concurrent Akt/mTor blockage to undergo apoptosis after histone deacetylase inhibitor treatment. Blood; 2006 Mar 1;107(5):2094-7
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  • [Title] FLT3-ITD-, but not BCR/ABL-transformed cells require concurrent Akt/mTor blockage to undergo apoptosis after histone deacetylase inhibitor treatment.
  • Leukemias are differentially sensitive to histone deacytelase inhibitor (HDI)-induced apoptosis, but molecular reasons for this remain unclear.
  • We here show that BCR/ABL-, but not FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD)-transformed 32D cells or primary acute myeloid leukemia (AML) blasts undergo apoptosis after treatment with the HDI valproic acid (VPA) plus all-trans retinoic acid (VPA/ATRA).
  • A particular VPA/ATRA responsiveness of Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (ALL) was confirmed in a therapy-refractory patient in vivo.
  • Conversely, separate blockage of the Akt/mTor-signaling pathway was a prerequisite for overcoming apoptosis resistance to VPA/ATRA in FLT3-ITD cells, and primary AML blasts (n = 9).
  • In conclusion, constitutive Akt activation causes apoptosis resistance to VPA/ATRA in AML, but not in Ph+ leukemia.
  • This warrants the application of HDI-based therapies in poor-risk Ph+ ALL, and the use of Akt/mTor inhibitors to overcome HDI resistance in AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Signal Transduction / drug effects. Tretinoin / pharmacology. Valproic Acid / pharmacology
  • [MeSH-minor] Caspases / metabolism. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / metabolism. Histone Deacetylase Inhibitors. Humans. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Mutation. Oncogene Protein v-akt / antagonists & inhibitors. Oncogene Protein v-akt / metabolism. Philadelphia Chromosome. Protein Kinases / metabolism. TOR Serine-Threonine Kinases. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 16304046.001).
  • [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 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.4.22.- / Caspases
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20. Thomas X, Campos L, Mounier C, Cornillon J, Flandrin P, Le QH, Piselli S, Guyotat D: Expression of heat-shock proteins is associated with major adverse prognostic factors in acute myeloid leukemia. Leuk Res; 2005 Sep;29(9):1049-58
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  • [Title] Expression of heat-shock proteins is associated with major adverse prognostic factors in acute myeloid leukemia.
  • To identify prognostic factors alternative or additional to drug-resistance and apoptosis proteins, we studied the impact of the expression of heat-shock proteins (HSPs) in 98 newly diagnosed acute myeloid leukemia (AML).
  • HSP90 and HSP110 were correlated with FAB subtype and karyotypic grouping.
  • Median disease-free survival (DFS) of the 68 remitters was 18.1 months with a 3-year DFS rate of 41%.
  • [MeSH-major] Heat-Shock Proteins / metabolism. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Bone Marrow Cells / metabolism. Disease-Free Survival. Female. Flow Cytometry. Humans. Male. Multivariate Analysis. Prognosis


21. Advani AS, Shadman M, Ali-Osman F, Barker A, Rybicki L, Kalaycio M, Sekeres MA, de Castro CM, Diehl LF, Moore JO, Beaven A, Copelan E, Sobecks R, Talea P, Rizzieri DA: A Phase II trial of gemcitabine and mitoxantrone for patients with acute myeloid leukemia in first relapse. Clin Lymphoma Myeloma Leuk; 2010 Dec;10(6):473-6
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  • [Title] A Phase II trial of gemcitabine and mitoxantrone for patients with acute myeloid leukemia in first relapse.
  • INTRODUCTION: We evaluated the complete remission (CR) rate in patients with acute myeloid leukemia (AML) in first relapse treated with fixed-dose-rate gemcitabine and mitoxantrone.
  • Higher sum total of ABCC4 and SLC29A2 expression measured by RT-PCR was associated with not achieving CR (20.6 vs. 12.1; P = .006).
  • In addition, there was a trend for higher expression of the sum total of the 10 MDR genes (measured by RT-PCR) and not achieving CR (P = .06).
  • The high expression of GSTP1 suggests that this may be a therapeutic target for relapsed AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / drug effects. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Drug Resistance, Multiple / genetics. Equilibrative-Nucleoside Transporter 2 / genetics. Equilibrative-Nucleoside Transporter 2 / metabolism. Female. Fever / chemically induced. Gene Expression Regulation, Leukemic / genetics. Glutathione S-Transferase pi / genetics. Glutathione S-Transferase pi / metabolism. Humans. Immunohistochemistry. Infusions, Intravenous. K562 Cells. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Multidrug Resistance-Associated Proteins / genetics. Multidrug Resistance-Associated Proteins / metabolism. Recurrence. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. U937 Cells

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  • (PMID = 21156465.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [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 / ABCC4 protein, human; 0 / Equilibrative-Nucleoside Transporter 2; 0 / Multidrug Resistance-Associated Proteins; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BZ114NVM5P / Mitoxantrone; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
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22. Miller G, Bertelli L, Little T, Guilmette RA: Internal dosimetry verification and validation database. Radiat Prot Dosimetry; 2007;127(1-4):361-9
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  • Simulated-data internal dosimetry cases for use in intercomparison exercises or as a software verification and validation tool have been published on the internet (www.lanl.gov/bayesian/software Bayesian software package II).
  • Simulated data are generated for all the assumed biokinetic models, both for incidents, where the time of intake is known, and for non-incidents, where it is not.
  • For the dose calculations, the route of intake, but not the biokinetic model, is considered to be known.

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  • (PMID = 18325930.001).
  • [ISSN] 0144-8420
  • [Journal-full-title] Radiation protection dosimetry
  • [ISO-abbreviation] Radiat Prot Dosimetry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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23. Dorsey WC, Tchounwou PB, Ford BD: Neuregulin 1-Beta cytoprotective role in AML 12 mouse hepatocytes exposed to pentachlorophenol. Int J Environ Res Public Health; 2006 Mar;3(1):11-22
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  • [Title] Neuregulin 1-Beta cytoprotective role in AML 12 mouse hepatocytes exposed to pentachlorophenol.
  • Accumulating evidence has shown that neuregulins have cyto- and neuroprotective properties in various cell types.
  • In particular, the neuregulin-1 Beta (NRG1-Beta) isoform is well documented for its antiinflammatory properties in rat brain after acute stroke episodes.
  • Previous investigations from our laboratory have demonstrated that PCP exerts both cytotoxic and mitogenic effects in human liver carcinoma (HepG2) cells, primary catfish hepatocytes and AML 12 mouse hepatocytes.
  • In the present study, we hypothesize that NRG1-Beta will exert its cytoprotective effects in PCP-treated AML 12 mouse hepatocytes by its ability to suppress the toxic effects of PCP.
  • To test this hypothesis, we performed the MTT-cell respiration assay to assess cell viability, and Western-blot analysis to assess stress-related proteins as a consequence of PCP exposure.
  • Data obtained from 48 h-viability studies demonstrated a biphasic response; showing a dose-dependent increase in cell viability within the range of 0 to 3.87 microg/mL, and a gradual decrease within the concentration range of 7.75 to 31.0 microg/mL in concomitant treatments of NRG1-Beta+PCP and PCP.
  • Cell viability percentages indicated that NRG1-Beta+PCPtreated cells were not significantly impaired, while PCP-treated cells were appreciably affected; suggesting that NRG1-Beta has the ability to suppress the toxic effects of PCP.
  • Western Blot analysis demonstrated the potential of PCP to induce oxidative stress and inflammatory response (c-fos), growth arrest and DNA damage (GADD153), proteotoxic effects (HSP70), cell cycle arrest as consequence of DNA damage (p53), mitogenic response (cyclin- D1), and apoptosis (caspase-3).
  • NRG1-Beta exposure attenuated stress-related protein expression in PCP-treated AML 12 mouse hepatocytes.
  • Here we provide clear evidence that NRG1-Beta exerts cytoprotective effects in AML 12 mouse hepatocytes exposed to PCP.

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  • (PMID = 16823072.001).
  • [ISSN] 1661-7827
  • [Journal-full-title] International journal of environmental research and public health
  • [ISO-abbreviation] Int J Environ Res Public Health
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Ddit3 protein, mouse; 0 / HSP70 Heat-Shock Proteins; 0 / Neuregulin-1; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Suppressor Protein p53; 0 / neuregulin beta; 136601-57-5 / Cyclin D1; 147336-12-7 / Transcription Factor CHOP; D9BSU0SE4T / Pentachlorophenol; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC3785675
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24. Szczepanski MJ, Szajnik M, Welsh A, Foon KA, Whiteside TL, Boyiadzis M: Interleukin-15 enhances natural killer cell cytotoxicity in patients with acute myeloid leukemia by upregulating the activating NK cell receptors. Cancer Immunol Immunother; 2010 Jan;59(1):73-9
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  • [Title] Interleukin-15 enhances natural killer cell cytotoxicity in patients with acute myeloid leukemia by upregulating the activating NK cell receptors.
  • Interleukin-15 (IL-15) has a major role in NK-cell homeostasis.
  • Modulation of the relative frequency and expression intensity of the NK-cell receptors by IL-15 may increase NK cell-mediated cytotoxicity in cancer patients.
  • We investigated the receptor repertoire and measured NK-cell activity in newly diagnosed AML patients and evaluated the ex vivo effects of IL-15.
  • The expression of the activating NK cell receptors was significantly decreased in the AML patients compared to that in NK cells of healthy donors.
  • When NK cells obtained from AML patients were cultured with IL-15, expression of the activating receptors was significantly upregulated compared to pre-culture levels.
  • This IL-15 induced increase in activity was blocked by neutralizing antibodies specific for the NK cell activating receptors.
  • These pre-clinical data support the future use of IL-15 for NK cell- based therapies for AML patients.

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  • (PMID = 19526239.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / N01HB37165; United States / NCI NIH HHS / CA / P01 CA109688; United States / NHLBI NIH HHS / HB / N01-HB-37165; United States / NCI NIH HHS / CA / P01-CA109688
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Interleukin-15; 0 / Receptors, Natural Killer Cell
  • [Other-IDs] NLM/ NIHMS489247; NLM/ PMC3721322
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25. Choudhary C, Brandts C, Schwable J, Tickenbrock L, Sargin B, Ueker A, Böhmer FD, Berdel WE, Müller-Tidow C, Serve H: Activation mechanisms of STAT5 by oncogenic Flt3-ITD. Blood; 2007 Jul 1;110(1):370-4
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  • Mutations in the receptor tyrosine kinase Flt3 represent a very common genetic lesion in acute myeloid leukemia (AML).
  • Oncogenic activation of Flt3 by ITD mutations is known to activate aberrant signaling including activation of STAT5 and repression of myeloid transcription factors Pu.1 and c/EBP-alpha.
  • Using small molecule inhibitors and cell lines deficient for Src family kinases or Jak2 or Tyk2, here we show that Flt3-ITD-induced STAT5 activation is independent of Src or Jak kinases.
  • Also, overexpression of SOCS1, an inhibitor of Jak kinases, inhibited IL-3- but not Flt3-ITD-mediated STAT5 activation.
  • [MeSH-minor] Animals. Cell Line. Janus Kinase 2. Mice. Mice, Knockout. Mutation. Suppressor of Cytokine Signaling Proteins. TYK2 Kinase

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  • (PMID = 17356133.001).
  • [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 / STAT5 Transcription Factor; 0 / Socs1 protein, mouse; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / Tyk2 protein, mouse
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26. Lasa A, Carricondo M, Estivill C, Bussaglia E, Gich I, Brunet S, Aventin A, Sierra J, Nomdedéu JF: WT1 monitoring in core binding factor AML: comparison with specific chimeric products. Leuk Res; 2009 Dec;33(12):1643-9
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  • [Title] WT1 monitoring in core binding factor AML: comparison with specific chimeric products.
  • Minimal residual disease may help to establish clinical decisions in patients with AML.
  • To compare the value of chimeric specific quantitative PCR with WT1 PCR in CBF acute leukemia, 445 samples from 96 AML (49 AML1-ETO+ and 47 CBFB-MYH11+) cases were included in the study.
  • The majority of CBF samples showed rises in WT1 levels (88.7%) at diagnosis.
  • WT1 mutation was not detected in any case (70 diagnostic samples).
  • We found correlation between WT1 levels at diagnosis and the CD34 blast population estimated by flow cytometry in CBFB-MYH11+ cases.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics. Monitoring, Physiologic

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  • (PMID = 19427034.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; 63231-63-0 / RNA
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27. Valcárcel D, Martino R, Caballero D, Martin J, Ferra C, Nieto JB, Sampol A, Bernal MT, Piñana JL, Vazquez L, Ribera JM, Besalduch J, Moraleda JM, Carrera D, Brunet MS, Perez-Simón JA, Sierra J: Sustained remissions of high-risk acute myeloid leukemia and myelodysplastic syndrome after reduced-intensity conditioning allogeneic hematopoietic transplantation: chronic graft-versus-host disease is the strongest factor improving survival. J Clin Oncol; 2008 Feb 1;26(4):577-84
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  • [Title] Sustained remissions of high-risk acute myeloid leukemia and myelodysplastic syndrome after reduced-intensity conditioning allogeneic hematopoietic transplantation: chronic graft-versus-host disease is the strongest factor improving survival.
  • PURPOSE: Reduced-intensity conditioning (RIC) for allogeneic stem-cell transplantation (allo-SCT) reduces nonrelapse mortality (NRM).
  • This reduction makes it possible for patients who are ineligible for high-dose myeloablative conditioning allo-SCT to benefit from graft-versus-leukemia reaction.
  • In this multicenter, prospective study of patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS), we investigated the efficacy of RIC allo-SCT from a human leukocyte antigen-identical sibling by using a regimen that uses fludarabine and busulfan.
  • PATIENTS AND METHODS: Ninety-three patients with AML (n = 59) and MDS (n = 34) were included, and the median age was of 53 years.
  • Graft-versus-host disease (GVHD) prophylaxis consisted of cyslosporine and methotrexate or mycophenolate mofetil.
  • The 1- and 4-year relapse cumulative incidences were 23% and 37%, respectively, and leukemia recurrence was the main cause of death.
  • The 4-year disease-free survival (DFS) and overall survival (OS) rates were 43% and 45%, respectively.
  • CONCLUSION: Our results confirm the capacity of this RIC regimen to obtain long-term remissions in patients ineligible for a conventional allo-SCT.
  • [MeSH-major] Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Transplantation Conditioning
  • [MeSH-minor] Adult. Aged. Busulfan / administration & dosage. Chronic Disease. Disease-Free Survival. Drug Therapy, Combination. Female. Humans. Immunosuppressive Agents / administration & dosage. Male. Middle Aged. Multivariate Analysis. Myeloablative Agonists / administration & dosage. Prospective Studies. Remission Induction. Survival Analysis. Transplantation, Homologous. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives


28. 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


29. Sellick GS, Spendlove HE, Catovsky D, Pritchard-Jones K, Houlston RS: Further evidence that germline CEBPA mutations cause dominant inheritance of acute myeloid leukaemia. Leukemia; 2005 Jul;19(7):1276-8
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  • [Title] Further evidence that germline CEBPA mutations cause dominant inheritance of acute myeloid leukaemia.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Genes, Dominant / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child, Preschool. DNA Mutational Analysis. Female. Germ-Line Mutation. Humans. Male. Pedigree

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  • (PMID = 15902292.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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30. Dusenbery KE, Bellairs EE, Potish RA, Twiggs LB, Boente MP: Twenty-five year outcome of sequential abdominal radiotherapy and melphalan:implications for future management of epithelial carcinoma of the ovary. Gynecol Oncol; 2005 Feb;96(2):307-13
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  • Disease-free survival was 48% at 5 years and remained at 45% from 10 to 25 years.
  • Stage and the presence of palpable postoperative disease were significant prognostic factors.
  • Disease-free survivals were 95% from 5 to 25 years for stage I, 70% at 5 years and 60% at 25 years for stage II, and 20% from 5 to 25 years for stage III (P < 0.0001).
  • Stage III patients without postoperative palpable tumor achieved a 47% 25-year disease-free survival.
  • Acute toxicity was acceptable, and 98% of patients completed radiation therapy.
  • Chronic toxicity included a 12% small bowel obstruction rate and a 3% fatal second malignancy/hematological toxicity rate (two cases of acute myelocytic leukemia, one case of thrombocytopenia).
  • CONCLUSIONS: The long-term disease-free survival obtained with abdominopelvic radiotherapy followed by single alkylating agent chemotherapy has not been exceeded by three subsequent decades of multiagent chemotherapy trials.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Disease-Free Survival. Epithelial Cells / pathology. Female. Follow-Up Studies. Humans. Hysterectomy. Middle Aged. Neoplasm Staging. Treatment Outcome

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  • (PMID = 15661213.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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31. Wilking N, Lidbrink E, Wiklund T, Erikstein B, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Bergh J: Long-term follow-up of the SBG 9401 study comparing tailored FEC-based therapy versus marrow-supported high-dose therapy. Ann Oncol; 2007 Apr;18(4):694-700
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  • Ten patients in the tailored FEC regimen developed acute myeloid leukaemia (AML)/myelodysplasia (MDS).
  • CONCLUSION: The update of this study shows an improved outcome linked to the tailored FEC treatment in relation to breast cancer relapse, but also an increased incidence of AML/MDS.

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  • (PMID = 17301072.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
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32. Travaglino E, Benatti C, Malcovati L, Della Porta MG, Gallì A, Bonetti E, Rosti V, Cazzola M, Invernizzi R: Biological and clinical relevance of matrix metalloproteinases 2 and 9 in acute myeloid leukaemias and myelodysplastic syndromes. Eur J Haematol; 2008 Mar;80(3):216-26
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  • [Title] Biological and clinical relevance of matrix metalloproteinases 2 and 9 in acute myeloid leukaemias and myelodysplastic syndromes.
  • We analysed by immunocytochemistry metalloproteinase (MMP)-2 and MMP-9 expression in bone marrow cells from 54 acute myeloid leukaemia (AML) patients, 153 myelodysplastic syndrome (MDS) patients, and 52 non-haemopathic subjects, in order to evaluate whether MMP expression abnormalities were associated with relevant laboratory or clinical findings.
  • In normal samples MMP-2 was detected in rare myeloid cells, MMP-9 in most maturing myeloid cells.
  • In MDS MMP-2 myeloid levels were higher than in controls (P < 0.0001); MMP-2 and MMP-9 were often co-expressed.
  • There was a positive correlation between MMP-2 erythroblast expression and erythroid dysplasia (P = 0.002) and an inverse correlation between MMP-2 or MMP-9 myeloid expression and blast cell percentage (P = 0.05 and P = 0.04 respectively).
  • High MMP levels in myeloid cells were associated with longer overall survival (P = 0.03) and evolution-free survival (P = 0.04).
  • In AML MMP-2 levels were lower than in MDS (P < 0.0001) and MMP-9 levels lower than in MDS and controls (P < 0.0001).
  • MMP levels did not predict response to therapy.
  • The release of active MMPs was detected by colorimetric analysis in cell cultures from representative MDS and AML cases.
  • In conclusion, we have demonstrated an abnormal MMP expression in AML as well as in MDS.
  • The production and release of these enzymes may influence haematopoietic cell behaviour.
  • In MDS, the detection of MMP deregulated expression may be important also from the clinical point of view: it may provide a useful tool for diagnosis, prognosis and a possible target for experimental treatments.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 9 / biosynthesis. Myelodysplastic Syndromes / enzymology
  • [MeSH-minor] Aged. Aged, 80 and over. Apoptosis / physiology. Bone Marrow / blood supply. Bone Marrow / enzymology. Bone Marrow / pathology. Cell Proliferation. Cells, Cultured. Erythroblasts / enzymology. Erythroblasts / pathology. Female. Humans. Male. Middle Aged. Myeloid Cells / enzymology. Myeloid Cells / pathology. Neoplasm Invasiveness. Phenotype. Tumor Cells, Cultured


33. Lei HY, Zhao XL: [Clinical significance of NF-kappaB continual activity and expression of WT1 and MDR1 in acute nonlymphocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):253-7
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  • [Title] [Clinical significance of NF-kappaB continual activity and expression of WT1 and MDR1 in acute nonlymphocytic leukemia].
  • The study was aimed to explore the NF-kappaB continual activity and the expression of WT1 and MDR1 in acute non-lymphocytic leukemia (ANLL) patients, and to investigate if the three factors affect the curative effect of ANLL together as to provide some theoretical basis for finding new measures to improve the curative effect of refractory ANLL.
  • The bone marrow samples of 45 ANLL patients was collected.
  • 45 patients including 20 primary ANLL patients (A group) and 25 refractory ANLL patients.
  • Refractory ANLL patients were divided into 2 sub-groups (B, C groups).
  • The results showed that the activity of NF-kappaB and the expressions of WT1, MDR1 were not detected in 15 samples of simply iron deficiency anemia subjects.
  • But the NF-kappaB continual activity, the expression of WT1 gene and MDR1 gene were not significantly different between group B and group C (P>0.05).
  • By assaying the relativity between the them the NF-kappaB continual activity and the expression of WT1 or MDR1 had positive correlation in ANLL patients.
  • It is concluded that the NF-kappaB continual activity, the overexpression of WT1 and MDR1 may be one of the reasons causing poor curative effect in acute non-lymphocytic leukemia.
  • The NF-kappaB continual activity and the expression of WT1, MDR1, all show positive correlation in ANLL patients.

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  • (PMID = 17493326.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / NF-kappa B; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / WT1 Proteins
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34. Lim SH, Hulsey M, Esler WV: Resolution of Behcet's disease after non-myeloablative allogeneic stem cell transplant for acute myeloid leukaemia. Rheumatology (Oxford); 2009 Jan;48(1):88-9
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  • [Title] Resolution of Behcet's disease after non-myeloablative allogeneic stem cell transplant for acute myeloid leukaemia.
  • [MeSH-major] Behcet Syndrome / therapy. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy


35. Steinbach D, Schramm A, Eggert A, Onda M, Dawczynski K, Rump A, Pastan I, Wittig S, Pfaffendorf N, Voigt A, Zintl F, Gruhn B: Identification of a set of seven genes for the monitoring of minimal residual disease in pediatric acute myeloid leukemia. Clin Cancer Res; 2006 Apr 15;12(8):2434-41
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  • [Title] Identification of a set of seven genes for the monitoring of minimal residual disease in pediatric acute myeloid leukemia.
  • BACKGROUND: Monitoring of minimal residual disease (MRD) has become a strong diagnostic tool in acute lymphoblastic leukemia.
  • In acute myeloid leukemia (AML), there is still a need for more suitable MRD markers.
  • EXPERIMENTAL DESIGN: A stepwise approach which combined genome-wide expression profiling, TaqMan low density arrays, and a TaqMan real-time PCR-based screening was used to identify new markers for the monitoring of MRD in AML.
  • Leukemic cells from 52 children with AML and 145 follow-up samples from 25 patients were analyzed.
  • RESULTS: Seven genes were identified which are vastly overexpressed in many patients with AML compared with healthy bone marrow: CCL23, GAGED2, MSLN, SPAG6, and ST18 as well as the previously described markers WT1 and PRAME.
  • CONCLUSIONS: This set of genes should allow a sensitive and specific monitoring of MRD in AML.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, Neoplasm / blood. Antigens, Neoplasm / genetics. Biomarkers, Tumor / blood. Biomarkers, Tumor / genetics. Bone Marrow / metabolism. Chemokines, CC / blood. Chemokines, CC / genetics. Child. Child, Preschool. DNA-Binding Proteins / blood. DNA-Binding Proteins / genetics. Female. GPI-Linked Proteins. Humans. Infant. Infant, Newborn. Male. Membrane Glycoproteins / blood. Membrane Glycoproteins / genetics. Microtubule Proteins / blood. Microtubule Proteins / genetics. Oligonucleotide Array Sequence Analysis / methods. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction. WT1 Proteins / blood. WT1 Proteins / genetics

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  • (PMID = 16638849.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CCL23 protein, human; 0 / Chemokines, CC; 0 / DNA-Binding Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Microtubule Proteins; 0 / PRAME protein, human; 0 / Repressor Proteins; 0 / SPAG6 protein, human; 0 / ST18 protein, human; 0 / WT1 Proteins; 0 / XAGE1A protein, human; 0 / mesothelin
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36. Gesundheit B, Shapira MY, Resnick IB, Amar A, Kristt D, Dray L, Budowski E, Or R: Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation. Am J Hematol; 2009 Mar;84(3):188-90
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  • [Title] Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation.
  • Acute myeloid leukemia (AML) is an extremely aggressive disease with a high relapse rate even after allogeneic hematopoietic stem cell transplantation (HSCT).
  • We report the successful outcome of cell-mediated cytokine-activated immunotherapy in a high-risk pediatric AML patient who relapsed shortly after allogeneic HSCT.
  • Donor lymphocyte infusion along with interferon induced a graft-versus-leukemia effect, presenting as a reversible episode of graft-versus-host disease, which led to stable complete donor chimerism and total eradication of AML for over 24 months, at the time of this report.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Lymphocyte Transfusion. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Child. Graft vs Host Disease. Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Factors / administration & dosage. Immunotherapy. Interferon-alpha / administration & dosage. Male. Recombinant Proteins

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  • (PMID = 19105234.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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37. Gorello P, Brandimarte L, La Starza R, Pierini V, Bury L, Rosati R, Martelli MF, Vandenberghe P, Wlodarska I, Mecucci C: t(3;11)(q12;p15)/NUP98-LOC348801 fusion transcript in acute myeloid leukemia. Haematologica; 2008 Sep;93(9):1398-401
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  • [Title] t(3;11)(q12;p15)/NUP98-LOC348801 fusion transcript in acute myeloid leukemia.
  • In a case of acute myeloid leukemia we report molecular cytogenetic findings of a t(3;11)(q12;p15), characterized as a new NUP98 translocation rearranging with LOC348801 at chromosome 3.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Recombinant Fusion Proteins / genetics. Transcription, Genetic / genetics

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  • (PMID = 18603550.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Recombinant Fusion Proteins; 0 / nuclear pore complex protein 98
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38. Weiss JR, Baer MR, Ambrosone CB, Blanco JG, Hutson A, Ford LA, Moysich KB: Concordance of pharmacogenetic polymorphisms in tumor and germ line DNA in adult patients with acute myeloid leukemia. Cancer Epidemiol Biomarkers Prev; 2007 May;16(5):1038-41
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  • [Title] Concordance of pharmacogenetic polymorphisms in tumor and germ line DNA in adult patients with acute myeloid leukemia.
  • However, genotypes determined in tumor and somatic tissues may differ due to cytogenetic and molecular changes associated with malignant transformation and progression.
  • Discordance between germ line and tumor genotypes may be particularly relevant in leukemia because cytogenetic abnormalities are frequent.
  • We compared genotypes determined in DNA extracted from paired pretreatment bone marrow and buccal samples from 80 adult patients with acute myeloid leukemia (AML).
  • Paired AML and buccal DNA samples were genotyped for polymorphisms (21 single nucleotide polymorphisms and 2 gene deletions) on genes encoding proteins involved in drug metabolism (CYP3A4, CYP2C8, CDA, and GSTP1), oxidative stress mechanisms (CAT, MnSOD, GSTT1, GSTM1, GSTA1, and GPX1), drug transport (MDR1, MRP1, and BCRP), and DNA repair (MGMT, XPD, and XRCC1).
  • Concordance of genotypes was tested by kappa statistics. kappa statistics for paired AML and buccal DNA samples ranged between 0.94 and 1.00, indicating excellent agreement.
  • Agreement was also excellent for genes at AML chromosome deletion and translocation breakpoints, including MDR1 at 7q21.1 and MRP1 at 16p13.1.
  • Based on these data, genotypes derived from archived AML bone marrow samples were not likely to differ from those from genomic DNA, and archived bone marrow samples may be useful for the conduct of retrospective pharmacogenetic studies.
  • [MeSH-major] Bone Marrow Cells / pathology. DNA, Neoplasm / analysis. Leukemia, Myeloid, Acute / genetics. Mouth Mucosa / cytology. Pharmacogenetics. Polymorphism, Genetic


39. Khanim FL, Hayden RE, Birtwistle J, Lodi A, Tiziani S, Davies NJ, Ride JP, Viant MR, Gunther UL, Mountford JC, Schrewe H, Green RM, Murray JA, Drayson MT, Bunce CM: Combined bezafibrate and medroxyprogesterone acetate: potential novel therapy for acute myeloid leukaemia. PLoS One; 2009;4(12):e8147
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  • [Title] Combined bezafibrate and medroxyprogesterone acetate: potential novel therapy for acute myeloid leukaemia.
  • BACKGROUND: The majority of acute myeloid leukaemia (AML) patients are over sixty years of age.
  • In particular, therapies that have anti-leukaemic activity but that, unlike conventional chemotherapy, do not impair normal haemopoiesis.
  • PRINCIPAL FINDINGS: Here we demonstrate the potent anti-leukaemic activity of the combination of the lipid-regulating drug bezafibrate (BEZ) and the sex hormone medroxyprogesterone acetate (MPA) against AML cell lines and primary AML cells.
  • B/M treatment resulted in growth arrest, apoptosis and cell differentiation in both AML cell lines and primary AML cells and these actions were recapitulated by treatment with 15d-PGJ(2).
  • Importantly, the actions of B/M had little effect on the survival of normal adult myeloid progenitors.
  • SIGNIFICANCE: Collectively our data demonstrate that B/M treatment of AML cells elevated ROS and delivered the anti-neoplastic actions of 15d-PGJ(2).
  • These observations provide the mechanistic rationale for the redeployment of B/M in elderly and relapsed AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bezafibrate / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Medroxyprogesterone Acetate / therapeutic use
  • [MeSH-minor] 3-Hydroxysteroid Dehydrogenases / antagonists & inhibitors. Antigens, CD34 / metabolism. Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Cholecalciferol / metabolism. Drug Screening Assays, Antitumor. Glutathione / metabolism. Humans. Hydroxyprostaglandin Dehydrogenases / antagonists & inhibitors. I-kappa B Proteins / metabolism. PPAR gamma / metabolism. Prostaglandin D2 / analogs & derivatives. Prostaglandin D2 / metabolism. Reactive Oxygen Species / metabolism. Vitamin A / metabolism

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  • (PMID = 19997560.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 15-deoxyprostaglandin J2; 0 / Antigens, CD34; 0 / I-kappa B Proteins; 0 / PPAR gamma; 0 / Reactive Oxygen Species; 11103-57-4 / Vitamin A; 1C6V77QF41 / Cholecalciferol; C2QI4IOI2G / Medroxyprogesterone Acetate; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; GAN16C9B8O / Glutathione; RXY07S6CZ2 / Prostaglandin D2; Y9449Q51XH / Bezafibrate
  • [Other-IDs] NLM/ PMC2785482
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40. Szczepanek J, Pogorzala M, Konatkowska B, Juraszewska E, Badowska W, Olejnik I, Kuzmicz M, Stanczak E, Malinowska I, Stefaniak J, Sobol G, Szczepanski T, Czyzewski K, Wysocki M, Styczynski J: Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia. Anticancer Res; 2010 Jun;30(6):2119-24
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  • [Title] Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia.
  • The objective of this study was the analysis of the ex vivo activity of bortezomib in paediatric acute lymphoblastic leukaemia (ALL), in comparison to paediatric acute myeloid leukaemia (AML).
  • A total of 159 patients entered the study, including 106 ALL (including 86 precursor-B-cell ALL, and 20 T-cell ALL) and 53 AML children.
  • Paediatric AML samples were more resistant than paediatric ALL samples to most of the tested drugs, except for cytarabine and thioguanine.
  • With respect to immunophenotype, ex vivo drug resistance in T-cell ALL (T-ALL) was higher for most of the drugs.
  • No differences in drug resistance between T-ALL and common/pre-B-cell-ALL were found for daunorubicin, mitoxantrone and 6-thioguanine.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrazines / therapeutic use

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  • (PMID = 20651360.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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41. Martens JH, Stunnenberg HG: The molecular signature of oncofusion proteins in acute myeloid leukemia. FEBS Lett; 2010 Jun 18;584(12):2662-9
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  • [Title] The molecular signature of oncofusion proteins in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) associated translocations often cause gene fusions that encode oncofusion proteins.
  • Although many of the breakpoints involved in chromosomal translocations have been cloned, in most cases the role of the chimeric proteins in tumorigenesis is not elucidated.
  • Here we will discuss the fusion proteins of the 4 most common translocations associated with AML as well as the common molecular mechanisms that these four and other fusion proteins utilize to transform progenitor cells.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Epigenesis, Genetic. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Receptors, Cytoplasmic and Nuclear / metabolism. Signal Transduction. Transcription, Genetic. Translocation, Genetic

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  • [Copyright] Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20388510.001).
  • [ISSN] 1873-3468
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytoplasmic and Nuclear; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 73
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42. Bradstock K: Chemotherapy for patients with acute myeloid leukemia in first remission. Curr Hematol Malig Rep; 2006 Jun;1(2):108-13
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  • [Title] Chemotherapy for patients with acute myeloid leukemia in first remission.
  • Although the majority of patients with acute myeloid leukemia (AML) achieve a complete remission with induction chemotherapy, most will ultimately relapse.
  • Therefore, the optimal postremission therapy for AML remains to be defined, and further improvements in treatment strategies are required.
  • Autologous and allogeneic stem cell transplantation in first remission are also valid alternatives, but the value of low-dose maintenance treatment seems confined to acute promyelocytic leukemia.
  • Further improvement in the treatment of AML is likely to depend on the development of new strategies, such as molecularly targeted or immune therapies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Clinical Trials as Topic. Combined Modality Therapy. Cytarabine / administration & dosage. Drug Administration Schedule. Hematopoietic Stem Cell Transplantation. Humans. Immunotherapy. Middle Aged. Multicenter Studies as Topic. Remission Induction

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  • (PMID = 20425340.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine
  • [Number-of-references] 31
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43. Norde WJ, Overes IM, Maas F, Fredrix H, Vos JC, Kester MG, van der Voort R, Jedema I, Falkenburg JH, Schattenberg AV, de Witte TM, Dolstra H: Myeloid leukemic progenitor cells can be specifically targeted by minor histocompatibility antigen LRH-1-reactive cytotoxic T cells. Blood; 2009 Mar 5;113(10):2312-23
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  • [Title] Myeloid leukemic progenitor cells can be specifically targeted by minor histocompatibility antigen LRH-1-reactive cytotoxic T cells.
  • CD8(+) T cells recognizing minor histocompatibility antigens (MiHAs) on leukemic stem and progenitor cells play a pivotal role in effective graft-versus-leukemia reactivity after allogeneic stem cell transplantation (SCT).
  • We found that P2X5 is significantly expressed in CD34(+) leukemic subpopulations from chronic myeloid leukemia (CML) and acute myeloid leukemia (AML) patients.
  • Here, we demonstrate that LRH-1-specific CD8(+) T-cell responses are frequently induced in myeloid leukemia patients following donor lymphocyte infusions.
  • Patients with high percentages of circulating LRH-1-specific CD8(+) T cells had no or only mild graft-versus-host disease.
  • Functional analysis showed that LRH-1-specific cytotoxic T lymphocytes (CTLs) isolated from 2 different patients efficiently target LRH-1-positive leukemic CD34(+) progenitor cells from both CML and AML patients, whereas mature CML cells are only marginally lysed due to down-regulation of P2X5.
  • Furthermore, we observed that relative resistance to LRH-1 CTL-mediated cell death due to elevated levels of antiapoptotic XIAP could be overcome by IFN-gamma prestimulation and increased CTL-target ratios.
  • These findings provide a rationale for use of LRH-1 as immunotherapeutic target antigen to treat residual or persisting myeloid malignancies after allogeneic SCT.
  • [MeSH-major] DNA-Binding Proteins / immunology. Leukemia, Myeloid / immunology. Neoplastic Stem Cells / immunology. T-Lymphocytes, Cytotoxic / immunology. Transcription Factors / immunology
  • [MeSH-minor] Adult. Antigens, CD34 / immunology. Antigens, CD34 / metabolism. Female. Flow Cytometry. Gene Expression. Graft vs Host Disease / immunology. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. RNA, Messenger / analysis. Receptors, Purinergic P2 / genetics. Receptors, Purinergic P2X5. Reverse Transcriptase Polymerase Chain Reaction. X-Linked Inhibitor of Apoptosis Protein / biosynthesis. X-Linked Inhibitor of Apoptosis Protein / genetics

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  • (PMID = 19074734.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA-Binding Proteins; 0 / P2RX5 protein, human; 0 / RNA, Messenger; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X5; 0 / Transcription Factors; 0 / X-Linked Inhibitor of Apoptosis Protein
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44. Wu YJ, Li JY, Zhu MQ, Song JH, Zheng WJ: [Application of a four antibody (cMPO/cCD79aalpha/cCD3/CD45) combination to the diagnosis of acute leukemia expressing cross-lineage antigens]. Zhonghua Xue Ye Xue Za Zhi; 2006 Jul;27(7):449-51
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  • [Title] [Application of a four antibody (cMPO/cCD79aalpha/cCD3/CD45) combination to the diagnosis of acute leukemia expressing cross-lineage antigens].
  • OBJECTIVE: To explore the diagnostic value of intracellular antibody combination in acute leukemia (AL) expressing cross-lineage cell-surface antigens.
  • RESULTS: Fifty-four of 269 previously untreated adult AL patients who expressed only one kind of intracellular antigen were diagnosed as cross-lineage AL, the percentage of cross-lineage AL in T cell acute lymphoblastic leukemia (T-ALL), B-ALL and acute myeloid leukemia (AML) was 28.6%, 43.6% and 13.4%, respectively.
  • The positive rate of CD7, CD19, CD5 and CD20 in cross-lineage AML was 65.4%, 15.4%, 11.5%, and 7.7%, respectively.
  • Six (2.3%) patients expressed two-lineage intracellular antigens were diagnosed as biphenotypic AL: 2 of T/B type and 4 B/M (B/myeloid) type.
  • [MeSH-major] Antibodies, Monoclonal. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17147246.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD3; 0 / Antigens, CD79; 0 / Antigens, Surface; EC 3.1.3.48 / Antigens, CD45
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45. Boissel N, Leroy H, Brethon B, Philippe N, de Botton S, Auvrignon A, Raffoux E, Leblanc T, Thomas X, Hermine O, Quesnel B, Baruchel A, Leverger G, Dombret H, Preudhomme C, Acute Leukemia French Association (ALFA), Leucémies Aiguës Myéloblastiques de l'Enfant (LAME) Cooperative Groups: Incidence and prognostic impact of c-Kit, FLT3, and Ras gene mutations in core binding factor acute myeloid leukemia (CBF-AML). Leukemia; 2006 Jun;20(6):965-70
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  • [Title] Incidence and prognostic impact of c-Kit, FLT3, and Ras gene mutations in core binding factor acute myeloid leukemia (CBF-AML).
  • In core binding factors (CBF) acute myeloid leukemia (AML), the disruption of CBFalpha/beta genes impairs normal hematopoietic differentiation and is supposed to cooperate with additional mutations promoting proliferation.
  • The incidence and the prognosis of receptor tyrosine kinase (RTK) c-Kit and FLT3 mutations and Ras mutations were evaluated in 103 pediatric and adult patients with CBF-AML. c-Kit mutations were present in 17% patients. c-Kit exon 8 mutations were more frequent in inv(16) than in t(8;21) subset (20 versus 6%).
  • Only one patient had FLT3-ITD but FLT3-D835 was as frequent as reported in AML population (7%).
  • RTK mutations were associated with a higher white blood cell count (WBC) (36 versus 21 G/L, P=0.05).
  • FLT3 mutations were significantly associated with a shorter EFS and survival (P<0.0001 and P=0.0002) owing to an excess of early events. c-Kit mutations were associated with a shorter EFS and RFS (P=0.002 and P=0.003) in t(8;21) but not inv(16) patients.
  • As previously observed, Ras mutations did not affect prognosis.
  • [MeSH-major] Core Binding Factors / genetics. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins p21(ras) / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Exons. Female. Humans. Infant. Male. Middle Aged. Mutation. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 16598313.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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46. Zebisch A, Staber PB, Delavar A, Bodner C, Hiden K, Fischereder K, Janakiraman M, Linkesch W, Auner HW, Emberger W, Windpassinger C, Schimek MG, Hoefler G, Troppmair J, Sill H: Two transforming C-RAF germ-line mutations identified in patients with therapy-related acute myeloid leukemia. Cancer Res; 2006 Apr 1;66(7):3401-8
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  • [Title] Two transforming C-RAF germ-line mutations identified in patients with therapy-related acute myeloid leukemia.
  • In a screen of 82 acute myeloid leukemia (AML) samples, 45 (55%) showed activated ERK and thus were further analyzed for mutations in B-RAF and C-RAF.
  • Two C-RAF germ-line mutations, S427G and I448V, were identified in patients with therapy-related AML in the absence of alterations in RAS and FLT3.
  • In vitro and in vivo kinase assays revealed significantly increased activity for (S427G)C-RAF but not for (I448V)C-RAF.
  • The involvement of the S427G C-RAF mutation in constitutive activation of ERK was further confirmed through demonstration of activating phosphorylations on C-RAF, MEK, and ERK in neoplastic cells, but not in nonneoplastic cells.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Germ-Line Mutation. Leukemia, Myeloid / genetics. Neoplasms, Second Primary / genetics. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Animals. Apoptosis / genetics. Base Sequence. COS Cells. Cercopithecus aethiops. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation, Leukemic / genetics. Genes, ras. HL-60 Cells. Humans. MAP Kinase Signaling System. Mice. Molecular Sequence Data. NIH 3T3 Cells. Pedigree. Phosphorylation. Proto-Oncogene Proteins B-raf / genetics. Sequence Alignment. fms-Like Tyrosine Kinase 3 / genetics


47. Sanderson RN, Johnson PR, Moorman AV, Roman E, Willett E, Taylor PR, Proctor SJ, Bown N, Ogston S, Bowen DT: Population-based demographic study of karyotypes in 1709 patients with adult acute myeloid leukemia. Leukemia; 2006 Mar;20(3):444-50
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  • [Title] Population-based demographic study of karyotypes in 1709 patients with adult acute myeloid leukemia.
  • Few large demographic studies of acute myeloid leukemia (AML) are derived from population-based registries.
  • Demographic and karyotypic data were provided for AML cases from two regional leukemia registry databases in Scotland and the Northern Region of England.
  • Complex karyotypes not involving chromosomes 5 or 7 represented 30% of all complex karyotypes, occurred in younger patients than those involving chromosomes 5 and 7, and frequently included additional trisomy 8 (26%).
  • [MeSH-major] Leukemia, Myeloid / genetics. Population Surveillance
  • [MeSH-minor] Acute Disease. Adult. Demography. Female. Humans. Male. Registries


48. Mesa RA, Li CY, Ketterling RP, Schroeder GS, Knudson RA, Tefferi A: Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases. Blood; 2005 Feb 1;105(3):973-7
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  • [Title] Leukemic transformation in myelofibrosis with myeloid metaplasia: a single-institution experience with 91 cases.
  • Among 2333 consecutive patients with myelofibrosis with myeloid metaplasia (MMM) seen at our institution, 91 fulfilled the World Health Organization (WHO) criteria for leukemic transformation (LT).
  • All episodes of LT were myeloid in origin (acute myeloid leukemia [AML]) with all French-American-British (FAB) subtypes represented except M3; the most frequent subtypes were M7 (25.4%), M0 (22.4%), and M2 (17.9%).
  • Cytogenetic studies during LT were available in 56 patients and revealed a clonal abnormality in 51 (91%): 30 patients had complex karyotype, 2 had core-binding factor gene lesions, and 18 had abnormalities of chromosome 5 or 7.
  • Twenty-four patients received AML-like induction chemotherapy that resulted in no complete remission: 41% reverted into chronic-phase disease and the incidence of treatment-related mortality was 33%.
  • [MeSH-major] Leukemia / drug therapy. Leukemia / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Myelodysplastic Syndromes / pathology. Primary Myelofibrosis / pathology
  • [MeSH-minor] Adult. Age of Onset. Aged. Aged, 80 and over. Cell Transformation, Neoplastic. Female. Humans. Male. Middle Aged. Reference Values. Treatment Outcome


49. Breems DA, Löwenberg B: Acute myeloid leukemia and the position of autologous stem cell transplantation. Semin Hematol; 2007 Oct;44(4):259-66
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  • [Title] Acute myeloid leukemia and the position of autologous stem cell transplantation.
  • Most adult patients with acute myeloid leukemia (AML) who reach a complete remission (CR) after induction chemotherapy will relapse if they do not receive further therapy.
  • Autologous stem cell transplantation (SCT) represents one of the options of postremission therapy in AML.
  • Meta-analyses of published randomized trials using bone marrow as the source of stem cells show a modest improvement of disease-free survival as compared to nonmyeloablative chemotherapy.
  • Subsequently, the value of autologous SCT in different prognostic subsets of AML is discussed.
  • Autologous mobilized peripheral blood stem cell (PBSC) transplantation offers a much faster hematopoietic recovery and is associated with reduced morbidity and treatment-related mortality.
  • To fully appreciate the role of autologous PBSC transplantation, the results of a recently closed randomized trial must be awaited.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Adult. Combined Modality Therapy. Disease-Free Survival. Evidence-Based Medicine. Hematopoietic Stem Cell Transplantation. Humans. Randomized Controlled Trials as Topic. Risk Assessment / methods. Transplantation, Autologous. Transplantation, Homologous


50. Zeng Z, Sarbassov dos D, Samudio IJ, Yee KW, Munsell MF, Ellen Jackson C, Giles FJ, Sabatini DM, Andreeff M, Konopleva M: Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML. Blood; 2007 Apr 15;109(8):3509-12
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  • [Title] Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML.
  • We investigated the molecular effects of mTOR inhibition by the rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in acute myeloid leukemia (AML) cells.
  • Unexpectedly, RDs not only inhibited the mTOR complex 1 (mTORC1) containing mTOR and raptor with decreased p70S6K, 4EPB1 phosphorylation, and GLUT1 mRNA, but also blocked AKT activation via inhibition of mTORC2 formation.
  • This resulted in suppression of phosphorylation of the direct AKT substrate FKHR and decreased transcription of D-cyclins in AML cells.
  • Our study provides the first evidence that rapamycin derivatives inhibit AKT signaling in primary AML cells both in vitro and in vivo, and supports the therapeutic potential of mTOR inhibition strategies in leukemias.

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  • (PMID = 17179228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 55164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA 49639; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / Cyclin D; 0 / Cyclins; 0 / Glucose Transporter Type 1; 0 / Immunosuppressive Agents; 0 / Protein Kinase Inhibitors; 0 / Proteins; 0 / RICTOR protein, human; 0 / RNA, Messenger; 0 / RPTOR protein, human; 0 / SLC2A1 protein, human; 624KN6GM2T / temsirolimus; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1852241
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51. Jiang J, Zhou J, Shen Y: Acute myeloblastic leukemia with initial manifestations in the central airway. J Thorac Oncol; 2009 Mar;4(3):409-10
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  • [Title] Acute myeloblastic leukemia with initial manifestations in the central airway.
  • [MeSH-major] Airway Obstruction / diagnosis. Carcinoma, Small Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Aged. Biopsy, Needle. Blood Chemical Analysis. Bone Marrow / pathology. Bronchoscopy. Catheterization. Cough / diagnosis. Cough / etiology. Diagnosis, Differential. Disease Progression. Dyspnea / diagnosis. Dyspnea / etiology. Fatal Outcome. Humans. Male. Stents. Tomography, X-Ray Computed. Treatment Refusal

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  • (PMID = 19247088.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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52. Heinzelmann F, Ottinger H, Müller CH, Allgaier S, Faul C, Bamberg M, Belka C: Total-body irradiation--role and indications: results from the German Registry for Stem Cell Transplantation (DRST). Strahlenther Onkol; 2006 Apr;182(4):222-30
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  • [Title] Total-body irradiation--role and indications: results from the German Registry for Stem Cell Transplantation (DRST).
  • BACKGROUND AND PURPOSE: Total-body irradiation (TBI) is a key part of the conditioning regimen before hematopoietic stem cell transplantation (HSCT).
  • In order to determine the relevance of TBI, the status of TBI utilization was analyzed on the basis of a nationwide registry.
  • MATERIAL AND METHODS: 14,371 patients (1998-2002) documented in the German Stem Cell Transplantation Registry (DRST) were analyzed regarding TBI utilization prior to autologous or allogeneic transplantation, underlying disorder, type of donor, stem cell source, and size of the treatment center.
  • RESULTS: For autologous HSCT approximately 10% of the patients (873/8,167) received TBI, with chronic lymphocytic leukemia (CLL, approximately 80%, 171/214) and low-grade non-Hodgkin's lymphoma (l-NHL, approximately 35%, 330/929) being the most important disorders.
  • In the allogeneic setting 50% of the patients (2,399/4,904) received TBI, with acute lymphocytic leukemia (ALL, 85%, 794/930), acute myeloid leukemia (AML, 45%, 662/1,487) and chronic myeloid leukemia (CML, 49%, 561/1,156) being the key indications.
  • The type of donor, stem cell source and center size did not strongly influence the use of TBI.
  • The use of TBI is generally accepted for ALL, whereas approximately half of the patients with CML or AML received TBI.
  • [MeSH-major] Registries. Stem Cell Transplantation. Transplantation Conditioning. Whole-Body Irradiation
  • [MeSH-minor] Acute Disease. Germany. Histocompatibility Testing. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid / therapy. Lymphoma, Non-Hodgkin / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Tissue Donors. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 16622624.001).
  • [ISSN] 0179-7158
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Röntgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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53. Aleskog A, Höglund M, Pettersson J, Hermansson M, Larsson R, Lindhagen E: In vitro activity of the flt3-inhibitor su5614 and standard cytotoxic agents in tumour cells from patients with wild type and mutated flt3 acute myeloid leukaemia. Leuk Res; 2005 Sep;29(9):1079-81
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  • [Title] In vitro activity of the flt3-inhibitor su5614 and standard cytotoxic agents in tumour cells from patients with wild type and mutated flt3 acute myeloid leukaemia.
  • The correlation between drug sensitivity in vitro and the mutation status of the FLT3 receptor gene was evaluated in tumour cells from 17 previously untreated AML patients.
  • Tumour cells with internal tandem duplication (ITD) in the FLT3 receptor gene were significantly more sensitive to the FLT3 inhibitor SU5614 than tumour cells with wild type FLT3.
  • Our results suggest that the FLT3 inhibitor SU5614 may have a therapeutic potential, especially in combination with other cytotoxic agents, in patients with FLT3-ITD positive AML.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Indoles / pharmacology. Leukemia, Myeloid / drug therapy. Proto-Oncogene Proteins / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Humans. Point Mutation. Polymerase Chain Reaction. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3

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  • (PMID = 16038735.001).
  • [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 / Antineoplastic Agents; 0 / Indoles; 0 / Proto-Oncogene Proteins; 0 / SU 5614; 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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54. Johnson KJ, Soler JT, Puumala SE, Ross JA, Spector LG: Parental and infant characteristics and childhood leukemia in Minnesota. BMC Pediatr; 2008;8:7
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  • [Title] Parental and infant characteristics and childhood leukemia in Minnesota.
  • BACKGROUND: Leukemia is the most common childhood cancer.
  • With the exception of Down syndrome, prenatal radiation exposure, and higher birth weight, particularly for acute lymphoid leukemia (ALL), few risk factors have been firmly established.
  • Translocations present in neonatal blood spots and the young age peak of diagnosis suggest that early-life factors are involved in childhood leukemia etiology.
  • METHODS: We investigated the association between birth characteristics and childhood leukemia through linkage of the Minnesota birth and cancer registries using a case-cohort study design.
  • Cases included 560 children with ALL and 87 with acute myeloid leukemia (AML) diagnoses from 28 days to 14 years.
  • RESULTS: Male sex (HR = 1.41, 95% CI 1.16-1.70), white race (HR = 2.32, 95% CI 1.13-4.76), and maternal birth interval > or = 3 years (HR = 1.31, 95% CI 1.01-1.70) increased ALL risk, while maternal age increased AML risk (HR = 1.21/5 year age increase, 95% CI 1.0-1.47).
  • Higher birth weights (>3798 grams) (HRALL = 1.46, 1.08-1.98; HRAML = 1.97, 95% CI 1.07-3.65), and one minute Apgar scores < or = 7 (HRALL = 1.30, 95% CI 1.05-1.61; HRAML = 1.62, 95% CI 1.01-2.60) increased risk for both types of leukemia.
  • Sex was not a significant modifier of the association between ALL and other covariates, with the exception of maternal education.
  • We have also provided data that supports an increased risk for AML following higher birth weights, and demonstrated an association with low Apgar scores.
  • [MeSH-major] Leukemia / epidemiology

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  • (PMID = 18298855.001).
  • [ISSN] 1471-2431
  • [Journal-full-title] BMC pediatrics
  • [ISO-abbreviation] BMC Pediatr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2292161
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55. Li Z, Godinho FJ, Klusmann JH, Garriga-Canut M, Yu C, Orkin SH: Developmental stage-selective effect of somatically mutated leukemogenic transcription factor GATA1. Nat Genet; 2005 Jun;37(6):613-9
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  • Acquired mutations in the hematopoietic transcription factor GATA binding protein-1 (GATA1) are found in megakaryoblasts from nearly all individuals with Down syndrome with transient myeloproliferative disorder (TMD, also called transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M7).
  • These mutations lead to production of a variant GATA1 protein (GATA1s) that is truncated at its N terminus.
  • To understand the biological properties of GATA1s and its relation to DS-AMKL and TMD, we used gene targeting to generate Gata1 alleles that express GATA1s in mice.
  • We show that the dominant action of GATA1s leads to hyperproliferation of a unique, previously unrecognized yolk sac and fetal liver progenitor, which we propose accounts for the transient nature of TMD and the restriction of DS-AMKL to infants.
  • Our observations raise the possibility that the target cells in other leukemias of infancy and early childhood are distinct from those in adult leukemias and underscore the interplay between specific oncoproteins and potential target cells.
  • [MeSH-minor] Adult. Age Factors. Animals. Cell Differentiation. Cells, Cultured. Down Syndrome / genetics. Embryo, Mammalian. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. Gene Targeting. Hematopoiesis / genetics. Humans. Infant. Leukemia, Megakaryoblastic, Acute / genetics. Liver / cytology. Liver / embryology. Megakaryocytes. Mice. Transfection


56. Malaise M, Steinbach D, Corbacioglu S: Clinical implications of c-Kit mutations in acute myelogenous leukemia. Curr Hematol Malig Rep; 2009 Apr;4(2):77-82
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  • [Title] Clinical implications of c-Kit mutations in acute myelogenous leukemia.
  • This finding culminated in a two-class model integrating constitutive activating and maturation arrest-inducing mutations as key elements for the pathogenesis of acute myelogenous leukemia (AML).
  • c-Kit is expressed by myeloblasts in about 60% to 80% of patients, and the most frequently observed activating RTK mutations in AML (next to FLT3) are mutations or internal tandem duplications in c-Kit, with an overall incidence of 17%.
  • The identification of small-molecule tyrosine kinase inhibitors capable of blocking key kinase switches introduced a paradigm change in the treatment of diseases like gastrointestinal stromal tumors and chronic myelogenous leukemia.
  • Despite encouraging preclinical data, it appears that a complex clonal disease like AML will probably benefit from a synergistic approach of targeted drugs used (at least for now) in combination with conventional chemotherapy.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gene Expression Regulation, Leukemic. Humans. Prognosis. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome


57. Garcia-Manero G, Stoltz ML, Ward MR, Kantarjian H, Sharma S: A pilot pharmacokinetic study of oral azacitidine. Leukemia; 2008 Sep;22(9):1680-4
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  • Azacitidine has been shown to have survival benefits in patients with high-risk myelodysplastic syndrome (MDS), and has activity in the treatment of acute myelogenous leukemia (AML).
  • It is administered by subcutaneous (s.c.) or intravenous (i.v.) injection daily at a dose of 75 mg/m(2) for 7 days every 4 weeks.
  • Development of a film-coated formulation has circumvented this difficulty.
  • In a formulation feasibility pilot study, four subjects with solid malignant tumors, AML or MDS received single oral doses of 60 or 80 mg azacitidine.
  • Subjects demonstrated measurable plasma concentrations of azacitidine, allowing bioavailability comparisons to be made to historical pharmacokinetic data for s.c. azacitidine.


58. Busse A, Letsch A, Scheibenbogen C, Nonnenmacher A, Ochsenreither S, Thiel E, Keilholz U: Mutation or loss of Wilms' tumor gene 1 (WT1) are not major reasons for immune escape in patients with AML receiving WT1 peptide vaccination. J Transl Med; 2010 Jan 21;8:5
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  • [Title] Mutation or loss of Wilms' tumor gene 1 (WT1) are not major reasons for immune escape in patients with AML receiving WT1 peptide vaccination.
  • Here, we analyzed 10 HLA-A2 positive patients with acute myeloid leukemia (AML) for loss or mutations of the WT1 epitope or epitope flanking sequences that may abolish proper T cell recognition or epitope presentation.
  • METHODS: All patients had been enrolled in a WT1 peptide phase II vaccination trial (NCT00153582) and ultimately progressed despite induction of a WT1 specific T cell response.
  • RESULTS: Only in one patient, downregulation of WT1 mRNA by 1 log and loss of WT1 detection on protein level at time of disease progression was observed.
  • CONCLUSION: Defects in antigen presentation caused by loss or mutation of WT1 or downregulation of HLA molecules are not the major basis for escape from the immune response induced by WT1 peptide vaccination.
  • [MeSH-major] Cancer Vaccines / immunology. Leukemia, Myeloid, Acute. Tumor Escape. Vaccines, Subunit / immunology. WT1 Proteins / genetics. Wilms Tumor
  • [MeSH-minor] Antigen Presentation / immunology. Clinical Trials, Phase II as Topic. Disease Progression. Epitopes. HLA-A2 Antigen / genetics. HLA-A2 Antigen / immunology. Humans. Mutation. T-Lymphocytes / immunology

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  • (PMID = 20092642.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A2 Antigen; 0 / Vaccines, Subunit; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2844374
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59. Gündogdu MS, Liu H, Metzdorf D, Hildebrand D, Aigner M, Aktories K, Heeg K, Kubatzky KF: The haematopoietic GTPase RhoH modulates IL3 signalling through regulation of STAT activity and IL3 receptor expression. Mol Cancer; 2010;9:225
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  • Its expression is restricted to the haematopoietic lineage, where it serves as a positive regulator for T cell selection and mast cell function and as a negative regulator for growth-related functions in other lineages.
  • RESULTS: Using the murine IL3-dependent cell line BaF3 we investigated the influence of RhoH protein expression levels on IL3-mediated cellular responses.
  • SiRNA-mediated repression of RhoH gene expression led to an increase in proliferation and STAT5 activity which correlated with an increased number of IL3 receptor α chain molecules, also known as CD123, expressed at the cell surface.
  • Interestingly, these findings could be reproduced using human THP-1 cells as a model system for acute myeloid leukaemia, where low RhoH levels are known to be an unfavourable prognostic marker.
  • STAT1 is known to induce apoptosis or cell cycle arrest and we detected an upregulation of cyclin-dependent kinase inhibitors (CDKI) p21Cip1 and p27Kip1 in RhoH overexpressing BaF3 cells.
  • Low RhoH levels on the other hand led to an upregulation of IL3-dependent cell growth, STAT5 activity and an increase of CD123 surface expression, linking RhoH to a CD123/STAT5 phenotype that has been described in AML patients.
  • [MeSH-minor] Animals. Cell Line. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Mice. Up-Regulation

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  • (PMID = 20738848.001).
  • [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 / Cdkn1a protein, mouse; 0 / Cdkn1b protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Interleukin-3; 0 / Receptors, Interleukin-3; 0 / RhoH protein, mouse; 0 / STAT Transcription Factors; 0 / Transcription Factors; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2936343
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60. Boissel N, Nibourel O, Renneville A, Gardin C, Reman O, Contentin N, Bordessoule D, Pautas C, de Revel T, Quesnel B, Huchette P, Philippe N, Geffroy S, Terre C, Thomas X, Castaigne S, Dombret H, Preudhomme C: Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group. J Clin Oncol; 2010 Aug 10;28(23):3717-23
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  • [Title] Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group.
  • PURPOSE: Recently, whole-genome sequencing in acute myeloid leukemia (AML) identified recurrent isocitrate dehydrogenase enzyme isoform (IDH1) mutations (IDH1m), previously reported to be involved in gliomas as well as IDH2 mutations (IDH2m).
  • The prognosis of both IDH1m and IDH2m in AML remains unclear.
  • PATIENTS AND METHODS: The prevalence and the prognostic impact of R132 IDH1 and R172 IDH2 mutations were evaluated in a cohort of 520 adults with AML homogeneously treated in the French Acute Leukemia French Association (ALFA) -9801 and -9802 trials.
  • In patients with CN-AML, IDH1m were associated with NPM1m (P = .008), but exclusive of CEBPAm (P = .03).
  • In CN-AML patients, IDH1m were found in 19% of favorable genotype ([NPM1m or CEBPAm] without fms-related tyrosine kinase 3 [FLT3] internal tandem duplication [ITD]) and were associated with a higher risk of relapse (RR) and a shorter overall survival (OS).
  • Favorable genotype in CN-AML could thus be defined by the association of NPM1m or CEBPAm with neither FLT3-ITD nor IDH1m.
  • In IDH2m CN-AML patients, we observed a higher risk of induction failure, a higher RR and a shorter OS.
  • CONCLUSION: Contrarily to what is reported in gliomas, IDH1m and IDH2m in AML are associated with a poor prognosis.
  • Screening of IDH1m could help to identify high-risk patients within the subset of CN-AML with a favorable genotype.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20625116.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00880243/ NCT00931138
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
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61. Rigamonti F, Beris P, Sanchez-Pareja A, Meyer P, Ashrafpoor G, Zaza S, Passweg J, Chalandon Y: Atypical presentation of acute myeloid leukemia: cardiac myeloid sarcoma. Int J Hematol; 2009 Jun;89(5):693-8
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  • [Title] Atypical presentation of acute myeloid leukemia: cardiac myeloid sarcoma.
  • We present the case of a 52-year-old man with a 2-month history of dyspnea, bilateral pleural effusion and cardiomegaly of rapid onset.
  • Flow cytometry analysis of the blood and immunohistochemistry study of the pleural liquid showed a blast population of CD34+, CD33+, CD13+ and HLA-DR+ cells; a percutaneous cardiac biopsy showed CD34+ cells in the pericardium which led to the diagnosis of extramedullary acute myeloid leukemia (AML).
  • This case illustrates a rare presentation of cardiac extramedullary AML.
  • [MeSH-major] Heart Neoplasms / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Sarcoma, Myeloid / diagnosis


62. Rubant SA, Ludwig RJ, Diehl S, Hardt K, Kaufmann R, Pfeilschifter JM, Boehncke WH: Dimethylfumarate reduces leukocyte rolling in vivo through modulation of adhesion molecule expression. J Invest Dermatol; 2008 Feb;128(2):326-31
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  • [Title] Dimethylfumarate reduces leukocyte rolling in vivo through modulation of adhesion molecule expression.
  • However, the molecular mechanisms of DMF action are not completely understood.
  • Here, we investigate the effects of DMF on lymphocyte adhesion molecule expression in vitro and interactions with endothelial cells in vivo.
  • DMF dose-dependently reduced superantigen-induced expression of CD25, human leukocyte antigen-DR, and cutaneous lymphocyte antigen by 27, 22, and 48% on CD3-positive cells, respectively.
  • DMF led to a significant reduction in binding of human peripheral blood mononuclear cells (PBMCs) to E-selectin (72%), P-selectin (36%), and vascular cell adhesion molecule-1 (33%) in vitro.
  • Intravital microscopy of PBMCs in ear vasculature of wild-type and knockout mice showed that rolling was mainly P-selectin-dependent and could be reduced by 61% through DMF incubation.
  • We provide early evidence that DMF affects adhesion molecule expression on human leukocytes and their rolling behavior in vivo, indicating that DMF directly affects the initial step of leukocyte extravasation.
  • [MeSH-major] Cell Adhesion / drug effects. Cell Adhesion Molecules / metabolism. Fumarates / pharmacology. Immunosuppressive Agents / pharmacology. Leukocyte Rolling / drug effects
  • [MeSH-minor] Animals. Bacterial Toxins / pharmacology. Cells, Cultured. Dimethyl Fumarate. Down-Regulation / drug effects. Down-Regulation / immunology. E-Selectin / genetics. E-Selectin / metabolism. Enterotoxins / pharmacology. Humans. In Vitro Techniques. Leukocytes, Mononuclear / cytology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. P-Selectin / genetics. P-Selectin / metabolism. Solubility. Superantigens / pharmacology. Vascular Cell Adhesion Molecule-1 / genetics. Vascular Cell Adhesion Molecule-1 / metabolism. Venules / cytology

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  • (PMID = 17671516.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Cell Adhesion Molecules; 0 / E-Selectin; 0 / Enterotoxins; 0 / Fumarates; 0 / Immunosuppressive Agents; 0 / P-Selectin; 0 / Superantigens; 0 / Vascular Cell Adhesion Molecule-1; 0 / enterotoxin F, Staphylococcal; FO2303MNI2 / Dimethyl Fumarate
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63. Palomero T, McKenna K, O-Neil J, Galinsky I, Stone R, Suzukawa K, Stiakaki E, Kalmanti M, Fox EA, Caligiuri MA, Aster JC, Look AT, Ferrando AA: Activating mutations in NOTCH1 in acute myeloid leukemia and lineage switch leukemias. Leukemia; 2006 Nov;20(11):1963-6
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  • [Title] Activating mutations in NOTCH1 in acute myeloid leukemia and lineage switch leukemias.
  • Activating mutations in NOTCH1 are found in over 50% of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here, we report the analysis for activating NOTCH1 mutations in a large number of acute myeloid leukemia (AML) primary samples and cell lines.
  • We found activating mutations in NOTCH1 in a single M0 primary AML sample, in three (ML1, ML2 and CTV-1) out of 23 AML cell lines and in the diagnostic (myeloid) and relapsed (T-lymphoid) clones in a patient with lineage switch leukemia.
  • Importantly, the ML1 and ML2 AML cell lines are derived from an AML relapse in a patient initially diagnosed with T-ALL.
  • Overall, these results demonstrate that activating mutations in NOTCH1 are mostly restricted to T-ALL and are rare in AMLs.
  • The presence of NOTCH1 mutations in myeloid and T-lymphoid clones in lineage switch leukemias establishes the common clonal origin of the diagnostic and relapse blast populations and suggests a stem cell origin of NOTCH1 mutations during the molecular pathogenesis of these tumors.
  • [MeSH-major] Cell Lineage / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Receptor, Notch1 / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. Cell Line, Tumor. Gene Deletion. Hematopoietic Stem Cells / pathology. Hematopoietic Stem Cells / physiology. Humans. Point Mutation. Recurrence. T-Lymphocytes / pathology

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  • (PMID = 17008890.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109901; United States / NCI NIH HHS / CA / CA68484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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64. Olsson H, Magnusson S, Bladström A: Lower breast cancer survival in mothers of children with a malignancy: a national study. Br J Cancer; 2008 Jun 3;98(11):1876-8
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  • Those having a child with a childhood malignancy had a significantly worse survival than other women, relative risk (RR)=1.25, 95% CI 1.02-1.55, P<0.04, adjusted for age at diagnosis, year of diagnosis, parity and time since last pregnancy.
  • Childhood sarcomas or acute myeloid leukaemia seemed to be most associated with a worse survival in the mother (RR=1.38 and 1.69, respectively).

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  • (PMID = 18458676.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2410117
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65. Katsumoto T, Yoshida N, Kitabayashi I: Roles of the histone acetyltransferase monocytic leukemia zinc finger protein in normal and malignant hematopoiesis. Cancer Sci; 2008 Aug;99(8):1523-7
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  • [Title] Roles of the histone acetyltransferase monocytic leukemia zinc finger protein in normal and malignant hematopoiesis.
  • Histone-modified enzymes are involved in various cell functions, including proliferation, differentiation, cell death and carcinogenesis.
  • The protein MOZ (monocytic leukemia zinc finger protein) is a Myst (MOZ, Ybf2 (Sas3), Sas2, Tip60)-type histone acetyltranseferase (HAT) that generates fusion genes, such as MOZ-TIF2, MOZ-CBP and MOZ-p300, in acute myeloid leukemia (AML) by chromosomal translocation.
  • Gene targeting in mice has revealed that MOZ is essential for the generation and maintenance of hematopoietic stem cells (HSC) and for the appropriate development of myeloid, erythroid and B-lineage cell progenitors.
  • In AML, MOZ fusion genes lead to repressed differentiation, hyper-proliferation, and self-renewal of myeloid progenitors through deregulation of MOZ-regulated target gene expression.
  • It is therefore necessary to analyze the roles of MOZ and MOZ fusion genes in normal and malignant hematopoiesis to elucidate the mechanisms underlying and develop therapies for MOZ-related AML.
  • [MeSH-major] Gene Fusion. Hematopoiesis / genetics. Histone Acetyltransferases / metabolism. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Animals. Cell Death / genetics. Cell Differentiation / genetics. Cell Proliferation. Gene Expression. Humans. Mice

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  • (PMID = 18754862.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  • [Number-of-references] 59
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66. Zhang J, Harrison JS, Uskokovic M, Danilenko M, Studzinski GP: Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors. Hematol Oncol; 2010 Sep;28(3):124-32
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  • [Title] Silibinin can induce differentiation as well as enhance vitamin D3-induced differentiation of human AML cells ex vivo and regulates the levels of differentiation-related transcription factors.
  • Induction of terminal differentiation is a conceptually attractive approach for the therapy of neoplastic diseases.
  • Although vitamin D derivatives (deltanoids) can induce differentiation of AML cells in vitro, so far deltanoids have not been successfully brought to the clinic, due to the likelihood of life-threatening hypercalcemia.
  • Here, we incubated freshly obtained blood cells from patients with AML with a plant antioxidant (PAOx), silibinin (SIL), alone or together with a deltanoid.
  • Twenty patients with AML (all subtypes except M3) were available for this study, and in 14 (70%), SIL (60 µM) either induced differentiation ex vivo, or enhanced differentiation induced by deltanoids, or both.
  • Interestingly, SIL acting alone induced differentiation only in cases in which chromosome aberrations could not be detected.
  • In eleven samples sufficient material was available for a limited analysis of the underlying events.
  • This suggests that although the presence of SIL may not always be sufficient to induce differentiation, it can serve as a differentiation enabling factor for blasts obtained from a large proportion of patients with AML.
  • Thus, SIL/deltanoid combinations warrant further consideration as preventive/therapeutic regimens in human leukaemia.

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  • [Copyright] © 2009 John Wiley & Sons, Ltd.
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  • (PMID = 19866452.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA044722-19; United States / NCI NIH HHS / CA / R01 CA117942-02; United States / NCI NIH HHS / CA / R01-CA 044722; United States / NCI NIH HHS / CA / R01 CA117942; United States / NCI NIH HHS / CA / CA044722-19; United States / NCI NIH HHS / CA / CA117942-02; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01-CA 117942
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; 0 / Retinoid X Receptor alpha; 0 / Silymarin; 0 / Transcription Factors; 1C6V77QF41 / Cholecalciferol; 4RKY41TBTF / silybin
  • [Other-IDs] NLM/ NIHMS170018; NLM/ PMC2889217
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67. Al-Anazi K, Al-Jasser A: Candidaemia in patients with haematological disorders and stem cell transplant. Libyan J Med; 2006 Nov 21;1(2):140-55
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  • [Title] Candidaemia in patients with haematological disorders and stem cell transplant.
  • The incidence of non-albicans species of Candida has recently increased, especially in patients with malignant haematological disorders receiving fluconazole prophylaxis.
  • Twenty-four episodes were caused by non-albicans species of Candida and only 7 episodes were caused by C.albicans.
  • The most frequent underlying haematological disorders were acute myeloid leukaemia (AML) followed by acute lymphoblastic leukaemia (ALL).
  • The main predisposing factors for the development of candidaemia were: broad spectrum antibiotics, central venous catheters, neutropenia, cytotoxic chemotherapy, coexisting bacterial infections, steroid therapy, relapsing or untreated primary disease and fluconazole prophylaxis.Eight episodes were complicated by chronic disseminated candidiasis.
  • The highest mortality rate was encountered with C.tropicalis infections.Candidaemia is an important cause of mortality and morbidity in patients with malignant haematological disorders and stem cell transplant.
  • The predominance of non-albicans species of Candida especially C.krusei and C.tropicalis is alarming.

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  • (PMID = 21526012.001).
  • [ISSN] 1993-2820
  • [Journal-full-title] The Libyan journal of medicine
  • [ISO-abbreviation] Libyan J Med
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3081354
  • [Keywords] NOTNLM ; Candida / acute lymphoblastic leukaemia / acute myeloid leukaemia / chronic disseminated candidiasis / stem cell transplant
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68. Ullah K, Ahmed P, Raza S, Satti TM, Chaudhry QU, Akhtar F, Kamal MK, Akhtar FM, Khan B: Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi. J Pak Med Assoc; 2007 Sep;57(9):434-9
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  • [Title] Management of acute myeloid leukaemia--5 years experience at Armed Forces Bone Marrow Transplant Centre, Rawalpindi.
  • OBJECTIVE: To evaluate the outcome in denovo AML patients treated with different remission induction and consolidation chemotherapy regimens in our population.
  • METHODS: A retrospective study on acute myeloid leukaemia (AML) patients was carried out at Armed Forces Bone Marrow Transplant Centre Rawalpindi Pakistan between July 2001 and June 2006.
  • During 5 years period 46 patients received treatment for AML at our centre.
  • These 46 patients were categorized into two groups on the basis of type of leukaemia and chemotherapy given.
  • In group-I 40 patients (group Ia: 23 patients of M1-M6, less M3 group Ib: 17 patients of AML M3) received anthracycline and cytarabin based chemotherapy.
  • In group-II, six patients (AML- M3) received all trans retinoic acid (ATRA) based chemotherapy.
  • Survival in AML-M3 patients treated with ATRA based chemotherapy is significantly superior than anthracycline based chemotherapy (66.6% vs. 29.4%).
  • [MeSH-major] Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Military Medicine. Military Personnel. Treatment Outcome. Tretinoin / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Child. Disease Progression. Female. Humans. Male. Middle Aged. Pakistan. Retrospective Studies. Time Factors


69. Elmas SA, Cetin M, Tuncer M, Hiçsönmez G: Myeloprotective effect of short-course high-dose methylprednisolone treatment before consolidation therapy in children with acute myeloblastic leukemia. Am J Hematol; 2005 Sep;80(1):1-5
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  • [Title] Myeloprotective effect of short-course high-dose methylprednisolone treatment before consolidation therapy in children with acute myeloblastic leukemia.
  • In our previous studies, short-course high-dose methylprednisolone (HDMP) has been shown to shorten the chemotherapy-induced neutropenic period by stimulating the CD34(+) hematopoietic progenitor cells in children with acute leukemia.
  • In this study, we investigate the role of short-course HDMP on induction of a myeloprotective effect when administered before consolidation therapy consisting of high-dose cytosine arabinoside and daunorubicin.
  • Thirty-four consecutive newly diagnosed children with acute myeloblastic leukemia (AML) who received 64 courses of consolidation regimen were entered into the study.
  • The control group did not receive HDMP (group B).
  • There were no differences in the white blood cell (WBC) and absolute neutrophil counts (ANC) between group A (at day -4) and group B (at day 0) at the beginning of the study (medians: 3 x 10(9)/L vs. 3.2 x 10(9)/L and 1.5 x 10(9)/L vs. 1.7 x 10(9)/L, respectively).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glucocorticoids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Methylprednisolone / therapeutic use

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138333.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; X4W7ZR7023 / Methylprednisolone
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70. Oyekunle AA, Kröger N, Zabelina T, Ayuk F, Schieder H, Renges H, Fehse N, Waschke O, Fehse B, Kabisch H, Zander AR: Allogeneic stem-cell transplantation in patients with refractory acute leukemia: a long-term follow-up. Bone Marrow Transplant; 2006 Jan;37(1):45-50
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  • [Title] Allogeneic stem-cell transplantation in patients with refractory acute leukemia: a long-term follow-up.
  • We examined retrospectively 44 patients with refractory acute leukemia (acute myeloid leukemia (AML)/acute lymphoblastic leukemia=25/19) who underwent allogeneic transplantation at our center between 11/1990 and 04/2004.
  • All patients had graft-versus-host disease (GVHD) prophylaxis with cyclosporin and methotrexate.
  • Severe acute-GVHD and chronic-GVHD appeared in eight and 14 patients, respectively.
  • We conclude that patients with refractory leukemia can benefit from allogeneic BMT, especially with < or =20% marrow blast.
  • [MeSH-major] Blast Crisis / therapy. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Busulfan / administration & dosage. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Retrospective Studies. Transplantation, Homologous. Whole-Body Irradiation / methods

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  • (PMID = 16258531.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloablative Agonists; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan
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71. Stone R, Sekeres M, Garcia-Manero G: Evolving strategies in the treatment of MDS and AML. Clin Adv Hematol Oncol; 2009 Aug;7(8):1-14; quiz 2 p following 14
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  • [Title] Evolving strategies in the treatment of MDS and AML.
  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder characterized by a hyperproliferative bone marrow, cellular dysplasia, and ineffective hematopoiesis.
  • This heterogeneous malignancy is composed of several subtypes, the classification of which has evolved over several years.
  • The treatment of MDS involves improving patient survival and quality of life while decreasing the likelihood of progression to acute myelogenous leukemia (AML).
  • In addition to supportive care with transfusions and hematopoietic growth factors as well as stem cell transplantation, three chemotherapeutic agents have been approved to treat MDS--lenalidomide, azacitidine, and decitabine.
  • In addition, multiple agents and novel combinations are currently in development to treat both MDS AML.
  • Several clinical studies which have investigated these therapeutic approaches, as well as the incorporation of new tools used in the diagnosis of MDS, have been published since the 2008 American Society of Hematology (ASH) Annual Meeting and Exposition, and are discussed here.
  • [MeSH-major] Education, Medical, Continuing. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


72. Kügler M, Stein C, Kellner C, Mentz K, Saul D, Schwenkert M, Schubert I, Singer H, Oduncu F, Stockmeyer B, Mackensen A, Fey GH: A recombinant trispecific single-chain Fv derivative directed against CD123 and CD33 mediates effective elimination of acute myeloid leukaemia cells by dual targeting. Br J Haematol; 2010 Sep;150(5):574-86
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  • [Title] A recombinant trispecific single-chain Fv derivative directed against CD123 and CD33 mediates effective elimination of acute myeloid leukaemia cells by dual targeting.
  • Two trivalent constructs consisting of single-chain Fv antibody fragments (scFvs) specific for the interleukin-3 receptor alpha chain (CD123), CD33 and the Fcgamma-receptor III (CD16) were designed and characterized for the elimination of acute myeloid leukaemia (AML) cells.
  • Both constructs induced potent antibody-dependent cellular cytotoxicity (ADCC) of two different AML-derived CD33- and CD123 double-positive cell lines in the low picomolar range using isolated mononuclear cells (MNCs) as effector cells.
  • In these experiments the dual targeting molecule produced significantly stronger lysis than the mono targeting agent.
  • In addition, the sctbs showed a high potency in mediating ADCC of primary leukaemia cells isolated from peripheral blood or bone marrow of seven AML patients.
  • Hence, these novel molecules displayed potent anti-leukaemic effects against AML cells in vitro and represent attractive candidates for further preclinical development.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Interleukin-3 Receptor alpha Subunit / immunology. Leukemia, Myeloid, Acute / immunology. Single-Chain Antibodies / immunology
  • [MeSH-minor] Antibody-Dependent Cell Cytotoxicity / immunology. GPI-Linked Proteins. Humans. Immunoglobulin Fragments / immunology. Killer Cells, Natural / immunology. Receptors, IgG / immunology. Recombinant Proteins / immunology. Sialic Acid Binding Ig-like Lectin 3. Tumor Cells, Cultured

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  • (PMID = 20636437.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / IL3RA protein, human; 0 / Immunoglobulin Fragments; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, IgG; 0 / Recombinant Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Single-Chain Antibodies; 0 / immunoglobulin Fv
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73. Imahashi N, Inamoto Y, Seto A, Watanabe K, Nishiwaki S, Yanagisawa M, Shinba M, Yasuda T, Kuwatsuka Y, Atsuta Y, Kodera Y, Miyamura K: Impact on relapse of corticosteroid therapy after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia. Clin Transplant; 2010 Nov-Dec;24(6):772-7
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  • [Title] Impact on relapse of corticosteroid therapy after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia.
  • Corticosteroids are often used following allogeneic hematopoietic stem cell transplantation (HSCT) to control complications such as graft-versus-host disease (GVHD).
  • However, there is some concern that corticosteroids may suppress the graft-versus-leukemia effect and increase leukemia relapse.
  • To evaluate the effect of corticosteroids on relapse, we analyzed 112 adult patients who received their first allogeneic HSCT for acute myeloid leukemia at our institution between 1997 and 2007.
  • In multivariate analysis, with corticosteroid administration entered as a time-dependent covariate, corticosteroid administration was not a risk factor for relapse (p = 1.00, hazard ratio [HR] 1.00, 95% confidence interval [CI] 0.53-1.88), but it was associated with higher non-relapse mortality (NRM) (p < 0.001, HR 55.5, 95% CI 7.42-416) and lower overall survival (p < 0.001, HR 2.68, 95% CI 1.56-4.61).
  • [MeSH-major] Glucocorticoids / therapeutic use. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Neoplasm Recurrence, Local


74. Corso A, Varettoni M, Mangiacavalli S, Zappasodi P, Klersy C, Rusconi C, Colucci E, Lorenzi A, Troletti D, Consensi E, Lazzarino M: Bone marrow CD34+ cell count is predictive for adequate peripheral progenitor cell collection. Leuk Res; 2005 Feb;29(2):159-63
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  • [Title] Bone marrow CD34+ cell count is predictive for adequate peripheral progenitor cell collection.
  • We studied 90 patients with multiple myeloma (MM) (41 patients), non-Hodgkin's lymphoma (NHL) (25 patients) or acute myeloid leukaemia (AML) (24 patients), mobilised with chemotherapy and growth factor.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Blood Cell Count. Bone Marrow Cells / cytology. Hematopoietic Stem Cell Mobilization / methods. Hematopoietic Stem Cells / cytology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Female. Filgrastim. Granulocyte Colony-Stimulating Factor / adverse effects. Granulocyte Colony-Stimulating Factor / pharmacology. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / drug therapy. Lymphoma, Non-Hodgkin / blood. Lymphoma, Non-Hodgkin / drug therapy. Male. Middle Aged. Multiple Myeloma / blood. Multiple Myeloma / drug therapy. Multivariate Analysis. Predictive Value of Tests. Recombinant Proteins

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  • (PMID = 15607364.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; PVI5M0M1GW / Filgrastim
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75. Zhao J, Yin YM, Zhao YL, Sun Y, Wang JB, Zhong J, Zhang X, Fei XH, Shan FX, Liu HX, Wang T, Wang H, Tong CR, Wu T, Lu DP: [Clinical and molecular biologic characteristics of 36 cases of leukemia with 11q23/mll]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1381-5
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  • [Title] [Clinical and molecular biologic characteristics of 36 cases of leukemia with 11q23/mll].
  • This study was aimed to analyze the clinical and cytogenetic characteristics of acute leukemia with 11q23/mll rearrangement and explore the reasonable therapeutic principles.
  • Characteristics in general situation, morphology, immunology, molecular biology, cytogenetics, treatment and overall survival of 36 cases of acute leukemias with mll gene rearrangement were studied and analyzed.
  • The results showed that 36 cases with mll gene rearrangement were found positive (7.2%) in 494 patients with acute leukemia.
  • Among the 36 cases of mll rearrangement positive, 32 cases were diagnosed as acute myeloid leukemia (AML) with myeloid antigen expression, of which 5 cases expressed lymphoblastic differentiation antigen; 4 cases were classified as B-lineage acute lymphoblastic leukemia (ALL), of which non-lineage myeloid expression pattern were found in 3 cases.
  • Of the responded patients, 10 cases relapsed within 6 months, with a recurrence rate of 40%; 9 cases received hematopoietic stem cell transplantation (HSCT), 7 cases of which survived after transplantation.
  • It is concluded that acute leukemia patients with mll gene rearrangement show poor response to chemotherapy, high recurrence rate and poor prognosis.
  • Hematopoietic stem cell transplantation may be a reasonable treatment principle to improve these patients' survival situation.

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  • (PMID = 21176334.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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76. Lengfelder E, Saussele S, Weisser A, Büchner T, Hehlmann R: Treatment concepts of acute promyelocytic leukemia. Crit Rev Oncol Hematol; 2005 Nov;56(2):261-74
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  • [Title] Treatment concepts of acute promyelocytic leukemia.
  • In the past, acute promyelocytic leukemia (APL) was associated with a high risk of early mortality resulting from severe coagulopathy, frequently inducing fatal cerebral hemorrhage.
  • With the introduction of the differentiating agent all-trans retinioc acid (ATRA) APL has changed to the best curable subtype of acute myeloid leukemia (AML).
  • PML/RARalpha, the molecular fusion transcript of the specific translocation t(15;17) represents not only the target for ATRA but also permits a precise diagnosis and provides a marker for the identification of minimal residual or recurrent disease (MRD).
  • Currently, arsenic compounds and transplantation procedures seem to be the most promising options in relapsed disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / therapy. Stem Cell Transplantation

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  • (PMID = 16236522.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 121
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77. Creutzig U, Zimmermann M, Ritter J, Reinhardt D, Hermann J, Henze G, Jürgens H, Kabisch H, Reiter A, Riehm H, Gadner H, Schellong G: Treatment strategies and long-term results in paediatric patients treated in four consecutive AML-BFM trials. Leukemia; 2005 Dec;19(12):2030-42
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  • [Title] Treatment strategies and long-term results in paediatric patients treated in four consecutive AML-BFM trials.
  • A total of 1111 children with acute myeloblastic leukaemia (AML) were treated in four consecutive Berlin-Frankfurt-Münster (BFM) studies from 1978 to 1998.
  • The first cooperative trial AML-BFM 78 established intensive chemotherapy with seven drugs, CNS irradiation and 2-year maintenance, achieving a long-term survival (overall survival (OS)) of 40%.
  • Induction intensification in AML-BFM 83 resulted in significant improvement of disease-free survival (DFS).
  • In AML-BFM 87, the benefit of CNS irradiation in preventing CNS/systemic relapses was demonstrated.
  • In AML-BFM 93, the introduction of idarubicin during first induction followed by intensification with HAM increased the 5-year EFS, DFS and OS to 50+/-2, 61+/-3 and 57+/-2%, respectively.
  • Stem cell transplantation (SCT), as applied in high-risk patients with a matched related donor, did not significantly improve the outcome compared to chemotherapy alone.
  • The AML-BFM studies performed in three European countries with >70 cooperating centres have significantly improved the outcome in AML children; nevertheless, increasing experience with these intensive treatment regimens is of fundamental importance to reduce fatal complications.
  • [MeSH-major] Antineoplastic Protocols / standards. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cranial Irradiation. Dose-Response Relationship, Drug. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Hemorrhage / etiology. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Risk Assessment. Secondary Prevention. Treatment Outcome

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  • (PMID = 16304570.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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78. Hijiya N, Metzger ML, Pounds S, Schmidt JE, Razzouk BI, Rubnitz JE, Howard SC, Nunez CA, Pui CH, Ribeiro RC: Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):63-9
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  • [Title] Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia.
  • BACKGROUND: Life-threatening pulmonary complications that coincide with cell lysis during early chemotherapy and that mimic systemic inflammatory response syndrome (SIRS) have been reported in patients with acute myeloid leukemia (AML).
  • METHODS: We reviewed the records of patients with de novo AML, excluding M3 and Down syndrome, treated at our institution between 1991 and 2002 to determine the prevalence of severe SIRS with grade 3/4 pulmonary complications and to identify AML subtypes associated with severe SIRS.
  • To examine the role of cell lysis, we compared leukocyte reduction in AML subtypes affected by severe SIRS with that in unaffected subtypes.
  • Severe SIRS was significantly more common in myelomonocytic or monocytic AML (M4/M4eo/M5) than in other subtypes (P = 0.010) and significantly more common in M4eo than in M4/M5 (P = 0.008).
  • CONCLUSIONS: Patients with M4/M4eo/M5 AML, especially M4eo, experience life-threatening cardiopulmonary complications of tumor lysis that meet the criteria for severe SIRS.
  • This observation may reflect more rapid cell reduction and the unique biology of this subtype.
  • [MeSH-major] Cell Death. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / drug therapy. Systemic Inflammatory Response Syndrome / etiology

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368547.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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79. Cushing T, Clericuzio CL, Wilson CS, Taub JW, Ge Y, Reichard KK, Winter SS: Risk for leukemia in infants without Down syndrome who have transient myeloproliferative disorder. J Pediatr; 2006 May;148(5):687-9
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  • [Title] Risk for leukemia in infants without Down syndrome who have transient myeloproliferative disorder.
  • Transient myeloproliferative disorder (TMD) occurs in 10% of infants with Down syndrome (DS).
  • Down syndrome infants with resolved TMD may later develop acute megakaryocytic leukemia (AMKL).
  • In these patients, AMKL is associated with somatic mutations in the X-linked transcription factor gene, GATA1.
  • AMKL also has been described after TMD in children without DS.
  • We report on a non-DS child identified with trisomy 21 mosaicism and a GATA1 mutation in the original blast cells who has been followed for 2 years without exhibiting AMKL.
  • Currently, the risk for such infants developing acute leukemia is uncertain.
  • [MeSH-major] GATA1 Transcription Factor / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Myeloproliferative Disorders / genetics

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  • [CommentIn] J Pediatr. 2007 Mar;150(3):e34 [17307526.001]
  • (PMID = 16737888.001).
  • [ISSN] 0022-3476
  • [Journal-full-title] The Journal of pediatrics
  • [ISO-abbreviation] J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor
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80. Balasooriya BL, Fonseka HF, Williams S, Premawardhena A: Oro-genital ulcers with a positive pathergy test in acute myeloid leukaemia. Ceylon Med J; 2009 Dec;54(4):131-2
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  • [Title] Oro-genital ulcers with a positive pathergy test in acute myeloid leukaemia.
  • [MeSH-major] Behcet Syndrome / diagnosis. Genital Diseases, Female / immunology. Leukemia, Myeloid, Acute / immunology. Oral Ulcer / immunology. Ulcer / immunology
  • [MeSH-minor] Adolescent. Diagnosis, Differential. Erythema Nodosum / diagnosis. Erythema Nodosum / immunology. Female. Humans

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  • (PMID = 20052857.001).
  • [ISSN] 0009-0875
  • [Journal-full-title] The Ceylon medical journal
  • [ISO-abbreviation] Ceylon Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sri Lanka
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81. Fisher BT, Zaoutis TE, Leckerman KH, Localio R, Aplenc R: Risk factors for renal failure in pediatric patients with acute myeloid leukemia: a retrospective cohort study. Pediatr Blood Cancer; 2010 Oct;55(4):655-61
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  • [Title] Risk factors for renal failure in pediatric patients with acute myeloid leukemia: a retrospective cohort study.
  • BACKGROUND: In children receiving treatment for acute myeloid leukemia (AML) there is often concern for the development of acute renal failure (ARF).
  • This study aims to evaluate the rate of ARF in AML patients and to delineate the impact of age, race, various co-morbid conditions and antimicrobial agents on the development of ARF.
  • METHODS: A cohort of newly diagnosed AML patients from children's hospitals across the United States was identified using the Pediatric Health Information Systems database.
  • Information regarding demographics, discharge diagnoses, pharmaceutical exposures, and hospital resource utilization were collected for each hospitalization for up to 1 year from AML diagnosis.
  • RESULTS: Within 1 year of AML diagnosis, 135 (16.2%) patients were diagnosed with ARF.
  • CONCLUSION: ARF is a relatively common problem in children with AML.
  • Empiric therapy with potentially nephrotoxic agents did not increase the risk of nephrotoxicity.
  • [MeSH-major] Acute Kidney Injury / etiology. Leukemia, Myeloid, Acute / complications

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
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  • (PMID = 20533519.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA133881
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS550157; NLM/ PMC3909928
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82. Akel S, Bertolette D, Petrow-Sadowski C, Ruscetti FW: Levels of Smad7 regulate Smad and mitogen activated kinases (MAPKs) signaling and controls erythroid and megakaryocytic differentiation of erythroleukemia cells. Platelets; 2007 Dec;18(8):566-78
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  • [Title] Levels of Smad7 regulate Smad and mitogen activated kinases (MAPKs) signaling and controls erythroid and megakaryocytic differentiation of erythroleukemia cells.
  • Smad and MAPK signaling cascades are involved in erythroid and megakaryocytic differentiation.
  • By modulating Smad7 expression, we attempted to delineate the relevance of Smad7 during erythro-megakaryocytic (E/M) differentiation of human erythroleukemia cells.
  • Smad7 transcripts were detected at low levels in different erythroleukemia cell lines (TF-1, HEL and K562).
  • High levels of Smad7 also interfered with hydroxyurea- and butyrate-, but not hemin-induced erythroid differentiation.
  • We showed here that: (a) low levels of endogenous Smad7 in erythroleukemia cells are physiologically relevant, and (b) high levels of Smad7 interferes with TGF-beta/activin-induced Smad/MAPK signaling and erythro-differentiation and promotes megakaryocytic differentiation, possibly by blocking autocrine TGF-beta.
  • [MeSH-major] Cell Differentiation. Erythroid Cells / cytology. Leukemia, Erythroblastic, Acute / pathology. Megakaryocytes / cytology. Signal Transduction. Smad7 Protein / analysis

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  • (PMID = 18041647.001).
  • [ISSN] 0953-7104
  • [Journal-full-title] Platelets
  • [ISO-abbreviation] Platelets
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CO / N01-CO-56000
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Smad Proteins; 0 / Smad7 Protein; 0 / Transforming Growth Factor beta; 104625-48-1 / Activins
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83. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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  • [Title] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • FOXM1 is an important cell cycle regulator and regulates cell proliferation.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In this study, we investigated the cellular and molecular function of FOXM1 in AML cells.
  • The FOXM1 messenger RNA (mRNA) expressed in AML cell lines was predominantly the FOXM1B isoform, and its levels were significantly higher than in normal high aldehyde dehydrogenase activity (ALDH(hi)) cells.
  • Reduction of FOXM1 expression in AML cells inhibited cell proliferation compared with control cells, through induction of G(2)/M cell cycle arrest, a decrease in the protein expression of Aurora kinase B, Survivin, Cyclin B1, S-phase kinase-associated protein 2 and Cdc25B and an increase in the protein expression of p21(Cip1) and p27(Kip1).
  • FOXM1 messenger RNA (mRNA) was overexpressed in all 127 AML clinical specimens tested (n = 21, 56, 32 and 18 for M1, M2, M4 and M5 subtypes, respectively).
  • Compared with normal ALDH(hi) cells, FOXM1 gene expression was 1.65- to 2.26-fold higher in AML cells.
  • Moreover, the FOXM1 protein was more strongly expressed in AML-derived ALDH(hi) cells compared with normal ALDH(hi) cells.
  • In addition, depletion of FOXM1 reduced colony formation of AML-derived ALDH(hi) cells due to inhibition of Cdc25B and Cyclin B1 expression.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • Thus, inhibition of FOXM1 expression represents an attractive target for AML therapy.
  • [MeSH-major] Cell Cycle. Cell Cycle Proteins / metabolism. Cell Proliferation. Forkhead Transcription Factors / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Aged. Aldehyde Dehydrogenase / genetics. Aldehyde Dehydrogenase / metabolism. Apoptosis. Aurora Kinase B. Aurora Kinases. Blotting, Western. Cells, Cultured. Cyclin B1 / genetics. Cyclin B1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Fluorescent Antibody Technique. Humans. Inhibitor of Apoptosis Proteins. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocytes / metabolism. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Middle Aged. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / metabolism

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  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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84. Goulden N, Virgo P, Grimwade D: Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now. Br J Haematol; 2006 Aug;134(3):273-82
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  • [Title] Minimal residual disease directed therapy for childhood acute myeloid leukaemia: the time is now.
  • The continued improvement in the prognosis of childhood acute myeloid leukaemia (AML) has been paralleled by the use of increasingly intensive therapy.
  • This annotation proposes that the introduction of protocols based on the measurement of minimal residual disease (MRD) holds the key to progression from an era of 'cure at all costs' to a more individualised approach.
  • The article illustrates which children may benefit most from MRD analysis in AML and explores practical issues that should be addressed in the design of clinical trials.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Neoplasm, Residual / drug therapy. Patient Selection. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Child. Clinical Trials as Topic. Drug Costs. Humans. Prognosis. Research Design. Risk Assessment. Salvage Therapy. Stem Cell Transplantation

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  • (PMID = 16848770.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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85. Nishida S, Hosen N, Shirakata T, Kanato K, Yanagihara M, Nakatsuka S, Hoshida Y, Nakazawa T, Harada Y, Tatsumi N, Tsuboi A, Kawakami M, Oka Y, Oji Y, Aozasa K, Kawase I, Sugiyama H: AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1. Blood; 2006 Apr 15;107(8):3303-12
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  • [Title] AML1-ETO rapidly induces acute myeloblastic leukemia in cooperation with the Wilms tumor gene, WT1.
  • AML1-ETO, a chimeric gene frequently detected in acute myelogenous leukemia (AML), inhibits the differentiation of myeloid progenitors by suppressing genes associated with myeloid differentiation and increases the replating ability of clonogenic myeloid progenitors.
  • However, AML1-ETO alone cannot induce AML and thus additional genetic events are required for the onset of AML.
  • The Wilms tumor gene (WT1), which has been identified as the gene responsible for Wilms tumor, is expressed at high levels in almost all human leukemias.
  • AML1-ETO-transduced bone marrow (BM) cells from WT1-Tg mice exhibited inhibition of myeloid differentiation at more immature stages and higher in vitro colony-forming ability compared with AML1-ETO-transduced BM cells from wild-type mice.
  • Most importantly, all of the mice that received a transplant of AML1-ETO-transduced BM cells from the WT1-Tg mice rapidly developed AML.
  • [MeSH-major] Cell Differentiation / genetics. Cell Transformation, Neoplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid Progenitor Cells / metabolism. Oncogene Proteins, Fusion / genetics. WT1 Proteins / genetics

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  • (PMID = 16380455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / WT1 Proteins
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86. Yoshida T, Gan Q, Shang Y, Owens GK: Platelet-derived growth factor-BB represses smooth muscle cell marker genes via changes in binding of MKL factors and histone deacetylases to their promoters. Am J Physiol Cell Physiol; 2007 Feb;292(2):C886-95
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  • [Title] Platelet-derived growth factor-BB represses smooth muscle cell marker genes via changes in binding of MKL factors and histone deacetylases to their promoters.
  • A hallmark of smooth muscle cell (SMC) phenotypic switching is suppression of SMC marker gene expression.
  • 1) MKL factors contribute to the expression of SMC marker genes in cultured SMCs; and 2) platelet-derived growth factor-BB (PDGF-BB)-induced repression of SMC marker genes is mediated by suppression of MKL factors.
  • Results of gain- and loss-of-function experiments showed that MKL factors regulated the expression of single and multiple CArG [CC(AT-rich)(6)GG]-containing SMC marker genes, such as smooth muscle (SM) alpha-actin and telokin, but not CArG-independent SMC marker genes such as smoothelin-B.
  • However, of interest, PDGF-BB induced the dissociation of MKL factors from the CArG-containing region of SMC marker genes, as determined by chromatin immunoprecipitation assays.
  • This dissociation was caused by the competition between MKL factors and phosphorylated Elk-1 at early time points, but subsequently by the reduction in acetylated histone H4 levels at these promoter regions mediated by histone deacetylases, HDAC2, HDAC4, and HDAC5.
  • Results provide novel evidence that PDGF-BB-induced repression of SMC marker genes is mediated through combinatorial mechanisms, including downregulation of myocardin expression and inhibition of the association of myocardin/MKL factors with CArG-containing SMC marker gene promoters.

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  • (PMID = 16987998.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / P01-HL-19242; United States / NHLBI NIH HHS / HL / R01-HL-38854; United States / NHLBI NIH HHS / HL / R37-HL-57353
  • [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 / Actins; 0 / Biomarkers; 0 / Cytoskeletal Proteins; 0 / Muscle Proteins; 0 / Peptide Fragments; 0 / Peptides; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / RNA, Small Interfering; 0 / Smtn protein, rat; 0 / Transcription Factors; 0 / ets-Domain Protein Elk-1; 0 / platelet-derived growth factor BB; 0 / telokin; EC 2.7.11.18 / Myosin-Light-Chain Kinase; EC 3.5.1.98 / Histone Deacetylases
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87. Faderl S, Gandhi V, O'Brien S, Bonate P, Cortes J, Estey E, Beran M, Wierda W, Garcia-Manero G, Ferrajoli A, Estrov Z, Giles FJ, Du M, Kwari M, Keating M, Plunkett W, Kantarjian H: Results of a phase 1-2 study of clofarabine in combination with cytarabine (ara-C) in relapsed and refractory acute leukemias. Blood; 2005 Feb 1;105(3):940-7
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  • [Title] Results of a phase 1-2 study of clofarabine in combination with cytarabine (ara-C) in relapsed and refractory acute leukemias.
  • Clofarabine (2-chloro-2'-fluoro-deoxy-9-beta-D-arabinofuranosyladenine) is a second-generation nucleoside analog with activity in acute leukemias.
  • We conducted a phase 1-2 study of clofarabine plus ara-C in 32 patients with relapsed acute leukemia (25 acute myeloid leukemia [AML], 2 acute lymphoblastic leukemia [ALL]), 4 high-risk myelodysplastic syndrome (MDS), and 1 blast-phase chronic myeloid leukemia (CML).(1) Clofarabine was given as a 1-hour intravenous infusion for 5 days (days 2 through 6) followed 4 hours later by ara-C at 1 g/m(2) per day as a 2-hour intravenous infusion for 5 days (days 1 through 5).
  • Adverse events were mainly less than or equal to grade 2, including transient liver test abnormalities, nausea/vomiting, diarrhea, skin rashes, mucositis, and palmoplantar erythrodysesthesias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adenine Nucleotides. Aged. Arabinonucleosides / administration & dosage. Arabinonucleosides / therapeutic use. Arabinonucleosides / toxicity. Cytarabine / administration & dosage. Cytarabine / therapeutic use. Cytarabine / toxicity. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Karyotyping. Male. Middle Aged. Recurrence. Treatment Outcome

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  • (PMID = 15486072.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101354; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / CA57629
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 04079A1RDZ / Cytarabine; 762RDY0Y2H / clofarabine
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88. Scholl S, Theuer C, Scheble V, Kunert C, Heller A, Mügge LO, Fricke HJ, Höffken K, Wedding U: Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia. Eur J Haematol; 2008 Mar;80(3):208-15
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  • [Title] Clinical impact of nucleophosmin mutations and Flt3 internal tandem duplications in patients older than 60 yr with acute myeloid leukaemia.
  • BACKGROUND: Nucleophosmin (NPM1) and Flt3 internal tandem duplications (Flt3-ITD mutations) represent the most frequent molecular aberrations in patients with acute myeloid leukemia (AML).
  • While NPM1 mutations are associated with favourable prognosis in younger AML patients, Flt3-ITD mutations reflect an unfavourable prognostic factor in these patients.
  • So far, especially NPM1 mutations have not yet been evaluated exclusively in older patients.
  • PATIENTS AND METHODS: We retrospectively analysed the prevalence of NPM1 and Flt3-ITD mutations and its association with complete remission (CR), and survival in 99 elderly patients (median age 71 yr, range 60-85 yr) newly diagnosed for AML.
  • Interestingly, there is no significant difference in overall survival between group 1 and group 2 (Log-rank test P = 0.22, median 440 d vs. 1125 d).
  • In contrast, patients carrying a Flt3-ITD mutation had a significant worse overall survival compared to wildtype patients (P = 0.03, median 210 d for group 3 + 4 vs. 634 d for group 1 + 2) while no difference of CR rate could be observed (42.8% vs. 48.9%, P = 0.91).
  • CONCLUSION: As elderly but medically fit patients with AML carrying a NPM1 mutation have a high CR rate, age itself should not be a barrier for induction treatment.
  • However, new therapeutic concepts of postremission therapy (e.g. allogeneic stem cell transplantation after dose-reduced conditioning) should be considered for these patients in first CR.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Cohort Studies. Disease-Free Survival. Female. Gene Frequency. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies

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  • (PMID = 18081718.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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89. Marcucci G, Mrózek K, Bloomfield CD: Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics. Curr Opin Hematol; 2005 Jan;12(1):68-75
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  • [Title] Molecular heterogeneity and prognostic biomarkers in adults with acute myeloid leukemia and normal cytogenetics.
  • PURPOSE OF REVIEW: Patients with acute myeloid leukemia (AML) and normal karyotype constitute the single largest cytogenetic group of AML, estimated to account for 45% of adults with de novo AML.
  • RECENT FINDINGS: Four prognostic biomarkers-the internal tandem duplication and point mutations in the FLT3 gene, partial tandem duplication of the MLL gene, mutations of the CEBPA gene, and overexpression of the BAALC gene-have been found to predict outcome in patients with AML and normal cytogenetics.
  • In addition, one study using gene expression profiling identified two subgroups of AML patients with a normal karyotype whose survival differs significantly.
  • SUMMARY: Considerable progress has been made in molecular characterization of AML patients with normal cytogenetics.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 15604894.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30CA16058
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 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
  • [Number-of-references] 65
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90. Vundinti BR, Kerketta L, Madkaikar M, Jijina F, Ghosh K: Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22. Indian J Cancer; 2008 Jan-Mar;45(1):30-2
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  • [Title] Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22.
  • The t(8;21)(q22;q22) is one of the most frequent chromosomal abnormality associated with acute myeloid leukemia (AML) M2 sub type.
  • We report a case of AML-M2 with t(X;8;21)(p22;q22;q22) associated with loss of Y chromosome.
  • The patient did not respond to therapy and follow-up of cytogenetics revealed same chromosome abnormality.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18453738.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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91. Romero AI, Thorén FB, Brune M, Hellstrand K: NKp46 and NKG2D receptor expression in NK cells with CD56dim and CD56bright phenotype: regulation by histamine and reactive oxygen species. Br J Haematol; 2006 Jan;132(1):91-8
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  • The cytotoxicity of natural killer (NK) cells is dependent on the interaction between target cell ligands and a series of stimulatory receptors on NK cells.
  • Two of these triggering receptors, the NKp46 natural cytotoxicity receptor (NKp46) and the major histocompatibility complex (MHC) class I-interactive NKG2D receptor, are deficiently expressed by NK cells recovered from patients with acute myeloid leukaemia (AML), but little is known regarding the regulation of NKp46 and NKG2D expression.
  • Here we report that mononuclear and polymorphonuclear phagocytes downregulate the cell surface density of NKp46 and NKG2D on NK cells with CD56(dim) phenotype in vitro by a mechanism that is dependent on the availability of phagocyte-derived reactive oxygen species (ROS).
  • Our findings are suggestive of a novel mechanism of relevance to the regulation of NKp46/NKG2D receptor expression.
  • Moreover, our findings suggest that the previously reported action of histamine on NK cell-mediated killing of leukaemic cells may be related to the preservation of activatory NK-cell receptors.
  • [MeSH-major] Antigens, CD56 / analysis. Killer Cells, Natural / metabolism. Membrane Glycoproteins / metabolism. Receptors, Immunologic / metabolism
  • [MeSH-minor] Apoptosis / immunology. Cells, Cultured. Down-Regulation / immunology. Flow Cytometry. Histamine / pharmacology. Humans. Immunophenotyping. NK Cell Lectin-Like Receptor Subfamily K. Natural Cytotoxicity Triggering Receptor 1. Neutrophil Activation / immunology. Neutrophils / immunology. Phagocytes / immunology. Reactive Oxygen Species / pharmacology. Receptors, Natural Killer Cell. Up-Regulation / immunology

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  • (PMID = 16371024.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / KLRK1 protein, human; 0 / Membrane Glycoproteins; 0 / NCR1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Natural Cytotoxicity Triggering Receptor 1; 0 / Reactive Oxygen Species; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell; 820484N8I3 / Histamine
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92. Takahashi S, Harigae H, Kameoka J, Sasaki T, Kaku M: AML1B transcriptional repressor function is impaired by the Flt3-internal tandem duplication. Br J Haematol; 2005 Aug;130(3):428-36
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  • Fms-like tyrosine kinase 3 (Flt3) is a type III receptor tyrosine kinase.
  • The internal tandem duplication (ITD) of the juxtamembrane region of this receptor is the most prevalent mutation in acute myeloid leukaemia (AML).
  • We recently reported that Flt3-ITD interferes with the transcriptional and biological action of promyelocytic leukaemia zinc finger transcriptional repressor by dissociating it from SMRT.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Gene Duplication. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences. Transcription Factors / metabolism
  • [MeSH-minor] Acute Disease. Animals. COS Cells. Core Binding Factor Alpha 2 Subunit. Humans. Mice. Nuclear Receptor Co-Repressor 2. RNA, Messenger / analysis. Repressor Proteins / metabolism. Transcription, Genetic. Transfection. Two-Hybrid System Techniques. fms-Like Tyrosine Kinase 3

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  • (PMID = 16042694.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / NCOR2 protein, human; 0 / Ncor2 protein, mouse; 0 / Nuclear Receptor Co-Repressor 2; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Runx1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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93. Guilloton F, Jean C, de Thonel A, Laurent G, Quillet-Mary A: Granzyme B induction signalling pathway in acute myeloid leukemia cell lines stimulated by tumor necrosis factor alpha and Fas ligand. Cell Signal; 2007 Jun;19(6):1132-40
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  • [Title] Granzyme B induction signalling pathway in acute myeloid leukemia cell lines stimulated by tumor necrosis factor alpha and Fas ligand.
  • Acute myeloid leukemia (AML) cell lines treated by genotoxic agents or by Tumor Necrosis Factor alpha (TNFalpha) acquire potent cytotoxicity towards myeloid cells through activation of granzyme B (GrB)/perforin (PFN) system.
  • Moreover, we analyzed GrB induction signalling pathway in TNFalpha- and FasL-stimulated AML cells.
  • Otherwise, TNFalpha and FasL stimulation led to radical oxygen species (ROS) generation and ASK1 (Apoptosis-signal-regulating-kinase-1) activation.
  • Altogether, our results suggest that TNFalpha- and FasL-stimulated AML cell lytic induction is regulated by a signalling pathway involving sequentially, ROS generation, Trx oxidation, ASK1 activation, p38MAPK stimulation and GrB induction at mRNA and protein levels.
  • [MeSH-major] Fas Ligand Protein / pharmacology. Granzymes / biosynthesis. Granzymes / genetics. Leukemia, Myeloid, Acute / pathology. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Line, Tumor. Enzyme Activation / drug effects. Enzyme Induction / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Hydrogen Peroxide / pharmacology. MAP Kinase Kinase Kinase 5 / metabolism. Membrane Glycoproteins / metabolism. Mice. Perforin. Pore Forming Cytotoxic Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reactive Oxygen Species / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 17258890.001).
  • [ISSN] 0898-6568
  • [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 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Pore Forming Cytotoxic Proteins; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 126465-35-8 / Perforin; BBX060AN9V / Hydrogen Peroxide; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; EC 2.7.11.25 / MAP3K5 protein, human; EC 3.4.21.- / Granzymes
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94. Girgis EH, Mahoney JP, Khalil RH, Soliman MR: Effect of thalidomide and arsenic trioxide on the release of tumor necrosis factor-α and vascular endothelial growth factor from the KG-1a human acute myelogenous leukemia cell line. Oncol Lett; 2010 Jul;1(4):663-667
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  • [Title] Effect of thalidomide and arsenic trioxide on the release of tumor necrosis factor-α and vascular endothelial growth factor from the KG-1a human acute myelogenous leukemia cell line.
  • Studies conducted in our lab have indicated that thalidomide cytotoxicity in the KG-1a human acute myelogenous leukemia (AML) cell line was enhanced by combining it with arsenic trioxide.
  • The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) from this cell line in an attempt to clarify its possible cytotoxic mechanism(s).
  • Human AML cell line KG-1a was used in this study.
  • Results obtained indicate that the levels of TNF-α in the supernatant of KG-1a cell cultures incubated with thalidomide, arsenic trioxide, or combination were statistically lower than those observed in the supernatant of control cells (2.89, 5.07, 4.15 and 16.88 pg/ml, respectively).
  • Arsenic trioxide, whether alone or in combination with thalidomide, did not produce any statistically significant difference in the levels of VEGF as compared to the control or thalidomide-treated cell supernatant.

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  • (PMID = 22966360.001).
  • [ISSN] 1792-1074
  • [Journal-full-title] Oncology letters
  • [ISO-abbreviation] Oncol Lett
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR003020
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] Greece
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95. Giles F, Verstovsek S, Garcia-Manero G, Thomas D, Ravandi F, Wierda W, Ferrajoli A, Kornblau S, Jabbour E, Shan J, O'brien S, Albitar M, Kantarjian H: Validation of the European Prognostic Index for younger adult patients with acute myeloid leukaemia in first relapse. Br J Haematol; 2006 Jul;134(1):58-60
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  • [Title] Validation of the European Prognostic Index for younger adult patients with acute myeloid leukaemia in first relapse.
  • In order to validate the European Prognostic Index (EPI) for patients <or=60 years with acute myeloid leukaemia in first relapse, a cohort of 599 such patients, treated between 1980 and 2004 at the MD Anderson Cancer Center, were assessed using this prognostic index.
  • [MeSH-major] Leukemia, Myeloid / immunology
  • [MeSH-minor] Acute Disease. Adult. Cohort Studies. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Proportional Hazards Models. Recurrence. Risk. Survival Rate

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  • (PMID = 16803568.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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96. Onsten T, Girardi FM, Coelho GM, Lima Frey MC, Paskulin G: Cytogenetic and morphological findings in 166 patients with de novo acute myeloid leukemia in southern Brazil. Cancer Genet Cytogenet; 2006 Oct 15;170(2):167-70
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  • [Title] Cytogenetic and morphological findings in 166 patients with de novo acute myeloid leukemia in southern Brazil.
  • Some of these chromosomal abnormalities are found in individuals from specific geographical areas and ethnic groups.
  • A high incidence of t(15;17) translocation has been observed, for example, in the Hispanic populations of the United States and Spain.
  • We performed a cytogenetic analysis of 166 patients at the Division of Hematology of Hospital de Clínicas de Porto Alegre between 1990 and 2002.
  • Those patients who met the criteria for de novo acute myeloid leukemia (AML) and whose karyotypes could be successfully determined were included in the study.
  • The karyotypes of each patient and the French-American-British (FAB) criteria for the diagnosis of AML were reviewed.
  • Abnormalities were significantly more common in the FAB-M3 group (70.3%).
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Brazil. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Female. Humans. Infant. Male. Middle Aged. Translocation, Genetic

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  • (PMID = 17011990.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. Darling TN, Pacheco-Rodriguez G, Gorio A, Lesma E, Walker C, Moss J: Lymphangioleiomyomatosis and TSC2-/- cells. Lymphat Res Biol; 2010 Mar;8(1):59-69
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  • The cells comprising pulmonary lymphangioleiomyomatosis (LAM) and renal angiomyolipomas (AMLs) are heterogeneous, with variable mixtures of cells exhibiting differentiation towards smooth muscle, fat, and vessels.
  • Cells grown from LAM and AMLs have likewise tended to be heterogeneous.
  • The discovery that LAM and AMLs contain cells with mutations in the TSC1 or TSC2 genes is allowing investigators to discriminate between "two-hit" cells and neighboring cells, providing insights into disease pathogenesis.
  • In rare cases, it has been possible to derive cells from human tumors, including AMLs and TSC skin tumors that are highly enriched for TSC2(-/-) cells.
  • Cells derived from an Eker rat uterine leiomyoma (ELT3 cells) are Tsc2-null and these have been used in a rodent cell models for LAM.
  • Further improvements in the ability to reliably grow well-characterized TSC2(-/-) cells from human tumors are critical to developing in vitro and in vivo model systems for studies of LAM pathogenesis and treatment.

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