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1. Dorsey WC, Ford BD, Roane L, Haynie DT, Tchounwou PB: Induced mitogenic activity in AML-12 mouse hepatocytes exposed to low-dose ultra-wideband electromagnetic radiation. Int J Environ Res Public Health; 2005 Apr;2(1):24-30
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  • [Title] Induced mitogenic activity in AML-12 mouse hepatocytes exposed to low-dose ultra-wideband electromagnetic radiation.
  • In the present study, we hypothesized that low-dose UWB electromagnetic radiation (UWBR) could elicit a mitogenic effect in AML-12 mouse hepatocytes, in vitro.
  • To test this hypothesis, we exposed AML-12 mouse hepatocytes, to UWBR in a specially constructed gigahertz transverse electromagnetic mode (GTEM) cell.
  • UWB pulses were triggered by an external pulse generator for UWBR exposure but were not triggered for the sham exposure.
  • We performed an MTT Assay to assess cell viability for UWBR-treated and sham-exposed hepatocytes.
  • UWBR exerted a statistically significant (p < 0.05) dose-dependent response in cell viability in both serum-treated and serum free medium (SFM) -treated hepatocytes.
  • Western blot analysis of hepatocyte lysates demonstrated that cyclin A protein was induced in hepatocytes, suggesting that increased MTT activity after UWBR exposure was due to cell proliferation.
  • This study indicates that UWBR has a mitogenic effect on AML-12 mouse hepatocytes and implicates a possible role for UWBR in hepatocarcinoma.
  • [MeSH-minor] Animals. Cell Proliferation / radiation effects. Cell Survival / radiation effects. Cells, Cultured. Cyclin A / biosynthesis. Mice

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  • (PMID = 16705798.001).
  • [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; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cyclin A
  • [Other-IDs] NLM/ PMC3814693
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2. Schwäble J, Choudhary C, Thiede C, Tickenbrock L, Sargin B, Steur C, Rehage M, Rudat A, Brandts C, Berdel WE, Müller-Tidow C, Serve H: RGS2 is an important target gene of Flt3-ITD mutations in AML and functions in myeloid differentiation and leukemic transformation. Blood; 2005 Mar 1;105(5):2107-14
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  • [Title] RGS2 is an important target gene of Flt3-ITD mutations in AML and functions in myeloid differentiation and leukemic transformation.
  • Activating fetal liver tyrosine kinase 3 (Flt3) mutations represent the most common genetic aberrations in acute myeloid leukemia (AML).
  • Most commonly, they occur as internal tandem duplications in the juxtamembrane domain (Flt3-ITD) that transform myeloid cells in vitro and in vivo and that induce aberrant signaling and biologic functions.
  • We identified RGS2, a regulator of G-protein signaling, as a gene specifically repressed by Flt3-ITD.
  • RGS2 was repressed after forced expression of activating Flt3 mutations in 2 myeloid cell lines (32Dcl3 and NB4).
  • Furthermore, RGS2 was repressed in Flt3-mutation-positive AML cases in comparison to Flt3-mutation-negative cases, especially in Flt3-ITD-positive cases with a high ITD-to-wild-type (WT) ratio.
  • Expression analyses in myeloid cell lines revealed induction of RGS2 during granulocytic but not during monocytic differentiation.
  • Taken together, RGS2 is a novel mediator of myeloid differentiation, and its repression is an important event in Flt3-ITD-induced transformation.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Myeloid / genetics. Mutation. Myeloid Cells / pathology. Proto-Oncogene Proteins / genetics. RGS Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Acute Disease. Cell Differentiation. Cell Line. Cell Proliferation. Glycogen Synthase Kinase 3 / metabolism. HL-60 Cells. Humans. Phosphorylation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt. Repressor Proteins. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3

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  • (PMID = 15536149.001).
  • [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 / Proto-Oncogene Proteins; 0 / RGS Proteins; 0 / RGS2 protein, human; 0 / Repressor 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; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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3. Carter BZ, Mak DH, Woessner R, Gross S, Schober WD, Estrov Z, Kantarjian H, Andreeff M: Inhibition of KSP by ARRY-520 induces cell cycle block and cell death via the mitochondrial pathway in AML cells. Leukemia; 2009 Oct;23(10):1755-62
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  • [Title] Inhibition of KSP by ARRY-520 induces cell cycle block and cell death via the mitochondrial pathway in AML cells.
  • Kinesin spindle protein (KSP), a microtubule-associated motor protein essential for cell cycle progression, is overexpressed in many cancers and is a potential anti-tumor target.
  • We found that inhibition of KSP by a selective inhibitor, ARRY-520, blocked cell cycle progression, leading to apoptosis in acute myeloid leukemia cell lines that express high levels of KSP.
  • Knockdown of p53, overexpression of XIAP and mutation in caspase-8 did not significantly affect sensitivity to ARRY-520, suggesting that the response is independent of p53, XIAP and the extrinsic apoptotic pathway.
  • Although ARRY-520 induced mitotic arrest in both HL-60 and Bcl-2-overexpressing HL-60Bcl-2 cells, cell death was blunted in HL-60Bcl-2 cells, suggesting that the apoptotic program is executed through the mitochondrial pathway.
  • ARRY-520 significantly inhibited tumor growth of xenografts in SCID mice and inhibited AML blast but not normal colony formation, supporting a critical role for KSP in proliferation of leukemic progenitor cells.
  • These results demonstrate that ARRY-520 potently induces cell cycle block and subsequent death in leukemic cells via the mitochondrial pathway and has the potential to eradicate AML progenitor cells.

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  • (PMID = 19458629.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / P01 CA49639; 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] England
  • [Chemical-registry-number] 0 / ARRY 520; 0 / Antineoplastic Agents; 0 / KIF11 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Thiadiazoles; 0 / Tumor Suppressor Protein p53; 0 / X-Linked Inhibitor of Apoptosis Protein; EC 3.4.22.- / Caspase 8; EC 3.6.1.- / Kinesin
  • [Other-IDs] NLM/ NIHMS445013; NLM/ PMC3593228
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4. Reindl C, Bagrintseva K, Vempati S, Schnittger S, Ellwart JW, Wenig K, Hopfner KP, Hiddemann W, Spiekermann K: Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML. Blood; 2006 May 1;107(9):3700-7
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  • [Title] Point mutations in the juxtamembrane domain of FLT3 define a new class of activating mutations in AML.
  • In acute myeloid leukemia (AML), two clusters of activating mutations are known in the FMS-like tyrosine kinase-3 (FLT3) gene: FLT3-internal tandem duplications (FLT3-ITDs) in the juxtamembrane (JM) domain in 20% to 25% of patients, and FLT3 point mutations in the tyrosine-kinase domain (FLT3-TKD) in 7% to 10% of patients, respectively.
  • Expression of 4 FLT3-JM-PMs in interleukin-3 (IL-3)-dependent Ba/F3 cells led to factor-independent growth, hyperresponsiveness to FLT3 ligand, and resistance to apoptotic cell death.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis. Base Sequence. Cell Line. DNA, Neoplasm / genetics. Enzyme Activation / genetics. Humans. In Vitro Techniques. Interleukin-3 / pharmacology. Mice. Models, Molecular. Molecular Sequence Data. Mutagenesis, Site-Directed. Phosphorylation. Protein Structure, Tertiary. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. STAT5 Transcription Factor / metabolism. Staurosporine / analogs & derivatives. Staurosporine / pharmacology. Tyrosine / chemistry

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  • (PMID = 16410449.001).
  • [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 / DNA, Neoplasm; 0 / Interleukin-3; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 120685-11-2 / 4'-N-benzoylstaurosporine; 42HK56048U / Tyrosine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine
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5. Andersson BS, de Lima M, Thall PF, Wang X, Couriel D, Korbling M, Roberson S, Giralt S, Pierre B, Russell JA, Shpall EJ, Jones RB, Champlin RE: Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS. Biol Blood Marrow Transplant; 2008 Jun;14(6):672-84
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  • [Title] Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS.
  • We postulated that fludarabine (Flu) instead of cyclophosphamide (Cy) combined with i.v. busulfan (Bu) as preconditioning for allogeneic hematopoietic stem cell transplantation (HSCT) would improve safety and retain antileukemic efficacy.
  • To account for improved supportive care and other unidentified factors that may affect outcome ("period" effects), 78 acute myelogenous leukemia (AML) patients receiving Melphalan-Flu (MF), treated in parallel during this time (1997-2004) were used to estimate the period effect.
  • These results support replacing BuCy +/- ATG with Bu-Flu +/- rabbit-antithymocyte globulin (ATG), and warrant a prospective comparison between allogeneic HSCT and conventional induction/consolidation chemotherapy for AML in CR1.

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  • (PMID = 18489993.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164-160020; United States / NCI NIH HHS / CA / 2P30CA16672-26; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS52878; NLM/ PMC4230823
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6. Lee E, Jung H, Radivojac P, Kim JW, Lee D: Analysis of AML Genes in Dysregulated Molecular Networks. Summit Transl Bioinform; 2009;2009:1-18

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  • [Title] Analysis of AML Genes in Dysregulated Molecular Networks.
  • BACKGROUND: Identifying disease causing genes and understanding their molecular mechanisms are essential to developing effective therapeutics.
  • Thus, several computational methods have been proposed to prioritize candidate disease genes by integrating different data types, including sequence information, biomedical literature, and pathway information.
  • Recently, molecular interaction networks have been incorporated to predict disease genes, but most of those methods do not utilize invaluable disease-specific information available in mRNA expression profiles of patient samples.
  • RESULTS: Through the integration of protein-protein interaction networks and gene expression profiles of acute myeloid leukemia (AML) patients, we identified subnetworks of interacting proteins dysregulated in AML and characterized known mutation genes causally implicated to AML embedded in the subnetworks.
  • The analysis shows that the set of extracted subnetworks is a reservoir rich in AML genes reflecting key leukemogenic processes such as myeloid differentiation, CONCLUSION: We showed that the integrative approach both utilizing gene expression profiles and molecular networks could identify AML causing genes most of which were not detectable with gene expression analysis alone due to their minor changes in mRNA.

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  • (PMID = 21347161.001).
  • [ISSN] 2153-6430
  • [Journal-full-title] Summit on translational bioinformatics
  • [ISO-abbreviation] Summit Transl Bioinform
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3041561
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7. Candoni A, Martinelli G, Toffoletti E, Chiarvesio A, Tiribelli M, Malagola M, Piccaluga PP, Michelutti A, Simeone E, Damiani D, Russo D, Fanin R: Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years. Leuk Res; 2008 Dec;32(12):1800-8
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  • [Title] Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years.
  • INTRODUCTION: The addition of gemtuzumab-ozogamicin (GO) to an induction regimen including synergistic drugs, such as intermediate dose of cytarabine (Ara-C), idarubicin and fludarabine (FLAI), could reduce treatment failure in acute myeloid leukemia (AML) patients.
  • Nevertheless, the role and safety of this antibody target-therapy in first-line chemotherapy in patients younger than 65 years has not yet been defined.
  • Thirty consecutive AML patients were included.
  • The M/F ratio was 16/14 and 21/30 (70%) of patients were poor-risk at diagnosis.
  • Hematopoietic stem cell transplant (HSCT) was planned for all high risk AML patients in first complete remission (CR) after consolidation with intermediate doses of Ara-C and idarubicin (IDAC-IDA).
  • Cytogenetic, multidrug-resistance phenotype, FLT3 mutation status, and WT1 quantitative expression analyses were performed at diagnosis in all patients.
  • WT1 expression and cytogenetic (in positive cases) analyses were performed after induction to detect and follow minimal residual disease.
  • The toxicity of FLAI-GO was acceptable; 57% of patients experienced transient and reversible GO infusion-related adverse events (especially fever and chills), but no cases of veno-occlusive disease occurred during CHT or after HSCT.
  • CONCLUSIONS: These preliminary results suggest that FLAI-GO is an effective and well tolerated induction regimen for CD33 positive AML patients younger than 65 years, with a high complete response rate, favourable safety profile, low DDI.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18621416.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Recombinant Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin
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8. Perea G, Lasa A, Aventín A, Domingo A, Villamor N, Queipo de Llano MP, Llorente A, Juncà J, Palacios C, Fernández C, Gallart M, Font L, Tormo M, Florensa L, Bargay J, Martí JM, Vivancos P, Torres P, Berlanga JJ, Badell I, Brunet S, Sierra J, Nomdedéu JF, Grupo Cooperativo para el Estudio y Tratamiento de las Leucemias Agudas y Miel: Prognostic value of minimal residual disease (MRD) in acute myeloid leukemia (AML) with favorable cytogenetics [t(8;21) and inv(16)]. Leukemia; 2006 Jan;20(1):87-94
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  • [Title] Prognostic value of minimal residual disease (MRD) in acute myeloid leukemia (AML) with favorable cytogenetics [t(8;21) and inv(16)].
  • Most patients with acute myeloid leukemia (AML) and t(8;21) or inv(16) have a good prognosis with current anthracycline- and cytarabine-based protocols.
  • The mean amount of minimal residual disease (MRD) detected by FC in relapsed and nonrelapsed patients was markedly different: 0.3 vs 0.08% (P=0.002) at the end of treatment.
  • The mean number of fusion transcript copies/ ABL x 10(4) also differed between relapsed and non-relapsed patients: 2385 vs 122 (P=0.001) after induction, 56 vs 7.6 after intensification (P=0.0001) and 75 vs 3.3 (P=0.0001) at the end of chemotherapy.
  • Combined use of FC and RQ-PCR may improve MRD detection, and provide useful clinical information on relapse kinetics in AML patients.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Neoplasm, Residual / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Inversion. Cytogenetic Analysis. Female. Flow Cytometry. Follow-Up Studies. Humans. Kinetics. Male. Middle Aged. Prognosis. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Rate


9. Vehreschild JJ, Böhme A, Buchheidt D, Arenz D, Harnischmacher U, Heussel CP, Ullmann AJ, Mousset S, Hummel M, Frommolt P, Wassmer G, Drzisga I, Cornely OA: A double-blind trial on prophylactic voriconazole (VRC) or placebo during induction chemotherapy for acute myelogenous leukaemia (AML). J Infect; 2007 Nov;55(5):445-9
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  • [Title] A double-blind trial on prophylactic voriconazole (VRC) or placebo during induction chemotherapy for acute myelogenous leukaemia (AML).
  • We conducted a trial to analyze the efficacy and safety of voriconazole in the prevention of lung infiltrates during induction chemotherapy for acute myelogenous leukaemia (AML).
  • METHODS: This was a prospective, randomised, double-blind, placebo-controlled phase III trial in AML patients undergoing remission induction chemotherapy.
  • Oral voriconazole 200 mg twice daily or placebo was administered until detection of a lung infiltrate or end of neutropenia.
  • Adverse events and toxicity did not differ between the two treatment groups.
  • CONCLUSION: In AML patients undergoing induction chemotherapy, prophylactic oral voriconazole 200 mg twice daily resulted in trends towards reduced incidences of lung infiltrates and hepatosplenic candidiasis.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / prevention & control. Mycoses / prevention & control. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Triazoles / adverse effects. Triazoles / therapeutic use

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  • (PMID = 17822770.001).
  • [ISSN] 1532-2742
  • [Journal-full-title] The Journal of infection
  • [ISO-abbreviation] J. Infect.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Placebos; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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10. de Oliveira FM, Tone LG, Simões BP, Falcão RP, Brassesco MS, Sakamoto-Hojo ET, dos Santos GA, Marinato AF, Jácomo RH, Rego EM: Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1. Cancer Genet Cytogenet; 2007 Jan 15;172(2):154-7
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  • [Title] Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1.
  • We report a case of acute myeloid leukemia (AML) subtype M2, with t(5;11)(q35;q13), in a 30-year-old man.
  • Conventional cytogenetic, spectral karyotyping, and fluorescence in situ hybridization (FISH) studies on bone marrow sample obtained at diagnosis revealed an abnormal karyotype in all cells examined.
  • Similar to the 11q23 region, 11q13 changes can be found in both myeloid and lymphoid neoplasias with different chromosomes serving as donors in translocations.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Cyclin D1 / biosynthesis. Cyclin D1 / genetics. Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. Leukemia, Myelomonocytic, Acute. Male


11. Schiffer CA: Molecular characterization of AML: a significant advance or just another prognostic factor? Best Pract Res Clin Haematol; 2008 Dec;21(4):621-8
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  • [Title] Molecular characterization of AML: a significant advance or just another prognostic factor?
  • Although there have been several major laboratory advances which have been helpful diagnostically and in the general classification of risk groups, they have not resulted in improvement in the overall outcome for patients with AML and, with occasional exceptions, have not provided clues about new therapeutic directions.
  • Gene expression profiling and the identification of a number of unique mutations in leukemia cells may help discriminate among the heterogeneous outcomes observed both in patients with the same karyotypic abnormality and in patients with normal cytogenetics.
  • However, the mechanism(s) by which these new molecular markers affect prognosis are poorly understood, and as more mutations and other patient subgroups are discovered, identifying new, non-empiric therapies and designing efficient clinical trials, becomes even more complicated.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 19041601.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 32
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12. Mato AR, Riccio BE, Qin L, Heitjan DF, Carroll M, Loren A, Porter DL, Perl A, Stadtmauer E, Tsai D, Gewirtz A, Luger SM: A predictive model for the detection of tumor lysis syndrome during AML induction therapy. Leuk Lymphoma; 2006 May;47(5):877-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A predictive model for the detection of tumor lysis syndrome during AML induction therapy.
  • In acute myelogenous leukemia (AML), TLS frequency, risk stratification, monitoring, and management strategies are based largely on case series and data from other malignancies.
  • A single-center, retrospective cohort study was conducted to estimate TLS incidence and identify TLS predictive factors in a patient population undergoing myeloid leukemia induction chemotherapy.
  • This study included 194 patients, aged 18-86 years, with AML or advanced myelodysplastic syndrome undergoing primary myeloid leukemia induction chemotherapy.
  • In univariate analysis, elevated pre-chemotherapy values for uric acid (P < 0.0001), creatinine (P = 0.0025), lactate dehydrogenase (LDH) (P = 0.0001), white blood cell (P = 0.0058), gender (P = 0.0064) and chronic myelomonocytic leukemia history (P = 0.0292) were significant predictors.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Predictive Value of Tests. Tumor Lysis Syndrome / diagnosis

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  • [CommentIn] Leuk Lymphoma. 2006 May;47(5):782-5 [16753859.001]
  • (PMID = 16753873.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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13. Olivieri A, Capelli D, Troiani E, Poloni A, Montanari M, Offidani M, Discepoli G, Leoni P: A new intensive induction schedule, including high-dose Idarubicin, high-dose Aracytin and Amifostine, in older AML patients: feasibility and long-term results in 42 patients. Exp Hematol; 2007 Jul;35(7):1074-82
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  • [Title] A new intensive induction schedule, including high-dose Idarubicin, high-dose Aracytin and Amifostine, in older AML patients: feasibility and long-term results in 42 patients.
  • OBJECTIVE: We evaluated the feasibility of a new regimen in elderly patients with acute myeloid leukemia (AML).
  • The main end points were overall response rate (ORR) and toxicity; secondary end points were feasibility of peripheral blood stem cells (PBSC) collection, leukemia-free survival, and overall survival (OS).
  • Patients with unfavorable cytogenetic and those with secondary AML had poorer OS; about 40% of patients could mobilize a sufficient amount of PBSC for autologous stem cell transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 17588476.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; M487QF2F4V / Amifostine; ZRP63D75JW / Idarubicin
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14. Schmitt C, Ghazi B, Bellier F, Bensussan A: Identification and analysis of the human CD160 promoter: implication of a potential AML-1 binding site in promoter activation. Genes Immun; 2009 Oct;10(7):616-23

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and analysis of the human CD160 promoter: implication of a potential AML-1 binding site in promoter activation.
  • CD160 is a glycosylphosphatidylinositol-anchored multimer expressed at the cell surface of subsets of cytotoxic T-lymphocytes and natural killer cells.
  • Although CD160 is an important molecule for the control of cell-mediated cytotoxic responses, the mechanisms of regulation of its expression is unknown.
  • Sequential deletion analysis led to the identification of a 371 bp sequence, located between -314 and +57 relative to the TSS, as the core promoter sequence driving CD160 gene transcription.
  • Sequence alignment of the mouse and human CD160 genomic promoter region revealed a strong homology in the 371 bp sequence identified and pointed out to three conserved transcription factor binding sites for acute myelogenous leukemia-1 (AML-1), FREAC-4 and Sox17.
  • Site-directed mutagenesis showed that the predicted AML-1 site is essential for the regulation of CD160 gene expression.

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  • (PMID = 19626042.001).
  • [ISSN] 1476-5470
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD160 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / FOXD1 protein, human; 0 / Forkhead Transcription Factors; 0 / GPI-Linked Proteins; 0 / RUNX1 protein, human; 0 / Receptors, Immunologic; 0 / SOX17 protein, human; 0 / SOXF Transcription Factors
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15. Cashen AF, Shah AK, Todt L, Fisher N, DiPersio J: Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Cancer Chemother Pharmacol; 2008 Apr;61(5):759-66
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  • [Title] Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • PURPOSE: In this study, pharmacokinetics (PK) of decitabine administered as a 3-h intravenous infusion of 15 mg/m2 every 8 h for 3 days (cycles repeated every 6 weeks) was evaluated in patients with MDS or AML.
  • METHODS: The PK of this dosing regimen was evaluated in sixteen patients with MDS or AML.
  • RESULTS: The mean maximum observed plasma concentration (Cmax), 64.8-77.0 ng/ml, and the mean area under the plasma concentration-time curve (AUC0-infinity), 152-163 ng h/ml, were unchanged during dosing of decitabine for 3 days.
  • The mean values for terminal phase elimination half-life (0.62-0.78 h), total body clearance (125-132 l/h per m2), and volume of distribution at steady state (62.7-89.2 l/m2), remained unchanged during the every 8 h dosing (P>0.05).
  • Cycles 1 and 2 Cmax values for days 1, 2, and 3 were not significantly different as determined by paired two-tailed t test (P>0.05).
  • CONCLUSIONS: Decitabine dosed at 15 mg/m2 iv every 8 h for 3 days resulted in a predictable and manageable toxicity profile in patients with MDS/AML.
  • The repeated dosing did not result in systemic accumulation of the drug, and decitabine PK remained unchanged from cycle to cycle.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Area Under Curve. Bone Marrow / drug effects. Bone Marrow / pathology. Chromatography, High Pressure Liquid. Drug Administration Schedule. Female. Half-Life. Humans. Infusions, Intravenous. Male. Mass Spectrometry. Middle Aged. Sepsis / etiology. Tissue Distribution


16. Bhushan B, Ahuja D, Verma S, Saluja S, Siddiqui S, Kapur S: Relation of cell viability and apoptosis with clinical remission following induction chemotherapy in ALL and AML. J Exp Clin Cancer Res; 2007 Sep;26(3):313-21
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  • [Title] Relation of cell viability and apoptosis with clinical remission following induction chemotherapy in ALL and AML.
  • Evaluation of in vitro spontaneous apoptosis of acute leukemic blast cells after incubating for different time period and its correlation with clinical outcome is well documented in the literature.
  • However, there is insufficient information available on the flowcytometric determination of cell viability immediately after separating blast cells and its correlation with the clinical response.
  • Cell viability was evaluated in freshly isolated leukemic cells from 84 patients with acute leukemia (AL) using 7-Amino-Actinomycin D and was correlated with the clinical response following induction chemotherapy.
  • Patients with ALL who achieved complete remission (CR) had significantly lower mean live cell (70.9%) compared to those patients who did not achieve CR (93.3%) (p=0.02).
  • Furthermore, ALL responders had also significantly higher mean early apoptotic cell (19.4%) as compared to non responders (5%) (p=0.04).
  • No significant difference was found in the mean live / early apoptotic cell count of responders and non responders of AML patients.
  • The probability of obtaining CR in ALL patients was 3.7 and 2.7 times higher in those who had mean live cell count less than 70% and apoptotic cell count more than 10%, respectively.
  • A lower cell viability and higher apoptosis in freshly isolated leukemic cells at the time of diagnosis may indicate a favorable response in patients with ALL but may not provide any sufficient information in predicting the response in AML patients to induction chemotherapy.
  • [MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Cell Survival. Flow Cytometry. Humans. Remission Induction. Tumor Cells, Cultured

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  • (PMID = 17987789.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
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17. Schneider F, Hoster E, Unterhalt M, Schneider S, Dufour A, Benthaus T, Mellert G, Zellmeier E, Bohlander SK, Feuring-Buske M, Buske C, Braess J, Fritsch S, Heinecke A, Sauerland MC, Berdel WE, Buechner T, Woermann BJ, Hiddemann W, Spiekermann K: NPM1 but not FLT3-ITD mutations predict early blast cell clearance and CR rate in patients with normal karyotype AML (NK-AML) or high-risk myelodysplastic syndrome (MDS). Blood; 2009 May 21;113(21):5250-3
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  • [Title] NPM1 but not FLT3-ITD mutations predict early blast cell clearance and CR rate in patients with normal karyotype AML (NK-AML) or high-risk myelodysplastic syndrome (MDS).
  • Mutations in the NPM1 gene represent the most frequent genetic alterations in patients with acute myeloid leukemia (AML) and are associated with a favorable outcome.
  • In 690 normal karyotype (NK) AML patients the complete remission rates (CRs) and the percentage of patients with adequate in vivo blast cell reduction 1 week after the end of the first induction cycle were significantly higher in NPM1(+) (75% and 80%, respectively) than in NPM1(-) (57% and 57%, respectively) patients, but were unaffected by the FLT3-ITD status.
  • Multivariate analyses revealed the presence of a NPM1 mutation as an independent positive prognostic factor for the achievement of an adequate day-16 blast clearance and a CR.
  • These findings provide insight into the pathophysiology and help to understand the favorable clinical outcome of patients with NPM1(+) AML.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics


18. Tam WF, Gary Gilliland D: Can FLT3 inhibitors overcome resistance in AML? Best Pract Res Clin Haematol; 2008 Mar;21(1):13-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Can FLT3 inhibitors overcome resistance in AML?
  • The identification of FLT3 mutations across a range of the cytogenetic subgroups of AML has opened up the possibility of a targeted therapeutic approach with broad applicability.
  • Four agents are currently in clinical trials, at least 3 of which have both sufficient activity against AML and sufficiently acceptable toxicity profiles to support continued efforts to refine their inclusion into therapeutic regimens for AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Design. Leukemia, Myeloid, Acute / drug therapy. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors

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  • (PMID = 18342808.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; 0 / Piperazines; 0 / Quinazolines; DO989GC5D1 / lestaurtinib; E1IO3ICJ9A / tandutinib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine
  • [Number-of-references] 24
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19. Liu CF, Liu GL, Zhang LP, Cheng YF, Lu AD, Tian KG, Liu YR, Qin YZ: [Clinical significance of detection of AML1/ETO fusion transcripts in childhood AML using real-time quantitative reverse transcription polymerase chain reaction]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Feb;13(1):76-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical significance of detection of AML1/ETO fusion transcripts in childhood AML using real-time quantitative reverse transcription polymerase chain reaction].
  • Fourteen AML1/ETO positive children out of 52 AML children were selected.
  • AML1/ETO was quantified according to the expression of the GAPDH housekeeping gene at new diagnosis and during/after chemotherapy and transplantation.
  • The results showed that the ratio of AML1/ETO: GAPDH expression level at new diagnosis varied in the range 0.219-2.080 (median 0.648) among the patients, without relevance with percentage of blasts.
  • It is concluded that real-time RT-PCR is a suitable approach for quantifying AML1/ETO transcripts in monitoring of AML patients with t(8;21) during/after chemotherapy and provides data of diagnostic relevance.

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  • (PMID = 15748440.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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20. Tabe Y, Jin L, Contractor R, Gold D, Ruvolo P, Radke S, Xu Y, Tsutusmi-Ishii Y, Miyake K, Miyake N, Kondo S, Ohsaka A, Nagaoka I, Andreeff M, Konopleva M: Novel role of HDAC inhibitors in AML1/ETO AML cells: activation of apoptosis and phagocytosis through induction of annexin A1. Cell Death Differ; 2007 Aug;14(8):1443-56
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  • [Title] Novel role of HDAC inhibitors in AML1/ETO AML cells: activation of apoptosis and phagocytosis through induction of annexin A1.
  • We analyzed the transcriptional changes in t(8;21) Kasumi-1 AML cells in response to the HDAC inhibitors, depsipeptide (FK228) and suberoylanilide hydroxamic acid (SAHA), which induced marked growth inhibition and apoptosis.
  • This led to increase in the N-terminal cleaved isoform of ANXA1 protein and accumulation of ANXA1 on cell membrane.
  • Neutralization with anti-ANXA1 antibody or gene silencing with ANXA1 siRNA inhibited FK228-induced apoptosis, suggesting that the upregulation of endogenous ANXA1 promotes cell death.
  • FK228-induced ANXA1 expression was associated with massive increase in cell attachment and engulfment of Kasumi-1 cells by human THP-1-derived macrophages, which was completely abrogated with ANXA1 knockdown via siRNA transfection or ANXA1 neutralization.
  • [MeSH-major] Annexin A1 / biosynthesis. Core Binding Factor Alpha 2 Subunit / metabolism. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Acetylation. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Base Sequence. Cell Line, Tumor. Cell Proliferation / drug effects. DNA, Complementary / genetics. Depsipeptides / pharmacology. Histones / metabolism. Humans. Hydroxamic Acids / pharmacology. Macrophages / physiology. Phagocytosis / drug effects. Up-Regulation / drug effects

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  • (PMID = 17464329.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Annexin A1; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Complementary; 0 / Depsipeptides; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Oncogene Proteins, Fusion; 58IFB293JI / vorinostat; CX3T89XQBK / romidepsin
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21. Pigazzi M, Manara E, Baron E, Beghin A, Basso G: The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e22045

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  • [Title] The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia.
  • CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription.
  • ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression.
  • We hypothesized that ICER restoration deserves a special consideration for playing a role in CREB oncogenic feature and in modeling leukemic cell phenotype.
  • We monitored transcription and translation of a series of genes involved in different pathways by quantitative gene expression and western blot analysis.
  • We investigate ICER's role in cell death after treatment with chemotherapic drugs.
  • RESULTS: We revealed that ICER was able to control gene expression in leukemia, principally of genes involved in cell death and survival.
  • Cell cycle analyses revealed a block in G2 phase, a lowered cell proliferation and clonogenic potential with respect to HL60 treated at the same conditions.

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  • (PMID = 27963227.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Giles FJ, O'Brien S, Rizzieri DA, Vey N, Krug U, Sekeres M, Jacobsen TF, Nilsson BI, Staudacher K: A phase II study with CP-4055 in patients with second salvage AML. J Clin Oncol; 2009 May 20;27(15_suppl):7047

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  • [Title] A phase II study with CP-4055 in patients with second salvage AML.
  • : 7047 Background: CP-4055 (cytarabine 5'-elaidic acid ester) is a novel derivative of cytarabine, independent of nucleoside transporters to enter the cell.
  • The aim of this study was to assess efficacy and safety of CP-4055 when given as second salvage therapy to patients (pts) with acute myeloid leukemia (AML).
  • METHODS: Adult pts who received two previous chemotherapy regimens and who had refractory/relapsed AML (CR after first salvage therapy lasting less than 6 months) were enrolled.
  • 6 pts had previous transplant, the majority of the pts had previous ara-C based therapy, 12 pts had not obtained CR1 or CR2.
  • Only 1 pt did not receive d1-5 dosing.
  • Most frequently reported related AE ≥ grade 3 (CTCAE v3.0) were myelosuppression, abdominal pain, colitis, diarrhoea, nausea, fatigue, liver function test (LFT) elevation.
  • Clinical activity (IWG criteria for AML), 2 CR (1 with no CR1 or CR2), and 1 CRp (CR rate 15%), were reported.
  • CONCLUSIONS: CP-4055 given as second salvage therapy to AML pts show manageable toxicity when administered at 2,000 mg/m<sup>2</sup>/d, 24 h CIV, in a d1-5 q3w schedule.
  • Clinical activity (2 CR and 1 CRp) has been reported among the first 20 late stage AML pts.

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  • (PMID = 27961426.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Chan L, Hardwick N, Darling D, Galea-Lauri J, Gäken J, Devereux S, Kemeny M, Mufti G, Farzaneh F: IL-2/B7.1 (CD80) fusagene transduction of AML blasts by a self-inactivating lentiviral vector stimulates T cell responses in vitro: a strategy to generate whole cell vaccines for AML. Mol Ther; 2005 Jan;11(1):120-31
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  • [Title] IL-2/B7.1 (CD80) fusagene transduction of AML blasts by a self-inactivating lentiviral vector stimulates T cell responses in vitro: a strategy to generate whole cell vaccines for AML.
  • However, poor rates of gene transfer and inefficient expression of multiple transgenes encoded by single vectors have hampered the development of such autologous tumor cell vaccines for clinical trials in acute myeloid leukemia (AML) patients.
  • Here we describe the development of a self-inactivating lentiviral vector encoding B7.1 and IL-2 as a single fusion protein postsynthetically cleaved to generate biologically active membrane-anchored B7.1 and secreted IL-2.
  • This enables the efficient transduction of both established and primary AML blasts, resulting in expression of the transgenes in up to 98% of the cells following a single round of infection at an m.o.i. of 10.
  • The combined expression of IL-2 and B7.1 in AML blasts enables increased stimulation of both allogeneic and autologous T cells.
  • The stimulated lymphocytes secrete greater levels of Th1 cytokines and show evidence of specificity, as indicated by their increased proliferation in the presence of autologous AML compared to remission bone marrow cells.
  • [MeSH-major] Antigens, CD80 / metabolism. Cancer Vaccines / immunology. Interleukin-2 / metabolism. Lentivirus / genetics. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / metabolism. T-Lymphocytes / immunology
  • [MeSH-minor] Bone Marrow Cells / immunology. Bone Marrow Cells / pathology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Cell Proliferation. Cells, Cultured. Gene Expression Regulation, Neoplastic. Genetic Vectors / genetics. Humans. Lymphocyte Activation. Th1 Cells / immunology. Th1 Cells / metabolism. Transduction, Genetic

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  • (PMID = 15585413.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Cancer Vaccines; 0 / Interleukin-2
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24. Shman TV, Fedasenka UU, Savitski VP, Aleinikova OV: CD34+ leukemic subpopulation predominantly displays lower spontaneous apoptosis and has higher expression levels of Bcl-2 and MDR1 genes than CD34- cells in childhood AML. Ann Hematol; 2008 May;87(5):353-60
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  • [Title] CD34+ leukemic subpopulation predominantly displays lower spontaneous apoptosis and has higher expression levels of Bcl-2 and MDR1 genes than CD34- cells in childhood AML.
  • In view of obscure clinical and biological significance of leukemic cells heterogeneity, we studied the efficacy of apoptosis, proliferation, and expression levels of the Bcl-2, MDR1, LRP, and BCRP genes in sorted CD34+ and CD34- subpopulations of childhood AML leukemic samples.
  • Significant differences in the patterns of genes expression between patients do not allow us to conclude that the CD34+ fractions have more resistant phenotype than the CD34- subpopulations.
  • [MeSH-major] Antigens, CD34. Apoptosis / physiology. Leukemia, Myeloid, Acute. Lymphocyte Subsets / metabolism. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism

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  • [CommentIn] Ann Hematol. 2008 Dec;87(12):1017-8 [18629500.001]
  • (PMID = 18228020.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Antigens, CD34; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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25. Licciulli S, Cambiaghi V, Scafetta G, Gruszka AM, Alcalay M: Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation. Leukemia; 2010 Feb;24(2):429-37
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  • [Title] Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation.
  • Terminal differentiation of blood cells requires the concerted action of a series of transcription factors that are expressed at specific stages of maturation and function in a cell-type and dosage-dependent manner.
  • Pirin (PIR) is a putative transcriptional regulator whose expression is silenced in cells bearing the acute myeloid leukemia-1 eight-twenty-one (AML1/ETO) and promyelocytic leukemia/retinoic acid receptor (PML/RAR) leukemogenic fusion proteins.
  • A role for PIR in myeloid differentiation has not to date been reported.
  • In this study we show that PIR expression is significantly repressed in a large proportion of acute myeloid leukemias (AMLs), regardless of subtype or underlying karyotypic abnormalities.
  • We show that PIR expression increases during in vitro myeloid differentiation of primary hematopoietic precursor cells, and that ablation of PIR in the U937 myelomonocytic cell line or in murine primary hematopoietic precursor cells results in impairment of terminal myeloid differentiation.
  • Our results suggest that PIR is required for terminal myeloid maturation, and its downregulation may contribute to the differentiation arrest associated with AML.
  • [MeSH-major] Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Differentiation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism


26. Kim HJ, Min WS, Cho BS, Eom KS, Kim SY, Kim YJ, Lee S, Min CK, Cho SG, Lee JW, Kim CC: Overcoming various comorbidities by G-CSF-primed unmanipulated BM SCT in adult patients with AML. Bone Marrow Transplant; 2009 Sep;44(6):345-51
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  • [Title] Overcoming various comorbidities by G-CSF-primed unmanipulated BM SCT in adult patients with AML.
  • We examined whether the use of G-CSF-primed unmanipulated bone marrow (pBM) permits successful transplantation in patients with adverse comorbid pretransplantation conditions.
  • A total of 33 patients at variable risk of AML undergoing allogeneic SCT from an HLA-identical sibling participated.
  • No particular finding in the context of CMV infection or other post transplant complication was observed.
  • [MeSH-major] Bone Marrow / drug effects. Bone Marrow Transplantation / adverse effects. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Body Weight. Comorbidity. Confidence Intervals. Donor Selection. Female. Follow-Up Studies. Graft vs Host Disease / prevention & control. Humans. Living Donors. Male. Middle Aged. Quality of Life. Siblings. Survival Analysis. Time Factors. Treatment Outcome. Young Adult

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  • (PMID = 19270728.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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27. Schnittger S, Bacher U, Haferlach C, Kern W, Haferlach T: Rare CBFB-MYH11 fusion transcripts in AML with inv(16)/t(16;16) are associated with therapy-related AML M4eo, atypical cytomorphology, atypical immunophenotype, atypical additional chromosomal rearrangements and low white blood cell count: a study on 162 patients. Leukemia; 2007 Apr;21(4):725-31
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  • [Title] Rare CBFB-MYH11 fusion transcripts in AML with inv(16)/t(16;16) are associated with therapy-related AML M4eo, atypical cytomorphology, atypical immunophenotype, atypical additional chromosomal rearrangements and low white blood cell count: a study on 162 patients.
  • The spectrum of CBFB-MYH11 fusion transcripts in acute myeloid leukemia (AML) M4eo with inv(16)/t(16;16) is heterogeneous.
  • In this study, a molecular characterization of CBFB-MYH11 transcripts in 162 patients with CBFB-MYH11 positive AML at diagnosis was performed.
  • Rare fusion transcripts were found more frequently in therapy-related AML (P=0.0106).
  • Median white blood cell (WBC) count was higher in type A (35.4 G/l; range=1.1-279 G/l) than in cases with rare types (7.8 G/l; range=0.8-148.0 G/l) (P<0.0001).
  • Rare fusion transcripts were correlated with an atypical cytomorphology not primarily suggestive for the FAB subtype M4eo (P=0.0203).
  • However, the type of fusion was not an independent prognostic parameter.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. Core Binding Factor beta Subunit / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Leukocytes / pathology. Myosin Heavy Chains / genetics. Transcription, Genetic. Translocation, Genetic

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  • (PMID = 17287858.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; EC 3.6.4.1 / Myosin Heavy Chains
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28. Barbaric D, Alonzo TA, Gerbing RB, Meshinchi S, Heerema NA, Barnard DR, Lange BJ, Woods WG, Arceci RJ, Smith FO: Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961. Blood; 2007 Mar 15;109(6):2314-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961.
  • To assess the impact of minimally differentiated acute myeloid leukemia (AML-M0) morphology in children, we analyzed 2 sequential Children's Cancer Group AML clinical trials.
  • We compared presenting characteristics and outcomes of 82 CCG-2891 and CCG-2961 patients with de novo, non-Down syndrome (DS) AML-M0 with those of 1620 patients with non-M0 AML, and of 10 CCG-2891 patients with DS-associated AML-M0 with those of 179 with DS-associated non-M0 AML.
  • The non-DS AML-M0 children had a lower white blood cell (WBC) count (P = .001) than their non-M0 counterparts and a higher incidence of chromosome 5 deletions (P = .002), nonconstitutional trisomy 21 (P = .027), and hypodiploidy (P = .002).
  • Outcome analyses considering all children with non-DS AML demonstrated no significant differences between M0 and non-M0 patients.
  • Analyses restricted to intensive-timing CCG-2891 and CCG-2961 demonstrated comparable complete response (CR) rates (79% and 78%) between non-DS M0 and non-M0 patients.
  • Overall survival (OS) from diagnosis (38% +/- 14% versus 51% +/- 3%; P = .160) was not significantly different between the 2 groups.
  • OS from end of induction (45% +/- 17% versus 63% +/- 3%; P = .038), event-free survival (EFS; 23% +/- 11% versus 41% +/- 3%; P = .018), and disease-free survival (DFS; 31% +/- 14% versus 52% +/- 3%; P = .009) were inferior in the M0 group.
  • There was no significant outcome difference between DS-associated AML-M0 and non-M0 children.
  • This study suggests that intensively treated non-DS-associated AML-M0 children have an inferior outcome compared with children with non-M0 AML.

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  • (PMID = 17158236.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 98413; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1852193
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29. Lee E, Jung H, Radivojac P, Kim JW, Lee D: Analysis of AML genes in dysregulated molecular networks. BMC Bioinformatics; 2009;10 Suppl 9:S2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of AML genes in dysregulated molecular networks.
  • BACKGROUND: Identifying disease causing genes and understanding their molecular mechanisms are essential to developing effective therapeutics.
  • Thus, several computational methods have been proposed to prioritize candidate disease genes by integrating different data types, including sequence information, biomedical literature, and pathway information.
  • Recently, molecular interaction networks have been incorporated to predict disease genes, but most of those methods do not utilize invaluable disease-specific information available in mRNA expression profiles of patient samples.
  • RESULTS: Through the integration of protein-protein interaction networks and gene expression profiles of acute myeloid leukemia (AML) patients, we identified subnetworks of interacting proteins dysregulated in AML and characterized known mutation genes causally implicated to AML embedded in the subnetworks.
  • The analysis shows that the set of extracted subnetworks is a reservoir rich in AML genes reflecting key leukemogenic processes such as myeloid differentiation.
  • CONCLUSION: We showed that the integrative approach both utilizing gene expression profiles and molecular networks could identify AML causing genes most of which were not detectable with gene expression analysis alone due to the minor changes in mRNA level.
  • [MeSH-major] Computational Biology / methods. Gene Expression Profiling / methods. Gene Regulatory Networks. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 19761572.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2745689
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30. Alcalay M, Tiacci E, Bergomas R, Bigerna B, Venturini E, Minardi SP, Meani N, Diverio D, Bernard L, Tizzoni L, Volorio S, Luzi L, Colombo E, Lo Coco F, Mecucci C, Falini B, Pelicci PG: Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance. Blood; 2005 Aug 1;106(3):899-902
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance.
  • Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal.
  • These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, FLT3 mutations, and multilineage involvement.
  • We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 without major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM.
  • Unsupervised clustering clearly separated NPMc+ from NPMc- AMLs, regardless of the presence of FLT3 mutations or non-major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity.
  • The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem-cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor.
  • [MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Nuclear Proteins / analysis. Up-Regulation / genetics
  • [MeSH-minor] Acute Disease. Cell Lineage. DNA Mutational Analysis. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hematopoietic Stem Cells. Neoplasm Proteins / analysis. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. fms-Like Tyrosine Kinase 3

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  • (PMID = 15831697.001).
  • [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 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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31. Chaubey R, Sazawal S, Mahapatra M, Saxena R: Low frequency of RAS and absence of FLT3-ITD gene mutations in patients with Myelodysplastic Syndromes in India: AIIMS experience. J Clin Oncol; 2009 May 20;27(15_suppl):e22231

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e22231 Background: Chromosomal abnormalities and molecular detection has potential importance for diagnosis and prognosis of MDS, although the mechanisms underlying the development of MDS and their progressive evolution to AML are still largely unknown.
  • Since, no studies have been reported from India on the prevalence of N-RAS, K- RAS point mutation in codon 12 and FLT3-ITD mutations in patients with MDS, we undertook this study.
  • PCR-RFLP and nested PCR-RFLP were used for the detection of point mutation in codon 12 of N-RAS and K-RAS.
  • One out of 53 patients (2%) was found positive for N-RAS and four patients were positive for K-RAS (8%) mutation.
  • The presence of N-RAS codon 12 mutation was associated with the poor survival.
  • FLT3-ITD mutation was not observed in any of our cases, which is in contrast to 3% reported from the West.

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  • (PMID = 27964108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Sierra J, Harms R, Mo M, Vogel CL: Evaluation of reported bone pain in patients (pts) receiving chemotherapy in pegfilgrastim clinical trials. J Clin Oncol; 2009 May 20;27(15_suppl):9621

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Some authors have suggested that pegfilgrastim-induced bone pain is unpredictable and refractory to analgesics (Kirshner 2007), though that impression may not be uniformly accepted.
  • The incidence of bone pain was determined by treatment (pegfilgrastim, filgrastim, or placebo), chemotherapy (taxane-containing or not), cycle, severity, age, and body surface area (BSA).
  • In studies comparing pegfilgrastim (n=74) and filgrastim (n==7) in pts with AML and NHL, 52% were female, and the mean (SD) age was 50 (15.1) years.

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  • (PMID = 27963898.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Sekeres M, Kantarjian H, Fenaux P, Becker P, Boruchov A, Guerci-Bresler A, Hu K, Franklin J, Berger D: Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7009

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  • Five pts experienced serious AEs, and there were 2 cases of disease progression to AML: one pt in the QWSC cohort who received romiplostim for 4 weeks and one in the Q2WSC cohort who received romiplostim for 20 weeks.
  • For pts who completed 8 weeks treatment, 15/23 (65%) achieved a plt response, defined by IWG 2006 criteria, and 14/23 (61%) did not require a plt transfusion during this period.

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  • (PMID = 27961381.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Mueller BU, Pabst T: Lineage-specific transcription factor aberrations in AML. Cancer Treat Res; 2010;145:109-25
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  • [Title] Lineage-specific transcription factor aberrations in AML.
  • This is particularly important in that a block in terminal differentiation is the key contributing factor in acute leukemias.
  • Consistent with the role of transcription factors in hematopoietic lineage commitment is the frequent finding of aberrations in transcription factors in AML patients.
  • Here, we intend to review recent findings on aberrations in lineage-restricted transcription factors as observed in patients with acute myeloid leukemia (AML).
  • [MeSH-major] Cell Lineage. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Transcription Factors / physiology
  • [MeSH-minor] Animals. CCAAT-Enhancer-Binding Proteins / physiology. Cell Differentiation. Hematopoietic Stem Cells / pathology. Humans. Mice. Mutation. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / physiology. Phosphorylation. Protein Processing, Post-Translational

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  • (PMID = 20306248.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
  • [Number-of-references] 90
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35. Vercauteren S, Zapf R, Sutherland H: Primitive AML progenitors from most CD34(+) patients lack CD33 expression but progenitors from many CD34(-) AML patients express CD33. Cytotherapy; 2007;9(2):194-204
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  • [Title] Primitive AML progenitors from most CD34(+) patients lack CD33 expression but progenitors from many CD34(-) AML patients express CD33.
  • BACKGROUND: AML blast populations are heterogeneous in their phenotype and functional properties, and contain a small subset of cells that regenerate leukemia in immunocompromised mice or produce clonogenic progeny in long-term cultures.
  • This suggests the existence of a hierarchy of AML progenitor cells.
  • CD33 is a myeloid marker absent on normal hematopoietic stem cells but expressed in about 75% of AML patients, and has been used for BM purging strategies and Ab-targeted therapies.
  • These CD33 Ab therapies benefit only a minority of AML patients, suggesting that AML stem cells are heterogeneous in their CD33 expression.
  • METHODS: In order to evaluate this question, we determined expression levels of CD34 and CD33 on AML progenitors with long-term in vitro proliferative ability and NOD/SCID engrafting ability.
  • This proliferation was leukemic from the CD34(+) AML patients, however from the CD34(-) AML patients only normal progenitors were detected in this fraction in some cases.
  • DISCUSSION: These data suggest that most leukemic progenitors of CD34(+) patients do not express CD33.
  • In contrast, CD34(-) AML primitive leukemic progenitors may be CD33(+).
  • CD34(-) AML patients could potentially benefit most from CD33-targeted therapies or purging.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Leukemia, Myeloid, Acute / blood. Neoplastic Stem Cells / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Cell Separation / methods. Flow Cytometry. Humans. Immunophenotyping. Mice. Mice, Inbred NOD. Mice, SCID. Sialic Acid Binding Ig-like Lectin 3. Stem Cell Transplantation / methods

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  • (PMID = 17453971.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Sialic Acid Binding Ig-like Lectin 3
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36. Diermayr S, Himmelreich H, Durovic B, Mathys-Schneeberger A, Siegler U, Langenkamp U, Hofsteenge J, Gratwohl A, Tichelli A, Paluszewska M, Wiktor-Jedrzejczak W, Kalberer CP, Wodnar-Filipowicz A: NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities. Blood; 2008 Feb 1;111(3):1428-36
Hazardous Substances Data Bank. VALPROIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities.
  • This study exploited alloreactivity of natural killer (NK) cells for augmenting the recognition of human acute myeloid leukemia (AML).
  • To circumvent the inhibitory effect of killer immunoglobulin receptor (KIR) signaling, we generated NK-cell lines with single KIR specificities for major human leukocyte antigen (HLA) class I allotypes.
  • We demonstrated efficient cytolysis of KIR-HLA class I-mismatched primary AML blasts even at low effector-to-target ratios.
  • To define the impact of tumor-associated activating NKG2D-ligands (NKG2D-L), 66 AML patients at diagnosis were analyzed.
  • NKG2D-L were selectively expressed on monoblastic cells in AML M4 and M5 yet absent or weakly expressed on myeloblastic cells in all AML subtypes.
  • Paucity of cell-surface NKG2D-L was not the result of shedding because levels of soluble ULBP1 ligand measured in AML plasma were in the normal range.
  • Notably, purified NKG2D-L(+) monoblastic cells were more susceptible to NK-mediated killing than NKG2D-L(-) myeloblastic cells.
  • Accordingly, induction of cell-surface NKG2D-L by treatment with the histone deacetylase inhibitor, valproic acid, rendered cells more sensitive to NK cytolysis.
  • These data suggest that adoptive transfer of selected populations of alloreactive HLA class I-mismatched NK cells in combination with pharmacologic induction of NKG2D-L merits clinical evaluation as novel approaches to immunotherapy of human AML.
  • [MeSH-major] HLA Antigens / immunology. Histone Deacetylase Inhibitors. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / metabolism. Receptors, Immunologic / metabolism. Valproic Acid / analogs & derivatives
  • [MeSH-minor] Cell Line. Cell Survival. Cytotoxicity, Immunologic / immunology. Enzyme Inhibitors / pharmacology. GPI-Linked Proteins. Histocompatibility Antigens Class I / immunology. Histocompatibility Antigens Class I / metabolism. Histone Deacetylases / metabolism. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Ligands. Membrane Proteins / metabolism. NK Cell Lectin-Like Receptor Subfamily K. Receptors, Natural Killer Cell. Sensitivity and Specificity. Solubility. Up-Regulation / drug effects

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  • (PMID = 17993609.001).
  • [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 / Enzyme Inhibitors; 0 / GPI-Linked Proteins; 0 / HLA Antigens; 0 / Histocompatibility Antigens Class I; 0 / Histone Deacetylase Inhibitors; 0 / Intracellular Signaling Peptides and Proteins; 0 / KLRK1 protein, human; 0 / Ligands; 0 / MHC class I-related chain A; 0 / Membrane Proteins; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell; 0 / ULBP1 protein, human; 0 / valpronic acid; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Histone Deacetylases
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37. Hardwick N, Chan L, Ingram W, Mufti G, Farzaneh F: Lytic activity against primary AML cells is stimulated in vitro by an autologous whole cell vaccine expressing IL-2 and CD80. Cancer Immunol Immunother; 2010 Mar;59(3):379-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lytic activity against primary AML cells is stimulated in vitro by an autologous whole cell vaccine expressing IL-2 and CD80.
  • Despite being of the myeloid lineage, acute myeloid leukaemia (AML) blasts are of low immunogenicity, probably because they lack the costimulatory molecule CD80 and secrete immunosuppressive factors.
  • We have previously shown that in vitro stimulation of autologous peripheral blood mononuclear cells (PBMCs) with primary AML cells modified to express CD80 and IL-2 promotes proliferation, secretion of Th1 cytokines and expansion of activated CD8(+) T cells.
  • In this study, we show that allogeneic effector cells (from a healthy donor or AML patients) when stimulated with IL-2/CD80 modified AML blasts were able to induce the lysis of unmodified AML blasts.
  • Effector cells stimulated with IL-2/CD80AML blasts had higher lytic activity than cells stimulated with AML cells expressing CD80 or IL-2 alone.
  • Similarly, AML patient PBMCs primed with autologous IL-2/CD80 AML cells had a higher frequency of IFN-gamma secreting cells and show cytotoxicity against autologous, unmodified blasts.
  • Crucially, the response appears to be leukaemia specific, since stimulated patient PBMCs show higher frequencies of IFN-gamma secreting effector cells in response to AML blasts than to remission bone marrow cells from the same patients.
  • Although studied in a small number of heterogeneous patient samples, the data are encouraging and support the continuing development of vaccination for poor prognosis AML patients with autologous cells genetically modified to express IL-2/CD80.
  • [MeSH-major] Antigens, CD80 / genetics. Interleukin-2 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 19711075.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D014301/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E005896/1; United Kingdom / Department of Health / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Interleukin-2
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38. Gupta A, Singh M, Singh H, Kumar L, Sharma A, Bakhshi S, Raina V, Thulkar S: Febrile neutropenia during acute myeloid leukemia therapy: Single institution experience from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):e18000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Febrile neutropenia during acute myeloid leukemia therapy: Single institution experience from a developing country.
  • : e18000 Background: Febrile neutropenia poses a major challenge during treatment of acute myeloid leukaemia (AML).
  • METHODS: Episodes of febrile neutropenia in 104 consecutive patients of AML admitted to the medical oncology ward between May 2001 and December 2006 were studied.
  • RESULTS: 402 febrile episodes including 363 episodes of febrile neutropenia (180 in induction, 183 in consolidation) and 39 non-neutropenic episodes (18 in induction, 21 in consolidation) occurred.
  • Prompt and proper institution of antibiotics and antifungals besides considering alternative diagnosis peculiar to the region (e.g. tuberculosis, malaria) may aid in better management.

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  • (PMID = 27964014.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Choi CH, Bark H, Chung JM, Park EK, Kim SH: Elevated reactive oxygen species but not glutathione regulate mercury resistance to AML-2/DX100 cells. Immunopharmacol Immunotoxicol; 2006;28(3):545-55
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  • [Title] Elevated reactive oxygen species but not glutathione regulate mercury resistance to AML-2/DX100 cells.
  • This study was designed to investigate the role of reactive oxygen species (ROS) and glutathione on the resistance of AML-2/DX100 cells to mercuric chloride.
  • The MRP1 overexpressing cells (AML-2/DX100) cells showed less scavenging activity to ROS induced by mercury while no difference in the basal glutathione levels between AML-2/WT and AML-2/DX100 cells.
  • Mercury induced the activation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) but not c-jun-N-terminal kinase in AML-2/DX100 cells.
  • The specific inhibitor for p38 MAPK and ERK, and antioxidant decreased the production of MRP1 and therefore resistance of AML-2/DX100 cells against mercury exposure.
  • These results suggest that induction of ROS and downstream p38 MAPK and ERK were involved in the resistance of cells to mercury by expression MRP1 in AML-2/DX100 cells.
  • [MeSH-minor] Acetylcysteine / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Flavonoids / pharmacology. Humans. Hydrogen Peroxide / pharmacology. Imidazoles / pharmacology. Multidrug Resistance-Associated Proteins / metabolism. Probenecid / pharmacology. Pyridines / pharmacology. Pyrrolidines / pharmacology. Signal Transduction / drug effects. Thiocarbamates / pharmacology. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 16997801.001).
  • [ISSN] 0892-3973
  • [Journal-full-title] Immunopharmacology and immunotoxicology
  • [ISO-abbreviation] Immunopharmacol Immunotoxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Imidazoles; 0 / Multidrug Resistance-Associated Proteins; 0 / Pyridines; 0 / Pyrrolidines; 0 / Reactive Oxygen Species; 0 / SB 203580; 0 / Thiocarbamates; 0 / multidrug resistance-associated protein 1; 25769-03-3 / pyrrolidine dithiocarbamic acid; 53GH7MZT1R / Mercuric Chloride; BBX060AN9V / Hydrogen Peroxide; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; GAN16C9B8O / Glutathione; PO572Z7917 / Probenecid; WYQ7N0BPYC / Acetylcysteine
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40. Shimada A, Taki T, Tabuchi K, Taketani T, Hanada R, Tawa A, Tsuchida M, Horibe K, Tsukimoto I, Hayashi Y: Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group. Pediatr Blood Cancer; 2008 Feb;50(2):264-9
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  • [Title] Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.
  • BACKGROUND: Mixed-lineage leukemia (MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult acute myeloid leukemia (AML), but its relationship to pediatric AML is unknown.
  • PROCEDURE: One hundred fifty-eight newly diagnosed AML patients, including 13 FAB-M3 and 10 Down syndrome (DS) patients, who were treated on the Japanese Childhood AML Cooperative Treatment Protocol AML 99 were analyzed for MLL-PTD, as well as internal tandem duplication (ITD) and the kinase domain mutation (D835Mt) in the FLT3 gene.
  • RESULTS: We found MLL-PTD in 21 (13.3%) of 158 AML patients, but not in FAB-M3 or DS patients.
  • The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018), disease-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.
  • CONCLUSION: AML patients with FLT3-ITD, but not D835Mt, showed a poor prognosis.
  • AML patients with MLL-PTD were also correlated with poor prognosis in this study.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763464.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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41. Manzoor NF, Azim S, Fadoo Z: Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2). J Pak Med Assoc; 2010 Nov;60(11):977-9
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  • [Title] Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2).
  • He was diagnosed with Acute Mycloid Leukemia (AML-M2).
  • This case shows the efficacy and safety of combined antifungal therapy, including voriconazole, for invasive aspergillosis complicating AML.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Leukemia, Myeloid, Acute / microbiology. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 21375212.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; JFU09I87TR / Voriconazole
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42. Trobaugh-Lotrario AD, Kletzel M, Quinones RR, McGavran L, Proytcheva MA, Hunger SP, Malcolm J, Schissel D, Hild E, Giller RH: Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT). Bone Marrow Transplant; 2005 Jan;35(2):143-9
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  • [Title] Monosomy 7 associated with pediatric acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS): successful management by allogeneic hematopoietic stem cell transplant (HSCT).
  • Pediatric acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) with monosomy 7 is associated with poor disease-free survival when treated by conventional chemotherapy, immunosuppression or supportive measures.
  • Hematopoietic stem cell transplant (HSCT) may improve outcomes; however, data to support this are limited.
  • To better understand the curative potential of HSCT in these patients, all cases of AML and MDS with monosomy 7 treated by two transplant programs (1992 to present) were reviewed.
  • Primary diagnoses were MDS (N = 5), therapy-related MDS (N = 3), AML (N = 5) and therapy-related AML (N = 3).
  • Toxicity caused deaths of the five nonsurviving patients, four of whom were transplanted with active leukemia.
  • Allogeneic HSCT is effective therapy for childhood AML and MDS associated with monosomy 7, particularly for patients with AML in complete remission and MDS.
  • [MeSH-major] Chromosomes, Human, Pair 7. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Monosomy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Cause of Death. Child. Child, Preschool. Disease Management. Female. Humans. Male. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous. Treatment Outcome


43. Gondek LP, Tiu R, O'Keefe CL, Sekeres MA, Theil KS, Maciejewski JP: Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML. Blood; 2008 Feb 1;111(3):1534-42
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal lesions and uniparental disomy detected by SNP arrays in MDS, MDS/MPD, and MDS-derived AML.
  • We hypothesized that with new precise methods more cryptic karyotypic lesions can be uncovered that may show important clinical implications.
  • We have applied 250K single nucleotide polymorphisms (SNP) arrays (SNP-A) to study chromosomal lesions in samples from 174 patients (94 MDS, 33 secondary acute myeloid leukemia [sAML], and 47 myelodysplastic/myeloproliferative disease [MDS/MPD]) and 76 controls.
  • Previously unrecognized lesions were detected in patients with normal MC and in those with known lesions.
  • Moreover, segmental uniparental disomy (UPD) was found in 20% of MDS, 23% of sAML, and 35% of MDS/MPD patients, a lesion resulting in copy-neutral loss of heterozygosity undetectable by MC.
  • The potential clinical significance of abnormalities detected by SNP-A, but not seen on MC, was demonstrated by their impact on overall survival.

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  • (PMID = 17954704.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2214746
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44. Haferlach C, Mecucci C, Schnittger S, Kohlmann A, Mancini M, Cuneo A, Testoni N, Rege-Cambrin G, Santucci A, Vignetti M, Fazi P, Martelli MP, Haferlach T, Falini B: AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features. Blood; 2009 Oct 1;114(14):3024-32
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  • [Title] AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features.
  • Acute myeloid leukemia (AML) with mutated NPM1 usually carries normal karyotype (NK), but it may harbor chromosomal aberrations whose significance remains unclear.
  • We addressed this question in 631 AML patients with mutated/cytoplasmic NPM1.
  • Chromosome aberrations in NPM1-mutated AML were similar to, but occurred less frequently than additional chromosome changes found in other AML with recurrent cytogenetic abnormalities according to WHO classification.
  • Four of the 31 NPM1-mutated AML patients karyotyped at different time points had NK at diagnosis but AK at relapse: del(9q) (n = 2), t(2;11) (n = 1), inv(12) (n = 1).
  • NPM1-mutated AML with NK or AK showed overlapping morphologic, immunophenotypic (CD34 negativity), and gene expression profile (down-regulation of CD34 and up-regulation of HOX genes).
  • No difference in survival was observed among NPM1-mutated AML patients independently of whether they carried a NK or an AK, the NPM1-mutated/FLT3-ITD negative cases showing the better prognosis.
  • Findings in our patients point to chromosomal aberrations as secondary events, reinforce the concept that NPM1 mutation is a founder genetic lesion, and indicate that NPM1-mutated AML should be clinically handled as one entity, irrespective of the karyotype.
  • [MeSH-major] Antigens, CD34 / metabolism. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Mutation / genetics. Nuclear Proteins / genetics

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  • [CommentIn] Blood. 2009 Nov 12;114(20):4601-2; author reply 4602-3 [19965707.001]
  • (PMID = 19429869.001).
  • [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 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 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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45. Siendones E, Barbarroja N, Torres LA, Buendía P, Velasco F, Dorado G, Torres A, López-Pedrera C: Inhibition of Flt3-activating mutations does not prevent constitutive activation of ERK/Akt/STAT pathways in some AML cells: a possible cause for the limited effectiveness of monotherapy with small-molecule inhibitors. Hematol Oncol; 2007 Mar;25(1):30-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Flt3-activating mutations does not prevent constitutive activation of ERK/Akt/STAT pathways in some AML cells: a possible cause for the limited effectiveness of monotherapy with small-molecule inhibitors.
  • The Flt3 receptor tyrosine kinase is a critical mediator in the pathogenesis of acute myeloid leukaemia (AML).
  • Flt3-activating mutations have been associated with poor prognosis and decreased overall survival of AML patients, thus Flt3 constitutes an ideal target for drug treatment of such disease.
  • Unfortunately, the monotherapy with small-molecule tyrosine kinase inhibitors in clinical trials shows that remission is not permanent, presumably by resistance of Flt3 mutants to inhibitors.
  • An alternative approach for treatment is based on the cooperation between Flt3 and additional intracellular pathways for AML transformation in some patients.
  • Thus, the inhibition of both Flt3 and such pathways may be exploited for successful treatment of the disease.
  • We investigated the importance of Flt3-activating mutations for the constitutive activation of intracellular pathways in primary AML cells, and their effect on cell survival.
  • We found that the main compounds involved in the differentiation, proliferation and survival of AML (MAPK/AKT/STAT) were constitutively activated.
  • Surprisingly, contrary to previous reports, we found that inhibition of ITD/Flt3 activity did not prevent the phosphorylation of ERK, STAT5 or Akt in some primary AML cells.
  • In parallel, we found that in these cells, Flt3 and ERK or Akt cooperate to regulate cell survival.
  • Our results support the hypothesis that the optimal therapeutic treatment of AML may require not only the oncogenic tyrosine kinase, but also the appropriate combination of different specific inhibitors, thus providing a more effective approach to reverse leukaemogenesis.
  • Thus, we propose that each AML patient should have an individually tailored combination treatment.
  • [MeSH-minor] Acute Disease. Cell Survival. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Leukemia, Myeloid / pathology. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. STAT Transcription Factors / metabolism. Tandem Repeat Sequences. Tumor Cells, Cultured

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  • (PMID = 17128418.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / STAT Transcription Factors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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46. Nicoloso MS, Jasra B, Calin GA: MicroRNAs: new players in AML pathogenesis. Cancer Treat Res; 2010;145:169-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNAs: new players in AML pathogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. MicroRNAs / physiology

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  • (PMID = 20306251.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins
  • [Number-of-references] 49
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47. Seo M, Park M, Yook Y, Kwon YS, Suh YJ, Kim MJ, Cho D, Park JH: IL-18 gene expression pattern in exogenously treated AML cells. BMB Rep; 2008 Jun 30;41(6):461-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IL-18 gene expression pattern in exogenously treated AML cells.
  • IL-18 production may enhance immune system defense against KG-1 cells ; NB4 cells, which are associated with good prognosis, do not produce IL-18.
  • Following exogenous exposure of KG-1 cells to IL-18, expression of CRYGC, NF(kappa)BIA and NACA gene were monitored.
  • NF(kappa)BIA is an inhibitor of NF(kappa)B, and affects growth regulation, apoptosis and hypoxic stress.
  • Studies, such as this one, are beginning to clarify the differences between cells associated with good and bad cancer prognoses, which may ultimately assist in medical treatment for acute myeloid leukemia.
  • [MeSH-major] Gene Expression / drug effects. Interleukin-18 / genetics. Interleukin-18 / pharmacology. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Down-Regulation. Gene Expression Profiling. Humans. NF-kappa B / metabolism. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18593530.001).
  • [ISSN] 1976-6696
  • [Journal-full-title] BMB reports
  • [ISO-abbreviation] BMB Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Interleukin-18; 0 / NF-kappa B
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48. Foss B, Tronstad KJ, Bruserud Ø: Connexin-based signaling in acute myelogenous leukemia (AML). Biochim Biophys Acta; 2010 Jan;1798(1):1-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Connexin-based signaling in acute myelogenous leukemia (AML).
  • Normal and malignant hematopoiesis are regulated by intercellular communication in the hematopoietic microenvironments, and both soluble mediators as well as direct cell-cell contact play important functional roles.
  • Gap junctions are complex membrane structures that transfer molecules between neighboring cells and thereby alter intracellular signaling and metabolism.
  • Connexins are furthermore involved in cell regulation as single molecules by modulating intracellular pathways and possibly gene transcription.
  • The role of connexins in leukemogenesis and leukemic cell functions are not well characterized.
  • In this review, we describe the known effects of gap junctions and connexins in acute myelogenous leukemia and the diverse potential of connexins in acute myelogenous leukemia chemosensitivity, intracellular signaling and cell death regulation.
  • [MeSH-major] Connexins / metabolism. Leukemia, Myeloid / metabolism. Signal Transduction
  • [MeSH-minor] Acute Disease. Apoptosis. Cell Communication. Gap Junctions / metabolism. Humans. Models, Biological

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  • (PMID = 19883623.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Connexins
  • [Number-of-references] 103
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49. Mochiduki Y, Amemiya T, Yabe M: [Brain abscess induced by Bacillus licheniformis complications in acute myeloid leukemia (AML)]. Kansenshogaku Zasshi; 2007 Sep;81(5):592-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Brain abscess induced by Bacillus licheniformis complications in acute myeloid leukemia (AML)].
  • A 64-year-old woman with acute myeloid leukemia, headache, vomiting, and fever exceeding 38.5 degrees C on day 15 during severe neutropenia while undergoing second consolidation chemotherapy presented the next day, with an altered mental state.
  • A space-occupying lesion with ring enhancement was detected in her right frontal lobe on CT, indicting a brain abscess.
  • The patient's general condition improved without neurological complications, and her enhanced brain lesion disappeared on day 185. B. licheniformis is often encountered in diagnostic laboratory culture and usually dismissed as a contaminant, but must be considered as a causative agents for brain abscesses in immunocompromised hosts.
  • [MeSH-major] Brain Abscess / complications. Gram-Positive Bacterial Infections / etiology. Leukemia, Myeloid, Acute / complications. Opportunistic Infections

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  • (PMID = 17966643.001).
  • [ISSN] 0387-5911
  • [Journal-full-title] Kansenshōgaku zasshi. The Journal of the Japanese Association for Infectious Diseases
  • [ISO-abbreviation] Kansenshogaku Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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50. Dombret H, Gardin C: An old AML drug revisited. N Engl J Med; 2009 Sep 24;361(13):1301-3
Hazardous Substances Data Bank. DAUNORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An old AML drug revisited.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Daunorubicin / administration & dosage. Leukemia, Myelomonocytic, Acute / drug therapy

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  • [CommentOn] N Engl J Med. 2009 Sep 24;361(13):1249-59 [19776406.001]
  • [CommentOn] N Engl J Med. 2009 Sep 24;361(13):1235-48 [19776405.001]
  • (PMID = 19776412.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; ZS7284E0ZP / Daunorubicin
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51. Ma Y, Tong HX, Deng X, Zhao Y, Liu ZG, Zhang JH: [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):12-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)].
  • This study was purposed to investigate the acute myeloid leukemia with complex karyotype t(2;21;8)(p12;q22;q22) (AML-M(2)) by using morphologic, immunologic, cytogenetic and molecular biologic classification technique (MICM) and to analyze the MICM characteristics of AML-M(2) and their diagnostic significance.
  • The FAB typing of bone marrow cells (BMCs) was performed by Wright-Giemsa staining and histochemical staining of BM smears; the immunophenotype of leukemic cells was detected by flow cytometry; the karyotypes of chromosome samples prepared by short-term (48 hours) conventional culture of fresh BMCs were analyzed by RHG banding technique; the FISH signaling in mitotic metaphase was determined by dual color and dual fusion AML/ETO probe and chromosome painting probe, and was compared with results of conventional cytogenetic assay; the AML/ETO fusion transcripts were detected by nested RT-PCR.
  • Case 2 accorded with AML-M(2b) in which abnormal increase of myelocytes mainly appeared.
  • It is concluded that application of MICM has an important significance for correct diagnostic typing of AML-M2 with complex karyotype variant of t(8; 21)(p12;q22;q22).

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  • (PMID = 19236738.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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52. Advani AS, Rodriguez C, Jin T, Jawde RA, Saber W, Baz R, Kalaycio M, Sobecks R, Sekeres M, Tripp B, Hsi E: Increased C-kit intensity is a poor prognostic factor for progression-free and overall survival in patients with newly diagnosed AML. Leuk Res; 2008 Jun;32(6):913-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased C-kit intensity is a poor prognostic factor for progression-free and overall survival in patients with newly diagnosed AML.
  • C-kit, a tyrosine kinase receptor, is expressed on most myeloid blasts and is thought to be important in the pathogenesis of AML.
  • Activation of the c-kit receptor leads to phosphorylation and activation of downstream signaling proteins, which are important for cell survival and proliferation.
  • Here, we discuss the prognostic impact of c-kit intensity, measured using the mean fluorescent index (MFI) in patients with newly diagnosed AML.
  • On multivariate analysis, c-kit MFI>20.3 correlated with a decreased progression-free survival and overall survival, independent of known prognostic factors (age, white blood count at diagnosis and cytogenetics).
  • Whether inhibiting c-kit in patients with AML will alter prognosis is the basis of ongoing clinical trials.
  • [MeSH-major] Flow Cytometry. Leukemia, Myeloid, Acute / metabolism. Proto-Oncogene Proteins c-kit / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Disease Progression. Disease-Free Survival. Female. Fluorescence. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate

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  • [CommentIn] Leuk Res. 2008 Jun;32(6):845-6 [18023867.001]
  • (PMID = 17928050.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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53. Stock W: Clinical trials in adult AML. Clin Adv Hematol Oncol; 2009 Jun;7(6):8-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trials in adult AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Drugs, Investigational / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Double-Blind Method. Hematopoietic Stem Cell Transplantation. Humans. Middle Aged. Multicenter Studies as Topic. Randomized Controlled Trials as Topic. Treatment Outcome

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  • (PMID = 19645130.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational
  • [Number-of-references] 30
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54. Estey EH: Advances in the management of AML in the elderly. Clin Adv Hematol Oncol; 2007 Mar;5(3):185-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in the management of AML in the elderly.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adenine Nucleotides / therapeutic use. Aged. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Cause of Death. Humans. Hydrazines / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 17519879.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Hydrazines; 0 / Sulfonamides; 14J2G0U3NQ / laromustine; 762RDY0Y2H / clofarabine
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55. Mikulásová Z, Ilencíková D, Slamka T, Durovcíková D: [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)]. Klin Onkol; 2010;23(6):401-7
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  • [Title] [Acute myeloblastic leukaemia with alternations of MLL proto-oncogene protein (11q23/MLL+ AML)].
  • [Transliterated title] Akútna myeloblastová leukémia s alteráciami MLL protoonkogénu (11q23/MLL+ AML).
  • One of the most common chromosomal breakpoint regions in acute myeloid leukaemia is the chromosome band 11q23.
  • The above work gives well arranged information about different types of genetic tests and their outcomes, which can help oncologists in predicting the prognosis, in minimal residual disease monitoring and in modifying oncological patient treatment.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 21351416.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] slo
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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56. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • OBJECTIVES: This study analyzes changes in the degree of global methylationlevel in myelodysplastic syndrome during progression of the disease.
  • The genome wide hypermethylation of MDS is a distinct feature of this disease.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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57. Seedhouse CH, Pallis M, Grundy M, Shang S, Russell NH: FLT3-ITD expression levels and their effect on STAT5 in AML with and without NPM mutations. Br J Haematol; 2009 Dec;147(5):653-61
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  • [Title] FLT3-ITD expression levels and their effect on STAT5 in AML with and without NPM mutations.
  • We studied FLT3-associated biological parameters in 322 acute myeloid leukaemia samples to establish their importance.
  • Whilst phosphorylated signal transducer and activator of transcription 5 (phospho-STAT5) was not confined to FLT3-ITD samples, within the FLT3-ITD group phosphorylation correlated with adjusted FLT3-ITD levels assessed by determining the total transcripts and proportion of FLT3-ITD within a sample.
  • Expression of the STAT5 downstream target Bcl-xl (an isoform of BCL2L1) was strongly correlated with FLT3 total and adjusted FLT3-ITD levels in FLT3-ITD samples (P < 0.001), however there was no association between Bcl-xl and phospho-STAT5 levels suggesting that STAT5 is not the sole regulator of Bcl-xl in FLT3-ITD cells.
  • We further stratified our cohort by the presence/absence of a cytoplasmic nucleophosmin NPMc+ mutation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. STAT5 Transcription Factor / metabolism. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19775300.001).
  • [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 / BCL2L1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / STAT5 Transcription Factor; 0 / bcl-X Protein; 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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58. Bhayat F, Das-Gupta E, Hubbard R: Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study. BMC Cancer; 2010;10:514
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  • [Title] Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study.
  • BACKGROUND: We have previously shown that in the UK mortality in people with Acute Myeloid Leukaemia (AML) was nearly 50% greater among the most socio-economically deprived.
  • The aim of this study was to determine whether AML patients from lower socioeconomic classes had a lower chance of receiving a bone marrow transplant.
  • METHODS: Using Hospital Episode Statistics (HES) data, we identified all incident cases of AML admitted to UK hospitals between 1998 and 2007.
  • We calculated the number of bone marrow transplantations undertaken in AML patients, stratifying our results by gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity.
  • We used logistic regression to calculate odds ratios for bone marrow transplantation, adjusting for gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity score.
  • RESULTS: We identified a total of 23 910 incident cases of AML over this 10-year time period, of whom 1 140 (4.8%) underwent BMT.
  • Bone marrow transplantation declined with increasing socioeconomic deprivation (p for trend < 0.001) such that people in the most deprived socioeconomic quintile were 40% less likely to have a transplant than those in the most advantaged group (Odds Ratio 0.60, 95% confidence interval 0.49, 0.73), even after adjusting for gender, age at diagnosis, year of diagnosis and co-morbidity.
  • CONCLUSION: This large cohort study demonstrates that AML patients from lower socioeconomic classes are less likely to undergo bone marrow transplantation than their better off counter-parts.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 20920158.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
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59. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • As the proportion of leukemic blast cells is critical for exact cytochemical analysis, study was restricted to the evaluation of 48 adult and pediatric patients with newly diagnosed AMLs with 80% or more blasts in analyzed samples.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
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60. Saito Y, Uchida N, Tanaka S, Suzuki N, Tomizawa-Murasawa M, Sone A, Najima Y, Takagi S, Aoki Y, Wake A, Taniguchi S, Shultz LD, Ishikawa F: Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML. Nat Biotechnol; 2010 Mar;28(3):275-80
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  • [Title] Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML.
  • Cancer stem cells have been proposed to be important for initiation, maintenance and recurrence of various malignancies, including acute myeloid leukemia (AML).
  • We have previously reported that CD34+CD38- human primary AML stem cells residing in the endosteal region of the bone marrow are relatively chemotherapy resistant.
  • Using a NOD/SCID/IL2rgamma(null) mouse model of human AML, we now show that the AML stem cells in the endosteal region are cell cycle quiescent and that these stem cells can be induced to enter the cell cycle by treatment with granulocyte colony-stimulating factor (G-CSF).
  • In combination with cell cycle-dependent chemotherapy, G-CSF treatment significantly enhances induction of apoptosis and elimination of human primary AML stem cells in vivo.
  • The combination therapy leads to significantly increased survival of secondary recipients after transplantation of leukemia cells compared with chemotherapy alone.

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  • (PMID = 20160717.001).
  • [ISSN] 1546-1696
  • [Journal-full-title] Nature biotechnology
  • [ISO-abbreviation] Nat. Biotechnol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA020408; United States / NCI NIH HHS / CA / CA20408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS519081; NLM/ PMC3857633
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61. Storb R: Can reduced-intensity allogeneic transplantation cure older adults with AML? Best Pract Res Clin Haematol; 2007 Mar;20(1):85-90
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  • [Title] Can reduced-intensity allogeneic transplantation cure older adults with AML?
  • Development of nonablative and reduced-intensity conditioning regimens has enabled older or medically infirm patients with myeloid malignancies to be treated with allogeneic hematopoietic cell transplantation (HCT).
  • These regimens rely largely on graft-versus-leukemia effects rather than high-dose therapy to eliminate malignant cells.
  • This review summarizes the outcome in recent studies of patients with myeloid malignancies who received HCT following nonmyeloablative or reduced-intensity conditioning.
  • Toxicity is a major problem in the elderly who have comorbid conditions, but otherwise the patient has a similar outcome, again emphasizing the graft-versus-leukemia effect.
  • These studies have demonstrated encouraging overall survival and nonrelapse mortalities with evidence for graft-versus-leukemia responses in elderly patients with hematologic malignancies.
  • Relapse and progressive disease continued to be problems, particularly in patients with large tumor burdens at time of HCT.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Graft vs Leukemia Effect. Humans. Meta-Analysis as Topic. Middle Aged. Neoplasm, Residual. Survival Analysis. Transplantation, Homologous. Tumor Burden

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  • (PMID = 17336258.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 11
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62. Owonikoko T, Agha M, Balassanian R, Smith R, Raptis A: Gemtuzumab therapy for isolated extramedullary AML relapse following allogeneic stem-cell transplant. Nat Clin Pract Oncol; 2007 Aug;4(8):491-5
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  • [Title] Gemtuzumab therapy for isolated extramedullary AML relapse following allogeneic stem-cell transplant.
  • BACKGROUND: A 19-year-old male with primary refractory acute myeloid leukemia received salvage therapy with mitoxantrone and cytarabine combination.
  • He received consolidation therapy 3 months later with a matched-unrelated-donor stem-cell transplant.
  • The disease relapsed in the bone marrow (BM) 9 months after the initial stem-cell transplant, and was successfully treated by repeat transplant from the same donor.
  • Ten months following repeat transplant, the patient presented with an increasing number of extramedullary sites of biopsy-proven disease relapse (i.e. cranial and peripheral nerves, tongue, abdominal wall and chest wall).
  • Repeated biopsy of the BM and chimera study showed no morphologic evidence of leukemic infiltrate with 100% donor-cell population.
  • DIAGNOSIS: Isolated extramedullary relapse of acute myeloid leukemia after stem-cell transplant.
  • MANAGEMENT: Primary leukemia treatment with idarubicin, cytarabine, etoposide, dexamethasone, tioguanine on protocol and salvage therapy with mitoxantrone and cytarabine combination for primary refractory disease.
  • A matched-unrelated-donor stem-cell transplant for consolidation and donor-lymphocyte infusions were performed, followed by repeat unrelated-donor transplant for leukemia relapse in the marrow, radiation therapy and gemtuzumab ozogamicin for multiple sites of extramedullary leukemia relapse.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Neoplasm Recurrence, Local / drug therapy. Sarcoma, Myeloid / drug therapy

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  • (PMID = 17657254.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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63. Messner H: Current status of blood and marrow transplantation for patients with AML. Bone Marrow Transplant; 2008 Aug;42 Suppl 1:S14-S17
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  • [Title] Current status of blood and marrow transplantation for patients with AML.
  • Reduced intensity preparations have resulted in lower morbidity and mortality during the pre-engraftment period, but have not reduced later occurring infections, GVHD and relapse.
  • Outcome-determining risk factors that characterize patients at diagnosis as well as during their course include age, cytogenetic configuration, hematopoietic elements and a previous history of myelodysplasia or cytoreductive therapy for a pre-existing malignancy.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy


64. Fiskus W, Wang Y, Sreekumar A, Buckley KM, Shi H, Jillella A, Ustun C, Rao R, Fernandez P, Chen J, Balusu R, Koul S, Atadja P, Marquez VE, Bhalla KN: Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor panobinostat against human AML cells. Blood; 2009 Sep 24;114(13):2733-43
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  • [Title] Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor panobinostat against human AML cells.
  • In this study, we demonstrate that treatment with the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanocin A (DZNep) depletes EZH2 levels, and inhibits trimethylation of lysine 27 on histone H3 in the cultured human acute myeloid leukemia (AML) HL-60 and OCI-AML3 cells and in primary AML cells.
  • In addition, DZNep treatment induced apoptosis in cultured and primary AML cells.
  • Furthermore, compared with treatment with each agent alone, cotreatment with DZNep and the pan-histone deacetylase inhibitor panobinostat caused more depletion of EZH2, induced more apoptosis of AML, but not normal CD34(+) bone marrow progenitor cells, and significantly improved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia.
  • These findings indicate that the combination of DZNep and panobinostat is effective and relatively selective epigenetic therapy against AML cells.

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  • (PMID = 19638619.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA123207; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R01 CA123207-03; United States / NCI NIH HHS / CA / CA123207-03; United States / NCI NIH HHS / CA / R01 CA116629
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Indoles; 0 / Nuclear Proteins; 0 / SUZ12 protein, human; 0 / Transcription Factors; 102052-95-9 / 3-deazaneplanocin; 9647FM7Y3Z / panobinostat; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Polycomb Repressive Complex 2; K72T3FS567 / Adenosine
  • [Other-IDs] NLM/ PMC2756128
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65. Goemans BF, Zwaan CM, Cloos J, de Lange D, Loonen AH, Reinhardt D, Hählen K, Gibson BE, Creutzig U, Kaspers GJ: FLT3 and KIT mutated pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to the tyrosine kinase inhibitor SU11657. Leuk Res; 2010 Oct;34(10):1302-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FLT3 and KIT mutated pediatric acute myeloid leukemia (AML) samples are sensitive in vitro to the tyrosine kinase inhibitor SU11657.
  • New treatment strategies to improve the outcome of pediatric acute myeloid leukemia (AML) are required as 40% of children diagnosed with AML do not survive.
  • Around 30% of pediatric AML patients harbour a mutation in the tyrosine kinases FLT3 (+/-20%) or KIT (+/-10%).
  • In this study we investigated whether pediatric AML samples (N=61) were sensitive to the tyrosine kinase inhibitor SU11657 (similar to the clinically available drug sunitinib) in vitro, and whether sensitivity was related to expression of, and mutations in, FLT3 and KIT.
  • Inclusion in clinical trials should not be restricted to patients with FLT3 or KIT mutations.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Mutation. Organic Chemicals / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Female. Humans. Male

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20435347.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organic Chemicals; 0 / SU 11657; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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66. Savani BN: Transplantation in AML CR1. Blood; 2010 Sep 16;116(11):1822-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transplantation in AML CR1.

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  • [CommentOn] Blood. 2010 Sep 16;116(11):1839-48 [20538804.001]
  • (PMID = 20847206.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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67. Palanisamy N: Chromosomal translocations in AML: detection and prognostic significance. Cancer Treat Res; 2010;145:41-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal translocations in AML: detection and prognostic significance.
  • [MeSH-major] Chromosomes, Human / ultrastructure. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 20306244.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R43CA091532-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 61
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68. Mahmud M, Stebbing J: Epigenetic modifications in AML and MDS. Leuk Res; 2010 Feb;34(2):139-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic modifications in AML and MDS.
  • [MeSH-major] Epigenesis, Genetic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


69. Silva FP, Morolli B, Storlazzi CT, Zagaria A, Impera L, Klein B, Vrieling H, Kluin-Nelemans HC, Giphart-Gassler M: ETV6 mutations and loss in AML-M0. Leukemia; 2008 Aug;22(8):1639-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6 mutations and loss in AML-M0.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18305557.001).
  • [ISSN] 1476-5551
  • [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 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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70. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 8. Clone Cells. Disease Progression. Humans. Male. Mutation. Neoplasms, Second Primary. Trisomy

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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71. Graf M, Reif S, Hecht K, Pelka-Fleischer R, Pfister K, Schmetzer H: High expression of urokinase plasminogen activator receptor (UPA-R) in acute myeloid leukemia (AML) is associated with worse prognosis. Am J Hematol; 2005 May;79(1):26-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of urokinase plasminogen activator receptor (UPA-R) in acute myeloid leukemia (AML) is associated with worse prognosis.
  • CD87) is a membrane protein responsible for plasmin expression on cells facilitating cellular extravasations and tissue invasions.
  • We studied the expression of the UPA-R on bone marrow (BM) cells of 93 patients with acute myeloid leukemia at first diagnosis and 8 healthy probands as controls by FACS analysis using phycoerythrin (PE)-conjugated antibodies.
  • Whereas none of the 8 healthy BM samples was positive for the UPA-R, 32 (34%) of the 93 AML samples were UPA-R+.
  • Expression of UPA-R was heterogeneous in different FAB types, however, with the highest expression rates in monocytic subtypes (FAB M4/M5): 18%/19%/30% of UPA-R+ cases were found in M1/M2 or M3, and 58%/80% of cases with M4 or M5 were UPA-R+.
  • Proportions of UPA-R+ cells varied between 1% and 98% of the mononuclear cell fractions, with the highest proportions in M4/M5 subtypes (on average 27%/40% UPA-R+ cells) and the lowest expression in AML M2 (11% UPA-R+ cells).
  • The density of expressed UPA-R, estimated as mean channel fluorescence activity, was highest in cases with AML M1 (mFI: 124) followed by M4 and M5 (mFI: 78/77) and lowest in AML M2 (mFI: 43).
  • Separating our patients' cohort in cytogenetic risk groups, we could not detect significant differences in the UPA-R expression profiles.
  • For evaluations of the clinical course of AML, only patients treated by the AML-CG protocol (n = 65) were included.
  • In the group of patients who did not respond to AML-CG therapy, significantly higher proportions of UPA-R+ cells (31% vs. 14%, P = 0.0015, t-test) were found.
  • In summary, our data show a high expression of the UPA-R in AML, especially in (myelo)monocytoid subtypes.
  • Cases with higher proportions of UPA-R+ cells were characterized by a significant lower remission rate after AML-CG therapy and a higher risk for relapse.
  • UPA-R positivity may identify subtypes of AML associated with a more aggressive clinical course.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Receptors, Cell Surface / genetics

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 15849776.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Genetic Markers; 0 / PLAUR protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator
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72. Lakshmikuttyamma A, Scott SA, DeCoteau JF, Geyer CR: Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition. Oncogene; 2010 Jan 28;29(4):576-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reexpression of epigenetically silenced AML tumor suppressor genes by SUV39H1 inhibition.
  • In support of this model, we found in acute myeloid leukemia cells with hypermethylated p15INK4B and E-cadherin promoters that the DNMT inhibitor, 5-aza-2'-deoxycytidine, induced p15INK4B and E-cadherin expression, and decreased levels of DNA methylation, histone H3 lysine 9 (H3K9) methylation and SUV39H1 associated with p15INK4B and E-cadherin promoters.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Methyltransferases / metabolism. RNA Interference. Repressor Proteins / metabolism
  • [MeSH-minor] Apoptosis. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cadherins / genetics. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p15 / genetics. DNA Methylation / drug effects. DNA Modification Methylases / antagonists & inhibitors. DNA Modification Methylases / metabolism. Enzyme Inhibitors / pharmacology. Humans. Promoter Regions, Genetic

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  • (PMID = 19881540.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cadherins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Enzyme Inhibitors; 0 / Repressor Proteins; 776B62CQ27 / decitabine; EC 2.1.1. / SUV39H1 protein, human; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.- / Methyltransferases; M801H13NRU / Azacitidine
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73. Miyawaki S: [The state-of-the-art chemotherapy for AML]. Rinsho Ketsueki; 2010 Oct;51(10):1328-37
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  • [Title] [The state-of-the-art chemotherapy for AML].
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Humans. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 20962465.001).
  • [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
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74. Abboud CN: Another nail in the AML coffin. Blood; 2009 Jun 11;113(24):6045-6

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  • [Title] Another nail in the AML coffin.

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  • [CommentOn] Blood. 2009 Jun 11;113(24):6206-14 [19050309.001]
  • [CommentOn] Blood. 2009 Jun 11;113(24):6215-24 [18955566.001]
  • (PMID = 19520813.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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75. Rowe JM: Closer to the truth in AML. Blood; 2009 Apr 30;113(18):4129-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Closer to the truth in AML.

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  • [CommentOn] Blood. 2009 Apr 30;113(18):4179-87 [19008455.001]
  • (PMID = 19406994.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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76. Lannert H, Lenze M, Able T, Park BJ, Lenze A, Meissner S, Eckstein V, Ho AD, Leicht S, Franz T: Changes in phosphorylation and dephosphorylation status of cytoskeleton and their regulator proteins in CD34+ stem cells after G-CSF stimulation and in AML. J Clin Oncol; 2009 May 20;27(15_suppl):e22067

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes in phosphorylation and dephosphorylation status of cytoskeleton and their regulator proteins in CD34+ stem cells after G-CSF stimulation and in AML.
  • It is a dynamic structure that maintains cell shape, enables cellular motion.
  • In this study we investigated the expression of cytoskeleton proteins in native hematopoietic CD34+ stem cells from BM in comparison to mobilized peripheral blood stem cells (mPBSCs) from G-CSF stimulated donors as well as CD34+ cells from AML.
  • METHODS: An Auto-MACS (Miltenyi) and FACS Vantage SE cell sorter (Becton Dickinson) was used to process high enriched (>99%) CD34+ cells fractions from MNCs.
  • Stathmin is overexpressed in G-CSF mobilized hematopoietic stem cells and in AML in his active 'dephosphorylated' form.
  • Our results show, that mobilized stem cells "in vivo" and AML cells increase cytoskeleton proteins expression and cause a complex phosphorylation status, which may explain the regulation of migration and metastasis.

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  • (PMID = 27963210.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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77. Wakui M, Kuriyama K, Miyazaki Y, Hata T, Taniwaki M, Ohtake S, Sakamaki H, Miyawaki S, Naoe T, Ohno R, Tomonaga M: Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol. Int J Hematol; 2008 Mar;87(2):144-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.
  • We reviewed and categorized 638 of 809 patients who were registered in the Japan Adult Leukemia Study Group acute myeloid leukemia (AML)-97 protocol using morphological means.
  • Patients with the M3 subtype were excluded from the study group.
  • According to the WHO classification, 171 patients (26.8%) had AML with recurrent genetic abnormalities, 133 (20.8%) had AML with multilineage dysplasia (MLD), 331 (51.9%) had AML not otherwise categorized, and 3 (0.5%) had acute leukemia of ambiguous lineage.
  • The platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in AML with MLD than in the other WHO categories.
  • Overall survival (OS) did not significantly differ between nine patients with t(9;11) and 23 with other 11q23 abnormalities (P = 0.22).
  • Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with AML, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries


78. Pinheiro RF, Moreira Ede S, Silva MR, Greggio B, Alberto FL, Chauffaille Mde L: FLT3 mutation and AML/ETO in a case of Myelodysplastic syndrome in transformation corroborates the two hit model of leukemogenesis. Leuk Res; 2007 Jul;31(7):1015-8
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  • [Title] FLT3 mutation and AML/ETO in a case of Myelodysplastic syndrome in transformation corroborates the two hit model of leukemogenesis.
  • The aim of this report is to present a case of Myelodysplastic syndrome (MDS) who presented, during AML transformation, a step-wise genetic progression that corroborates the two hit model of leukemogenesis.
  • A RCDM-RS (WHO)/RARS (FAB) patient with normal karyotype at diagnosis, evolved into AML after six months of follow up.
  • At transformation, AML/ETO fusion was detected, although marrow blast cells were not increased until 21 days later, when FLT3-ITD was also demonstrated pointing out that the overgrowth of the FLT3/ITD clone was concomitant with the outburst of marrow blasts.
  • These findings corroborates the two hit model of leukemogenesis in which one class of mutations (Class I) (FLT3/ITD) confers a proliferative or survival advantage to cells, and a second class of mutations (Class II) (AML/ETO) interferes with hematopoietic differentiation.
  • [MeSH-major] Cell Transformation, Neoplastic. Core Binding Factor Alpha 2 Subunit / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics. Oncogene Proteins, Fusion / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Bone Marrow / pathology. Disease Progression. Female. Humans. Middle Aged. Tandem Repeat Sequences

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  • (PMID = 17079011.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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79. Damiani D, Tiribelli M, Raspadori D, Michelutti A, Gozzetti A, Calistri E, Candoni A, Chiarvesio A, Lenoci M, Russo D, Fanin R: The role of MDR-related proteins in the prognosis of adult acute myeloid leukaemia (AML) with normal karyotype. Hematol Oncol; 2007 Mar;25(1):38-43
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  • [Title] The role of MDR-related proteins in the prognosis of adult acute myeloid leukaemia (AML) with normal karyotype.
  • Cytogenetic abnormalities are among the most important factors affecting the outcome of patients with acute myeloid leukaemia (AML), but approximately 40-50% of AML cases display a normal karyotype at diagnosis.
  • Multidrug resistance (MDR) proteins overexpression is associated with worse prognosis in acute leukaemias, but its role in normal karyotype AML is less defined.
  • We analysed the expression of P-glycoprotein (PGP), MDR-related protein (MRP) and lung resistance protein (LRP) in 135 adult patients with normal karyotype AML and its correlation with other biological features of the disease, to evaluate the impact of MDR proteins on response to therapy and on survival.
  • Our data confirm the prognostic role of MDR proteins, in particular of PGP, also in AML patients with normal karyotype at diagnosis.
  • This finding could be used to stratify patients with different prognosis and to design risk-adapted therapeutic strategies.
  • [MeSH-major] Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. P-Glycoproteins / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Cytogenetic Analysis. Disease-Free Survival. Female. Humans. Karyotyping. Male. Middle Aged. Multidrug Resistance-Associated Proteins / analysis. P-Glycoprotein / analysis. Prognosis. Remission Induction

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  • (PMID = 17200981.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins
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80. Didier C, Cavelier C, Quaranta M, Galcera MO, Demur C, Laurent G, Manenti S, Ducommun B: G2/M checkpoint stringency is a key parameter in the sensitivity of AML cells to genotoxic stress. Oncogene; 2008 Jun 19;27(27):3811-20
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  • [Title] G2/M checkpoint stringency is a key parameter in the sensitivity of AML cells to genotoxic stress.
  • Acute myeloid leukemia (AML) cells exposed to genotoxic agents arrest their cell cycle at the G2/M checkpoint and are inherently chemoresistant.
  • To understand the mechanism of this chemoresistance, we compared the ability of immature CD34+ versus mature CD34- AML cell lines (KG1a and U937, respectively) to recover from a DNA damage-induced cell cycle checkpoint in G2.
  • We show that in both cell types, the CDC25B phosphatase participates in the G2/M checkpoint recovery and that its expression is upregulated.
  • Similarly, UCN-01 treatment potentializes genotoxic-induced inhibition of colony formation efficiency of primary leukemic cells from AML patients.
  • Altogether, our results demonstrate that checkpoint stringency varies during the maturation process and indicate that targeting checkpoint mechanisms might represent an attractive therapeutic opportunity for chemoresistant immature AML cells.
  • [MeSH-major] Cell Division. G2 Phase. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD34 / analysis. Antineoplastic Agents / toxicity. Cell Line, Tumor. Colony-Forming Units Assay. Humans. Mitosis / drug effects. Nocodazole / pharmacology. Staurosporine / analogs & derivatives. Staurosporine / toxicity. U937 Cells. cdc25 Phosphatases / metabolism

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  • (PMID = 18212737.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 7BU5H4V94A / 7-hydroxystaurosporine; EC 3.1.3.48 / cdc25 Phosphatases; H88EPA0A3N / Staurosporine; SH1WY3R615 / Nocodazole
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81. Petrovici K, Graf M, Hecht K, Reif S, Pfister K, Schmetzer H: Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis. Cancer Genomics Proteomics; 2010 Jul-Aug;7(4):173-80
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  • [Title] Use of NG2 (7.1) in AML as a tumor marker and its association with a poor prognosis.
  • We analyzed 70 bone marrow (BM) samples from acute myeloid leukemia (AML) patients for 11q23 aberrations and reactivity with the monoclonal antibody NG2.
  • We detected NG2(+) cells in AML cases with normal karyotype, however, not in healthy BM cells.
  • This means that NG2 qualifies as a reliable AML blast tumor marker, enabling monitoring of the course of AML independently of, although often associated with, 11q23-aberrations.
  • While 31% of the patients with NG2(+) cells responded to chemotherapy, 58% of the group with NG2(+) cells did not respond (p=0.047).
  • In conclusion, NG2 detects many, but not all 11q23 aberrations and other cases without 11q23 aberrations.
  • However, it does not react with healthy BM cells, thereby contributing to the detection of patients with poor prognosis.
  • [MeSH-major] Antigens / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Proteoglycans / analysis

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  • (PMID = 20656983.001).
  • [ISSN] 1790-6245
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens; 0 / Biomarkers, Tumor; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4
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82. Willasch AM, Gruhn B, Coliva T, Kalinova M, Schneider G, Kreyenberg H, Steinbach D, Weber G, Hollink IH, Zwaan CM, Biondi A, van der Velden VH, Reinhardt D, Cazzaniga G, Bader P, Trka J, European Study Group on WT1 Expression in Childhood AML: Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study. Leukemia; 2009 Aug;23(8):1472-9
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  • [Title] Standardization of WT1 mRNA quantitation for minimal residual disease monitoring in childhood AML and implications of WT1 gene mutations: a European multicenter study.
  • A standardized, sensitive and universal method for minimal residual disease (MRD) detection in acute myeloid leukemia (AML) is still pending.
  • Although hyperexpression of Wilms' tumor (WT1) gene transcript has been frequently proposed as an MRD marker in AML, wide comparability of the various methods used for evaluating WT1 expression has not been given.
  • We established and standardized a multicenter approach for quantifying WT1 expression by quantitative reverse transcriptase PCR (qRT-PCR), on the basis of a primer/probe set combination at exons 6 and 7.
  • In a series of quality-control rounds, we analyzed 69 childhood AML samples and 47 normal bone marrow (BM) samples from 4 participating centers.
  • Differences in the individual WT1 expressions levels ranged within <0.5 log of the mean in 82% of the cases.
  • In AML samples, the median WT1/1E+04 Abelson (ABL) expression was 3.5E+03 compared with that of 2.3E+01 in healthy BM samples.
  • As 11.5% of childhood AML samples in this cohort harbored WT1 mutations in exon 7, the effect of mutations on WT1 expression has been investigated, showing that mutated cases expressed significantly higher WT1 levels than wild-type cases.
  • [MeSH-major] Bone Marrow Examination / standards. Genes, Wilms Tumor. Leukemia, Myeloid / pathology. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / standards
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Cohort Studies. DNA Primers. Exons / genetics. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Male. Middle Aged. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm, Residual. Sensitivity and Specificity. WT1 Proteins / biosynthesis. Young Adult

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  • (PMID = 19322206.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
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83. van den Heuvel-Eibrink MM, van der Holt B, Burnett AK, Knauf WU, Fey MF, Verhoef GE, Vellenga E, Ossenkoppele GJ, Löwenberg B, Sonneveld P: CD34-related coexpression of MDR1 and BCRP indicates a clinically resistant phenotype in patients with acute myeloid leukemia (AML) of older age. Ann Hematol; 2007 May;86(5):329-37
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  • [Title] CD34-related coexpression of MDR1 and BCRP indicates a clinically resistant phenotype in patients with acute myeloid leukemia (AML) of older age.
  • Clinical resistance to chemotherapy in acute myeloid leukemia (AML) is associated with the expression of the multidrug resistance (MDR) proteins P-glycoprotein, encoded by the MDR1/ABCB1 gene, multidrug resistant-related protein (MRP/ABCC1), the lung resistance-related protein (LRP), or major vault protein (MVP), and the breast cancer resistance protein (BCRP/ABCG2).
  • The clinical value of MDR1, MRP1, LRP/MVP, and BCRP messenger RNA (mRNA) expression was prospectively studied in 154 newly diagnosed AML patients >or=60 years who were treated in a multicenter, randomized phase 3 trial.
  • Expression of MDR1 and BCRP showed a negative whereas MRP1 and LRP showed a positive correlation with high white blood cell count (respectively, p < 0.05, p < 0.001, p < 0.001 and p < 0.001).
  • Higher BCRP mRNA was associated with secondary AML (p < 0.05).
  • When adjusted for other prognostic actors, only CD34-related MDR1/BCRP coexpression remained significantly associated with a lower CR rate (p = 0.03), thereby identifying a clinically resistant subgroup of elderly AML patients.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Multidrug Resistance-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Antigens, CD34 / metabolism. Disease-Free Survival. Humans. Middle Aged. Phenotype. Prospective Studies. RNA, Messenger / metabolism. Vault Ribonucleoprotein Particles / metabolism


84. Adhya AK, Varma N, Varma S: Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases. Indian J Pathol Microbiol; 2007 Jul;50(3):655-8
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  • [Title] Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases.
  • Bone marrow mastocytosis, though infrequently documented in Indian patients, may be observed in association with many non mast cell hematological neoplasms, including acute myeloblastic leukemia (AML) and myelodysplastic syndromes (MDS).
  • We report three cases of acute myeloid leukemia with excess of mast cells in the bone marrow (BM) samples.
  • Mast cell hyperplasia may remain under diagnosed due to shortcoming of morphological identification and diagnostic workup.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Mast Cells / pathology. Mastocytosis, Systemic / pathology


85. de Jonge HJ, de Bont ES, Valk PJ, Schuringa JJ, Kies M, Woolthuis CM, Delwel R, Veeger NJ, Vellenga E, Löwenberg B, Huls G: AML at older age: age-related gene expression profiles reveal a paradoxical down-regulation of p16INK4A mRNA with prognostic significance. Blood; 2009 Oct 1;114(14):2869-77
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  • [Title] AML at older age: age-related gene expression profiles reveal a paradoxical down-regulation of p16INK4A mRNA with prognostic significance.
  • Acute myeloid leukemia (AML) has a different clinical and biologic behavior in patients at older age.
  • After validation with 2 independent AML cohorts, the 969 differentially regulated probe sets on aging could be pointed to 41 probe sets, including the tumor-suppressor gene CDKN2A (encoding p16(INK4A)).
  • In contrast to the induced p16(INK4A) expression that is associated with physiologic aging, p16(INK4A) is down-regulated in AML samples of patients with increasing age.
  • However, this was only noticed in the intermediate- and unfavorable-risk group and not in the favorable-risk group and the molecularly defined subset "NPM1 mutant without FLT3-ITD."
  • We conclude that, in addition to altered clinical and biologic characteristics, AML presenting at older age shows different gene expression profiles.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics

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  • (PMID = 19667402.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger
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86. Schmelz K, Sattler N, Wagner M, Lübbert M, Dörken B, Tamm I: Induction of gene expression by 5-Aza-2'-deoxycytidine in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) but not epithelial cells by DNA-methylation-dependent and -independent mechanisms. Leukemia; 2005 Jan;19(1):103-11
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  • [Title] Induction of gene expression by 5-Aza-2'-deoxycytidine in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) but not epithelial cells by DNA-methylation-dependent and -independent mechanisms.
  • The methylation inhibitor 5-Aza-2'-deoxycytidine (5-Aza-CdR, decitabine) has therapeutic efficacy in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Using microarray analysis, we investigated global changes in gene expression after 5-Aza-CdR treatment in AML.
  • In the AML cell line OCI-AML2, Aza-CdR induced the expression of 81 out of 22 000 genes; 96 genes were downregulated (> or =2-fold change in expression).
  • RT-PCR analysis of 10 randomly selected genes confirmed the changes of expression in AML cells.
  • Similar results were obtained with primary AML and MDS cells after treatment with 5-Aza-CdR ex vivo and in vivo, respectively.
  • DNA methylation inversely correlated with MPO expression in newly diagnosed untreated AML patients (P< or =0.004).
  • [MeSH-major] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. DNA Methylation. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Apoptosis / drug effects. Base Sequence. Cell Division / drug effects. DNA Primers. Epithelial Cells / drug effects. Humans. Polymerase Chain Reaction


87. Cárdenas-Blanco A, Olariou E, Cameron I: Poster - Thurs Eve-28: New brain diffusion analysis method: White matter grey matter dissasociation. Med Phys; 2008 Jul;35(7Part2):3406

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  • The significance of the present diffusion decay study lies in the combination of three novel procedures to provide a better characterization of the diffusion decay: i) the acquisition of a large number of b-values (96 b-values up to 10,000 s/mm<sup>2</sup> ), ii) the application of a noise correction technique (3) to the acquired data, and iii) the use of a Non Negative Least Squares (NNLS) fitting algorithm to evaluate the diffusion coefficients.
  • The NNLS algorithm is used to fit the corrected data instead of the more commonly used Levenberg-Marquardt algorithm since the NNLS algorithm does not require the number of components to be specified, nor does it need initial estimates of the fitting parameters as input; thus giving it more versatility as a fitting tool for the diffusion decay.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28512828.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Brain / Diffusion / Medical imaging / Medical magnetic resonance imaging / Neural information
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88. Imai N, Miwa H, Shikami M, Suganuma K, Gotoh M, Hiramatsu A, Wakabayashi M, Watarai M, Hanamura I, Imamura A, Mihara H, Shitara K, Shibuya M, Nitta M: Growth inhibition of AML cells with specific chromosome abnormalities by monoclonal antibodies to receptors for vascular endothelial growth factor. Leuk Res; 2009 Dec;33(12):1650-7
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  • [Title] Growth inhibition of AML cells with specific chromosome abnormalities by monoclonal antibodies to receptors for vascular endothelial growth factor.
  • By using neutralizing monoclonal antibodies to vascular endothelial growth factor receptor type 1 (VEGFR1) and VEGFR2, we have shown that acute myelogenous leukemia (AML) cells with specific chromosome abnormalities are dependent on VEGF/VEGFR system.
  • AML with t(8;21) is the most dependent subtype on VEGF with both VEGFR1 and VEGFR2. t(15;17)AML cells depend on VEGF with VEGFR1.
  • AML cells with 11q23 abnormalities showed variable dependence on VEGF.
  • The growth of t(11;19)AML cells are most extensively inhibited by anti-VEGFR1 antibody.
  • Then, the growth of Kasumi-1, a t(8;21) cell line was suppressed by either anti-VEGFR1 antibody (p=0.0022) or anti-VEGFR2 antibody (p=0.0029) in a dose-dependent manner.
  • The growth of NB4, a t(15;17) cell line was more potently suppressed by anti-VEGFR1 antibody (p=0.0111) than by anti-VEGFR2 antibody (p=0.0477).
  • As for downstream signals, we have shown that VEGFR2 transduce growth and survival signals through phosphorylation of Akt and MEK in leukemia cells (Kasumi-1).
  • Finally, our data suggested that autocrine pathway of VEGF and VEGFRs observed in AML cells with specific chromosomal translocations have contributed to leukemogenesis as activated signaling of receptor tyrosine kinase.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Cell Division / immunology. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Receptors, Vascular Endothelial Growth Factor / immunology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Proliferation. Humans. Phosphorylation

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  • (PMID = 19342098.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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89. Dunne J, Cullmann C, Ritter M, Soria NM, Drescher B, Debernardi S, Skoulakis S, Hartmann O, Krause M, Krauter J, Neubauer A, Young BD, Heidenreich O: siRNA-mediated AML1/MTG8 depletion affects differentiation and proliferation-associated gene expression in t(8;21)-positive cell lines and primary AML blasts. Oncogene; 2006 Oct 05;25(45):6067-78
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  • [Title] siRNA-mediated AML1/MTG8 depletion affects differentiation and proliferation-associated gene expression in t(8;21)-positive cell lines and primary AML blasts.
  • The chromosomal translocation t(8;21) is associated with 10-15% of all cases of acute myeloid leukaemia (AML).
  • We studied the effects of small interfering RNA (siRNA)-mediated AML1/MTG8 depletion on global gene expression in t(8;21)-positive leukaemic cell lines and in primary AML blasts using cDNA arrays, oligonucleotide arrays and real-time reverse transcription-polymerase chain reaction (RT-PCR).
  • Suppression of AML1/MTG8 results in the increased expression of genes associated with myeloid differentiation, such as AZU1, BPI, CTSG, LYZ and RNASE2 as well as of antiproliferative genes such as IGFBP7, MS4A3 and SLA both in blasts and in cell lines.
  • Furthermore, expression levels of several genes affiliated with drug resistance or indicative of poor prognosis AML (BAALC, CD34, PRG2, TSPAN7) are affected by AML1/MTG8 depletion.
  • In conclusion, siRNA-mediated suppression of AML1/MTG8 cause very similar changes in gene expression pattern in t(8;21)-positive cell lines and in primary AML blasts.
  • [MeSH-major] Cell Differentiation / genetics. Cell Proliferation. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / physiology. DNA-Binding Proteins / physiology. Gene Expression Regulation, Neoplastic / physiology. Leukemia, Myeloid / genetics. Proto-Oncogene Proteins / physiology. RNA, Small Interfering / physiology. Transcription Factors / physiology. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Base Sequence. Cell Line, Tumor. DNA Primers. Gene Expression Profiling. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16652140.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [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 Primers; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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90. Paulsson K, Heidenblad M, Strömbeck B, Staaf J, Jönsson G, Borg A, Fioretos T, Johansson B: High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia; 2006 May;20(5):840-6
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  • [Title] High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration.
  • Although trisomy 8 as the sole chromosome aberration is the most common numerical abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), little is known about its pathogenetic effects.
  • Considering that +8 is a frequent secondary change in AML/MDS, cryptic--possibly primary--genetic aberrations may occur in cases with trisomy 8 as the apparently single anomaly.
  • We performed a high-resolution genome-wide array-based comparative genome hybridization (array CGH) analysis of 10 AML/MDS cases with isolated +8, utilizing a 32K bacterial artificial chromosome array set, providing >98% coverage of the genome with a resolution of 100 kb.
  • Array CGH revealed intrachromosomal imbalances, not corresponding to known genomic copy number polymorphisms, in 4/10 cases, comprising nine duplications and hemizygous deletions ranging in size from 0.5 to 2.2 Mb.
  • A 1.8 Mb deletion at 7p14.1, which had occurred prior to the +8, was identified in MDS transforming to AML.
  • The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive AML/MDS cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Genome. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization / methods. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged


91. Berger M, Ferrero I, Vassallo E, Gastaldo L, Carraro F, Biasin E, Madon E, Fagioli F: Stem cell transplantation as consolidation therapy for children in first-remission AML: a single-center report. Pediatr Hematol Oncol; 2005 Oct-Nov;22(7):597-608
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  • [Title] Stem cell transplantation as consolidation therapy for children in first-remission AML: a single-center report.
  • A large number of patients affected by acute myeloid leukemia (AML) achieve complete remission following induction chemotherapy based on high-dose aracytin and anthracyclines.
  • Sixteen patients with newly diagnosed AML received induction chemotherapy according to the AIEOP LAM 92P/Mod protocol.
  • All patients were HLA-typed, and if no donor was identified within the family, patients underwent autologous stem cell transplantation (autoSCT) with mafosfamide-purged bone marrow.
  • Patients with very high-risk AML (cytogenetics with t(9;22), hyperleukocytosis (540x10(9)/L), and AML-M7 with trilineage myelodysplasia) underwent unrelated donor transplantation.
  • The median interval between diagnosis and transplant was 175 days (129-277).
  • Taking stem cell transplantation as the starting point, overall survival was 93%, disease-free survival (according to the chosen treatment) was 80%, the relapse rate was 20%, and transplant-related mortality was 0%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Antineoplastic Agents / administration & dosage. Bone Marrow Purging / methods. Child. Child, Preschool. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Infant. Male. Recurrence. Remission Induction. Retrospective Studies. Transplantation, Autologous. Transplantation, Homologous

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  • (PMID = 16166053.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
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92. Creutzig U, Zimmermann M, Lehrnbecher T, Graf N, Hermann J, Niemeyer CM, Reiter A, Ritter J, Dworzak M, Stary J, Reinhardt D: Less toxicity by optimizing chemotherapy, but not by addition of granulocyte colony-stimulating factor in children and adolescents with acute myeloid leukemia: results of AML-BFM 98. J Clin Oncol; 2006 Sep 20;24(27):4499-506
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  • [Title] Less toxicity by optimizing chemotherapy, but not by addition of granulocyte colony-stimulating factor in children and adolescents with acute myeloid leukemia: results of AML-BFM 98.
  • PURPOSE: To improve prognosis in children with acute myeloid leukemia (AML) by randomized comparisons of (1) two short consolidation cycles versus the Berlin-Frankfurt-Muenster (BFM) -type biphasic 6-week consolidation and (2) the prophylactic administration of granulocyte colony-stimulating factor (G-CSF) versus no G-CSF.
  • Further, therapy for standard risk patients was intensified by addition of a second induction, HAM (high-dose cytarabine and mitoxantrone).
  • PATIENTS AND METHODS: Four hundred seventy-three patients younger than 18 years with de novo AML were enrolled in trial AML-BFM 98.
  • Compared with trial AML-BFM 93, early deaths decreased from 7.4 to 3.2% (P = .005), and 5-year overall survival increased from 58% to 62% (log-rank P = .03).
  • G-CSF shortened neutropenia, but did not reduce the rate of severe infections.
  • Intensification of induction therapy did not improve prognosis of standard-risk patients (event-free survival, 62% v 67%).
  • CONCLUSION: Overall results were improved by neither the administration of G-CSF nor by cycle therapy; however, the latter was easier to perform.
  • Compared with study AML-BFM 93, therapy intensification with HAM in standard-risk patients did not result in improved prognosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cranial Irradiation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Idarubicin / administration & dosage. Idarubicin / adverse effects. Infant. Infection / etiology. Male. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Neutropenia / chemically induced. Neutropenia / prevention & control. Radiotherapy, Adjuvant. Risk Assessment. Risk Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 16983120.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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93. Ho PA, Alonzo TA, Kopecky KJ, Miller KL, Kuhn J, Zeng R, Gerbing RB, Raimondi SC, Hirsch BA, Oehler V, Hurwitz CA, Franklin JL, Gamis AS, Petersdorf SH, Anderson JE, Reaman GH, Baker LH, Willman CL, Bernstein ID, Radich JP, Appelbaum FR, Stirewalt DL, Meshinchi S: Molecular alterations of the IDH1 gene in AML: a Children's Oncology Group and Southwest Oncology Group study. Leukemia; 2010 May;24(5):909-13
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  • [Title] Molecular alterations of the IDH1 gene in AML: a Children's Oncology Group and Southwest Oncology Group study.
  • Recent whole-genome sequencing efforts led to the identification of IDH1(R132) mutations in acute myeloid leukemia (AML) patients.
  • We studied the prevalence and clinical implications of IDH1 genomic alterations in pediatric and adult AML.
  • Diagnostic DNA from 531 AML patients treated on Children's Oncology Group trial COG-AAML03P1 (N=257), and Southwest Oncology Group trials SWOG-9031, SWOG-9333 and SWOG-9500 (N=274), were tested for IDH1 mutations.
  • Patients with IDH1(R132) mutations trended toward higher median diagnostic white blood cell counts (59.2 x 10(9) vs 29.1 x 10(9) per liter, P=0.19) than those without mutations, but the two groups did not differ significantly in age, bone marrow blast percentage, overall survival or relapse-free survival.
  • IDH1 mutations were not detected in pediatric AML, and are uncommon in adult AML.

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  • [Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]
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  • (PMID = 20376086.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA027057; United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / U10 CA032102-30; United States / NCI NIH HHS / CA / U10 CA098543-03; United States / NCI NIH HHS / CA / CA12213; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / K23 CA92405; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / CA114563; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / N01 CA038926; United States / NCI NIH HHS / CA / N01 CA027057; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA020319; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA038926; United States / NCI NIH HHS / CA / R21 CA102624; United States / NCI NIH HHS / CA / CA27057; United States / NCI NIH HHS / CA / R01 CA114563-04; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Codon; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS184578; NLM/ PMC2945692
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94. Erikstein BS, McCormack E, Tronstad KJ, Schwede F, Berge R, Gjertsen BT: Protein kinase A activators and the pan-PPAR agonist tetradecylthioacetic acid elicit synergistic anti-leukaemic effects in AML through CREB. Leuk Res; 2010 Jan;34(1):77-84
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  • [Title] Protein kinase A activators and the pan-PPAR agonist tetradecylthioacetic acid elicit synergistic anti-leukaemic effects in AML through CREB.
  • We combined protein kinase A (PKA) activation with a pan-peroxisome proliferator-activated receptor (PPAR) activator tetradecylthioacetic acid, resulting in synergistic decrease in viability of AML cell lines.
  • PKA isoform II activation appeared to be involved in inhibition of proliferation but not induction of apoptosis in HL-60 cells.
  • Preclinical studies employing the rat AML model Brown Norwegian Myeloid Leukaemia also indicated anti-leukaemic activity of the combination therapy in vivo.
  • [MeSH-major] Cyclic AMP Response Element-Binding Protein / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Enzyme Activators / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Peroxisome Proliferator-Activated Receptors / agonists. Sulfides / therapeutic use

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19786302.001).
  • [ISSN] 1873-5835
  • [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 / Cyclic AMP Response Element-Binding Protein; 0 / Enzyme Activators; 0 / Peroxisome Proliferator-Activated Receptors; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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95. Miyawaki S, Emi N, Mitani K, Oyashiki K, Kitamura K, Morishita T, Ogawa H, Komatsu N, Soma T, Tamaki T, Kosugi H, Ohnishi K, Mizoguchi H, Hiraoka A, Kodera Y, Ueda R, Morishima Y, Nakagawa M, Tobita T, Sugimoto K, Chiba S, Inoue N, Hamaguchi M, Koga D, Tamaki H, Naoe T, Sugiyama H, Takaku F: [Clinical course of the disease and the level of WT1 mRNA in 191 patients with acute myeloid leukemia (AML): joint research by 23 institutions in Japan]. Rinsho Ketsueki; 2005 Dec;46(12):1279-87
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  • [Title] [Clinical course of the disease and the level of WT1 mRNA in 191 patients with acute myeloid leukemia (AML): joint research by 23 institutions in Japan].
  • We evaluated the clinical course of acute myeloid leukemia (AML) and the levels of WT1 mRNA in 191 AML patients.
  • Of 114 previously untreated patients with AML, 107 cases were positive for WT1 mRNA (93.9% : 107/114).
  • On the other hand, WT1 mRNA was expressed in 87.0% of non-remission cases (47/54), maintaining 50 copies/microg of RNA or higher ("positive").
  • In all 29 cases who relapsed during the follow-up observation period after achieving remission, WT1 mRNA levels declined transiently approximately around the time of achieving remission and then rose again when the disease relapsed.
  • In 79.3% of relapsed cases (23/29), WT1 mRNA levels rose above 200 copies/microg RNA, 43 days (median) before the diagnosis of "relapse".
  • Given the percent of the correct diagnosis, WT1 mRNA at 200 copies/microg RNA appeared to be a reasonable cut-off level for early detection of AML-relapse.
  • Taken together, these findings indicate that WT1 mRNA levels allow us to detect the presence of so-called "minimal residual disease" (leukemic cells) that cannot be detected by morphological examination.
  • Besides these promising data, this kit is suitable for routine monitoring of AML because this kit utilizes peripheral blood as a test specimen, reducing the patient's burden at the time of collection of clinical samples as compared with bone marrow aspirate.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid, Acute / diagnosis. RNA, Messenger / blood. RNA, Neoplasm / blood. WT1 Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Early Diagnosis. Female. Humans. Japan. Male. Middle Aged. Monitoring, Physiologic / methods. Neoplasm Recurrence, Local / diagnosis. Neoplasm, Residual / diagnosis. Polymerase Chain Reaction / methods. Reagent Kits, Diagnostic

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  • (PMID = 16447800.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Multicenter Study
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Reagent Kits, Diagnostic; 0 / WT1 Proteins
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96. Bachas C, Schuurhuis GJ, Hollink IH, Kwidama ZJ, Goemans BF, Zwaan CM, van den Heuvel-Eibrink MM, de Bont ES, Reinhardt D, Creutzig U, de Haas V, Assaraf YG, Kaspers GJ, Cloos J: High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine. Blood; 2010 Oct 14;116(15):2752-8
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  • [Title] High-frequency type I/II mutational shifts between diagnosis and relapse are associated with outcome in pediatric AML: implications for personalized medicine.
  • Although virtually all pediatric patients with acute myeloid leukemia (AML) achieve a complete remission after initial induction therapy, 30%-40% of patients will encounter a relapse and have a dismal prognosis.
  • To determine relevance of established AML type I/II mutations that may serve as therapeutic targets, we assessed frequencies of these mutations and their persistence during disease progression in a large group (n = 69) of paired diagnosis and relapse pediatric AML specimens.
  • In 26 of 42 patients (61%) harboring mutations at either stage of the disease, mutation status changed between diagnosis and relapse, particularly in FLT3, WT1, and RAS genes.
  • These findings suggest that mutational shifts affect disease progression.
  • We hence propose that risk stratification, malignant cell detection, and selection of personalized treatment should be based on status of type I/II mutations both at initial diagnosis and during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precision Medicine

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  • [CommentIn] Blood. 2010 Oct 14;116(15):2622-3 [20947687.001]
  • (PMID = 20592250.001).
  • [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 / Biomarkers, Tumor; 0 / DNA Primers; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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97. Faderl S, Ferrajoli A, Harris D, Van Q, Priebe W, Estrov Z: WP-1034, a novel JAK-STAT inhibitor, with proapoptotic and antileukemic activity in acute myeloid leukemia (AML). Anticancer Res; 2005 May-Jun;25(3B):1841-50
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  • [Title] WP-1034, a novel JAK-STAT inhibitor, with proapoptotic and antileukemic activity in acute myeloid leukemia (AML).
  • Cytokine stimulation induces proliferation and growth of acute myeloid leukemia (AML) blasts and high levels of cytokines have been associated with poor prognosis in AML.
  • We investigated whether WP-1034, a novel Jak-Stat inhibitor, is active against AML blasts.
  • OCIM2 and fresh AML cells were incubated with 1 to 6 microM WP-1034 to determine its effect on proliferation.
  • WP-1034 effectively inhibited proliferation of OCIM2 cells and fresh AML samples.
  • Analysis of cell cycle status by PI staining and flow cytometry showed that WP-1034 caused cell cycle arrest of OCIM2 cells in sub-Go phase.
  • Taken together, our data suggest that WP-1034 is a potent inhibitor of AML cell proliferation by inhibition of Stat 3 and 5 and induction of caspase-dependent apoptosis.
  • [MeSH-major] Acrylamides / pharmacology. Apoptosis / drug effects. DNA-Binding Proteins / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Milk Proteins / antagonists & inhibitors. Nitriles / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Trans-Activators / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Adult. Aged. Antineoplastic Agents / pharmacology. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Enzyme Activation / drug effects. Female. Humans. Janus Kinase 1. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / enzymology. Leukemia, Erythroblastic, Acute / pathology. Male. Protein Kinase Inhibitors / pharmacology. STAT3 Transcription Factor. STAT5 Transcription Factor. Signal Transduction / drug effects

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  • (PMID = 16158916.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Milk Proteins; 0 / Nitriles; 0 / Protein Kinase Inhibitors; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / WP-1034; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 1; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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98. Fatrai S, Schepers H, Tadema H, Vellenga E, Daenen SM, Schuringa JJ: Mucin1 expression is enriched in the human stem cell fraction of cord blood and is upregulated in majority of the AML cases. Exp Hematol; 2008 Oct;36(10):1254-65
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  • [Title] Mucin1 expression is enriched in the human stem cell fraction of cord blood and is upregulated in majority of the AML cases.
  • OBJECTIVE: Mucin1 is a membrane glycoprotein that is overexpressed in a variety of human cancers.
  • Here, we analyzed the role of Mucin1 in human hematopoietic stem/progenitor cells as well as in acute myeloid leukemia (AML) cells.
  • MATERIALS AND METHODS: Mucin1 expression was determined within the normal stem cell and progenitor compartment, as well as in the AML CD34+ and CD34- subfractions of patient samples.
  • Stem cells were enumerated in long-term culture-initiating cell (LTC-IC) assays in limiting dilution and progenitor frequencies in colony-forming cell (CFC) assays in methylcellulose, and consequences of elevated Mucin1 expression were studied using retroviral overexpression systems in cord blood (CB) CD34+ cells.
  • Retroviral overexpression of Mucin1 in CB CD34+ cells resulted in elevated stem cell and progenitor frequencies as determined in LTC-IC and CFC assays without affecting differentiation, which coincided with increased proliferation.
  • Overexpression of intercellular adhesion molecule-1, a ligand for Mucin1, in MS5 stromal cells further increased LTC-IC frequencies.
  • Mucin1 overexpression was associated with increased nuclear factor-kappaB p50 nuclear translocation, suggesting that Mucin1-induced phenotypes involve increased cell survival mechanisms.
  • Finally, we observed increased Mucin1 expression in 70% of the AML cases (n=24), suggesting that elevated Mucin1 levels might be involved in regulating the proliferative potential of the immature leukemic compartment as well.
  • CONCLUSIONS: Our data indicate that hematopoietic stem cells as well as CD34+ AML subfractions are enriched for Mucin1 expression, and that overexpression of Mucin1 in CB cells is sufficient to increase both progenitor and LTC-IC frequencies.
  • [MeSH-major] Fetal Blood / physiology. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Mucin-1 / genetics. Stem Cells / physiology
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD34 / analysis. Colony-Forming Units Assay. DNA Primers. Flow Cytometry. Humans. Infant, Newborn. Intercellular Adhesion Molecule-1 / genetics. Polymerase Chain Reaction. Retroviridae / genetics. Up-Regulation

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  • (PMID = 18640764.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / DNA Primers; 0 / MUC1 protein, human; 0 / Mucin-1; 126547-89-5 / Intercellular Adhesion Molecule-1
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99. Sonneck K, Mannhalter C, Krauth MT, Sperr WR, Schwarzinger I, Fonatsch C, Haas O, Geissler K, Valent P: An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase. Eur J Haematol; 2005 Jul;75(1):73-7
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  • [Title] An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase.
  • An unusual case of secondary acute myeloid leukemia (AML) with indolent clinical course is described.
  • The patient, a 67-yr-old female, had first been diagnosed to suffer from low-risk myelodysplastic syndrome, subtype refractory anemia with ringed sideroblasts, in 1992.
  • In 2001, transformation to secondary AML with an increase in bone marrow blasts (>20%) and thrombocytopenia, was found.
  • The patient did not require cytoreductive drugs.
  • Rather, during the following months, spontaneous improvement of peripheral blood cells with normalization of platelets and decrease in the red cell transfusion frequency, were noted.
  • However, the bone marrow still showed AML with >20% blasts.
  • We hypothesize that clonal stability may have contributed to the indolent course of the disease in this patient.
  • [MeSH-major] Leukemia, Myeloid, Acute / physiopathology. Myelodysplastic Syndromes / complications

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  • [Copyright] (c) Blackwell Munksgaard 2005.
  • (PMID = 15946315.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Receptors, Androgen
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100. Classen CF, Teigler-Schlegel A, Röttgers S, Reinhardt D, Döhner K, Debatin KM: AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid. Ann Hematol; 2005 Nov;84(12):774-80
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  • [Title] AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid.
  • We describe a case of acute myeloid leukemia (AML) bearing the translocation t(11;17)(q23;q21).
  • The morphological phenotype represented a monoblastic leukemia, AML French-American-British (FAB) M5a.
  • Further analysis of the translocation revealed an involvement of the mixed-lineage leukemia (MLL) gene and a region closely proximal to the retinoic acid (RA) receptor alpha (RARA) gene.
  • AMLs involving both a rearranged MLL and the 17q21 region, in which the RARA gene is located, have only been described in some individual cases.
  • Rearrangements of the MLL (11q23) gene in AML are usually related to the morphological phenotype FAB M5.
  • In acute promyelocytic leukemia, the translocation (15;17)(q22;q11-21) involving the RARA leads to a maturation arrest that can be overcome by RA, often inducing remission.
  • In other forms of AML, however, the effects of RA are limited and diverse.
  • To study whether RA might have a therapeutical potential in our case, we performed an in vitro analysis of RA effects on AML cells.
  • We found that RA leads to enhanced cell death and up-regulation of CD38 and CD117.
  • Our data indicate that in AML cells bearing the t(11;17)(q23;q21), a differentiation arrest that is overcome by RA is not present.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic. Tretinoin / pharmacology
  • [MeSH-minor] Antigens, CD38 / biosynthesis. Cell Death / drug effects. Cell Death / genetics. Child. Drug Screening Assays, Antitumor. Female. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Receptors, Retinoic Acid / therapeutic use. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 16044313.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MLL protein, human; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5688UTC01R / Tretinoin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.2.2.5 / Antigens, CD38
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