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1. Gutierrez-Aguirre CH, Cantú-Rodríguez OG, Gonzalez-Llano O, Salazar-Riojas R, Martinez-González O, Jaime-Pérez JC, Morales-Toquero A, Tarín-Arzaga LC, Ruiz-Argüelles GJ, Gómez-Almaguer D: Non-myeloablative hematopoietic stem cell transplantation is of limited value in advanced or refractory acute myeloblastic leukemia. The Mexican experience. Hematology; 2007 Jun;12(3):193-7
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  • [Title] Non-myeloablative hematopoietic stem cell transplantation is of limited value in advanced or refractory acute myeloblastic leukemia. The Mexican experience.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is an effective strategy for preventing relapse of acute myelogenous leukemia (AML).
  • We analyzed the outcome of 31 primary AML patients who received a reduced-intensity conditioning regimen for allogeneic HSCT in first or second remission.
  • Thirty-one AML patients, 20 in first complete remission (FCR), 8 in second complete remission (SCR) and 3 in a partial remission (SPR) were included.
  • All patients received cyclosporine-A (CsA) and methotrexate as graft vs. host disease (GvHD) prophylaxis.
  • All patients showed myeloid engraftment (neutrophils >0.5 x 10(9)/l) after a median of 13 days in FCR group and 15 days in SCR group.
  • Conclusions. Reduced-intensity conditioning followed by allogeneic HSCT can induce stable remission in primary AML patients transplanted in FCR.
  • A high relapse rate was documented in patients with refractory or relapsed AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Busulfan / administration & dosage. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Cyclosporine / administration & dosage. Graft Survival. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. Humans. Mexico. Middle Aged. Recurrence. Salvage Therapy / methods. Transplantation Conditioning / methods. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 17558694.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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2. Gra OA, Glotov AS, Kozhekbaeva Zhm, Makarova OV, Nasedkina TV: [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia]. Mol Biol (Mosk); 2008 Mar-Apr;42(2):214-25
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  • [Title] [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia].
  • It is known that presence of xenobiotic-metabolizing gene polymorphisms in some cases correlates with hereditary predisposition to the oncological diseases.
  • In the present work the frequencies of xenobiotic-metabolizing gene polymorphisms in 332 children with the diagnosis acute lymphoblastic leukemia (ALL), 71 children with the diagnosis acute myeloblastic leukemia (AML) and 490 healthy donors have been determined using allele-specific hybridization on the biochip.
  • Statistically significant increase in the frequency of GSTT1 "null" genotype (OR = 1.9, p = 4.7E-5) and GSTT1/GSTM1 double "null" genotype (OR = 3.1, p = 2.5E-8) in children with acute leukemia relative to healthy donors group has been revealed.
  • Also 1.8-fold increase in the frequency of NAT2 genotype 341T/T, 481C/C, 590G/G in children with acute leukemia relative to healthy donors group (p = 0.026) has been recognized.
  • Analysis of gene-gene interactions has showed that in patients with acute leukemia genotype NAT2 341T/T, 481C/C, 590G/G in combination with GSTT1 "null" and/or GSTM1 "null" genotype is significantly more frequent than in population control.
  • Besides the reduction of MTRR genotype 66G/G frequency in girls with acute leukemia relative to female healthy donors has been found (OR = 0.50, p = 0.0015).
  • Analysis of gene-gene interactions has shown that the presence of GSTT1 "null" and/or GSTM1 "null" genotype in combination with MTRR genotype 66A/- may consider as risk factor of acute leukemia in girls.
  • Thus, the studied polymorphic variants of genes GSTT1, GSTM1, NAT2 and MTRR can modulate the risk of childhood acute leukemia, residents of European part of Russia.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Ferredoxin-NADP Reductase / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18610829.001).
  • [ISSN] 0026-8984
  • [Journal-full-title] Molekuliarnaia biologiia
  • [ISO-abbreviation] Mol. Biol. (Mosk.)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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3. Jiang JL, Yan SK, Yang J, Cai Y, Wan LP, Qin YW, Wang C: [Allogeneic hematopoietic stem cell transplantation following reduced intensity conditioning regimen for treatment of refractory leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2008 Aug;29(8):517-21
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  • [Title] [Allogeneic hematopoietic stem cell transplantation following reduced intensity conditioning regimen for treatment of refractory leukemia].
  • OBJECTIVE: To evaluate the efficacy of allogeneic hematopoietic stem cell transplantation (allo-HSCT) following reduced intensity conditioning (RIC) regimen for treatment of refractory leukemia.
  • METHODS: Twenty patients with refractory leukemia received allo-HSCT following RIC regimen consisting of fludarabine plus small or moderate dose total body irradiation (TBI).
  • Graft versus host disease (GVHD) prophylaxis was CsA plus mycophenolate mofetil (MMF) or short-term MTX, or these three drugs combination; CD25 monoclone antibody(McAb) and ATG were also used in some of the patients.
  • The incidence of acute and chronic GVHD was 47.1% (8/17) and 38.5% (5/13) respectively.
  • Up to now, 7 patients relapsed and 9 were alive with leukemia free.
  • 3 +/- 14.2)% for all patients and (52.5 +/- 18.6)% for acute non-lymphocytic leukemia (ANLL) patients.
  • CONCLUSION: Allo-HSCT following fludarabine and TBI based RIC regimen can be used for treatment of refractory leukemia with well tolerance and low TRM and there is a better prognosis for ANLL patients than that for acute lymphocytic leukemia patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Child. Female. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19112913.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] China
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4. Fröhling S, Scholl C, Levine RL, Loriaux M, Boggon TJ, Bernard OA, Berger R, Döhner H, Döhner K, Ebert BL, Teckie S, Golub TR, Jiang J, Schittenhelm MM, Lee BH, Griffin JD, Stone RM, Heinrich MC, Deininger MW, Druker BJ, Gilliland DG: Identification of driver and passenger mutations of FLT3 by high-throughput DNA sequence analysis and functional assessment of candidate alleles. Cancer Cell; 2007 Dec;12(6):501-13
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  • Mutations in the juxtamembrane and kinase domains of FLT3 are common in AML, but it is not known whether alterations outside these regions contribute to leukemogenesis.
  • We used a high-throughput platform to interrogate the entire FLT3 coding sequence in AML patients without known FLT3 mutations and experimentally tested the consequences of each candidate leukemogenic allele.
  • This approach identified gain-of-function mutations that activated downstream signaling and conferred sensitivity to FLT3 inhibition and alleles that were not associated with kinase activation, including mutations in the catalytic domain.
  • These findings support the concept that acquired mutations in cancer may not contribute to malignant transformation and underscore the importance of functional studies to distinguish "driver" mutations underlying tumorigenesis from biologically neutral "passenger" alterations.

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  • (PMID = 18068628.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NCI NIH HHS / CA / CA113434; United States / NCI NIH HHS / CA / CA105423; United States / NCI NIH HHS / CA / T32 CA009172; United States / NHLBI NIH HHS / HL / HL082677
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mutant Proteins; 0 / Protein Kinase Inhibitors; 120685-11-2 / 4'-N-benzoylstaurosporine; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine
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5. Wald D, Vermaat JM, Peleg G, Tse W: Genetic abnormalities in acute myelogenous leukemia with normal cytogenetics. Curr Hematol Malig Rep; 2008 Apr;3(2):83-8
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  • [Title] Genetic abnormalities in acute myelogenous leukemia with normal cytogenetics.
  • Acute myelogenous leukemia (AML) results from a differentiation block of hematopoietic progenitor cells along with uncontrolled proliferation.
  • The cytogenetic abnormality at initial diagnosis is the single most important prognostic factor classifying AML patients into three prognostic categories: favorable, intermediate, and poor risk.
  • Currently, favorable-risk AML patients are usually treated with contemporary chemotherapy, and poor-risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist.
  • The approximately 40% of AML patients without identifiable cytogenetic abnormalities (NC AML) are classified as intermediate risk.
  • Emerging data recently suggested that molecular study of the mutations of NPM1, FLT3, MLL, and CEBPalpha and alterations in expression levels of BAALC, MN1, and ERG may identify poor-risk patients with NC AML.
  • Further prospective studies are needed to confirm whether NC AML patients with poor risk have improved clinical outcomes after more aggressive therapy.
  • [MeSH-major] Cytogenetic Analysis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] CCAAT-Enhancer-Binding Protein-alpha / genetics. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Proto-Oncogene Proteins c-ets / genetics. Tumor Suppressor Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20425451.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / MLL protein, human; 0 / MN1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / Tumor Suppressor Proteins; 117896-08-9 / nucleophosmin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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6. Vongchan P, Linhardt RJ: Expression of human liver HSPGs on acute myeloid leukemia. Clin Immunol; 2007 Feb;122(2):194-206
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  • [Title] Expression of human liver HSPGs on acute myeloid leukemia.
  • Heparan sulfate proteoglycans (HSPGs) play important biological roles in cell-matrix adhesion processes and are essential regulators of growth actions.
  • Human liver is a target for a number of pathogens, and HSPGs have been demonstrated in several cases to play a pivotal role in infectivity.
  • Despite HSPGs important biological functions, little is known about its cell-specific distribution patterns.
  • Human liver HSPG was isolated, and a specific monoclonal antibody (mAb) 1E4-1C2 was produced.
  • Distribution of HSPG reactive to this mAb was studied in normal blood cells, hematopoietic cell lines and blood cells isolated from patients with various hematologic disorders using indirect immunofluorescence.
  • There was no expression of molecules recognized by this mAb on lymphoid (Daudi, Jurkat, SupT-1) and monocytoid (U937) cell lines.
  • Peripheral blood cells, normal bone marrow, together with leukocytes isolated from patients with acute lymphoblastic leukemia, chronic myelocytic leukemia, Hodgkin's disease or Non-Hodgkin's lymphoma, were also negative.
  • In contrast, 1E4-1C2 showed significant positive results on human myeloid cell lines HL-60 and K562.
  • Moreover, it is interesting that this mAb also recognized epitopes on leukocytes isolated from acute myeloblastic leukemia.
  • These results suggest that malignancies of cells in myeloid lineage may cause expression of HSPGs that are detected by this specific mAb, making it a potential co-marker for the diagnosis of acute myeloid leukemia.

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  • (PMID = 17035092.001).
  • [ISSN] 1521-6616
  • [Journal-full-title] Clinical immunology (Orlando, Fla.)
  • [ISO-abbreviation] Clin. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL052622-09; United States / NHLBI NIH HHS / HL / R01 HL052622; United States / NHLBI NIH HHS / HL / HL052622-09; United States / NIGMS NIH HHS / GM / GM038060-19; United States / NIGMS NIH HHS / GM / R01 GM038060; United States / NIGMS NIH HHS / GM / R01 GM038060-19
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Heparan Sulfate Proteoglycans; 0 / Membrane Glycoproteins
  • [Other-IDs] NLM/ NIHMS75574; NLM/ PMC4142644
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7. Medina DJ, Gharibo M, Savage P, Cohler A, Kuriyan M, Balsara B, Anand M, Schaar D, Krimmel T, Saggiomo K, Manago J, Talty L, Dudek L, Grospe S, Rubin A, Strair RK: A pilot study of allogeneic cellular therapy for patients with advanced hematologic malignancies. Leuk Res; 2008 Dec;32(12):1842-8
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  • Allogeneic hematopoietic stem cell transplantation provides curative therapy for some patients with advanced hematologic malignancies.
  • Disease response after allogeneic transplant is, at least in part, mediated by donor immune cells.
  • Patients with persistent disease beyond 8 weeks could be further treated with infusions of irradiated haploidentical donor cells.
  • Two patients with resistant relapsed acute myelogenous leukemia (AML) had a disease response.
  • Analysis of T cell reactivity from one patient who achieved a complete response but did not have durable engraftment of donor cells indicated that disease response was associated with the generation of host-derived anti-leukemic cytotoxic CD8+ T cells that reacted with an AML-associated proteinase 3 epitope.
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD / blood. Antigens, CD3 / blood. Antigens, CD34 / blood. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. CD8-Positive T-Lymphocytes / immunology. Cell Transplantation. Female. Flow Cytometry. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / surgery. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / surgery. Male. Middle Aged. Pilot Projects. Tissue Donors. Tissue Expansion / methods. Tissue and Organ Harvesting / methods. Transplantation, Homologous

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  • (PMID = 18614230.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34
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8. Wang XB, Zheng JE, Gu JX, Yao JX, Yang J, Liu J, Li XQ, He YL, Yu JM, Wei J, Liu ZP, Huang SA: [Correlation of immunophenotype to cytogenetics and clinical features of adult acute myeloid leukemia]. Ai Zheng; 2005 Jun;24(6):667-71
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  • [Title] [Correlation of immunophenotype to cytogenetics and clinical features of adult acute myeloid leukemia].
  • BACKGROUND & OBJECTIVE: New WHO classification has been rapidly used in diagnosis of leukemia.
  • Based on coexpression and correlation of lineage-associated antigens, multiparameter high-resolution flow cytometry has been developed to precisely identify lineage characteristics of leukemia.
  • Some immunophenotypes correlate with cytogenetic abnormality and prognosis.
  • This study was to analyze immunophenotype of naive acute myeloid leukemia (AML), and explore its correlations to cytogenetics, clinical features, and FAB subtype of AML.
  • METHODS: Multiparameter high-resolution flow cytometry with a panel of 25 different monoclonal antibodies was used to analyze the surface and cytoplasmic antigens expressions of 96 adults with AML; G-binding technique was used to analyze karyotype of 73 of the 96 patients.
  • RESULTS: In these AML patients, some antigens were correlated with FAB subtypes:expression of CD2 was enhanced in AML-M3; HLA-DR, CD34, and CD56 were absent in AML-M3; expression of CD19 was increased in AML-M2; expressions of CD14 and CD56 were enhanced in AML-M5; MPO was absent in AML-M0.
  • Karyotype abnormality was detected in 40(54.8%) patients.
  • CD22, CD56, and TdT expressions were correlated with karyotype abnormality. t(8;.
  • 21) was only detected in 10 AML-M2 patients with high expressions of CD15, CD19, CD34, and CD56; no lymphoid lineage antigens were detected in 7 AML-M3 patients with t (15; 17).
  • Expressions of CD4 and TdT were positively correlated with patient's age; expressions of CD7 and CD14 were positively correlated with high white blood cell count; expressions of CD4, CD14, and CD56 were positively correlated with high platelet count.
  • CONCLUSIONS: The abnormal antigen expression of AML is tightly linked with karyotype abnormality.
  • Detection of immunophenotype may help to diagnose and classify AML.
  • [MeSH-major] Immunoglobulin Fab Fragments / immunology. Immunophenotyping. Leukemia, Myeloid, Acute / immunology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / metabolism. Chromosome Aberrations. Female. Humans. Karyotyping. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / immunology. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / immunology. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / immunology. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / immunology. Male. Middle Aged

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  • (PMID = 15946475.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Immunoglobulin Fab Fragments
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9. Gupta M, Raghavan M, Gale RE, Chelala C, Allen C, Molloy G, Chaplin T, Linch DC, Cazier JB, Young BD: Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia. Genes Chromosomes Cancer; 2008 Sep;47(9):729-39
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  • [Title] Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia.
  • The acquisition of uniparental disomy (aUPD) in acute myeloid leukemia (AML) results in homozygosity for known gene mutations.
  • We therefore aimed to develop a map of the regions of aUPD in AML.
  • Here, we have analyzed a large set of diagnostic AML samples (n = 454) from young adults (age: 15-55 years) using genotype arrays.
  • This study demonstrates aUPD is a frequent and significant finding in AML and pinpoints regions that may contain novel mutational targets.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Uniparental Disomy / genetics

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18506749.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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10. Porta G, Mattarucchi E, Maserati E, Pressato B, Valli R, Morerio C, Zecca M, Panarello C, Locatelli F, Lo Curto F, Pasquali F: Monitoring the isochromosome i(7)(q10) in the bone marrow of patients with Shwachman syndrome by real-time quantitative PCR. J Pediatr Hematol Oncol; 2007 Mar;29(3):163-5
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  • Clonal chromosome anomalies may be found in the bone marrow (BM) of patients with Shwachman syndrome, who are at risk to develop myelodysplastic syndromes and/or acute myeloid leukemias.
  • [MeSH-major] Abnormalities, Multiple / genetics. Bone Marrow Diseases / genetics. Chromosomes, Human, Pair 7 / genetics. Isochromosomes / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 17356395.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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11. Ward PS, Patel J, Wise DR, Abdel-Wahab O, Bennett BD, Coller HA, Cross JR, Fantin VR, Hedvat CV, Perl AE, Rabinowitz JD, Carroll M, Su SM, Sharp KA, Levine RL, Thompson CB: The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate. Cancer Cell; 2010 Mar 16;17(3):225-34
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  • [Title] The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate.
  • Here, we report that tumor 2HG is elevated in a high percentage of patients with cytogenetically normal acute myeloid leukemia (AML).
  • Furthermore, AML patients with IDH mutations display a significantly reduced number of other well characterized AML-associated mutations and/or associated chromosomal abnormalities, potentially implicating IDH mutation in a distinct mechanism of AML pathogenesis.


12. Kirwan M, Vulliamy T, Marrone A, Walne AJ, Beswick R, Hillmen P, Kelly R, Stewart A, Bowen D, Schonland SO, Whittle AM, McVerry A, Gilleece M, Dokal I: Defining the pathogenic role of telomerase mutations in myelodysplastic syndrome and acute myeloid leukemia. Hum Mutat; 2009 Nov;30(11):1567-73
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  • [Title] Defining the pathogenic role of telomerase mutations in myelodysplastic syndrome and acute myeloid leukemia.
  • The primary pathology in many cases of myelodysplasia (MDS) and acute myeloid leukemia (AML) remains unknown.
  • However, there are also other familial cases of MDS/AML where the genetic basis remains unknown.
  • Both MDS, and to a lesser extent AML, have been observed in cases of the bone marrow failure syndrome dyskeratosis congenita, in which telomerase mutations have been identified.
  • Recently, an increased incidence of telomerase reverse transcriptase mutations has been reported in a series of de novo AML.
  • We have now identified novel mutations in the telomerase RNA (TERC) or telomerase reverse transcriptase component (TERT) within 4 of 20 families presenting with familial MDS/AML.
  • These families, in conjunction with a review of previously published cases, help to further define the pathological role of telomerase mutations in MDS/AML and have implications for the biology, treatment and screening regimen of de novo cases.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. RNA / genetics. Telomerase / genetics


13. Lehner M, Bailo M, Stachel D, Roesler W, Parolini O, Holter W: Caspase-8 dependent apoptosis induction in malignant myeloid cells by TLR stimulation in the presence of IFN-alpha. Leuk Res; 2007 Dec;31(12):1729-35
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  • [Title] Caspase-8 dependent apoptosis induction in malignant myeloid cells by TLR stimulation in the presence of IFN-alpha.
  • Pro-apoptotic signalling upon toll-like receptor (TLR) stimulation in myeloid cells is normally antagonized by the simultaneous activation of anti-apoptotic pathways.
  • Based on these results we investigated whether similarly apoptosis can be cooperatively induced in myeloid tumor cells.
  • When testing established acute myeloid leukemia (AML) cell lines we found the monocytic cell line THP-1 to be sensitive to IFN-alpha plus LPS induced apoptosis, which was partially dependent on caspase-8 and was associated with an enhanced expression of Fas/CD95.
  • We extended our study to 29 short term blast lines from patients with AML and observed additive effects of IFN-alpha and LPS on cell death only with few samples indicating that sensitivity to IFN-alpha plus LPS inducible apoptosis is present in a fraction of AML samples only with no obvious correlation with certain FAB phenotypes.
  • [MeSH-major] Apoptosis. Caspase 8 / physiology. Interferon-alpha / pharmacology. Leukemia, Myeloid, Acute / pathology. Toll-Like Receptors / physiology
  • [MeSH-minor] Cell Line. Cell Line, Tumor. Humans. Lipopolysaccharides / pharmacology. Monocytes. Myeloid Cells

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  • (PMID = 17572490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Lipopolysaccharides; 0 / Toll-Like Receptors; EC 3.4.22.- / Caspase 8
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14. Appelbaum FR, Pearce SF: Hematopoietic cell transplantation in first complete remission versus early relapse. Best Pract Res Clin Haematol; 2006;19(2):333-9
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  • [Title] Hematopoietic cell transplantation in first complete remission versus early relapse.
  • Although data from a number of clinical trials can help guide the choice, the decision of whether patients with acute myeloid leukemia (AML) should undergo transplantation while in first remission or should have transplantation withheld until relapse is a particularly difficult one.
  • Current data suggest that patients with AML and unfavorable cytogenetics should undergo allogeneic transplantation while in first remission if at all possible.
  • Patients with AML and good risk cytogenetics can probably forgo transplantation until after first relapse.
  • For patients with intermediate risk disease, the decision of transplantation during first remission versus waiting until first relapse is particularly difficult and should be made only after considering additional individual risk factors.

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  • (PMID = 16516131.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 15704; United States / NHLBI NIH HHS / HL / HL 36444; United States / NCI NIH HHS / CA / CA 78902; United States / NCI NIH HHS / CA / P01 CA078902; United States / NCI NIH HHS / CA / CA 18029
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 17
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15. Raffegerst SH, Hoelzlwimmer G, Kunder S, Mysliwietz J, Quintanilla-Martinez L, Schendel DJ: Diverse hematological malignancies including hodgkin-like lymphomas develop in chimeric MHC class II transgenic mice. PLoS One; 2009;4(12):e8539
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  • The majority of malignancies were distributed equally between T and B cell neoplasms and included lymphoblastic T cell lymphoma (LTCL), lymphoblastic B cell lymphoma (LBCL), diffuse large B cell lymphoma (DLBCL), the histiocyte/T cell rich variant of DLBCL (DLBCL-HA/T cell rich DLBCL), splenic marginal zone lymphoma (SMZL), follicular B cell lymphoma (FBL) and plasmacytoma (PCT).
  • Most of these neoplasms were highly similar to human diseases.
  • Also, some non-lymphoid malignancies such as acute myeloid leukemia (AML) and histiocytic sarcoma were found.
  • Interestingly, composite lymphomas, including Hodgkin-like lymphomas, were also detected that had CD30(+) Hodgkin/Reed-Sternberg (H/RS)-like cells, representing a tumor type not previously described in mice.
  • Thus, this DR4 line is a useful model to investigate common molecular mechanisms that may contribute to important neoplastic diseases in man.
  • [MeSH-major] Chimerism. Hematologic Neoplasms / immunology. Hematologic Neoplasms / pathology. Histocompatibility Antigens Class II / immunology. Hodgkin Disease / immunology. Hodgkin Disease / pathology
  • [MeSH-minor] Animals. Antigens, CD30 / metabolism. Base Sequence. Lymphoma, B-Cell / pathology. Lymphoma, T-Cell / pathology. Mice. Mice, Transgenic. Molecular Sequence Data. Reed-Sternberg Cells / pathology. Survival Analysis. Transgenes / genetics

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  • (PMID = 20046882.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Histocompatibility Antigens Class II
  • [Other-IDs] NLM/ PMC2796171
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16. Skeete DH, Cesar-Rittenberg P, Jong R, Murray SK, Colgan TJ: Myeloid sarcoma of the vagina: a report of 2 cases. J Low Genit Tract Dis; 2010 Apr;14(2):136-41
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  • [Title] Myeloid sarcoma of the vagina: a report of 2 cases.
  • OBJECTIVE: To describe 2 cases of myeloid sarcoma of the vagina, in a patient without a history of acute myeloid leukemia (AML) and in another whose condition was previously diagnosed with AML.
  • MATERIALS AND METHODS: The clinical histories of 2 patients whose conditions were diagnosed with myeloid sarcoma of the vagina were obtained from their medical records.
  • The histopathologic specimen was evaluated on routine and immunohistochemical stains, and myeloid sarcoma was diagnosed after extensive immunohistochemical analysis.
  • She developed extensive myeloid sarcoma of the skin and AML 4.5 months later; she died 2 weeks later, 5 months after the initial presentation.
  • Case 2: A 36-year-old woman with a known history of AML who has had multiple leukemic and extramedullary recurrences presented with a pelvic mass.
  • Physical findings revealed large masses in the vagina and rectovaginal septum, which were confirmed as myeloid sarcoma after biopsy and histologic examination.
  • CONCLUSIONS: Myeloid sarcoma of the vagina is extremely rare.
  • Most patients have a poor prognosis and either have a history of or will subsequently develop AML.
  • [MeSH-major] Sarcoma, Myeloid / diagnosis. Vagina / pathology. Vaginal Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / complications. Skin Neoplasms / secondary

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  • (PMID = 20354424.001).
  • [ISSN] 1526-0976
  • [Journal-full-title] Journal of lower genital tract disease
  • [ISO-abbreviation] J Low Genit Tract Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / SAGE protein, human
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17. Boehrer S, Adès L, Braun T, Galluzzi L, Grosjean J, Fabre C, Le Roux G, Gardin C, Martin A, de Botton S, Fenaux P, Kroemer G: Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study. Blood; 2008 Feb 15;111(4):2170-80
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  • [Title] Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study.
  • Erlotinib, an inhibitor of the epidermal growth factor receptor (EGFR), induces differentiation, cell-cycle arrest, and apoptosis of EGFR-negative myeloblasts of patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), as well as in EGFR-negative cell lines representing these diseases (P39, KG-1, and HL 60).
  • Apoptosis induction coupled to mitochondrial membrane permeabilization occurred independently from phenotypic differentiation.
  • In apoptosis-sensitive AML cells, erlotinib caused a rapid (within less than 1 hour) nucleocytoplasmic translocation of nucleophosmin-1 (NPM-1) and p14(ARF).
  • Moreover, erlotinib reduced the growth of xenografted human AML cells in vivo.
  • Erlotinib also killed CD34(+) bone marrow blasts from MDS and AML patients while sparing normal CD34(+) progenitors.
  • One patient afflicted with both MDS and non-small cell lung cancer manifested hematologic improvement in response to erlotinib.
  • In summary, we here provide novel evidence in vitro, ex vivo, and in vivo for the potential therapeutic efficacy of erlotinib in the treatment of high-risk MDS and AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Erlotinib Hydrochloride. Female. Humans. Male. Middle Aged. Reference Values


18. Neudenberger J, Hotfilder M, Rosemann A, Langebrake C, Reinhardt D, Pieters R, Schrauder A, Schrappe M, Röttgers S, Harbott J, Vormoor J: Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11). Br J Haematol; 2006 May;133(3):337-44
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  • [Title] Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11).
  • Therefore, these leukaemic stem cells should be the target cells for therapy and for minimal residual disease (MRD) detection.
  • Six acute myeloid leukaemia (AML)/abn(11q23) and three acute lymphoblastic leukaemia (ALL)/t(4;11) samples were analysed by four-colour flow cytometry for NG2 expression on primitive cell populations.
  • Candidate leukaemic cell populations were defined by the antigen profiles CD34+CD38- in AML and CD34+CD19-CD117+ in ALL.
  • Surprisingly, in all patients these candidate stem cell populations were shown to lack expression of NG2.
  • Instead, a correlation between the expression of the myeloid differentiation marker CD33 and increasing levels of NG2 on maturing cells could be demonstrated.
  • Thus, NG2 appears to be upregulated with differentiation and not to be expressed on primitive disease-maintaining cells.
  • [MeSH-major] Antigens / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Neoplastic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteoglycans / metabolism
  • [MeSH-minor] Acute Disease. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Flow Cytometry / methods. Humans. Neoplasm Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Sialic Acid Binding Ig-like Lectin 3. Translocation, Genetic

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  • (PMID = 16643437.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / chondroitin sulfate proteoglycan 4
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19. Giori NJ: Unexpected finding of a fractured metal prosthetic femoral head in a nonmodular implant during revision total hip arthroplasty. J Arthroplasty; 2010 Jun;25(4):659.e13-5
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  • [Title] Unexpected finding of a fractured metal prosthetic femoral head in a nonmodular implant during revision total hip arthroplasty.
  • Though there are many reports of fractured femoral components after total hip arthroplasty; there are no reports of a fractured metal femoral head.
  • This is a report of a fractured metal femoral head in a nonmodular total hip replacement discovered unexpectedly during revision total hip arthroplasty for acetabular failure.
  • This surprise finding, which was not appreciated on preoperative x-rays, required unplanned extraction of a well-ingrown, fully porous coated cylindrical femoral stem.
  • Though rare, fracture of the metal femoral head in a DePuy (Warsaw, Ind.) monoblock Anatomic Medullary Locking (AML) component is possible, and one cannot expect the fracture to be apparent on preoperative radiographs as the 2 pieces may not necessarily dissociate.

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 20022458.001).
  • [ISSN] 1532-8406
  • [Journal-full-title] The Journal of arthroplasty
  • [ISO-abbreviation] J Arthroplasty
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Metals
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20. Liu Y, Ke XY, Ma J, Shen ZX, Zhang XH, Du X, Zhao YM, Lü JQ, Zhan ZM, Zeng XY, Xu XH, Lu ZS: [Multi-institutional randomized controlled clinical trial on China made 4-demethoxydaunokrubicin (IDA) in the treatment of acute leukemia]. Zhonghua Zhong Liu Za Zhi; 2005 Dec;27(12):750-2
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  • [Title] [Multi-institutional randomized controlled clinical trial on China made 4-demethoxydaunokrubicin (IDA) in the treatment of acute leukemia].
  • OBJECTIVE: To evaluate the efficacy and safety of IDA (Haizheng Parmacy, China) in the treatment of acute leukemia.
  • A total of 155 newly diagnosed patients with AML and ALL were enrolled.
  • In patients treated with IDA vs zevodas, the overall response rate (OR) was 78.1% vs 76.9%, CR was 68.8% vs 67.7%; in AML patients, OR was 82.4% vs 71.8%, and CR was 76.5% vs 64.1%; in ALL patients, OR was 80.0% vs 81.8%, and CR was 68.0% vs 68.2%.
  • There was no sitatistically significant difference in hematologic and non-hematologic toxicities between the two groups.
  • CONCLUSION: The efficacy of IDA in the treatment of acute leukemia is comparable to that of zevodas.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Idarubicin / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16483490.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; ZRP63D75JW / Idarubicin
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21. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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  • [Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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22. Göhring G, Giagounidis A, Büsche G, Kreipe HH, Zimmermann M, Hellström-Lindberg E, Aul C, Schlegelberger B: Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression. Ann Hematol; 2010 Apr;89(4):365-74
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  • [Title] Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression.
  • Thirty-six percent of patients progressed into acute myeloid leukaemia.
  • However, erythroid and cytogenetic responders had a significantly decreased risk of progression to acute myeloid leukaemia (p = 0.001 and p = 0.009, respectively) compared to non-responders.
  • Three and 5 years after study entry, the cumulative incidence of acute myeloid leukaemia for patients with a cytogenetic response was 10% and 21%, respectively, and for patients without cytogenetic response, it was 46% and 60%.
  • Patients with del(5q) myelodysplastic syndromes without erythroid or cytogenetic remission after treatment with lenalidomide have a high risk for clonal evolution and acute myeloid leukaemia progression.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Erythroid Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Remission Induction. Risk Factors. Treatment Failure


23. Grosveld GC: MN1, a novel player in human AML. Blood Cells Mol Dis; 2007 Nov-Dec;39(3):336-9
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  • [Title] MN1, a novel player in human AML.
  • The transcriptional coactivator MN1 has been identified as a gene overexpressed in certain types of human acute myeloid leukemia.
  • Upregulation is invariantly associated with inv(16) AML but is also found in other AML subtypes.
  • Overexpression of this gene is also associated with a worse prognosis and a shorter survival in AML patients with a normal karyotype.
  • In this short review, I will discuss the role of MN1 in myeloid leukemia.

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  • (PMID = 17698380.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA072996-11; United States / NCI NIH HHS / CA / R01 CA072996; United States / NCI NIH HHS / CA / R01 CA072996-11
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MN1 protein, human; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 26
  • [Other-IDs] NLM/ NIHMS32389; NLM/ PMC2387274
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24. Mori M, Ohta M, Miyata A, Higashihara M, Oshimi K, Kimura H, Yagasaki F, Sunami K: Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG). Leuk Lymphoma; 2006 Oct;47(10):2062-9
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  • [Title] Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG).
  • The feasibility and effects of combination chemotherapy for very elderly patients with acute myeloid leukemia was examined in 65 patients (including previous myelodysplastic syndrome) aged 76 years or morewith a performance status of 0 - 3.
  • Induction chemotherapy was performed with 30 mg/m2 daunorubicin on days 1 - 3, 150 mg/m2 behenoyl cytosine arabinoside on days 1 - 7, and 70 mg/m2 6-mercaptopurine with 300 mg allopurinol taken orally on days 1 - 7 (BHAC-DM).
  • The relapse rate of the 25 CR patients was 64.0% and disease-free survival at 2 and 5 years was 21.0% and 11.2%, respectively.
  • BHAC-DM is feasible and effective for selected very elderly acute myeloid leukemia patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Cytarabine / analogs & derivatives. Cytarabine / pharmacology. Disease-Free Survival. Female. Humans. Male. Remission Induction. Time Factors. Treatment Outcome

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  • (PMID = 17071477.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 9YVR68W306 / enocitabine
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25. Styczynski J, Czyzewski K, Wysocki M: Ex vivo activity of thalidomide in childhood acute leukemia. Leuk Lymphoma; 2006 Jun;47(6):1123-8
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  • [Title] Ex vivo activity of thalidomide in childhood acute leukemia.
  • Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias.
  • Ex vivo activity of thalidomide as a single agent and in combination with prednisolone or cytarabine in childhood acute leukemias was analyzed.
  • Forty samples of childhood acute lymphoblastic leukemia (ALL) and 13 acute myeloid leukemia (AML) were tested for cytotoxicity by the MTT assay and cell cycle phases by flow cytometry.
  • Control studies were performed on 9 samples of normal lymphocytes and 4 cell lines.
  • However, in the presence of thalidomide, cytotoxicity of prednisolone or cytarabine, increased 3.3-fold and 2.7-fold, respectively, in childhood ALL but was not changed in AML.
  • Thalidomide increased apoptosis in lymphoblasts, and modulated cell cycle arrest caused by prednisolone but not cytarabine in childhood acute lymphoblastic leukemia samples.
  • Thalidomide potentiated ex vivo sensitivity of childhood ALL cells to prednisolone and cytarabine, while no sensitization effect was observed in AML cells.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / pharmacology
  • [MeSH-minor] Cell Cycle. Child. Child, Preschool. Cytarabine / pharmacology. Female. Humans. Immunophenotyping. Infant. Male. Prednisolone / pharmacology. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology

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  • (PMID = 16840205.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; 4Z8R6ORS6L / Thalidomide; 9PHQ9Y1OLM / Prednisolone
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26. Li W, Mi YC, Wang Y, Lin D, Wei H, Liu XP, Bian SG, Wang JX: [Clinical features and prognosis of acute myeloid leukemia-M(4).]. Zhonghua Xue Ye Xue Za Zhi; 2010 Jan;31(1):6-10
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  • [Title] [Clinical features and prognosis of acute myeloid leukemia-M(4).].
  • OBJECTIVE: To investigate factors that affect survival and prognosis of acute myeloid leukemia (AML)-M(4).
  • METHODS: Seventy AML-M(4) patients were divided into three groups, neither eosinophilia nor inv(16)\[Eos(-)\], eosinophilia with inv (16)\[Eos(+) inv(16)(+)\], and eosinophilia with no inv(16)\[Eos(+) inv(16)(-)\].
  • The CR rate, CR after the first course of induction therapy and the median OS for the Eos(-) group were 76.9%, 61.5% and 11.2 (1.2 - 162.4) months; for the Eos(+) group were 96.8%, 89.6% and did not reach; for the Eos(+)inv16(+) group were 100%, 94.4% and did not reach; and for the Eos(+) inv(16)(-) group were 91.7%,69.2% and 14.3 months respectively.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute

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  • (PMID = 20302767.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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27. von Lilienfeld-Toal M, Hahn-Ast C, Kirchner H, Flieger D, Dölken G, Glasmacher A: A randomized comparison of immediate versus delayed application of G-CSF in induction therapy for patients with acute myeloid leukemia unfit for intensive chemotherapy. Haematologica; 2007 Dec;92(12):1719-20
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  • [Title] A randomized comparison of immediate versus delayed application of G-CSF in induction therapy for patients with acute myeloid leukemia unfit for intensive chemotherapy.
  • We randomized 66 elderly patients with AML unfit for conventional chemotherapy to receive GCSF from d6 or from d12 after induction-chemotherapy with cytarabine/idarubicin.
  • Delayed treatment can reduce the administration of G-CSF without adverse consequences.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18056004.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin
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28. 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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29. Lopes de Menezes DE, Peng J, Garrett EN, Louie SG, Lee SH, Wiesmann M, Tang Y, Shephard L, Goldbeck C, Oei Y, Ye H, Aukerman SL, Heise C: CHIR-258: a potent inhibitor of FLT3 kinase in experimental tumor xenograft models of human acute myelogenous leukemia. Clin Cancer Res; 2005 Jul 15;11(14):5281-91
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  • [Title] CHIR-258: a potent inhibitor of FLT3 kinase in experimental tumor xenograft models of human acute myelogenous leukemia.
  • PURPOSE: Fms-like tyrosine kinase 3 (FLT3) encodes a receptor tyrosine kinase (RTK) for which activating mutations have been identified in a proportion of acute myelogenous leukemia (AML) patients and associated with poor clinical prognosis.
  • Given the relevance of FLT3 mutations in AML, we investigated the activity of CHIR-258, an orally active, multitargeted small molecule, with potent activity against FLT3 kinase and class III, IV, and V RTKs involved in endothelial and tumor cell proliferation in AML models.
  • EXPERIMENTAL DESIGN: CHIR-258 was tested on two human leukemic cell lines in vitro and in vivo with differing FLT3 mutational status [MV4;11 cells express FLT3 internal tandem duplications (ITD) versus RS4;11 cells with wild-type (WT) FLT3].
  • Tumor regressions and eradication of AML cells from the bone marrow were shown in s.c. and bone marrow engraftment leukemic xenograft models.
  • Tumor responses were characterized by decreased cellular proliferation and positive immunohistochemical staining for active caspase-3 and cleaved poly(ADP-ribose) polymerase, suggesting cell death was mediated in part via apoptosis.
  • CONCLUSIONS: Our data indicate that CHIR-258 may be an effective therapy in FLT3-associated AML and warrants clinical trials.
  • [MeSH-major] Benzimidazoles / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Proto-Oncogene Proteins / genetics. Quinolones / pharmacology. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Animals. Cell Proliferation. DNA Mutational Analysis. Disease Models, Animal. Dose-Response Relationship, Drug. Female. Humans. Immunohistochemistry. Mice. Mice, SCID. Neoplasm Transplantation. Tandem Repeat Sequences. Transplantation, Heterologous. Tumor Cells, Cultured. fms-Like Tyrosine Kinase 3

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  • (PMID = 16033847.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one; 0 / Benzimidazoles; 0 / Proto-Oncogene Proteins; 0 / Quinolones; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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30. Luger SM: Treating the elderly patient with acute myelogenous leukemia. Hematology Am Soc Hematol Educ Program; 2010;2010:62-9
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  • [Title] Treating the elderly patient with acute myelogenous leukemia.
  • Decisions regarding the optimal treatment of acute myelogenous leukemia in the elderly patient requires the consideration of multiple factors.
  • Furthermore, not all patients are candidates for such therapy.
  • Consideration of patient and disease-related factors can help to determine the appropriateness of intensive therapy in a given patient.
  • For those patients for whom aggressive induction therapy does not seem to be in their best interest, novel agents are being investigated that will hopefully address the issues of induction death and early relapse associated with these patient populations.

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  • (PMID = 21239772.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Dos Santos C, Récher C, Demur C, Payrastre B: [The PI3K/Akt/mTOR pathway: a new therapeutic target in the treatment of acute myeloid leukemia]. Bull Cancer; 2006 May;93(5):445-7
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  • [Title] [The PI3K/Akt/mTOR pathway: a new therapeutic target in the treatment of acute myeloid leukemia].
  • [Transliterated title] La voie PI3K/Akt/mTOR: une nouvelle cible thérapeutique dans le traitement des leucémies aiguës myéloïdes.
  • Despite important progress in the therapy of acute myeloid leukaemia (AML) most patients relapse and die from the disease, underlying the need for potent and more specific drugs for the treatment of this pathology.
  • Recently, we demonstrated that the PI3-kinase-Akt-mTOR (mammalian target of rapamycin) pathway is constitutively activated in about 60% of AML patients cells.
  • The results of this preclinical study led us to investigate the activity of rapamycin in relapsed, refractory, or poor-risk AML patients.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / enzymology. Protein Kinases. Sirolimus / therapeutic use
  • [MeSH-minor] Acute Disease. Enzyme Inhibitors / therapeutic use. Humans. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / physiology. Signal Transduction. TOR Serine-Threonine Kinases

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  • (PMID = 16777621.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
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32. Qiu J, Wong J, Tweardy DJ, Dong S: Decreased intranuclear mobility of acute myeloid leukemia 1-containing fusion proteins is accompanied by reduced mobility and compartmentalization of core binding factor beta. Oncogene; 2006 Jun 29;25(28):3982-93
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  • [Title] Decreased intranuclear mobility of acute myeloid leukemia 1-containing fusion proteins is accompanied by reduced mobility and compartmentalization of core binding factor beta.
  • Acute myeloid leukemia 1 (AML1) gene on chromosome 21 is involved in several chromosomal translocations, including t(8;21) and t(16;21), that produce chimeric fusion proteins AML1-eight twenty-one (ETO) and AML-myeloid transforming gene chromosome 16 (MTG16), which contribute to leukemogenesis.
  • Therefore, AML1 fusion proteins may interfere with normal AML1 function due to aberrant nuclear dynamics, which leads to spatial and temporal sequestration of CBFbeta and perhaps other coregulators critical for myeloid differentiation.
  • [MeSH-major] Cell Compartmentation. Core Binding Factor Alpha 2 Subunit / metabolism. Core Binding Factor beta Subunit / metabolism
  • [MeSH-minor] Animals. Cell Line. Dimerization. Green Fluorescent Proteins / metabolism. Humans. Protein Transport. Xenopus

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  • (PMID = 16474840.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21 CA119080
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / RUNX1 protein, human; 147336-22-9 / Green Fluorescent Proteins
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33. Nagamura-Inoue T, Kodo H, Takahashi TA, Mugishima H, Tojo A, Asano S: Four cases of donor cell-derived AML following unrelated cord blood transplantation for adult patients: experiences of the Tokyo Cord Blood Bank. Cytotherapy; 2007;9(8):727-8
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  • [Title] Four cases of donor cell-derived AML following unrelated cord blood transplantation for adult patients: experiences of the Tokyo Cord Blood Bank.
  • [MeSH-major] Blood Donors. Cord Blood Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / etiology


34. Chen YX, Wang WP, Zhang PY, Zhang WG, Liu J, Ma XR: [Expression of genes psma6 and slc25a4 in patients with acute monocytic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1168-73
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  • [Title] [Expression of genes psma6 and slc25a4 in patients with acute monocytic leukemia].
  • The aim of this study was to investigate the expression levels of genes psma6 and slc25a4 in bone marrow of patients with acute monocytic leukemia and their correlation with clinical features and prognosis.
  • The expression levels of genes psma6 and slc25a4 in AML-M5 leukemia cells, normal blood cells and non-leukemia cells were detected by real-time quantitative RT-PCR and compared each other.
  • The results showed that the expression levels of psma6 mRNA in AML-M5 leukemia cells was lower than that in non AML-M5 leukemia cells, non-leukemia cells and normal blood cells.
  • The expression level of psma6 in AML-M5 patients with complete remission was higher than that in AML-M5 patients without remission.
  • The expression level of P27K protein in AML-M5 and AL correlated to leukocyte count in peripheral blood and LDH content.
  • The overexpression of slc25a4 mRNA was found in AML-M5, but there was no significant difference in slc25a4 mRNA expression between the patients with complete remission and those without remission.
  • It is concluded that the expression level of psma6 is probably a new prognostic indicator of acute monocytic leukemia, slc25a4 may be a novel gene of antigen associated with acute monocytic leukemia.

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  • (PMID = 19840444.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenine Nucleotide Translocator 1; EC 3.4.25.1 / PSMA6 protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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35. Clements D, Markwick LJ, Puri N, Johnson SR: Role of the CXCR4/CXCL12 axis in lymphangioleiomyomatosis and angiomyolipoma. J Immunol; 2010 Aug 1;185(3):1812-21
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  • Lymphangioleiomyomatosis (LAM) is a progressive disease caused by accumulation of metastatic (LAM) cells in the lungs, lymphatics, and the tumor angiomyolipoma (AML).
  • LAM cells have biallelic loss of either tuberous sclerosis complex gene (but predominantly TSC-2) and resultant dysregulation of the mammalian target of rapamycin (mTOR) pathway.
  • Chemokines are associated with neoplastic cell growth, survival, and homing to specific organs and may play similar roles in LAM.
  • Our objective was to study comprehensively the expression and function of chemokine receptors and how their function interacts with dysregulation of the mTOR pathway in LAM and AML.
  • We used RT-PCR and FACS to study receptor expression in primary AML cells and immunohistochemistry to investigate expression in tissues.
  • Chemokine receptor function was analyzed in AML cells by Western blotting of signaling proteins and cell proliferation and apoptosis assays.
  • Primary AML cells, LAM, and AML tissues expressed CCR3, CXCR4, CXCR6, and CXC3CR1.
  • In AML cells, their ligands CXCL12 CX3CL1, CCL11, CCL24, and CCL28 caused robust phosphorylation of p42/44 MAPK and Akt.
  • CXCL12 was expressed in type II pneumocytes covering LAM nodules and caused AML cell growth and protection from apoptosis, which was blocked by AMD3100, a CXCR4 inhibitor.
  • The mTOR inhibitor rapamycin, but not AMD3100, inhibited growth of AML tumor xenografts.
  • We conclude that the CXCL12/CXCR4 axis promotes, but is not absolutely required for, AML/LAM cell growth and survival.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / biosynthesis. Apoptosis Regulatory Proteins / metabolism. Apoptosis Regulatory Proteins / physiology. Cell Line, Transformed. Cell Movement / immunology. Cell Proliferation. Cell Survival / immunology. Female. Humans. Inflammation Mediators / physiology. Lung Neoplasms / immunology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Mice. Mice, Nude. Signal Transduction / immunology. Tumor Cells, Cultured. Tumor Suppressor Proteins / physiology. Xenograft Model Antitumor Assays

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  • (PMID = 20585037.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Inflammation Mediators; 0 / Receptors, CXCR4; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein
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36. Claus R, Almstedt M, Lübbert M: Epigenetic treatment of hematopoietic malignancies: in vivo targets of demethylating agents. Semin Oncol; 2005 Oct;32(5):511-20
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  • These provide a powerful rationale for using azanucleosides (and other small molecules being developed for DNA demethylation) as a novel means of pharmacologic targeting of cancer cells that is distinct from low-dose chemotherapy.
  • Encouraging response rates of about 50% in myelodysplasia with 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine or DAC) have resulted in a number of phase III studies being initiated in this disorder.
  • The development of such drugs for the treatment of acute myeloid leukemia (AML) is ongoing.
  • Thus, demethylating agents and histone deacetylase inhibitors may also induce a T-cell-mediated antileukemic or antitumor effect.
  • [MeSH-minor] Antigens, Neoplasm / metabolism. Antineoplastic Agents / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / chemistry. Cell Cycle Proteins / metabolism. Cyclin-Dependent Kinase Inhibitor p15. DNA / chemistry. DNA Methylation. Gene Silencing. Herpesvirus 4, Human / genetics. Humans. Leukemia, Myeloid, Acute / drug therapy. Membrane Proteins / metabolism. Models, Genetic. Neoplasms / genetics. Time Factors. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16210092.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CDKN2B protein, human; 0 / CTAG1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Membrane Proteins; 0 / Tumor Suppressor Proteins; 776B62CQ27 / decitabine; 9007-49-2 / DNA; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Number-of-references] 96
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37. Haus O, Kotlarek-Haus S, Potoczek S, Czarnecka M, Duszenko E, Makowska I, Mirowska N, Kuliczkowski K: Myelodysplastic syndromes according to FAB and WHO classification. Single center experience. Neoplasma; 2006;53(2):136-43
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  • [Title] Myelodysplastic syndromes according to FAB and WHO classification. Single center experience.
  • The results of clinical and laboratory observations of 119 MDS patients divided acc. to FAB, and - after excluding RAEB-t and CMML groups -- of 95 patients divided accordingly to WHO classification are presented.
  • The diagnosis of MDS was based on medical interview, physical examination, blood biochemistry, peripheral blood (PB) and bone marrow (BM) cytomorphology and cytochemistry, trephine biopsy and cytogenetic examination.
  • The progression to AML was more common in less favorable groups, with p=0.0001 for FAB and p=0.00016 for WHO.
  • The distribution of IPSS prognostic index among the groups showed statistically significant difference (p=0.0004 for FAB, and p=0.0001 for WHO), whereas the distribution of karyotypic abnormalities did not.
  • However, in univariate analysis statistically significant influence on ST showed, beside the both classification systems: cytogenetics, the presence of blasts in PB, age and IPSS index.
  • The authors conclude that the WHO classification offers a good prognostic tool for MDS patients.
  • [MeSH-major] Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / diagnosis. World Health Organization


38. Taussig DC, Vargaftig J, Miraki-Moud F, Griessinger E, Sharrock K, Luke T, Lillington D, Oakervee H, Cavenagh J, Agrawal SG, Lister TA, Gribben JG, Bonnet D: Leukemia-initiating cells from some acute myeloid leukemia patients with mutated nucleophosmin reside in the CD34(-) fraction. Blood; 2010 Mar 11;115(10):1976-84
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  • [Title] Leukemia-initiating cells from some acute myeloid leukemia patients with mutated nucleophosmin reside in the CD34(-) fraction.
  • Leukemia-initiating cells (LICs) in acute myeloid leukemia (AML) are believed to be restricted to the CD34(+) fraction.
  • However, one of the most frequently mutated genes in AML is nucleophosmin (NPM), and this is associated with low CD34 expression.
  • We, therefore, investigated whether NPM-mutated AMLs have LICs restricted to the CD34(+) fraction.
  • We transplanted sorted fractions of primary NPM-mutated AML into immunodeficient mice to establish which fractions initiate leukemia.
  • When samples were sorted based on CD34 and CD38 expression, multiple fractions initiated leukemia in primary and secondary recipients.
  • [MeSH-major] Antigens, CD34 / metabolism. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology. Nuclear Proteins / genetics
  • [MeSH-minor] Animals. Antigens, CD38 / metabolism. Cell Separation / methods. Erythroid Precursor Cells / metabolism. Erythroid Precursor Cells / pathology. Erythroid Precursor Cells / transplantation. Humans. Immunotherapy, Adoptive / methods. Mice. Mice, Inbred NOD. Mice, Knockout. Mice, SCID. Mutant Proteins / metabolism. Phenotype. Xenograft Model Antitumor Assays

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  • (PMID = 20053758.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501940; United States / NCI NIH HHS / CA / P01 CA095426; United States / NCI NIH HHS / CA / P01 CA95426; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Mutant Proteins; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 3.2.2.5 / Antigens, CD38
  • [Other-IDs] NLM/ PMC2837317
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39. Sanchez PV, Perry RL, Sarry JE, Perl AE, Murphy K, Swider CR, Bagg A, Choi JK, Biegel JA, Danet-Desnoyers G, Carroll M: A robust xenotransplantation model for acute myeloid leukemia. Leukemia; 2009 Nov;23(11):2109-17
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  • [Title] A robust xenotransplantation model for acute myeloid leukemia.
  • Xenotransplantation of human acute myeloid leukemia (AML) in immunocompromised animals has been critical for defining leukemic stem cells.
  • However, existing immunodeficient strains of mice have short life spans and low levels of AML cell engraftment, hindering long-term evaluation of primary human AML biology.
  • A recent study suggested that NOD/LtSz-scid IL2Rgammac null (NSG) mice have enhanced AML cell engraftment, but this relied on technically challenging neonatal injections.
  • Here, we performed extensive analysis of AML engraftment in adult NSG mice using tail vein injection.
  • Of the 35 AML samples analyzed, 66% showed bone marrow engraftment over 0.1%.
  • A 2-44-fold expansion of AML cells was often seen.
  • Secondary and tertiary recipients showed consistent engraftment, with most showing further AML cell expansion.
  • Engraftment did not correlate with French-American-British subtype or cytogenetic abnormalities.
  • Importantly, animals developed organomegaly and a wasting illness consistent with advanced leukemia.
  • We conclude that the NSG xenotransplantation model is a robust model for human AML cell engraftment, which will allow better characterization of AML biology and testing of new therapies.
  • [MeSH-major] Disease Models, Animal. Leukemia, Myeloid, Acute / pathology. Mice, Inbred NOD. Neoplasm Transplantation / methods. Transplantation, Heterologous / methods


40. Bäsecke J, Schwieger M, Griesinger F, Schiedlmeier B, Wulf G, Trümper L, Stocking C: AML1/ETO promotes the maintenance of early hematopoietic progenitors in NOD/SCID mice but does not abrogate their lineage specific differentiation. Leuk Lymphoma; 2005 Feb;46(2):265-72
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  • [Title] AML1/ETO promotes the maintenance of early hematopoietic progenitors in NOD/SCID mice but does not abrogate their lineage specific differentiation.
  • AML1-ETO is generated by the t(8;21) translocation found in approximately 12% of acute myelogenous leukemia.
  • Studies to delineate the mechanism by which AML1-ETO induces leukemia have primarily relied on transformed human cell lines or murine model systems.
  • The capacity for prolonged survival, however, did not abrogate maturation, as AML1-ETO cells gave rise to normal colonies in a CFU-assay.
  • AML1/ETO-expressing cells also contributed to myeloid (CD15, CD33), B-lymphoid (CD20), NK-cell (CD56) and erythroid (GPA) lineages in xenografted NOD/SCID mice.
  • Although able to engraft all major lineages, AML1/ETO transplanted cells were primarily found in less differentiated fractions as measured by cell surface markers CD34 and CD38.
  • In spite of a good engraftment and prolonged observation period none of the NOD/SCID-mice developed an acute myelogenous leukemia.
  • Our findings demonstrate that AML1/ETO promotes the maintenance of early human hematopoietic progenitors, but does not abrogate their physiologic differentiation.
  • Furthermore, the leukemogenic potential of AML1/ETO expressed in human progenitors is low, despite transcription levels equivalent to those found in AMLs.
  • [MeSH-major] Cell Differentiation. Hematopoietic Stem Cells / cytology. Oncogene Proteins, Fusion / physiology. Transcription Factors / physiology
  • [MeSH-minor] Animals. Cell Lineage. Cell Proliferation. Cells, Cultured. Core Binding Factor Alpha 2 Subunit. Hematopoietic Stem Cell Transplantation. Humans. Leukemia / etiology. Mice. Mice, Inbred NOD. Mice, SCID. Transfection. Transplantation, Heterologous

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  • (PMID = 15621811.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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41. Petropoulos K, Arseni N, Schessl C, Stadler CR, Rawat VP, Deshpande AJ, Heilmeier B, Hiddemann W, Quintanilla-Martinez L, Bohlander SK, Feuring-Buske M, Buske C: A novel role for Lef-1, a central transcription mediator of Wnt signaling, in leukemogenesis. J Exp Med; 2008 Mar 17;205(3):515-22
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  • Deregulation of this pathway has been linked to a large variety of cancers, including different subtypes of leukemia.
  • Here, we demonstrate Lef-1 expression in murine HSCs as well as its expression in human leukemia.
  • Mice transplanted with bone marrow retrovirally transduced to express Lef-1 or a constitutive active Lef-1 mutant showed a severe disturbance of normal hematopoietic differentiation and finally developed B lymphoblastic and acute myeloid leukemia (AML).
  • Lef-1-induced AMLs were characterized by immunoglobulin (Ig) DH-JH rearrangements and a promiscuous expression of lymphoid and myeloid regulatory factors.
  • Furthermore, single cell experiments and limiting dilution transplantation assays demonstrated that Lef-1-induced AML was propagated by a leukemic stem cell with lymphoid characteristics displaying Ig DH-JH rearrangements and a B220(+) myeloid marker(-) immunophenotype.
  • These data indicate a thus far unknown role of Lef-1 in the biology of acute leukemia, pointing to the necessity of balanced Lef-1 expression for an ordered hematopoietic development.
  • [MeSH-major] Leukemia / etiology. Lymphoid Enhancer-Binding Factor 1 / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Gene Expression. Hematopoiesis / genetics. Hematopoiesis / physiology. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mice. Neoplastic Stem Cells / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction

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  • (PMID = 18316418.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LEF1 protein, human; 0 / Lef1 protein, mouse; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / RNA, Messenger; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2275375
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42. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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43. Fröhling S, Schlenk RF, Krauter J, Thiede C, Ehninger G, Haase D, Harder L, Kreitmeier S, Scholl C, Caligiuri MA, Bloomfield CD, Döhner H, Döhner K: Acute myeloid leukemia with deletion 9q within a noncomplex karyotype is associated with CEBPA loss-of-function mutations. Genes Chromosomes Cancer; 2005 Apr;42(4):427-32
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  • [Title] Acute myeloid leukemia with deletion 9q within a noncomplex karyotype is associated with CEBPA loss-of-function mutations.
  • To assess the prevalence of mutations in the CEBPA gene, which encodes the myeloid transcription factor CEBPA in specific cytogenetic subgroups, we initially studied 125 patients with acute myeloid leukemia (AML).
  • Five of the eight patients with del(9q) as the sole aberration or in combination with a single additional abnormality other than t(8;21) had CEBPA mutations associated with loss of CEBPA function.
  • We have shown for the first time that AML with del(9q) in the context of a noncomplex karyotype is strongly associated with CEBPA loss-of-function mutations.
  • Loss of a critical segment of 9q, most likely in 9q22, and disruption of CEBPA function possibly cooperate in the pathogenesis of del(9q) AML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 9. Leukemia, Myeloid / genetics. Mutation. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Base Sequence. Cohort Studies. DNA Primers. Humans. Middle Aged

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15645492.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 10114 0; United States / NCI NIH HHS / CA / CA 16058; United States / NCI NIH HHS / CA / CA 77658
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Transcription Factors
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44. Klymenko SV, Ilyenko IN, Golarnik NA, Maznichenko OL, Breier A, Bazyka DA: Membrane transport and apoptosis-related proteins in radiation-associated acute myeloid leukemia following the Chornobyl accident. Gen Physiol Biophys; 2009 Mar;28(1):63-9
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  • [Title] Membrane transport and apoptosis-related proteins in radiation-associated acute myeloid leukemia following the Chornobyl accident.
  • We report on the results of multidrug-resistance transporters (P-glycoprotein, LRP, and MDR1), and apoptosis-related proteins (Fas, Bcl-2, Bax, p53, and Bcl-X(L)) expression analysis of 56 acute myeloid leukemia (AML) patients by flow cytometry.
  • Of these, there were 21 persons exposed to ionizing radiation due to the Chornobyl accident with radiation-associated and 35 patients with spontaneous AML.
  • Leukemic cells in patients with radiation-associated AML more often overexpressed antiapoptotic protein Bcl-2 (12/21 vs. 6/35, p < 0.005) and less often demonstrated expression of Fas receptor (12/21 vs. 30/35, p < 0.05).
  • Patients with radiation-associated AML compared to spontaneous cases more often were P-glycoprotein positive (12/20 vs. 9/31, p < 0.05).
  • P-glycoprotein overexpression significantly correlated with the resistance of the disease to chemotherapy in patients with radiation-associated AML (p < 0.05).
  • [MeSH-major] Apoptosis. Chernobyl Nuclear Accident. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / metabolism. Leukemia, Radiation-Induced / metabolism. Membrane Transport Proteins / metabolism

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  • (PMID = 19390138.001).
  • [ISSN] 0231-5882
  • [Journal-full-title] General physiology and biophysics
  • [ISO-abbreviation] Gen. Physiol. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / FAS protein, human; 0 / Membrane Transport Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
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45. Pedersen-Bjergaard J, Andersen MK, Andersen MT, Christiansen DH: Genetics of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2008 Feb;22(2):240-8
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  • [Title] Genetics of therapy-related myelodysplasia and acute myeloid leukemia.
  • Myelodysplasia (MDS) and acute myeloid leukemia (AML) are heterogeneous, closely associated diseases arising de novo or following chemotherapy with alkylating agents, topoisomerase II inhibitors, or after radiotherapy.
  • Whereas de novo MDS and AML are almost always subclassified according to cytogenetic characteristics, therapy-related MDS (t-MDS) and therapy-related AML (t-AML) are often considered as separate entities and are not subdivided.
  • Alternative genetic pathways were previously proposed in t-MDS and t-AML based on cytogenetic characteristics.
  • An increasing number of gene mutations are now observed to cluster differently in these pathways with an identical pattern in de novo and in t-MDS and t-AML.
  • Point mutations of AML1 and RAS seem to cooperate and predispose to progression from t-MDS to t-AML.
  • Their association and cooperation with point mutations of p53 and AML1, respectively, extend the scenario of cooperating genetic abnormalities in MDS and AML.
  • As de novo and t-MDS and t-AML are biologically identical diseases, they ought to be subclassified and treated similarly.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics


46. Ojima H, Hasegawa T, Matsuno Y, Sakamoto M: Extramedullary myeloid tumour (EMMT) of the gallbladder. J Clin Pathol; 2005 Feb;58(2):211-3
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  • [Title] Extramedullary myeloid tumour (EMMT) of the gallbladder.
  • This report describes a rare case of an extramedullary myeloid tumour (EMMT) of the gallbladder in a patient without leukaemia.
  • A percutaneous needle biopsy was attempted, but because adenocarcinoma could not be completely ruled out, the use of undue force was considered dangerous.
  • Under a preoperative diagnosis of gallbladder carcinoma, a hepatopancreatoduodenectomy was performed.
  • After surgery, the patient underwent combination chemotherapy as prescribed for cases of acute myeloblastic leukaemia.
  • The patient did not develop acute leukaemia during a follow up period of four years.
  • In conclusion, a correct diagnosis of EMMT can be made using appropriate immunohistochemical staining.
  • [MeSH-major] Gallbladder Neoplasms / diagnosis. Sarcoma, Myeloid / diagnosis

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  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
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47. Syampurnawati M, Tatsumi E, Ardianto B, Takenokuchi M, Nakamachi Y, Kawano S, Kumagai S, Saigo K, Matsui T, Takahashi T, Nagai K, Gunadi, Nishio H, Yabe H, Kondo S, Hayashi Y: DR negativity is a distinctive feature of M1/M2 AML cases with NPM1 mutation. Leuk Res; 2008 Jul;32(7):1141-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DR negativity is a distinctive feature of M1/M2 AML cases with NPM1 mutation.
  • Our previous observation of a higher incidence of FLT3-ITD in DR(-) M1/M2 AML than in DR(+) M1/M2 led to an investigation of NPM1 mutation in the same samples, since DR(-) AML and AML with NPM1 mutation share such characteristics as normal karyotype, the absence of CD34, and FLT3-ITD.
  • NPM1 mutation was found in 18 of 26 (69.2%) of DR(-) cases, but not in any of 28 DR(+) cases.
  • These findings point to DR negativity as another phenotypic feature of AML with NPM1 mutation.
  • [MeSH-major] HLA-DR Antigens / analysis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18180033.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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48. Strupp C, Knipp S, Hartmann J, Gattermann N, Haas R, Germing U: A pilot study of bendamustine in elderly patients with high-risk MDS and AML. Leuk Lymphoma; 2007 Jun;48(6):1161-6
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  • [Title] A pilot study of bendamustine in elderly patients with high-risk MDS and AML.
  • We examined the efficacy of bendamustine in 15 pretreated patients (12 men, 3 women, median age 69 years) with acute myeloid leukaemia (AML) or myelodysplastic syndromes (MDS) 3 AML, 5 sAML, 5 CMML II, 1 RAEB II.
  • Three patients showed no response, one patient with AML died due to progressive disease.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Nitrogen Mustard Compounds / therapeutic use
  • [MeSH-minor] Acute Disease. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Bendamustine Hydrochloride. Drug Evaluation. Female. Humans. Male. Pilot Projects

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  • [CommentIn] Leuk Lymphoma. 2007 Jun;48(6):1064-6 [17577766.001]
  • (PMID = 17577779.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 981Y8SX18M / Bendamustine Hydrochloride
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49. Thomas X, Elhamri M: Tipifarnib in the treatment of acute myeloid leukemia. Biologics; 2007 Dec;1(4):415-24
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  • [Title] Tipifarnib in the treatment of acute myeloid leukemia.
  • FTIs inhibit farnesylation of a wide range of target proteins.
  • In preclinical models, tipifarnib (R115777, Zarnestra(R)), a non-peptidomimetic competitive FTI, showed great potency against leukemic cells.
  • Although it has recently demonstrated clinical responses in adults with refractory and relapsed acute myeloid leukemia (AML), and in older adults with newly diagnosed poor-risk AML, its activity was far less than anticipated.
  • Much remains to be learned to optimize such therapy in patients with AML.

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  • (PMID = 19707311.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2721284
  • [Keywords] NOTNLM ; acute myeloid leukemia / farnesyltransferase inhibitor / prognosis / targeted therapy / tipifarnib
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50. Chapuis N, Tamburini J, Green AS, Vignon C, Bardet V, Neyret A, Pannetier M, Willems L, Park S, Macone A, Maira SM, Ifrah N, Dreyfus F, Herault O, Lacombe C, Mayeux P, Bouscary D: Dual inhibition of PI3K and mTORC1/2 signaling by NVP-BEZ235 as a new therapeutic strategy for acute myeloid leukemia. Clin Cancer Res; 2010 Nov 15;16(22):5424-35
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  • [Title] Dual inhibition of PI3K and mTORC1/2 signaling by NVP-BEZ235 as a new therapeutic strategy for acute myeloid leukemia.
  • PURPOSE: The growth and survival of acute myeloid leukemia (AML) cells are enhanced by the deregulation of signaling pathways such as phosphoinositide 3-kinase (PI3K)/Akt and mammalian target of rapamycin (mTOR).
  • Major efforts have thus been made to develop molecules targeting these activated pathways.
  • In AML, however, the translation process is deregulated and rapamycin resistant.
  • EXPERIMENTAL DESIGN: The activity of NVP-BEZ235 was tested in primary AML samples (n = 21) and human leukemic cell lines.
  • The antileukemic activity of NVP-BEZ235 was tested by analyzing its effects on leukemic progenitor clonogenicity, blast cell proliferation, and survival.
  • Furthermore, NVP-BEZ235 fully inhibits the rapamycin-resistant phosphorylation of 4E-BP1, resulting in a marked inhibition of protein translation in AML cells.
  • Hence, NVP-BEZ235 reduces the proliferation rate and induces an important apoptotic response in AML cells without affecting normal CD34(+) survival.
  • CONCLUSIONS: Our results clearly show the antileukemic efficiency of the NVP-BEZ235 compound, which therefore represents a promising option for future AML therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Imidazoles / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Kinase Inhibitors / pharmacology. Proteins / antagonists & inhibitors. Quinolines / pharmacology. Transcription Factors / antagonists & inhibitors
  • [MeSH-minor] Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Humans. Multiprotein Complexes. RNA Caps / antagonists & inhibitors. RNA Caps / genetics. Signal Transduction / drug effects. Structure-Activity Relationship. TOR Serine-Threonine Kinases. Tumor Cells, Cultured

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  • [Copyright] ©2010 AACR.
  • (PMID = 20884625.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CRTC2 protein, human; 0 / Imidazoles; 0 / Multiprotein Complexes; 0 / Protein Kinase Inhibitors; 0 / Proteins; 0 / Quinolines; 0 / RNA Caps; 0 / Transcription Factors; 0 / mechanistic target of rapamycin complex 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; RUJ6Z9Y0DT / dactolisib
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51. Britschgi A, Simon HU, Tobler A, Fey MF, Tschan MP: Epigallocatechin-3-gallate induces cell death in acute myeloid leukaemia cells and supports all-trans retinoic acid-induced neutrophil differentiation via death-associated protein kinase 2. Br J Haematol; 2010 Apr;149(1):55-64
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  • [Title] Epigallocatechin-3-gallate induces cell death in acute myeloid leukaemia cells and supports all-trans retinoic acid-induced neutrophil differentiation via death-associated protein kinase 2.
  • Acute promyelocytic leukaemia (APL) patients are successfully treated with all-trans retinoic acid (ATRA).
  • Earlier studies suggested that in haematopoietic neoplasms, the green tea polyphenol epigallocatechin-3-gallate (EGCG) induces cell death without adversely affecting healthy cells.
  • We aimed at deciphering the molecular mechanism of EGCG-induced cell death in acute myeloid leukaemia (AML).
  • A significant increase of death-associated protein kinase 2 (DAPK2) levels was found in AML cells upon EGCG treatment paralleled by increased cell death that was significantly reduced upon silencing of DAPK2.
  • EGCG toxicity of primary AML blasts correlated with 67 kDa laminin receptor (67LR) expression.
  • Pretreatment of AML cells with ATRA, causing downregulation of 67LR, rendered these cells resistant to EGCG-mediated cell death.
  • In summary, it was found that (i) DAPK2 is essential for EGCG-induced cell death in AML cells, (ii) ATRA and EGCG cotreatment significantly boosted neutrophil differentiation, and 67LR expression correlates with susceptibility of AML cells to EGCG.
  • We thus suggest that EGCG, by selectively targeting leukaemic cells, may improve differentiation therapies for APL and chemotherapy for other AML subtypes.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Catechin / analogs & derivatives. Leukemia, Myeloid, Acute / pathology. Neutrophils / drug effects. Tretinoin / pharmacology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis Regulatory Proteins / physiology. Calcium-Calmodulin-Dependent Protein Kinases / physiology. Cell Death / drug effects. Cell Differentiation / drug effects. Death-Associated Protein Kinases. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Gene Knockdown Techniques. Humans. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured. Up-Regulation / drug effects

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  • (PMID = 20096012.001).
  • [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 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 5688UTC01R / Tretinoin; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.11.1 / DAPK2 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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52. Löwenberg B, Ossenkoppele GJ, van Putten W, Schouten HC, Graux C, Ferrant A, Sonneveld P, Maertens J, Jongen-Lavrencic M, von Lilienfeld-Toal M, Biemond BJ, Vellenga E, van Marwijk Kooy M, Verdonck LF, Beck J, Döhner H, Gratwohl A, Pabst T, Verhoef G, Dutch-Belgian Cooperative Trial Group for Hemato-Oncology (HOVON), German AML Study Group (AMLSG), Swiss Group for Clinical Cancer Research (SAKK) Collaborative Group: High-dose daunorubicin in older patients with acute myeloid leukemia. N Engl J Med; 2009 Sep 24;361(13):1235-48
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  • [Title] High-dose daunorubicin in older patients with acute myeloid leukemia.
  • BACKGROUND: A complete remission is essential for prolonging survival in patients with acute myeloid leukemia (AML).
  • In older patients, it is usual to give daunorubicin at a dose of 45 to 50 mg per square meter of body-surface area.
  • METHODS: Patients in whom AML or high-risk refractory anemia had been newly diagnosed and who were 60 to 83 years of age (median, 67) were randomly assigned to receive cytarabine, at a dose of 200 mg per square meter by continuous infusion for 7 days, plus daunorubicin for 3 days, either at the conventional dose of 45 mg per square meter (411 patients) or at an escalated dose of 90 mg per square meter (402 patients); this treatment was followed by a second cycle of cytarabine at a dose of 1000 mg per square meter every 12 hours [DOSAGE ERROR CORRECTED] for 6 days.
  • Survival end points in the two groups did not differ significantly overall, but patients in the escalated-treatment group who were 60 to 65 years of age, as compared with the patients in the same age group who received the conventional dose, had higher rates of complete remission (73% vs. 51%), event-free survival (29% vs. 14%), and overall survival (38% vs. 23%).
  • CONCLUSIONS: In patients with AML who are older than 60 years of age, escalation of the dose of daunorubicin to twice the conventional dose, with the entire dose administered in the first induction cycle, effects a more rapid response and a higher response rate than does the conventional dose, without additional toxic effects. (Current Controlled Trials number, ISRCTN77039377; and Netherlands National Trial Register number, NTR212. )
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Daunorubicin / administration & dosage. Leukemia, Myelomonocytic, Acute / drug therapy
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Combined Modality Therapy. Cytarabine / administration & dosage. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Proportional Hazards Models. Remission Induction / methods. Stem Cell Transplantation. Survival Analysis

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  • [Copyright] 2009 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2009 Sep 24;361(13):1301-3 [19776412.001]
  • [ErratumIn] N Engl J Med. 2010 Mar 25;362(12):1155. Dosage error in published abstract; MEDLINE/PubMed abstract corrected; Dosage error in article text
  • (PMID = 19776405.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ISRCTN/ ISRCTN77039377
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
  • [Investigator] Ferrant A; Delannoy A; Maertens J; Verhoef G; Demuynck H; Bosly A; Graux C; Breems DA; Zachee P; Jaeger E; Beck J; Fischer T; von Lilienfeld-Toal M; Glasmacher A; Salwender HJ; Hartmann F; Goetze K; Grimminger W; Döhner H; Bargetzi M; Wernli M; Gratwohl A; Fey MF; Pabst T; Chapuis B; Herr A; Wuillemin WA; Jacky E; Schans U; Wittebol S; Van der Lelie J; Biemond BJ; De Valk B; Ossenkoppele GJ; Huijgens PC; Wijermans PW; Levin MD; Schaafsma MR; Daenen SM; Vellenga E; Voogt PJ; Schouten HC; Biesma DH; Sonneveld P; Zijlmans J; Jongen-Lavrencic M; De Greef GE; Löwenberg B; Verdonck LF; Kuball J; van Marwijk Kooy M; Milne A; Milligan DW; Pocock C; Burnett AK; Aldouri M; Dennis M
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53. Zimmer J, Michel T, Andrès E, Hentges F: Up-regulation of NKG2D ligands by AML cells to increase sensitivity to NK cells: the tumour might strike back. Comment on "differentiation-promoting drugs up-regulate NKG2D ligand expression and enhance the susceptibility of acute myeloid leukemia cells to natural killer cell-mediated lysis" by Rohner et al. [Leuk Res 2007;31:1393-402]. Leuk Res; 2008 Apr;32(4):676-7
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  • [Title] Up-regulation of NKG2D ligands by AML cells to increase sensitivity to NK cells: the tumour might strike back. Comment on "differentiation-promoting drugs up-regulate NKG2D ligand expression and enhance the susceptibility of acute myeloid leukemia cells to natural killer cell-mediated lysis" by Rohner et al. [Leuk Res 2007;31:1393-402].
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Differentiation. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / metabolism. Receptors, Immunologic / metabolism
  • [MeSH-minor] Humans. Ligands. NK Cell Lectin-Like Receptor Subfamily K. Receptors, Natural Killer Cell. Up-Regulation

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  • [CommentOn] Leuk Res. 2007 Oct;31(10):1393-402 [17391757.001]
  • (PMID = 17920678.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / KLRK1 protein, human; 0 / Ligands; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell
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54. 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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  • [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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55. Stahl T, Badbaran A, Kröger N, Klyuchnikov E, Zabelina T, Zeschke S, Schafhausen P, Schultz W, Asenova S, Smirnova A, Wolschke C, Ayuk F, Zander AR, Fehse B, Bacher U: Minimal residual disease diagnostics in patients with acute myeloid leukemia in the post-transplant period: comparison of peripheral blood and bone marrow analysis. Leuk Lymphoma; 2010 Oct;51(10):1837-43
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  • [Title] Minimal residual disease diagnostics in patients with acute myeloid leukemia in the post-transplant period: comparison of peripheral blood and bone marrow analysis.
  • Considering the high relapse rates of AML after allogeneic hematopoietic stem cell transplant, research aims to improve post-transplant surveillance.
  • To determine the value of peripheral blood (PB) for post-transplant minimal residual disease monitoring, we compared 38 PB and bone marrow (BM) sample pairs in 25 stem cell recipients with NPM1-mutated AML (12 males, 13 females, ages 21-73 years).
  • NPM1A mutation levels and chimerism ratios were determined in non-separated BM/PB.
  • In conclusion, MRD monitoring with qPCR for the NPM1 mutation and chimerism from non-separated PB contributes to surveillance in patients with AML in the post-transplant period, but even with highly sensitive qPCR there is a risk of failure to detect the mutation in PB.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / surgery. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow / metabolism. Bone Marrow / pathology. Disease-Free Survival. Female. Humans. Male. Middle Aged. Mutation. Nuclear Proteins / genetics. Polymerase Chain Reaction. Postoperative Period. Transplantation Chimera / blood. Transplantation, Homologous. Young Adult

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  • (PMID = 20849383.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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56. Dang L, Jin S, Su SM: IDH mutations in glioma and acute myeloid leukemia. Trends Mol Med; 2010 Sep;16(9):387-97
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  • [Title] IDH mutations in glioma and acute myeloid leukemia.
  • Subsequent studies have confirmed recurrent IDH1 and IDH2 mutations in up to 70% of low-grade glioma and secondary GBM, as well as in 10% of acute myeloid leukemia (AML) cases.
  • This review surveys the prevalence of IDH mutations in cancer and explores current mechanistic understanding of IDH mutations with implications for diagnostic and therapeutic development for the treatment of gliomas and AML.
  • [MeSH-major] Brain Neoplasms / enzymology. Glioma / enzymology. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / enzymology. Mutation


57. Nishioka C, Ikezoe T, Yang J, Komatsu N, Koeffler HP, Yokoyama A: Blockade of MEK signaling potentiates 5-Aza-2'-deoxycytidine-induced apoptosis and upregulation of p21(waf1) in acute myelogenous leukemia cells. Int J Cancer; 2009 Sep 1;125(5):1168-76
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  • [Title] Blockade of MEK signaling potentiates 5-Aza-2'-deoxycytidine-induced apoptosis and upregulation of p21(waf1) in acute myelogenous leukemia cells.
  • We have recently reported that the mitogen-activated protein kinase/ERK kinase (MEK) inhibitor AZD6244 (ARRY-142886) strikingly potentiated the effects of histone deacetylase inhibitor to induce growth arrest and apoptosis of acute myelogeneous leukemia (AML) cells in association with enhanced upregulation of p21(waf1).
  • This study examined the effects of the MEK inhibitor on the action of DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-AzadC), another epigenetic agent in AML cells.
  • AZD6244 significantly potentiated the ability of 5-AzadC to induce growth arrest and apoptosis of NB4, and freshly isolated AML cells.
  • In parallel, 5-AzadC induced expression of p21(waf1) in AML cells, which was potently enhanced in the presence of AZD6244.
  • Taken together, combination of 5-AzadC and the MEK inhibitor may be useful for treatment of individuals with a subset of AML.
  • [MeSH-major] Apoptosis / drug effects. Azacitidine / analogs & derivatives. Benzimidazoles / pharmacology. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Gene Expression Regulation / drug effects. Leukemia, Myeloid / genetics. MAP Kinase Kinase 1 / antagonists & inhibitors
  • [MeSH-minor] Acetylation. Aged. Blotting, Western. Cell Proliferation / drug effects. Chromatin Immunoprecipitation. DNA Modification Methylases / antagonists & inhibitors. Drug Synergism. Enzyme Inhibitors / pharmacology. Flow Cytometry. Histone Deacetylase Inhibitors. Histone Deacetylases / metabolism. Histones / metabolism. Humans. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Tumor Cells, Cultured

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  • [Copyright] 2009 UICC.
  • (PMID = 19422044.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AZD 6244; 0 / Benzimidazoles; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
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58. Kitawaki T, Kadowaki N, Kondo T, Ishikawa T, Ichinohe T, Teramukai S, Fukushima M, Kasai Y, Maekawa T, Uchiyama T: Potential of dendritic-cell immunotherapy for relapse after allogeneic hematopoietic stem cell transplantation, shown by WT1 peptide- and keyhole-limpet-hemocyanin-pulsed, donor-derived dendritic-cell vaccine for acute myeloid leukemia. Am J Hematol; 2008 Apr;83(4):315-7
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  • [Title] Potential of dendritic-cell immunotherapy for relapse after allogeneic hematopoietic stem cell transplantation, shown by WT1 peptide- and keyhole-limpet-hemocyanin-pulsed, donor-derived dendritic-cell vaccine for acute myeloid leukemia.
  • Induction of leukemia-specific immune responses is a promising treatment for acute myeloid leukemia.
  • A 58-year-old woman received Wilms' tumor 1 (WT1) peptide- and keyhole limpet hemocyanin (KLH)-pulsed, donor-derived dendritic cell (DC) vaccination for AML relapse after allogeneic stem cell transplantation.
  • The vaccination induced immune responses to the naive antigen KLH, whereas definitive immune responses to WT1 were not detected.
  • Leukemia gradually progressed despite of vaccination.
  • This study indicates that DC vaccination can induce an antigen-specific immune response in a patient after allogeneic stem cell transplantation, thus representing a viable strategy to induce antigen-specific immune responses in such patients.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Dendritic Cells / transplantation. Hemocyanin / immunology. Immunotherapy, Active. Leukemia, Myelomonocytic, Acute / therapy. Peptide Fragments / immunology. Salvage Therapy. WT1 Proteins / immunology
  • [MeSH-minor] Adjuvants, Immunologic. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease Progression. Female. Hematopoietic Stem Cell Transplantation. Humans. Immunosuppressive Agents / therapeutic use. Living Donors. Middle Aged. Phosphoproteins / immunology. Siblings. Transplantation, Homologous. Viral Matrix Proteins / immunology

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18081032.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Immunosuppressive Agents; 0 / Peptide Fragments; 0 / Phosphoproteins; 0 / Viral Matrix Proteins; 0 / WT1 Proteins; 0 / cytomegalovirus matrix protein 65kDa; 04079A1RDZ / Cytarabine; 9013-72-3 / Hemocyanin; FV4Y0JO2CX / keyhole-limpet hemocyanin; ZS7284E0ZP / Daunorubicin
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59. Schwonzen M, Diehl V, Dellanna M, Staib P: Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis. Leuk Res; 2007 Jan;31(1):113-6
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  • [Title] Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis.
  • Immunophenotyping of acute leukemia using flow cytometry after density gradient separation (dg-sep) of mononuclear cells is the international gold standard.
  • Both methods revealed congruent results in phenotyping of 26 cases of acute myeloid leukemias by testing CD4, CD7, CD11b, CD11c, CD13, CD14, CD15, CD33, CD34, CD65s, Glycophorin A and HLA-DR antigens.
  • Only low antigen expression of CD2 was missed in the phenotype of two AML cases by the wb-lysis (23 and 29% positive cells by the dg-sep).
  • [MeSH-major] Antigens, CD / analysis. Antigens, Surface / analysis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16730795.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Surface; 0 / Glycophorin; 0 / HLA-DR Antigens
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60. Hu J, Shekhter-Levin S, Shaw PH, Bay C, Kochmar S, Surti U: A case of myelodysplastic syndrome with acquired monosomy 7 in a child with a constitutional t(1;19) and a mosaicism for trisomy 21. Cancer Genet Cytogenet; 2005 Jan 1;156(1):62-7
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  • A mosaic abnormal female karyotype 46,XX, t(1;19)(q42; p13.1)c[12]/ 47,idem,+21c[3]/ 47,idem,-7,+21c,+mar[7] was obtained on G-banded metaphases from unstimulated bone marrow aspirate cell culture.
  • The presence of two cell lines in multiple cultures indicates that the patient is a true low-level mosaic for trisomy 21.
  • Because of the finding of monosomy 7 and a marker chromosome only in the trisomy 21 clone, we conclude that the leukemic clone arose from a hematopoietic precursor with constitutional trisomy 21.
  • Because acute myelogenous leukemia (AML) and MDS with Down syndrome (DS) have distinct biologic and clinical features, the identification of DS patients with a mild or normal phenotype in the AML/MDS population is of fundamental importance for clinical diagnosis and management.


61. Wheatley K, Brookes CL, Howman AJ, Goldstone AH, Milligan DW, Prentice AG, Moorman AV, Burnett AK, United Kingdom National Cancer Research Institute Haematological Oncology Clinical Studies Group and Acute Myeloid Leukaemia Subgroup: Prognostic factor analysis of the survival of elderly patients with AML in the MRC AML11 and LRF AML14 trials. Br J Haematol; 2009 Jun;145(5):598-605
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  • [Title] Prognostic factor analysis of the survival of elderly patients with AML in the MRC AML11 and LRF AML14 trials.
  • This analysis, of 2483 patients with acute myeloid leukaemia (AML) aged 60+ years entered into two UK trials, was performed to determine the baseline parameters related to survival and to develop a risk index.
  • The Medical Research Council (MRC) AML11 trial (n = 1071) was used to develop the index; this was validated using data from the Leukaemia Research fund (LRF) AML14 trial on 1137 intensively (AML14I) and 275 non-intensively (AML14NI) treated patients.
  • In AML11, cytogenetic group, age, white blood count, performance status and type of AML (de novo, secondary) were all highly significantly related to prognosis in multivariate analysis.
  • The risk factors for survival in older AML patients were similar to those in younger ones and discrimination of patient groups with relatively good to very poor prognosis was possible.
  • These risk groups apply to both intensively and non-intensively treated patients.
  • Randomized trials of intensive versus non-intensive therapy are needed to determine which types of patient should be given which type of treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality

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  • (PMID = 19344426.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300133
  • [Publication-type] Journal Article
  • [Publication-country] England
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62. La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, Mecucci C: Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia. Leukemia; 2006 Jun;20(6):958-64
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  • [Title] Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.
  • Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group.
  • In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7.
  • Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Sensitivity and Specificity


63. Campana D: Status of minimal residual disease testing in childhood haematological malignancies. Br J Haematol; 2008 Nov;143(4):481-9
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  • [Title] Status of minimal residual disease testing in childhood haematological malignancies.
  • In children with acute leukaemia, measurements of minimal residual disease (MRD) provide unique information on treatment response and have become a crucial component of contemporary treatment protocols.
  • In acute lymphoblastic leukaemia (ALL), the most useful MRD assays are based on polymerase chain reaction (PCR) amplification of antigen-receptor genes, and on flow cytometric detection of abnormal immunophenotypes.
  • The latter is the only MRD assay available for most patients with acute myeloid leukaemia (AML).
  • PCR amplification of chromosomal breakpoints and fusion transcripts can also be used to track MRD in a minority of patients with ALL or AML.
  • Treatment de-intensification for patients with early MRD clearance is also being tested.
  • The identification of new markers of leukaemia and the use of increasingly sophisticated technologies for detection of rare cells should further facilitate routine monitoring of MRD and elucidate the features of drug-resistant leukaemic cells.

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  • (PMID = 18710378.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115422-04; United States / NCI NIH HHS / CA / CA115422; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / U01 CA060419-04; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA060419-04; United States / NCI NIH HHS / CA / R01 CA115422-04; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Number-of-references] 72
  • [Other-IDs] NLM/ NIHMS154353; NLM/ PMC2784675
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64. Caughey RW, Michels KB: Birth weight and childhood leukemia: a meta-analysis and review of the current evidence. Int J Cancer; 2009 Jun 1;124(11):2658-70
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  • [Title] Birth weight and childhood leukemia: a meta-analysis and review of the current evidence.
  • A growing body of evidence suggests that childhood leukemia may be initiated in utero when lymphoid and myeloid cells are not fully differentiated and are particularly susceptible to malignant transformation.
  • A fixed effects meta-analysis examining the association between birth weight and childhood leukemia was conducted including 32 studies and 16,501 cases of all types of leukemia (OL), 10,974 cases of acute lymphoblastic leukemia (ALL), and 1,832 cases of acute myeloid leukemia (AML).
  • The odd ratios (OR) for the association of high birth weight with OL, ALL and AML were 1.35 (95% CI: 1.24, 1.48), 1.23 (95% CI: 1.15, 1.32), and 1.40 (95% CI: 1.11, 1.76), respectively, compared with normal birth weight.
  • Low birth weight was not associated with overall and ALL leukemia, but with AML (OR = 1.50; 95% CI: 1.05, 2.13).
  • The combined available evidence from observational studies suggests that high birth weight is associated with an increased risk of overall leukemia and ALL.
  • For AML the risk may be elevated at both high and low extremes of birth weight, suggesting a U-shaped association.
  • [MeSH-major] Birth Weight. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 19173295.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Number-of-references] 62
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65. Grüllich C, Bertz H, Spyridonidis A, Müller CI, Finke J: A fludarabine, thiotepa reduced toxicity conditioning regimen designed specifically for allogeneic second haematopoietic cell transplantation after failure of previous autologous or allogeneic transplantation. Bone Marrow Transplant; 2008 May;41(10):845-50
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  • [Title] A fludarabine, thiotepa reduced toxicity conditioning regimen designed specifically for allogeneic second haematopoietic cell transplantation after failure of previous autologous or allogeneic transplantation.
  • We present a phase II study of fludarabine 5 x 30 mg/m(2), thiotepa 3 x 5 mg/kg as preparative regimen specifically for allogeneic second haematopoietic stem cell transplantation (HCT) after failure of previous HCT.
  • Diagnoses were AML (n=18), ALL (n=3), multiple myeloma (n=11), lymphoma (n=16) and CML (n=1).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Thiotepa / administration & dosage. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Cyclosporine / therapeutic use. Female. Graft vs Host Disease / prevention & control. Humans. Leukemia, Myeloid, Acute / therapy. Lymphoma / therapy. Male. Middle Aged. Multiple Myeloma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Recurrence. Survival Rate. Transplantation, Autologous / adverse effects. Transplantation, Homologous / adverse effects. Treatment Failure

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  • (PMID = 18209719.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; 83HN0GTJ6D / Cyclosporine; 905Z5W3GKH / Thiotepa; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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66. Chen J, Schmitt A, Chen B, Rojewski M, Rübeler V, Fei F, Yu Y, Yu X, Ringhoffer M, von Harsdorf S, Greiner J, Götzz M, Guillaume P, Döhner H, Bunjes D, Schmitt M: Nilotinib hampers the proliferation and function of CD8+ T lymphocytes through inhibition of T cell receptor signalling. J Cell Mol Med; 2008 Oct;12(5B):2107-18
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  • [Title] Nilotinib hampers the proliferation and function of CD8+ T lymphocytes through inhibition of T cell receptor signalling.
  • The novel selective BCR-ABL Breakpoint cluster region--Abelson murine leukemia viral oncogene homolog 1 (BCR-AML) inhibitor nilotinib (AMN107) is a tyrosine kinase inhibitor that is more potent against leukaemia cells in vitro than imatinib.
  • As nilotinib might be used in the context of allogeneic stem cell transplantation where CD8+ T lymphocytes play a pivotal role in the graft-versus-leukaemia (GVL) effect, we investigated effects of nilotinib on this lymphocyte subpopulation.
  • The inhibition of CD8+ T lymphocytes specific for leukaemia or viral antigens through nilotinib was associated with a reduced expansion of antigen peptide specific CD8+ T lymphocytes and with a decreased release of interferon-gamma and granzyme B by these cells as analysed by flow cytometry and enzyme-linked immunospot (ELISPOT) assays.
  • Taken together, we observed a strong suppressive impact of nilotinib on the CD8+ T lymphocyte function which should be considered carefully in the framework of allogeneic stem cell transplantation or other T cell based immunotherapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. CD8-Positive T-Lymphocytes / drug effects. Cell Proliferation / drug effects. Pyrimidines / pharmacology. Receptors, Antigen, T-Cell / drug effects. Signal Transduction / drug effects
  • [MeSH-minor] Case-Control Studies. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • [CommentIn] J Cell Mol Med. 2009 Mar;13(3):599-601 [19374687.001]
  • (PMID = 18194453.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ PMC4506175
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67. Kameoka J, Horiuchi T, Miyamura K, Miura I, Okuda M, Nomura J, Hirokawa M, Sawada K, Sasaki T: [Acute monoblastic leukemia with tetrasomy 8]. Rinsho Ketsueki; 2006 Aug;47(8):770-6
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  • [Title] [Acute monoblastic leukemia with tetrasomy 8].
  • Tetrasomy 8 is a rare chromosomal abnormality in acute leukemia, and it has recently been considered as a poor prognostic factor.
  • The patient was diagnosed as having AML (M5a), and treatment with daunorubicin (70 mg x 5 days) and cytosine arabinoside (150 mg x 7 days) resulted in a complete remission.
  • Remission could not be achieved, and the patient underwent allogeneic peripheral blood stem cell transplantation from her HLA-identical mother.
  • Her clinical course was almost uneventful except for a phlegmon in the right leg, but on day 49 a relapse occurred, and she died of acute renal failure on day 73.
  • This case strongly illustrates the characteristic of tetrasomy 8 as a poor prognostic factor in acute leukemia.
  • [MeSH-major] Aneuploidy. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Karyotyping. Leukemia, Monocytic, Acute / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Fatal Outcome. Female. Humans. Peripheral Blood Stem Cell Transplantation

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  • (PMID = 16986717.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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68. Appelbaum FR: Incorporating hematopoietic cell transplantation (HCT) into the management of adults aged under 60 years with acute myeloid leukemia (AML). Best Pract Res Clin Haematol; 2008 Mar;21(1):85-92
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  • [Title] Incorporating hematopoietic cell transplantation (HCT) into the management of adults aged under 60 years with acute myeloid leukemia (AML).
  • Current strategies for incorporating hematopoietic cell transplantation into the treatment of adults with AML are based predominantly on pre-treatment patient, donor and disease characteristics.
  • Here we review the currently accepted indications for transplantation and raise the possibility that alternative approaches to incorporating transplantation into the management of adults with AML that rely predominantly on the measurement of minimal residual disease (MRD) could save additional lives without any major advance in chemotherapy or transplant technologies.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy


69. Maino P, Dullenkopf A, Bernet V, Weiss M: Nitrous oxide diffusion into the cuffs of disposable laryngeal mask airways. Anaesthesia; 2005 Mar;60(3):278-82
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  • The aim of this study was to investigate cuff pressure changes found in disposable size 3 laryngeal mask airways (LMAs) from different manufacturers during nitrous oxide exposure and to compare the results with the re-usable Classic LMA.
  • Cuff pressure increases within 5 min of nitrous oxide exposure were > 250% in the Classic LMA and were not significantly different from those found in the Marshall laryngeal mask airway.
  • Unlike the re-usable Classic LMA and the disposable Marshall laryngeal mask airway, which have silicone cuffs, the disposable Ambu, Intersurgical, Portex Soft Seal and Unique laryngeal mask airways have cuffs constructed from PVC, which seems to be less susceptible to hyperinflation caused by nitrous oxide diffusion.

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  • (PMID = 15710013.001).
  • [ISSN] 0003-2409
  • [Journal-full-title] Anaesthesia
  • [ISO-abbreviation] Anaesthesia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anesthetics, Inhalation; K50XQU1029 / Nitrous Oxide
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70. Meyer-Monard S, Parlier V, Passweg J, Mühlematter D, Hess U, Bargetzi M, Kühne T, Cabrol C, Gratwohl A, Jotterand M, Tichelli A: Combination of broad molecular screening and cytogenetic analysis for genetic risk assignment and diagnosis in patients with acute leukemia. Leukemia; 2006 Feb;20(2):247-53
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  • [Title] Combination of broad molecular screening and cytogenetic analysis for genetic risk assignment and diagnosis in patients with acute leukemia.
  • We evaluated the impact of genetic analysis combining cytogenetics and broad molecular screening on leukemia diagnosis according to World Health Organization (WHO) and on genetic risk assignment.
  • A total of 186 patients (104 males (56%), 174 adults (94%), 12 children (6%), 155 AML (83%), 31 ALL (17%)) characterized by morphology and immunophenotyping were included.
  • Of these 186 patients, 120 (65%) had a genetic abnormality.
  • Cryptic fusion transcripts in nine (5%) patients changed the genetic risk assignment in four and the WHO classification in four patients.
  • In 34 patients (18%), cytogenetics defined the risk assignment by revealing structural and numerical chromosomal abnormalities not detected by molecular screening.
  • Broad molecular screening and cytogenetics are complementary in the diagnosis and genetic risk assignment of acute leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cytogenetic Analysis / methods. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Molecular Diagnostic Techniques / methods. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Acute Disease. Adult. Child. Chromosome Aberrations. Cohort Studies. Female. Humans. Karyotyping. Male. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Risk Assessment. World Health Organization

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  • (PMID = 16408102.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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71. Liu LB, Li WM, He W, Zou P: [Expression of immune response molecules and function of fas ligand on surface of AML WEHI-3 cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):535-8
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  • [Title] [Expression of immune response molecules and function of fas ligand on surface of AML WEHI-3 cells].
  • The purpose of this study was to investigate the expression of Fas, Fas ligand (FasL) and CD80 and function of FasL on the surface of acute myelomonocytic leukemia cells from WEHI-3 line.
  • The expression of Fas, FasL and CD80 on the surface of WEHI-3 were detected by flow cytometry, the apoptosis of YAC-1 cell induced by FasL on the surface of WEHI-3 were detected by (3)H-TdR incorporation.
  • It is concluded that WEHI-3 cells have high expression of FasL and low expression of Fas and CD80 on their cell membrane, and can induce the apoptosis of Fas(+) YAC-1 cells.

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  • (PMID = 16800937.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD95; 0 / Fas Ligand Protein
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72. Giles F, O'Brien S, Cortes J, Verstovsek S, Bueso-Ramos C, Shan J, Pierce S, Garcia-Manero G, Keating M, Kantarjian H: Outcome of patients with acute myelogenous leukemia after second salvage therapy. Cancer; 2005 Aug 1;104(3):547-54
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  • [Title] Outcome of patients with acute myelogenous leukemia after second salvage therapy.
  • BACKGROUND: Although the prognosis is poor for patients with acute myelogenous leukemia (AML) who have disease recurrence after frontline therapy, this is a general reflection of first salvage therapies.
  • The outcome of patients undergoing second salvage therapy in relation to complete response (CR) rates and survival has not been documented.
  • The authors analyzed the outcome of patients with AML undergoing second salvage therapy, and identified prognostic factors associated with response and survival.
  • METHODS: The records of 594 patients with AML undergoing second salvage therapy from 1980 until 2004 were reviewed.
  • Salvage therapy included allogeneic stem cell transplantation (SCT) in 74 patients, standard-dose cytosine arabinoside (ara-C) combinations in 30 patients, high-dose ara-C combinations in 171 patients, non-ara-C combinations in 73 patients, and Phase I-II single agents in 246 patients.
  • A multivariate analysis of prognostic factors for CR identified the following 6 independent adverse factors: first CR duration < 6 months; second CR duration < 6 months; salvage therapy not including allogeneic SCT; non-inversion 16 AML; platelet counts < 50 x 10(9)/L, and leukocytosis > 50 x 10(9)/L.
  • CONCLUSIONS: The current analysis established the outcome and prognostic factors associated with second salvage therapy in AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / therapy. Salvage Therapy. Stem Cell Transplantation. Transplantation, Homologous


73. Nahi H, Selivanova G, Lehmann S, Möllgård L, Bengtzen S, Concha H, Svensson A, Wiman KG, Merup M, Paul C: Mutated and non-mutated TP53 as targets in the treatment of leukaemia. Br J Haematol; 2008 May;141(4):445-53
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  • [Title] Mutated and non-mutated TP53 as targets in the treatment of leukaemia.
  • TP53 is mutated in 10-20% of cases of chronic lymphocytic leukaemia (CLL) and 3-8% of cases of acute myeloid leukaemia (AML).
  • PRIMA-1 (p53-dependent reactivation and induction of massive apoptosis) restores the wild-type conformation of mutant TP53, whereas RITA (reactivation of p53 and induction of tumour cell apoptosis) increases intracellular levels of p53.
  • We evaluated the effects of RITA alone and in combination with PRIMA-1 or conventional cytostatics on leukaemic cells isolated from AML and CLL patients.
  • AML samples with -17, which are more resistant to daunorubicin and cytarabine compared with samples without -17, were effectively killed by PRIMA-1.
  • RITA, which stabilizes the function of wild-type p53, induced apoptosis in AML cells.
  • In contrast to that seen with PRIMA-1, AML patient samples without -17 were significantly more sensitive to RITA.
  • In both AML and CLL cells exposure to RITA resulted in induction of intracellular p53.
  • We conclude that small molecules targeting p53 might be of clinical importance in the future for treating drug-resistant leukaemia.
  • [MeSH-major] Genes, p53 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Death / drug effects. Chromosome Aberrations. Cytarabine / pharmacology. Daunorubicin / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Furans / pharmacology. Humans. Membrane Proteins / pharmacology. Nerve Tissue Proteins / pharmacology. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 18341636.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Furans; 0 / Membrane Proteins; 0 / NSC 652287; 0 / Nerve Tissue Proteins; 0 / PRIMA1 protein, human; 0 / Tumor Suppressor Protein p53; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZS7284E0ZP / Daunorubicin
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74. Yamada K, Mizusawa M, Harima A, Kajiwara K, Hamaki T, Hoshi K, Kozai Y, Kodo H: Induction of remission of relapsed acute myeloid leukemia after unrelated donor cord blood transplantation by concomitant low-dose cytarabine and calcitriol in adults. Eur J Haematol; 2006 Oct;77(4):345-8
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  • [Title] Induction of remission of relapsed acute myeloid leukemia after unrelated donor cord blood transplantation by concomitant low-dose cytarabine and calcitriol in adults.
  • Low-dose cytarabine and calcitriol (LDCA + VD3) combination therapy was performed in two adult patients with acute myeloid leukemia (AML) that relapsed within 1 yr after unrelated donor cord blood transplantation (URD CBT) performed in a relapse or non-remission stage.
  • Although LDCA + VD3 therapy is minimally intensive chemotherapy, it may prolong the survival time of patients with relapsed AML after URD CBT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cord Blood Stem Cell Transplantation. Leukemia, Myeloid / surgery. Remission Induction
  • [MeSH-minor] Aclarubicin / administration & dosage. Acute Disease. Calcitriol / administration & dosage. Cytarabine / administration & dosage. Dose-Response Relationship, Drug. Female. Humans. Middle Aged. Recurrence. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16930144.001).
  • [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] 04079A1RDZ / Cytarabine; 74KXF8I502 / Aclarubicin; FXC9231JVH / Calcitriol
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75. Al-Rahawan MM, Alter BP, Bryant BJ, Elghetany MT: Bone marrow cell cycle markers in inherited bone marrow failure syndromes. Leuk Res; 2008 Dec;32(12):1793-9
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  • [Title] Bone marrow cell cycle markers in inherited bone marrow failure syndromes.
  • Patients with inherited bone marrow failure syndromes (IBMFS) are at increased risk of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), possibly related to cell cycle dysregulation.
  • In a cross-sectional analysis of bone marrow from 77 IBMFS, 71 sporadic conditions (AML, MDS, acquired aplastic anemia) and 22 normal controls we found overexpression of p53 in IBMFS, AML, and MDS; of Ki-67 in IBMFS and AML; and of survivin in IBMFS compared with all other groups.
  • The patterns of expression of cell cycle markers in IBMFS are thus distinct.
  • [MeSH-major] Bone Marrow Cells / pathology. Bone Marrow Diseases / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Biomarkers / analysis. Biopsy. Cell Cycle. Fanconi Anemia / genetics. Fanconi Anemia / pathology. Humans. Inhibitor of Apoptosis Proteins. Ki-67 Antigen / analysis. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 18606449.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers; 0 / Inhibitor of Apoptosis Proteins; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS77574; NLM/ PMC2716700
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76. Tallman MS: New agents for the treatment of acute myeloid leukemia. Best Pract Res Clin Haematol; 2006;19(2):311-20
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  • [Title] New agents for the treatment of acute myeloid leukemia.
  • The heterogeneity of acute myeloid leukemia (AML) has been established by many new insights into the diagnosis, pathogenesis, clinical manifestations, treatment, and prognosis of patients with AML.
  • Morphology remains the foundation for the diagnosis.
  • However, additional diagnostic studies, including immunophenotyping, cytogenetic evaluation, and molecular genetic studies, are necessary to develop treatments because specific subtypes of AML can now be approached with targeted therapy.
  • Acute promyelocytic leukemia (APL), defined by a single molecular abnormality, is now treated with specific targeted therapy, all-trans retinoic acid (ATRA), and this subtype of AML is now highly curable.
  • Currently, a number of agents have been explored in AML, including anti-CD33 antibodies and immunoconjugate drugs, inhibitors of multidrug resistance proteins, farnesyl transferase inhibitors, tyrosine kinase inhibitors, anti-Bcl-2 transcription agents, and inhibitors of mammalian target of rapamycin (mTOR).
  • The plan for the future is to find therapeutic strategies that are specific for patients based on the specific biology of the disease.
  • Future studies will investigate combinations of targeted therapies with each other and with chemotherapies to maximize the inhibition of multiple pathways present in AML.
  • Additionally, evaluation of the identified prognostic factors and gene mutations will enable further pathologic classification of patients with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotherapy. Leukemia, Myeloid, Acute / drug therapy


77. Lemez P, Urbánek V: Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients. Neoplasma; 2005;52(5):398-401
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  • [Title] Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients.
  • The aim was to follow-up gonadal functions in long-term survivors of acute myeloid leukemias (AML) after intensive chemotherapy based on high-doses of cytosine arabinoside (Ara-C) and anthracyclines in the study UHKT-911.
  • Adult patients were treated with at least 3 cycles of chemotherapy including 1-3 courses of Ara-C 10 x 2000 mg/m2/12 h and daunorubicin (DNR) 2 x 45 mg/m2/d.
  • The semen of a 49-year-old patient contained normal numbers of spermatozoa with decreased velocity when examined 1 year after chemotherapy but 4 years later exhibited oligoasthenozoospermia.
  • The patient received 4 cycles of Ara-C and DNR plus one cycle with etoposide 350 mg/m2 and mitoxantrone 30 mg/m2.
  • Semen examination of two patients 55- and 59-year-old showed permanent oligoasthenozoospermia with only sporadic progressively motile spermatozoa which might not be compatible with fertilization by sexual intercourse.
  • They received the same chemotherapy including cumulative doses of etoposide 500 mg/m2 and mitoxantrone 36 mg/m2.
  • Permanent amenorrhea developed in two women (42- and 46-year-old) during chemotherapy with DNR, Ara-C, etoposide, and mitoxantrone which was not the case in three women (29-40 years old) treated without etoposide and mitoxantrone.
  • Intensive chemotherapy with high-doses of Ara-C and DNR plus one cycle of etoposide and mitoxantrone may cause permanent gonadal dysfunction in middle-aged patients with AML.
  • [MeSH-major] Amenorrhea / chemically induced. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / drug therapy. Spermatozoa / drug effects
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Transplantation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Oligospermia / chemically induced. Sperm Motility / drug effects

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  • (PMID = 16151584.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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78. Büchner T, Krug U, Berdel WE, Heinecke A, Sauerland MC, Wörmann B, Hiddemann W: Maintenance for acute myeloid leukemia revisited. Curr Treat Options Oncol; 2007 Aug;8(4):296-304
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  • [Title] Maintenance for acute myeloid leukemia revisited.
  • Maintenance treatment for AML is an approach to minimize residual disease, optimize quality of remission and prevent a leukemic regrowth over a longer period of time.
  • From our today's knowledge about the impact of various strategies, a lack of postremission therapy is not compatible with durable remissions.
  • Either single prospective trials or crosstrial networking by a common standard arm and general upfront randomization can further assess the relative value of maintenance for AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18058075.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 22
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79. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


80. Turgeman Y, Atar S, Feldman A, Jabaren M, Suleiman K, Bloch L, Rosenfeld T: 'Frozen' posterior mitral leaflet in rheumatic mitral stenosis: incidence and impact on outcome of balloon mitral commissurotomy. J Heart Valve Dis; 2005 May;14(3):282-5
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  • Anterior mitral leaflet (AML) mobility index (MI), chordae tendineae (CT) length, and mitral valve area (MVA) were evaluated.
  • CT lengths directed to the AML and PML were 15 +/- 2 mm and 8 +/- 2 mm, respectively (p < 0.05).
  • MI of the AML before and immediately after PBMC was 0.4 and 0.6, respectively (p < 0.05).
  • It is suggested that pre-procedure leaflet morphology and functional assessment should focus on the AML.
  • [MeSH-major] Catheterization. Mitral Valve / physiopathology. Mitral Valve Stenosis / therapy. Rheumatic Heart Disease / therapy

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  • (PMID = 15974519.001).
  • [ISSN] 0966-8519
  • [Journal-full-title] The Journal of heart valve disease
  • [ISO-abbreviation] J. Heart Valve Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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81. Matondo M, Bousquet-Dubouch MP, Gallay N, Uttenweiler-Joseph S, Recher C, Payrastre B, Manenti S, Monsarrat B, Burlet-Schiltz O: Proteasome inhibitor-induced apoptosis in acute myeloid leukemia: a correlation with the proteasome status. Leuk Res; 2010 Apr;34(4):498-506
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  • [Title] Proteasome inhibitor-induced apoptosis in acute myeloid leukemia: a correlation with the proteasome status.
  • The proteasome plays a critical role in the regulation of many cellular processes, including the cell cycle and tumor growth.
  • In this study, we investigated the induction of apoptosis by proteasome inhibitors in several human acute myeloid leukemia (AML) cell lines and in primary cells from patients.
  • We demonstrate that these drugs induce a high level of apoptosis in the KG1a cell line, in which the therapeutic drug daunorubicin is poorly active, compared to other AML cell lines.
  • Moreover, the level of 20S proteasome in KG1a cells was also high compared to other AML cell lines, suggesting a relationship between the high sensitivity to proteasome inhibitors and an elevated amount of 20S proteasome.
  • Altogether, our results suggest that various AML subtypes may present different responses to proteasome inhibitors, that these molecules can be potentially considered as interesting therapeutic alternatives for these pathologies, and that the amount of 20S proteasome in AML cells may be predictive of the cellular response to these inhibitors.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Myeloid, Acute / pathology. Protease Inhibitors / pharmacology. Proteasome Endopeptidase Complex / metabolism. Proteasome Inhibitors

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):411-2 [19819547.001]
  • (PMID = 19811823.001).
  • [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 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Leupeptins; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex; ZS7284E0ZP / Daunorubicin
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82. Kiyoi H, Yanada M, Ozekia K: Clinical significance of FLT3 in leukemia. Int J Hematol; 2005 Aug;82(2):85-92
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  • [Title] Clinical significance of FLT3 in leukemia.
  • FLT3/ITD and FLT3/KDM occur in 15% to 35% and 5% to 10%, respectively, of patients with AML.
  • FLT3 mutations are, therefore, the most frequent genetic alterations so far reported in AML.
  • The overexpression of FLT3 transcripts has been demonstrated in a pro-portion of the AML patients without FLT3 mutations, which are associated with a poor prognosis for overall survival.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16146837.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 90
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83. von Bubnoff N, Engh RA, Aberg E, Sänger J, Peschel C, Duyster J: FMS-like tyrosine kinase 3-internal tandem duplication tyrosine kinase inhibitors display a nonoverlapping profile of resistance mutations in vitro. Cancer Res; 2009 Apr 1;69(7):3032-41
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  • FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown activity in the treatment of acute myelogenous leukemia (AML).
  • Using a cell-based screening approach, we generated FLT3-internal tandem duplication (ITD)-expressing cell lines resistant to the FLT3 inhibitors SU5614, PKC412, and sorafenib.
  • A mutation at N676 recently has been reported in a case of PKC412-resistant AML.
  • Therefore, combinations of FLT3 inhibitors may be useful to prevent FLT3 resistance mutations in the setting of FLT3-ITD-positive AML.
  • [MeSH-minor] Animals. Benzenesulfonates / pharmacology. Cell Line. Drug Resistance. Indoles / pharmacology. Mice. Models, Molecular. Mutagenesis, Site-Directed. Niacinamide / analogs & derivatives. Phenylurea Compounds. Protein Structure, Tertiary. Pyridines / pharmacology. Receptors, Platelet-Derived Growth Factor / chemistry. Staurosporine / analogs & derivatives. Staurosporine / pharmacology. Tandem Repeat Sequences

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  • (PMID = 19318574.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzenesulfonates; 0 / Indoles; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / SU 5614; 120685-11-2 / 4'-N-benzoylstaurosporine; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.1.- / PDGF receptor tyrosine kinase; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; H88EPA0A3N / Staurosporine
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84. Ito Y: RUNX genes in development and cancer: regulation of viral gene expression and the discovery of RUNX family genes. Adv Cancer Res; 2008;99:33-76
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  • This viral regulatory region was considered as a potential probe for mouse cell differentiation.
  • Purification and cDNA cloning revealed that PEBP2 has two subunits, DNA-binding alpha (PEBP2alpha) and non-DNA-binding beta (PEBP2beta).
  • PEBP2alpha was found to be highly homologous to a Drosophila segmentation gene, runt, and a human gene AML1 that was identified as a part of the fusion gene, AML1/ETO (MTG8) generated by t(8;21) chromosome translocation associated with acute myelogenous leukemia (AML).
  • Core-binding factor (CBF), which interacts with a murine retrovirus enhancer, was found to be identical to PEBP2. runt, PEBP2alpha and AML1 are now termed RUNX family, which are involved in cell specification during development.
  • RUNX1 is essential for generation of hematopoietic stem cells and is involved in human leukemia.
  • [MeSH-minor] Animals. Evolution, Molecular. Humans. Leukemia / genetics. Mutation. Oncogenes. Polyomavirus. Rabbits

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  • (PMID = 18037406.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor alpha Subunits
  • [Number-of-references] 150
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85. Meyer M, Waldvogel S, Chalandon Y, Bongiovanni M, Pache JC, Van Delden C: Breakthrough invasive pulmonary aspergillosis despite empirical voriconazole therapy for febrile neutropenia: case report and review of the literature. Scand J Infect Dis; 2007;39(8):731-3
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  • We report the development of invasive pulmonary aspergillosis in a patient treated for acute myeloid leukaemia during empirical voriconazole therapy for febrile neutropenia.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / surgery. Drug Resistance, Fungal / drug effects. Lung Diseases, Fungal / surgery. Pyrimidines / therapeutic use. Triazoles / therapeutic use
  • [MeSH-minor] Acute Disease. Fever / microbiology. Humans. Leukemia, Myeloid / complications. Male. Middle Aged. Neutropenia / microbiology. Voriconazole

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  • (PMID = 17654353.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
  • [Number-of-references] 18
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86. Zander AR, Bacher U, Finke J: Allogeneic stem cell transplantation in acute myeloid leukemia: establishment of indications on the basis of individual risk stratification. Dtsch Arztebl Int; 2008 Sep;105(39):663-9
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  • [Title] Allogeneic stem cell transplantation in acute myeloid leukemia: establishment of indications on the basis of individual risk stratification.
  • INTRODUCTION: Acute myeloid leukemia (AML) is a heterogeneous disorder with subtypes that differ considerably in morphology and in their underlying chromosomal and molecular aberrations, which, in turn, determine their prognosis.
  • The establishment of the indications for allogeneic stem cell transplantation (SCT) therefore requires individualized risk stratification based on a combination of multiple diagnostic methods, including cytogenetic and molecular genetic studies, and immunophenotyping, as well as the sensitivity of the disease to chemotherapy.
  • METHODS: This article surveys the current strategies for establishing the indications for SCT in AML on the basis of a selective review of the relevant literature in the Medline database.
  • The balanced translocations t(15;17) and t(8;21), and the inversion inv(16) are prognostically favorable and are thus not considered an indication for SCT in first remission.
  • The establishment of indications for stem cell transplantation also depends on the residual leukemic cell burden (minimal residual disease, MRD) as determined by the quantitative polymerase chain reaction or by flow cytometry, as well as an insufficient response to induction chemotherapy.
  • Reduced-dose conditioning, a new technique that lessens acute toxicity, has been found to be associated with a 30% to over 50% two-year survival rate when used in the treatment of chemotherapeutically unresponsive or relapsing AML.
  • DISCUSSION: The indications for allogeneic SCT in AML should be further refined by more investigation in large studies.

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  • (PMID = 19626214.001).
  • [ISSN] 1866-0452
  • [Journal-full-title] Deutsches Ärzteblatt international
  • [ISO-abbreviation] Dtsch Arztebl Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2700644
  • [Keywords] NOTNLM ; indications / leukemia treatment / molecular medicine / myelopathy / stem cell therapy
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87. Musolino C, Sant'antonio E, Penna G, Alonci A, Russo S, Granata A, Allegra A: Epigenetic therapy in myelodysplastic syndromes. Eur J Haematol; 2010 Jun;84(6):463-73
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  • The wide spectrum of clonal hematopoietic disorders that fall under the broad diagnostic category of myelodysplastic syndromes (MDS) consist of a family of bone marrow malignancies - with ineffective, inadequate, and dysplastic hematopoiesis, and with an increased risk of life-threatening infections, bleeding, and progression to acute myeloid leukemia (AML) - that are characterized by a deep heterogeneity on the clinical, biologic and prognostic level.
  • The intrinsic complexity of this group of disorders and the frequent association with one or more comorbidities have limited for many years the number of effective treatment options available: most patients are, indeed, still managed by supportive care measures, with just a minority of them being eligible for allogeneic stem cell transplantation, which is still the only potentially curative modality.

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  • (PMID = 20192987.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
  • [Number-of-references] 76
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88. Rogers PC, Meacham LR, Oeffinger KC, Henry DW, Lange BJ: Obesity in pediatric oncology. Pediatr Blood Cancer; 2005 Dec;45(7):881-91
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  • [Title] Obesity in pediatric oncology.
  • A recent Children's Oncology Group symposium considered epidemiology of obesity, pharmacology of chemotherapy and outcomes in obese adults with cancer, excess mortality in obese pediatric patients with acute myeloid leukemia (AML), and complications in obese survivors.
  • In pediatric acute myeloblastic leukemia, obese patients have greater treatment-related mortality (TRM), similar toxicity and relapse rates, and inferior survival compared with patients who are not obese.
  • An excess of female survivors of childhood leukemia who received cranial irradiation are obese.
  • These findings call for measures to prevent obesity, retrospective and prospective studies of chemotherapy pharmacology of analyzed according to BMI and outcomes, additional studies of the obesity impact on outcomes in pediatric cancer, and promotion of a healthy lifestyle among survivors.
  • [MeSH-major] Leukemia, Myeloid, Acute. Obesity. Precursor Cell Lymphoblastic Leukemia-Lymphoma


89. 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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90. Kara IO, Sahin B, Paydas S, Kara B: Granulocytic sarcoma of the heart: extramedullary relapse of acute myeloblastic leukemia after allogeneic stem cell transplantation successfully treated by chemotherapy alone. Leuk Lymphoma; 2005 Jul;46(7):1081-4
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  • [Title] Granulocytic sarcoma of the heart: extramedullary relapse of acute myeloblastic leukemia after allogeneic stem cell transplantation successfully treated by chemotherapy alone.
  • We present a case of granulocytic sarcoma (GS) of the heart.
  • A 28-year-old man with relapsed acute myelogenous leukemia (AML-M2) had undergone a non-myeloablative allogeneic peripheral stem cell transplantation.
  • Three years following transplantation, masses were evidenced in his heart by echocardiography but had completely disappeared following a common chemotherapy etoposide, mitoxantrone, ara-C (EMA) regimen for relapsed AML.
  • The involvement of the heart with GS is very rare and this is the first case of extramedullary disease in the heart after allogeneic transplantation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation / adverse effects. Sarcoma, Myeloid / drug therapy. Sarcoma, Myeloid / etiology
  • [MeSH-minor] Adult. Cytarabine / administration & dosage. Etoposide / administration & dosage. Heart Neoplasms / diagnosis. Heart Neoplasms / drug therapy. Heart Neoplasms / etiology. Humans. Male. Mitoxantrone / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Remission Induction. Transplantation, Homologous

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  • (PMID = 16019562.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
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91. Qiu JY, Zhang Y, Lu DP, Lai YY, He Q, Shi Y: [Clinical and cytogenetical study on subacute myeloid leukemia in myelodysplastic syndromes]. Zhonghua Nei Ke Za Zhi; 2005 Jun;44(6):407-10
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  • [Title] [Clinical and cytogenetical study on subacute myeloid leukemia in myelodysplastic syndromes].
  • OBJECTIVE: To discuss from the clinical and cytogenetic aspect that part of patients now diagnosed as myelodysplastic syndromes (MDS) could be diagnosed early as leukemia and be classified as subacute myeloid leukemia (Sub-AML).
  • RESULTS: Among the detected chromosome aberrations, +8 was the most frequent (42.8%) and then -7/7q-(15.0%); 42 patients with +8 had median blast cell count of 0.08, within a median of 18 months follow-up period 40.0% of the patients evolved to frank leukemia (FL) and the median overall survival was 20 months.
  • 16 patients with -7/7q- had higher blast cell count of 0.135; 43.8% of them developed into FL and the median overall survival was only 10 months within a 20-month follow-up period.
  • 55 patients had normal karyotype but a median blast cell count of 0.148; 52.7% of them patients evolved to FL and the median overall survival was 34 months.
  • CONCLUSIONS: Both the +8 and -7/7q- groups have malignant leukemic cell clone, and run a subacute and progressive clinical course; it is suggested they might be classified into Sub-AML.
  • We should keep close watch on the patients who have normal karyotype yet more than 0.10 blast cells, part of whom might suffer from early Sub-AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


92. Keeshan K, Shestova O, Ussin L, Pear WS: Tribbles homolog 2 (Trib2) and HoxA9 cooperate to accelerate acute myelogenous leukemia. Blood Cells Mol Dis; 2008 Jan-Feb;40(1):119-21
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  • [Title] Tribbles homolog 2 (Trib2) and HoxA9 cooperate to accelerate acute myelogenous leukemia.
  • Mice reconstituted with hematopoietic stem cells (HSC) retrovirally expressing Trib2 uniformly developed fatal transplantable acute myelogenous leukemia (AML).
  • Trib2-induced AML was clonal and we sought to identify cooperating genes in Trib2-induced AML.
  • Mice reconstituted with HSC cotransduced with HoxA9 and Trib2 had accelerated onset of AML compared to either gene alone.
  • These data identify Trib2 and HoxA9 as cooperating genes in AML.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Homeodomain Proteins / pharmacology. Intracellular Signaling Peptides and Proteins / pharmacology. Leukemia, Myeloid, Acute / etiology. Protein-Serine-Threonine Kinases / pharmacology

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  • (PMID = 17988908.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Oncogene Proteins; 0 / homeobox protein HOXA9; 0 / tribbles 2 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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93. Castro-Malaspina H, Jabubowski AA, Papadopoulos EB, Boulad F, Young JW, Kernan NA, Perales MA, Small TN, Hsu K, Chiu M, Heller G, Collins NH, Jhanwar SC, van den Brink M, Nimer SD, O'Reilly RJ: Transplantation in remission improves the disease-free survival of patients with advanced myelodysplastic syndromes treated with myeloablative T cell-depleted stem cell transplants from HLA-identical siblings. Biol Blood Marrow Transplant; 2008 Apr;14(4):458-68
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  • [Title] Transplantation in remission improves the disease-free survival of patients with advanced myelodysplastic syndromes treated with myeloablative T cell-depleted stem cell transplants from HLA-identical siblings.
  • From 1985 to 2004, 49 patients with advanced myelodysplastic syndromes (MDS) (> or =5% blasts) or acute myeloid leukemia (AML) transformed from MDS underwent T cell depleted bone marrow or peripheral blood hematopoietic stem cell transplantation (HSCT) from HLA-identical siblings following conditioning with a myeloablative regimen that included total body irradiation (44 patients) or busulfan (5 patients).
  • Thirty-six patients received chemotherapy (3 low dose and 33 induction doses) before conditioning, and 13 patients did not receive any chemotherapy.
  • No post-transplantation pharmacologic prophylaxis for graft-versus-host disease (GVHD) was given.
  • Only 3 patients developed acute GVHD (aGVHD) (grades I and III) and 1 chronic GVHD (cGVHD).
  • The disease free survival (DFS) was 50%, 15% and 0% in each group respectively (P=.0008).
  • In multivariate analysis, disease status before cytoreduction remained highly correlated with DFS (P<.001).
  • The CI of non-relapse mortality at 2-yrs post-transplantation, for the responders was 23%; for the untreated group was 38%; and for the failures was 40%.
  • These results indicate that patients with advanced MDS who achieve and remain in remission or a second refractory cytopenia phase with chemotherapy before conditioning can achieve successful long-term remissions following a myeloablative T cell depleted allogeneic HSCT.
  • [MeSH-major] HLA Antigens / immunology. Lymphocyte Depletion. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / immunology. Transplantation, Isogeneic / methods
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Graft vs Host Disease / prevention & control. Humans. Middle Aged. Remission Induction. Retrospective Studies. Siblings. Transplantation Conditioning / methods. Treatment Outcome. Whole-Body Irradiation

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  • (PMID = 18342789.001).
  • [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 / P01 CA023766; United States / NCI NIH HHS / CA / P30 CA008748; United States / NHLBI NIH HHS / HL / R01 HL088134
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
  • [Other-IDs] NLM/ NIHMS43830; NLM/ PMC4498391
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94. Pereira GH, Pádua SS, Park MV, Muller RP, Passos RM, Menezes Y: Chronic meningitis by histoplasmosis: report of a child with acute myeloid leukemia. Braz J Infect Dis; 2008 Dec;12(6):555-7
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  • [Title] Chronic meningitis by histoplasmosis: report of a child with acute myeloid leukemia.
  • In leukemia, the impaired of the T cells function can predispose to the disseminated form.
  • We have described a child with acute myeloid leukemia (AML), that developed skin lesions and asymptomatic chronic meningitis, with a good evolution after prolonged treatment with amphotericin B deoxycholate followed by fluconazole.
  • [MeSH-major] Histoplasmosis / diagnosis. Leukemia, Myeloid / immunology. Meningitis, Fungal / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Chronic Disease. Deoxycholic Acid / therapeutic use. Drug Combinations. Drug Therapy, Combination. Fluconazole / therapeutic use. Humans. Immunocompromised Host. Male. Treatment Outcome

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  • (PMID = 19287853.001).
  • [ISSN] 1678-4391
  • [Journal-full-title] The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
  • [ISO-abbreviation] Braz J Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Drug Combinations; 005990WHZZ / Deoxycholic Acid; 7XU7A7DROE / Amphotericin B; 87687-70-5 / amphotericin B, deoxycholate drug combination; 8VZV102JFY / Fluconazole
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95. Schardt JA, Eyholzer M, Timchenko NA, Mueller BU, Pabst T: Unfolded protein response suppresses CEBPA by induction of calreticulin in acute myeloid leukaemia. J Cell Mol Med; 2010 Jun;14(6B):1509-19
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  • [Title] Unfolded protein response suppresses CEBPA by induction of calreticulin in acute myeloid leukaemia.
  • Here, we studied the induction of mediators of the UPR in leukaemic cells of AML patients.
  • Increased expression of the spliced variant of the X-box binding protein 1 (XBP1s) was detected in 17.4% (16 of 92) of AML patients.
  • Conditional expression of calreticulin in leukaemic U937 cells was found to increase calreticulin binding to the CEBPA mRNA thereby efficiently blocking translation of the myeloid key transcription factor CEBPA and ultimately affecting myeloid differentiation.
  • Consequently, leukaemic cells from AML patients with activated UPR and thus increased calreticulin levels showed in fact suppressed CEBPA protein expression.
  • Thus, we propose a model of the UPR being activated in a considerable subset of AML patients through induction of calreticulin along the ATF6 pathway, thereby ultimately suppressing CEBPA translation and contributing to the block in myeloid differentiation.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / metabolism. Calreticulin / metabolism. Leukemia, Myeloid, Acute / metabolism. Unfolded Protein Response
  • [MeSH-minor] Activating Transcription Factor 6 / metabolism. Alternative Splicing / genetics. CCAAT-Binding Factor / metabolism. Cell Line, Tumor. DNA-Binding Proteins / genetics. Endoplasmic Reticulum / pathology. Gene Expression Regulation, Leukemic. Heat-Shock Proteins / genetics. Heat-Shock Proteins / metabolism. Humans. Myeloid Cells / metabolism. Promoter Regions, Genetic / genetics. Protein Binding. Protein Biosynthesis. Transcription Factors / genetics. Transcription, Genetic. Transcriptional Activation / genetics. YY1 Transcription Factor / metabolism

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  • (PMID = 19659458.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Activating Transcription Factor 6; 0 / CCAAT-Binding Factor; 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Calreticulin; 0 / DNA-Binding Proteins; 0 / Heat-Shock Proteins; 0 / NFYA protein, human; 0 / Transcription Factors; 0 / YY1 Transcription Factor; 0 / molecular chaperone GRP78; 0 / regulatory factor X transcription factors
  • [Other-IDs] NLM/ PMC3829017
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96. Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Morice P, Bourquard P, Banzakour S, Le Calvez G, Marion V, Berthou C, De Braekeleer M: Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations. Cancer Genet Cytogenet; 2005 Mar;157(2):169-74
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  • [Title] Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations.
  • We report here 2 male adults in whom a diagnosis of acute myelomonoblastic leukemia (FAB M4) and acute monoblastic leukemia (FAB M5) was made.
  • Fourteen and 24 patients, including ours, with acute myeloblastic leukemia associated with a t(1;11)(p32;q23) and a t(11;17)(q23;q21), respectively have been reported in the literature.
  • Several patients with the latter translocation have also been identified to have acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15721641.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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97. Kaspers GJ, Reinhardt D, Fleischhack G, Armendariz H, Stark B, Zwaan CM, Zimmermann M, Creutzig U: Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML. Pediatr Blood Cancer; 2006 Oct 15;47(5):539-42
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  • [Title] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.
  • BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.
  • PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.
  • Therefore, the study was closed, concluding that the probability of a good response in this patient-group was most likely to be less than 30%.
  • By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.
  • CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.
  • However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use


98. Calhoun DA, Lacourcière Y, Chiang YT, Glazer RD: Triple antihypertensive therapy with amlodipine, valsartan, and hydrochlorothiazide: a randomized clinical trial. Hypertension; 2009 Jul;54(1):32-9
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  • The efficacy/safety of the dual combinations of valsartan (Val)/hydrochlorothiazide (HCTZ) and amlodipine (Aml)/Val in hypertension are well established.
  • This randomized, double-blind study evaluated the efficacy/safety of triple therapy with Aml/Val/HCTZ for moderate or severe hypertension (mean sitting systolic BP: > or =145 mm Hg; mean sitting diastolic BP: > or =100 mm Hg).
  • The study included a single-blind, placebo run-in period, followed by double-blind treatment for 8 weeks; patients were randomly assigned to 1 of 4 groups titrated to Aml/Val/HCTZ 10/320/25 mg, Val/HCTZ 320/25 mg, Aml/Val 10/320 mg, or Aml/HCTZ 10/25 mg once daily.
  • Those on triple therapy received Val/HCTZ 160.0/12.5 mg during week 1, Aml/Val/HCTZ 5.0/160.0/12.5 mg during week 2, and target doses of all 3 of the agents during week 3.
  • Aml/Val/HCTZ was well tolerated.
  • In conclusion, this study demonstrates the efficacy/safety of treating moderate and severe hypertension with Aml/Val/HCTZ 10/320/25 mg.

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  • [CommentIn] Hypertension. 2009 Jul;54(1):19-22 [19470871.001]
  • (PMID = 19470877.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Tetrazoles; 0J48LPH2TH / Hydrochlorothiazide; 1J444QC288 / Amlodipine; 80M03YXJ7I / Valsartan; HG18B9YRS7 / Valine
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99. Marcucci G, Baldus CD, Ruppert AS, Radmacher MD, Mrózek K, Whitman SP, Kolitz JE, Edwards CG, Vardiman JW, Powell BL, Baer MR, Moore JO, Perrotti D, Caligiuri MA, Carroll AJ, Larson RA, de la Chapelle A, Bloomfield CD: Overexpression of the ETS-related gene, ERG, predicts a worse outcome in acute myeloid leukemia with normal karyotype: a Cancer and Leukemia Group B study. J Clin Oncol; 2005 Dec 20;23(36):9234-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the ETS-related gene, ERG, predicts a worse outcome in acute myeloid leukemia with normal karyotype: a Cancer and Leukemia Group B study.
  • PURPOSE: To test the prognostic significance of ETS-related gene (ERG) expression in cytogenetically normal primary acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Pretreatment blood samples from 84 cytogenetically normal AML patients aged less than 60 years, who were characterized for BAALC expression, FLT3 internal tandem duplication (ITD), and MLL partial tandem duplication (PTD) and uniformly treated on Cancer and Leukemia Group B 9621 protocol, were analyzed for ERG expression by real-time reverse transcriptase polymerase chain reaction.
  • High ERG expression was associated with upregulation of 112 expressed-sequenced tags and named genes, many of which are involved in cell proliferation, differentiation, and apoptosis.
  • CONCLUSION: ERG overexpression in AML patients with normal cytogenetics predicts an adverse clinical outcome and seems to be associated with a specific molecular signature.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Gene Expression Profiling. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Trans-Activators / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Expressed Sequence Tags. Female. Humans. Karyotyping. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Up-Regulation

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  • (PMID = 16275934.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09512; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA102031; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA90469
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Trans-Activators
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100. Matsunaga T, Fukai F, Miura S, Nakane Y, Owaki T, Kodama H, Tanaka M, Nagaya T, Takimoto R, Takayama T, Niitsu Y: Combination therapy of an anticancer drug with the FNIII14 peptide of fibronectin effectively overcomes cell adhesion-mediated drug resistance of acute myelogenous leukemia. Leukemia; 2008 Feb;22(2):353-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination therapy of an anticancer drug with the FNIII14 peptide of fibronectin effectively overcomes cell adhesion-mediated drug resistance of acute myelogenous leukemia.
  • We investigated whether FNIII14, a 22-mer peptide derived from fibronectin (FN) that potently impairs interaction of FN with beta1-integrin, could overcome cell adhesion-mediated drug resistance (CAM-DR) induced by very late antigen (VLA)-4-to-FN interaction in acute myelogenous leukemia (AML).
  • Two AML cell lines, U937 cells and HL-60 cells, and fresh leukemic cells from six AML patients with high alpha4-integrin expression exhibited CAM-DR to cytosine arabinoside (Ara C) through VLA-4-to-FN interaction, while fresh leukemic cells from two AML patients with low alpha4-integrin expression did not display CAM-DR to Ara C.
  • In these CAM-DR leukemic cells, upregulation of Bcl-2, which was induced through the focal adhesion kinase/Akt signal pathway upon VLA-4-to-FN interaction, was inhibited by FNIII14 treatment.
  • In a mouse model of minimal residual disease (MRD) in bone marrow, 100% survival was achieved by combining FNIII14 with Ara C, whereas Ara C alone prolonged survival only slightly.
  • The myelosuppression induced by Ara C was not augmented by the combination of FNIII14 in mouse experiments.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance / drug effects. Fibronectins / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Neoplasm, Residual / drug therapy. Peptide Fragments / pharmacology
  • [MeSH-minor] Animals. Antigens, CD29. Bone Marrow / pathology. Cell Adhesion / drug effects. Cell Line, Tumor. Cytarabine / pharmacology. Cytarabine / therapeutic use. Drug Therapy, Combination. Humans. Mice. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Tumor Cells, Cultured






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