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1. Suárez L, Vidriales MB, Moreno MJ, López A, García-Laraña J, Pérez-López C, Tormo M, Lavilla E, López-Berges MC, de Santiago M, San Miguel JF, Orfao A, PETHEMA Cooperative Group: Differences in anti-apoptotic and multidrug resistance phenotypes in elderly and young acute myeloid leukemia patients are related to the maturation of blast cells. Haematologica; 2005 Jan;90(1):54-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in anti-apoptotic and multidrug resistance phenotypes in elderly and young acute myeloid leukemia patients are related to the maturation of blast cells.
  • BACKGROUND AND OBJECTIVES: Elderly patients with acute myeloid leukemia (AML) have a less favorable outcome, which has been related, among other factors, to multidrug resistance (MDR) phenotypes.
  • DESIGN AND METHODS: Freshly obtained erythrocyte-lysed bone marrow samples from 150 elderly patients (> 65 years) with de novo AML and 30 younger AML patients were analyzed using a 4-color immunofluorescence technique for quantitative expression of proteins associated with apoptosis (bcl-2, bax, APO2.7) and MDR (P-gp, MRP, LRP) in 3 blast cell subpopulations, defined according to their maturation stage.
  • [MeSH-major] Apoptosis / drug effects. Blast Crisis / pathology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Antigens, CD34. Drug Resistance, Multiple. Female. Genes, MDR / genetics. Genes, MDR / physiology. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged

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  • [CommentIn] Haematologica. 2005 Jan;90(1):3 [15644303.001]
  • (PMID = 15642669.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34
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2. Chang WR, Park IJ, Lee HW, Park JS, Kim HC, Kim HJ, Han JH, Cho SR: [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts]. Korean J Lab Med; 2009 Oct;29(5):390-5
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  • [Title] [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts].
  • One patient was a 24 yr-old male with acute myelomonocytic leukemia.
  • The other patient was a 72 yr-old male with acute myeloid leukemia without maturation.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Graft vs Host Disease / diagnosis. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19893346.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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3. Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K, Koboldt DC, Fulton RS, Delehaunty KD, McGrath SD, Fulton LA, Locke DP, Magrini VJ, Abbott RM, Vickery TL, Reed JS, Robinson JS, Wylie T, Smith SM, Carmichael L, Eldred JM, Harris CC, Walker J, Peck JB, Du F, Dukes AF, Sanderson GE, Brummett AM, Clark E, McMichael JF, Meyer RJ, Schindler JK, Pohl CS, Wallis JW, Shi X, Lin L, Schmidt H, Tang Y, Haipek C, Wiechert ME, Ivy JV, Kalicki J, Elliott G, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson MA, Baty J, Heath S, Shannon WD, Nagarajan R, Link DC, Walter MJ, Graubert TA, DiPersio JF, Wilson RK, Ley TJ: Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med; 2009 Sep 10;361(11):1058-66
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  • [Title] Recurring mutations found by sequencing an acute myeloid leukemia genome.
  • BACKGROUND: The full complement of DNA mutations that are responsible for the pathogenesis of acute myeloid leukemia (AML) is not yet known.
  • METHODS: We used massively parallel DNA sequencing to obtain a very high level of coverage (approximately 98%) of a primary, cytogenetically normal, de novo genome for AML with minimal maturation (AML-M1) and a matched normal skin genome.


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4. Chen W, Konoplev S, Medeiros LJ, Koeppen H, Leventaki V, Vadhan-Raj S, Jones D, Kantarjian HM, Falini B, Bueso-Ramos CE: Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation. Cancer; 2009 Dec 1;115(23):5481-9
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  • [Title] Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation.
  • BACKGROUND: A small subset of patients with acute myeloid leukemia (AML) have cuplike nuclei.
  • RESULTS: In total, 22 patients who had AML with cuplike nuclei were identified and were classified as AML without maturation (French-American-British classification M1) (AML M1).

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  • [Copyright] (c) 2009 American Cancer Society.
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  • (PMID = 19672946.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA 100632-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS140671; NLM/ PMC3378048
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5. Wagner M, Schmelz K, Wuchter C, Ludwig WD, Dörken B, Tamm I: In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia. Int J Cancer; 2006 Sep 15;119(6):1291-7
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  • [Title] In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia.
  • Survivin, a member of the inhibitor of apoptosis protein family, is expressed in most human cancers, but undetectable in normal differentiated adult tissue in vivo.
  • To determine the expression and prognostic role of survivin in acute myeloid leukemia (AML), we investigated the mRNA expression pattern of survivin and of the splice variants survivin-2B and survivin-DeltaEx3 in adult (n = 74) and children (n = 31) with de novo AML using RT-PCR.
  • Neither expression of survivin nor of any splice variant correlated with maturation stage (FAB subtypes, immunophenotype) or cytogenetic risk groups.
  • For AML cases treated according to AMLCG92 (adult) and AML-BFM93 (children) protocols, respectively, expression patterns were correlated with clinical data: in adult AML (n = 51), low expression of survivin-2B correlated with a better overall survival (p = 0.05; mean survival time 19 months vs. 9 months) and a better eventfree survival (p < or = 0.01; 27 months vs. 10 months).
  • We conclude that certain survivin splice variants have potential prognostic impact for long-term therapy outcome in adult as well as childhood de novo AML.
  • [MeSH-major] Alternative Splicing. Leukemia, Myeloid / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Apoptosis. Case-Control Studies. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Disease-Free Survival. Female. Humans. Immunophenotyping. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16619249.001).
  • [ISSN] 0020-7136
  • [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 / BIRC5 protein, human; 0 / DNA, Neoplasm; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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6. Gutiérrez NC, López-Pérez R, Hernández JM, Isidro I, González B, Delgado M, Fermiñán E, García JL, Vázquez L, González M, San Miguel JF: Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia. Leukemia; 2005 Mar;19(3):402-9
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  • [Title] Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia.
  • Bone marrow samples from 43 adult patients with de novo diagnosed acute myeloid leukemia (AML)--10 acute promyelocytic leukemias (APL) with t(15;17), four AML with inv(16), seven monocytic leukemias and 22 nonmonocytic leukemias--were analyzed using high-density oligonucleotide microarrays.
  • In the latter cluster, CD34 upregulation and serine proteases downregulation is consistent with a maturation arrest and lack of granulocytic differentiation.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cluster Analysis. Female. Humans. Leukemia, Monocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Phylogeny. Retrospective Studies

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  • (PMID = 15674361.001).
  • [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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7. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
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  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

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  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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8. Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I: Phenotypic quantitative features of patients with acute myeloid leukemia. Neoplasma; 2006;53(2):155-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenotypic quantitative features of patients with acute myeloid leukemia.
  • The recent WHO classification for acute myeloid leukemias (AML) separates entities by recurrent cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
  • We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo AML, using a 3-color two-step panel.
  • Predominant FAB types were M2 and M4.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis

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  • (PMID = 16575472.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
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9. Serrano E, Lasa A, Perea G, Carnicer MJ, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures. Acta Haematol; 2006;116(2):77-89
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  • [Title] Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by abnormal proliferation of myeloid precursors and a maturation block.
  • One hundred and thirty-two RNA samples obtained from de novo adult AML patients were tested for FLT3, FLT3-LG, NDST1, HDAC2, ATRX, FOS, DNMT1, DNMT3A, DNMT3B, NBS1, RAD50, MRE11A, Meis1 and Meis2 expression using quantitative PCR (qPCR) assays.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Karyotyping. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Prognosis. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16914901.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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10. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • As the proportion of leukemic blast cells is critical for exact cytochemical analysis, study was restricted to the evaluation of 48 adult and pediatric patients with newly diagnosed AMLs with 80% or more blasts in analyzed samples.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
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11. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion
  • [MeSH-minor] Adult. Aged. Chromosome Banding. Fatal Outcome. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping

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  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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12. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
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  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

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  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
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13. Runarsson G, Feltenmark S, Forsell PK, Sjöberg J, Björkholm M, Claesson HE: The expression of cytosolic phospholipase A2 and biosynthesis of leukotriene B4 in acute myeloid leukemia cells. Eur J Haematol; 2007 Dec;79(6):468-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of cytosolic phospholipase A2 and biosynthesis of leukotriene B4 in acute myeloid leukemia cells.
  • Here, we have studied the expression and activity of the enzymes involved in the synthesis of leukotriene B4 (LTB4) in acute myeloid leukemia (AML) cells (16 clones) and G-CSF mobilized peripheral blood CD34+ cells.
  • CD34+ cells from patients with non-myeloid malignancies expressed cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase activating protein (FLAP), and leukotriene A4 (LTA4) hydrolase but not 5-lipoxygenase (5-LO).
  • Taken together, these results indicate that LT synthesis is under development during early myelopoiesis and the capacity to produce LTs is gained upon maturation.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood. Leukotriene B4 / biosynthesis. Phospholipases A2, Cytosolic / biosynthesis
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / biosynthesis. Arachidonate 5-Lipoxygenase / biosynthesis. Calcimycin / pharmacology. Female. Granulocyte Colony-Stimulating Factor / metabolism. Humans. Ionophores / pharmacology. Male. Middle Aged. Models, Biological

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  • (PMID = 17976189.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ionophores; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 1HGW4DR56D / Leukotriene B4; 37H9VM9WZL / Calcimycin; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 3.1.1.4 / Phospholipases A2, Cytosolic
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14. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology

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  • (PMID = 20698144.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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15. Yin CC, Cortes J, Barkoh B, Hayes K, Kantarjian H, Jones D: t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy. Cancer; 2006 Apr 15;106(8):1730-8
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  • [Title] t(3;21)(q26;q22) in myeloid leukemia: an aggressive syndrome of blast transformation associated with hydroxyurea or antimetabolite therapy.
  • BACKGROUND: The t(3;21)(q26;q22) translocation is associated with myeloid leukemias and results in a chimeric oncoprotein containing AML1/RUNX1 variably fused to EAP, MDS1, and/or EVI1.
  • RESULTS: In all 16 patients with chronic myeloproliferative disorders, including 14 with chronic myelogenous leukemia (CML), the occurrence of t(3;21) heralded myeloid blast transformation.
  • Among 10 cases of t(3;21)-associated acute myeloid leukemia, 8 were secondary tumors after chemotherapy for other neoplasms that had been treated with regimens including fludarabine and 5-fluorouracil in 3 patients each and etoposide in 2 patients.
  • The immunophenotype of the blasts in all 22 tested cases was similar, with uniform expression of myeloid markers and CD34 and variable expression of CD7 and CD9, but minimal morphological myeloid maturation.
  • Among patients with acute myeloid leukemia/myelodysplastic syndrome, 7 died of disease (at a median of 2 mos) and 2 had persistent leukemia with short follow-up.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 21 / drug effects. Chromosomes, Human, Pair 3 / drug effects. Hydroxyurea / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Lymphocyte Activation / drug effects. Myeloproliferative Disorders / drug therapy. Oncogene Proteins, Fusion / analysis. Translocation, Genetic / drug effects
  • [MeSH-minor] Adult. Aged. Bone Marrow / pathology. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics

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  • [Copyright] 2006 American Cancer Society
  • (PMID = 16532439.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; X6Q56QN5QC / Hydroxyurea
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16. Flandrin P, Guyotat D, Duval A, Cornillon J, Tavernier E, Nadal N, Campos L: Significance of heat-shock protein (HSP) 90 expression in acute myeloid leukemia cells. Cell Stress Chaperones; 2008 Sep;13(3):357-64
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  • [Title] Significance of heat-shock protein (HSP) 90 expression in acute myeloid leukemia cells.
  • The 90-kDa heat shock protein (HSP90) is implicated in the conformational maturation and stabilization of a variety of client proteins with receptor and signal transduction functions.
  • The objective of this study was to assess its expression in primary acute myeloid leukemia (AML) cells and to evaluate its biological and clinical significance.
  • Targeted therapy with 17-AAG represents a promising antileukemic strategy in adult AML.
  • [MeSH-major] HSP90 Heat-Shock Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / metabolism. Benzoquinones / pharmacology. Humans. Lactams, Macrocyclic / pharmacology. Middle Aged. Myeloid Cells / cytology. Myeloid Cells / drug effects. Myeloid Cells / metabolism. Statistics as Topic. Survival Rate

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  • (PMID = 18386162.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 4GY0AVT3L4 / tanespimycin
  • [Other-IDs] NLM/ PMC2673940
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17. Royer PJ, Bougras G, Ebstein F, Leveque L, Tanguy-Royer S, Simon T, Juge-Morineau N, Chevallier P, Harousseau JL, Gregoire M: Efficient monocyte-derived dendritic cell generation in patients with acute myeloid leukemia after chemotherapy treatment: application to active immunotherapy. Exp Hematol; 2008 Mar;36(3):329-39
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  • [Title] Efficient monocyte-derived dendritic cell generation in patients with acute myeloid leukemia after chemotherapy treatment: application to active immunotherapy.
  • OBJECTIVE: While complete remission in acute myeloid leukemia (AML) can be achieved after chemotherapy (CT), relapses occur for the majority of patients, underlying the need to eliminate residual disease.
  • Based on dendritic cell (DC) vaccination, the triggering of an immune response against residual leukemia cells after CT could maintain patients in remission.
  • MATERIALS AND METHODS: We evaluated efficiency of the production, yields, maturation, and functional properties of DCs from 22 AML patients at different CT stages compared to those from 15 healthy donors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cancer Vaccines / therapeutic use. Dendritic Cells / cytology. Immunotherapy / methods. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes, Mononuclear / cytology
  • [MeSH-minor] Adult. Aged. Cell Differentiation. Chemotherapy, Adjuvant. Cytokines / secretion. Female. Humans. Male. Middle Aged. Receptors, CCR7 / biosynthesis. Remission Induction. Time Factors. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 18207305.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CCR7 protein, human; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Receptors, CCR7
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18. Walter RB, Gooley TA, van der Velden VH, Loken MR, van Dongen JJ, Flowers DA, Bernstein ID, Appelbaum FR: CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy. Blood; 2007 May 15;109(10):4168-70
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  • [Title] CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy.
  • Studying patients undergoing GO monotherapy for relapsed acute myeloid leukemia (AML), we now find that AML blasts of responders have a significantly higher mean CD33 level and lower P-glycoprotein (Pgp) activity compared with nonresponders.
  • The inverse relationship between CD33 and Pgp suggests a maturation-stage-dependent expression of both proteins, and offers the rationale for using cell differentiation-promoting agents to enhance GO-induced cytotoxicity.

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  • (PMID = 17227830.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA091 316
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / P-Glycoprotein; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Other-IDs] NLM/ PMC1885511
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19. Van Driessche A, Van de Velde AL, Nijs G, Braeckman T, Stein B, De Vries JM, Berneman ZN, Van Tendeloo VF: Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial. Cytotherapy; 2009;11(5):653-68
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  • [Title] Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial.
  • We report on a phase I dose-escalation trial using clinical-grade manufactured mature RNA-electroporated DC in acute myeloid leukemia (AML) patients.
  • We also validated a simplified DC maturation protocol yielding a consistent phenotype, migration and allogeneic T-cell stimulatory capacity in AML patients in remission.
  • [MeSH-major] Dendritic Cells / cytology. Electroporation. Immunotherapy, Adoptive / adverse effects. Immunotherapy, Adoptive / methods. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Aged. Cancer Vaccines / administration & dosage. Cell Count. Cell Differentiation. Cell Movement. Cell Separation. Cells, Cultured. Cryopreservation. Dose-Response Relationship, Immunologic. Female. Freezing. Humans. Immunophenotyping. Injections. Male. Middle Aged. RNA, Messenger / metabolism. Reproducibility of Results. T-Lymphocytes / immunology

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  • (PMID = 19530029.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / RNA, Messenger
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20. Serrano E, Carnicer MJ, Lasa A, Orantes V, Pena J, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias. Leuk Res; 2008 Jun;32(6):944-53
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  • [Title] Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by an abnormal proliferation of the myeloid precursors and a maturation block.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. DNA Methylation. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Biomarkers, Tumor / genetics. Chromatin Assembly and Disassembly. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Histone Deacetylase Inhibitors. Humans. Hydroxamic Acids / pharmacology. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / genetics. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic. Tumor Cells, Cultured. U937 Cells

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  • (PMID = 18206229.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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21. Maha A, Cheong SK, Leong CF, Seow HF: Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome. Hematology; 2008 Feb;13(1):13-20
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  • [Title] Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome.
  • Despite the advances in understanding the pathophysiology of acute myeloid leukaemia (AML), the cure rate for acute myeloid leukaemia patients remains low.
  • Acute myeloid leukaemia blasts demonstrated differing ability to survive in culture.
  • First, cells underwent maturation by increased expression of CD16 and down-regulated CD34 (a haemopoietic stem cell marker).
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Apoptosis. Cell Survival. Child. Child, Preschool. Cohort Studies. Female. Humans. In Vitro Techniques. Infant. Male. Middle Aged. Phenotype. Remission Induction. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 18534060.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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22. Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z: Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jan 15;188(2):95-8
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  • [Title] Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Acute myeloid leukemia with maturation (AML-M2 based on the French-American-British classification) is often accompanied by typical chromosomal changes such as t (8;21)(q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebral Hemorrhage / complications. Core Binding Factor Alpha 2 Subunit / genetics. Cytarabine / administration & dosage. Fatal Outcome. Female. Humans. Karyotyping. Mitoxantrone / administration & dosage. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • [RetractionIn] Cancer Genet Cytogenet. 2009 Jul;192(1):54 [19489159.001]
  • (PMID = 19100512.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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23. Babusíková O, Zelezníková T, Kirschnerová G, Kankuri E: Hematogones in acute leukemia during and after therapy. Leuk Lymphoma; 2008 Oct;49(10):1935-44
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  • [Title] Hematogones in acute leukemia during and after therapy.
  • After each leukemia therapy phase, characteristics of normal regenerating B-cells may be reminiscent of and mistaken for a relapse.
  • The three individual physiological maturation phases of B-lymphocytes (hematogone stages 1, 2, and 3) were studied by four-color flow cytometry in the course of bone marrow regeneration in leukemia patients.
  • The hematogones had an extremely high phenotypic stability unaffected by disease or therapy or by their coincidence with leukemia cells.
  • [MeSH-major] B-Lymphocytes / cytology. Bone Marrow / physiology. Leukemia / immunology. Leukemia, Myeloid, Acute / immunology. Regeneration
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow Examination. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Infant. Infant, Newborn. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • [CommentIn] Leuk Lymphoma. 2009 Apr;50(4):523-4 [19373647.001]
  • (PMID = 18452085.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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24. Kufner S, Zitzelsberger H, Kroell T, Pelka-Fleischer R, Salem A, de Valle F, Schweiger C, Nuessler V, Schmid C, Kolb HJ, Schmetzer HM: Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions. Scand J Immunol; 2005 Jul;62(1):86-98
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  • [Title] Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions.
  • Functional dendritic cells (DC) are professional antigen-presenting cells (APC) and can be generated in vitro from healthy as well as from leukaemic cells from acute myeloid leukemia (AML) patients giving rise to APC of leukaemic origin-presenting leukaemic antigens.
  • Whereas the addition of FL increases the DC harvest, the addition of autologous plasma in many cases has inhibitory influence on DC maturation.
  • [MeSH-major] Bone Marrow Cells / immunology. Cell Culture Techniques. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Middle Aged. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology. Vaccination / methods

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  • (PMID = 16091128.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Culture Media, Serum-Free; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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25. Baldus CD, Martus P, Burmeister T, Schwartz S, Gökbuget N, Bloomfield CD, Hoelzer D, Thiel E, Hofmann WK: Low ERG and BAALC expression identifies a new subgroup of adult acute T-lymphoblastic leukemia with a highly favorable outcome. J Clin Oncol; 2007 Aug 20;25(24):3739-45
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  • [Title] Low ERG and BAALC expression identifies a new subgroup of adult acute T-lymphoblastic leukemia with a highly favorable outcome.
  • PURPOSE: Expression of the genes ERG (v-ets erythroblastosis virus E26 oncogene homolog) and BAALC (brain and acute leukemia, cytoplasmic) shows similarity during hematopoietic maturation and predicts outcome in acute myeloid leukemia.
  • We hypothesized that like ERG, BAALC expression might be of prognostic significance in acute T-lymphoblastic leukemia (T-ALL) and that ERG and BAALC expression together would better identify the patient's risk profile.
  • RESULTS: High BAALC expression correlated with a higher frequency of early T-ALL (P < .0001), CD34 positivity (P < .0001), coexpression of myeloid markers (P = .0001), and high ERG expression (P = .03).
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Organotechnetium Compounds. Oximes. Survival Rate

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  • (PMID = 17646667.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Neoplasm Proteins; 0 / Organotechnetium Compounds; 0 / Oximes; 0 / Trans-Activators; 0 / technetium Tc 99m 4,9-diaza-3,3,10,10-tetramethyldodecan-2,11-dione dioxime
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26. Babusikova O, Stevulova L, Fajtova M: Immunophenotyping parameters as prognostic factors in T-acute leukemia patients. Neoplasma; 2009;56(6):508-13
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  • [Title] Immunophenotyping parameters as prognostic factors in T-acute leukemia patients.
  • The main aim of this study represents the extension of our studies using multiparametric flow cytometry analysis for exact definition of membrane and intracellular (cytoplasmic and nuclear) markers of acute leukemia cells of T-phenotype.
  • New knowledge of the T-cell maturation stages of hematopoietic cells in bone marrow and thymus has been applied, as each T-acute leukemia clone is representative of one blocked stage through maturation.
  • These patients had very distinctive immunophenotes, CD1a and CD8 markers completely negative, CD7 and cCD3 positive; CD5 was weakly expressed and myeloid markers CD33 and CD13 were coexpressed, or immature markers CD34, HLA-DR were coexpressed, together with myeloid markers CD13 and CD33 of weak positivity.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, T-Lymphocyte / immunology. Biomarkers, Tumor / immunology. HLA-DR Antigens / analysis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunophenotyping. Male. Middle Aged. Neoplasm, Residual / immunology. Phenotype. Prognosis. Young Adult

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  • (PMID = 19728759.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / HLA-DR Antigens
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27. Pendino F, Hillion J, Dudognon C, Delaunay J, Mourah S, Podgorniak MP, Lafon I, Chomienne C, Lanotte M, Dombret H, Rousselot P, Ségal-Bendirdjian E: Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL. Leukemia; 2006 Apr;20(4):599-603

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  • [Title] Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL.
  • Recently, we have shown that long-term treatment with all-trans retinoic acid (ATRA), a compound clinically approved for differentiation therapy of acute promyelocytic leukemia (APL), represses hTERT in differentiation-resistant APL cell lines leading to telomere shortening and death.
  • In contrast to differentiation-therapy, which is only successful in this subtype of leukemia, the telomerase-targeted pathway could also be of use in non-APL.
  • Here, we demonstrate that repression of hTERT occurs in fresh blasts cells from patients with myeloid leukemias of various subtypes exposed ex vivo to ATRA or synthetic retinoids.
  • These results support the idea that, by hTERT targeting, retinoids can induce telomere shortening and cell death and their integration in therapy protocols for myeloid leukemias refractory to maturation should be considered.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Retinoids / pharmacology. Telomerase / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Death / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / genetics. Structure-Activity Relationship. Telomere / drug effects. Telomere / genetics. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 16482212.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Retinoids; EC 2.7.7.49 / Telomerase
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28. Ge W, You SG, Wang YF, Li CH, Liu XF, He XP, Ma S, Qiu L: [Induction of efficient T-cell immunity against autologous leukemia cells by dendritic cells pulsed with the leukemia cell total RNA]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):461-4
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  • [Title] [Induction of efficient T-cell immunity against autologous leukemia cells by dendritic cells pulsed with the leukemia cell total RNA].
  • OBJECTIVE: To assess the feasibility and efficiency of eliciting leukemia-specific T cell responses in acute myeloid leukemia patients in complete remission (AML-CR) in vitro by dendritic cells (DC) pulsed with the leukemia cells total RNA.
  • Then the cells were incubated for another 24 h in a medium containing 10 ng/ml of TNF-alpha for maturation of DC.
  • CONCLUSION: Immunization with DC-leukemia cell RNA vaccines may be a simple, rapid and potent approach to elicitation of T cell-mediated anti-leukemia immunity.
  • [MeSH-major] Dendritic Cells / immunology. Leukemia, Myeloid, Acute / immunology. RNA / pharmacology. T-Lymphocytes / immunology
  • [MeSH-minor] Adolescent. Adult. Cell Communication. Cells, Cultured. Coculture Techniques. Female. Humans. Male. Middle Aged

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  • (PMID = 16383235.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 63231-63-0 / RNA
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29. Licciulli S, Cambiaghi V, Scafetta G, Gruszka AM, Alcalay M: Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation. Leukemia; 2010 Feb;24(2):429-37
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  • [Title] Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation.
  • Terminal differentiation of blood cells requires the concerted action of a series of transcription factors that are expressed at specific stages of maturation and function in a cell-type and dosage-dependent manner.
  • Pirin (PIR) is a putative transcriptional regulator whose expression is silenced in cells bearing the acute myeloid leukemia-1 eight-twenty-one (AML1/ETO) and promyelocytic leukemia/retinoic acid receptor (PML/RAR) leukemogenic fusion proteins.
  • A role for PIR in myeloid differentiation has not to date been reported.
  • In this study we show that PIR expression is significantly repressed in a large proportion of acute myeloid leukemias (AMLs), regardless of subtype or underlying karyotypic abnormalities.
  • We show that PIR expression increases during in vitro myeloid differentiation of primary hematopoietic precursor cells, and that ablation of PIR in the U937 myelomonocytic cell line or in murine primary hematopoietic precursor cells results in impairment of terminal myeloid differentiation.
  • Our results suggest that PIR is required for terminal myeloid maturation, and its downregulation may contribute to the differentiation arrest associated with AML.
  • [MeSH-major] Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Differentiation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Animals. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Bone Marrow / metabolism. Bone Marrow / pathology. Down-Regulation. Female. Gene Expression Profiling. Humans. Male. Mice. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells. Young Adult


30. Florian S, Sonneck K, Hauswirth AW, Krauth MT, Schernthaner GH, Sperr WR, Valent P: Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies. Leuk Lymphoma; 2006 Feb;47(2):207-22
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  • [Title] Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies.
  • Recent data suggest that myeloid neoplasms are organized hierarchically in terms of self-renewal and maturation of early progenitor cells, similar to normal myelopoiesis.
  • In acute myeloid leukemia (AML), the NOD/SCID mouse-repopulating leukemic stem cells usually co-express CD123 with CD34, but lack CD38.
  • In the present study, expression of target antigens on CD34+/CD38- cells was analysed by multi-color flow cytometry in patients with AML (n = 18), myelodysplastic syndromes (MDS, n = 6), chronic myeloid leukemia (CML, n = 8) and systemic mastocytosis (SM, n = 9).
  • In conclusion, neoplastic stem cells in various myeloid neoplasms appear to express a similar phenotype including target antigens such as CD13, CD33 and CD44.
  • [MeSH-major] Antigens, CD34 / analysis. Antigens, CD38 / analysis. Leukemia, Myeloid / diagnosis. Mastocytosis, Systemic / diagnosis. Myelodysplastic Syndromes / diagnosis. Stem Cells / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Chronic Disease. Female. Flow Cytometry. Gene Expression Regulation, Leukemic / genetics. Humans. Immunophenotyping. Male. Middle Aged


31. Savaşan S, Buck S, Raimondi SC, Becton DL, Weinstein H, Chang M, Ravindranath Y: CD36 (thrombospondin receptor) expression in childhood acute megakaryoblastic leukemia: in vitro drug sensitivity and outcome. Leuk Lymphoma; 2006 Oct;47(10):2076-83
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  • [Title] CD36 (thrombospondin receptor) expression in childhood acute megakaryoblastic leukemia: in vitro drug sensitivity and outcome.
  • The outcome for children with acute megakaryoblastic leukemia (AMKL) remains poor, except for cases associated with Down syndrome (DS).
  • CD36 expression in acute myeloid leukemia cases other than AMKL was not associated with increased in vitro drug sensitivity.
  • CD36 expression in AMKL may be an indicator of megakaryoblast maturation and chemotherapy sensitivity.
  • [MeSH-major] Antigens, CD36 / biosynthesis. Gene Expression Regulation, Neoplastic. Leukemia, Megakaryoblastic, Acute / complications. Leukemia, Megakaryoblastic, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor. Cell Membrane / metabolism. Child. Child, Preschool. Cytarabine / pharmacology. Daunorubicin / pharmacology. Down Syndrome / complications. Humans. Immunophenotyping. Infant. Infant, Newborn. Sensitivity and Specificity. Treatment Outcome

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  • [CommentIn] Leuk Lymphoma. 2006 Oct;47(10):2004-5 [17071466.001]
  • (PMID = 17071479.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / U10 CA 30969
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Biomarkers, Tumor; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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32. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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35. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Cytogenetics. Fatal Outcome. Female. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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36. Zeng LJ, Tan H: [In vitro anti-leukemia activity of cord blood original cytotoxic T lymphocytes]. Ai Zheng; 2005 Apr;24(4):419-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [In vitro anti-leukemia activity of cord blood original cytotoxic T lymphocytes].
  • BACKGROUND & OBJECTIVE: Cord blood transplantation (CBT) possesses graft-versus-leukemia (GVL) effect.
  • It is possible to cure leukemia if specific cytotoxic T lymphocytes (CTLs) can be induced from lymphocytes in cord blood (CB), and be used to eradicate minimal residual disease (MRD) in leukemia patients.
  • This study was to induce CTLs from cord blood, and explore its in vitro anti-leukemia activity.
  • Immature DCs were pulsed with apoptotic leukemia cells to present leukemic antigens to cord blood original lymphocytes to obtain CTLs.
  • The characteristics of maturation of DCs were evaluated by morphology and flow cytometry.
  • Anti-leukemia effect of CTLs was measured by lactate dehydrogenase release assay.
  • When E:T ratio was 50:1, CTLs showed far higher cytotoxicity to uncultured acute myeloid leukemia (AML) cells than to K562 cells, and to mononuclear cells of bone marrow from the corresponding patients in complete remission phase (CR-MNCs) [(52.6+/-21.0)% vs. (18.2+/-20.2)%, and (3.3+/-6.3)%, P < 0.05].
  • CONCLUSIONS: Mature DCs derived from cord blood, which loaded leukemia antigens, could induce leukemia-specific CTLs.
  • The CTLs have vigorous cytotoxicity to original leukemia cells rather than CR-MNCs.
  • [MeSH-major] Antigen Presentation / immunology. Dendritic Cells / immunology. Fetal Blood / immunology. Leukemia, Myeloid, Acute / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Adult. Aged. Antigens, CD / analysis. Antigens, CD1 / analysis. Antigens, CD86 / analysis. Apoptosis / immunology. Cells, Cultured. Cytotoxicity, Immunologic. Female. HLA-DR Antigens / analysis. Humans. Immunoglobulins / analysis. Immunophenotyping. Leukocytes, Mononuclear / cytology. Male. Membrane Glycoproteins / analysis. Middle Aged

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  • (PMID = 15820063.001).
  • [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 / Antigens, CD1; 0 / Antigens, CD86; 0 / CD1a antigen; 0 / CD83 antigen; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
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37. Putz G, Rosner A, Nuesslein I, Schmitz N, Buchholz F: AML1 deletion in adult mice causes splenomegaly and lymphomas. Oncogene; 2006 Feb 9;25(6):929-39
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  • [Title] AML1 deletion in adult mice causes splenomegaly and lymphomas.
  • AML1 is one of the most frequently mutated genes associated with human acute leukemia, suggesting that genetic alterations of the gene contribute to leukemogenesis.
  • AML1 was deleted in adult mice by inducing Cre activity to replicate AML1 deletions found in human MDS, familial platelet disorder and rare de novo human AML.
  • At a latency of 2 months after induction, the thymus was reduced in size and frequently populated by immature double negative thymocytes, indicating defective T-lymphocyte maturation, resulting in lymphatic diseases with 50% penetrance, including atypical hyperplasia and thymic lymphoma.
  • Mice also developed splenomegaly with an expansion of the myeloid compartment.


38. Curti A, Trabanelli S, Onofri C, Aluigi M, Salvestrini V, Ocadlikova D, Evangelisti C, Rutella S, De Cristofaro R, Ottaviani E, Baccarani M, Lemoli RM: Indoleamine 2,3-dioxygenase-expressing leukemic dendritic cells impair a leukemia-specific immune response by inducing potent T regulatory cells. Haematologica; 2010 Dec;95(12):2022-30
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  • [Title] Indoleamine 2,3-dioxygenase-expressing leukemic dendritic cells impair a leukemia-specific immune response by inducing potent T regulatory cells.
  • BACKGROUND: The immunoregulatory enzyme indoleamine 2,3-dioxygenase, which catalyzes the conversion of tryptophan into kynurenine, is expressed in a significant subset of patients with acute myeloid leukemia, resulting in the inhibition of T-cell proliferation and the induction of regulatory T cells.
  • Acute myeloid leukemia cells can be differentiated into dendritic cells, which have increased immunogenicity and have been proposed as vaccines against leukemia.
  • DESIGN AND METHODS: Leukemic dendritic cells were generated from acute myeloid leukemia cells and used as stimulators in functional assays, including the induction of regulatory T cells.
  • RESULTS: We demonstrate that, after differentiation into dendritic cells, both indoleamine 2,3-dioxygenase-negative and indoleamine 2,3-dioxygenase-positive acute myeloid leukemia samples show induction and up-regulation of indoleamine 2,3-dioxygenase gene and protein, respectively.
  • Indoleamine 2,3-dioxygenase-positive acute myeloid leukemia dendritic cells catabolize tryptophan into kynurenine metabolite and inhibit T-cell proliferation through an indoleamine 2,3-dioxygenase-dependent mechanism.
  • Purified CD4(+)CD25(+) T cells obtained from co-culture with indoleamine 2,3-dioxygenase-positive leukemic dendritic cells act as regulatory T cells as they inhibit naive T-cell proliferation and impair the complete maturation of normal dendritic cells.
  • Importantly, leukemic dendritic cell-induced regulatory T cells are capable of in vitro suppression of a leukemia-specific T cell-mediated immune response, directed against the leukemia-associated antigen, Wilms' tumor protein.
  • CONCLUSIONS: These data identify indoleamine 2,3-dioxygenase-mediated catabolism as a tolerogenic mechanism exerted by leukemic dendritic cells and have clinical implications for the use of these cells for active immunotherapy of leukemia.
  • [MeSH-major] Dendritic Cells / enzymology. Indoleamine-Pyrrole 2,3,-Dioxygenase / metabolism. Leukemia, Myeloid / enzymology. T-Lymphocytes, Regulatory / metabolism
  • [MeSH-minor] Acute Disease. Adult. Biocatalysis. Blotting, Western. CD4-Positive T-Lymphocytes / cytology. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Cell Proliferation / drug effects. Cells, Cultured. Coculture Techniques. Flow Cytometry. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Leukemic. Humans. Immunophenotyping. Kynurenine / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tryptophan / analogs & derivatives. Tryptophan / metabolism. Tryptophan / pharmacology. Tumor Cells, Cultured

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  • (PMID = 20801903.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 343-65-7 / Kynurenine; 8DUH1N11BX / Tryptophan
  • [Other-IDs] NLM/ PMC2995559
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39. Schnittger S, Haferlach C, Ulke M, Alpermann T, Kern W, Haferlach T: IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status. Blood; 2010 Dec 16;116(25):5486-96
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  • Mutations in the IDH1 gene at position R132 coding for the enzyme cytosolic isocitrate dehydrogenase are known in glioma and have recently been detected also in acute myeloid leukemia (AML).
  • IDH1-mutated cases more often had AML without maturation/French-American-British M1 (P < .001), an immature immunophenotype, and female sex (8.7% vs 4.7% in male, P = .003) compared with IDH1wt cases.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. DNA, Neoplasm / genetics. Female. Genotype. Humans. Immunophenotyping. Karyotyping. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Risk Factors. Survival Rate. Young Adult

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  • (PMID = 20805365.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
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40. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
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  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • The quality/quantity of DC generated was estimated by flow cytometry studying (co) expressions of "DC"antigens, costimulatory, maturation, and blast-antigens.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigen Presentation / drug effects. Antigens, Differentiation / metabolism. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. Cell Differentiation / drug effects. Cell Separation. Culture Media, Serum-Free. Cytokines / metabolism. Cytokines / pharmacology. Cytotoxicity, Immunologic. Female. Flow Cytometry. Humans. Male. Middle Aged. Picibanil / pharmacology. Poly I-C / pharmacology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
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41. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
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  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.
  • [MeSH-minor] Adult. Cells, Cultured. Dimerization. Drug Resistance. Female. Gene Expression. Humans. Infant, Newborn. Ligands. Male. Parents. Point Mutation. Signal Transduction / drug effects. Signal Transduction / immunology

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  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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42. Campioni D, Secchiero P, Corallini F, Melloni E, Capitani S, Lanza F, Zauli G: Evidence for a role of TNF-related apoptosis-inducing ligand (TRAIL) in the anemia of myelodysplastic syndromes. Am J Pathol; 2005 Feb;166(2):557-63
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  • We focused our study on the cytokine TRAIL (TNF-related apoptosis-inducing ligand), which has been shown to exhibit an anti-differentiation activity on erythroid maturation.
  • Immunocytochemical analysis of bone marrow mononuclear cells (BMMC) showed an increased expression of TRAIL in MDS patients with respect to acute myeloid leukemia (AML) patients and normal BM donors.
  • TRAIL expression was increased predominantly in myeloid precursors of granulocytic lineage and in a subset of monocytes and pro-erythroblasts.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Apoptosis. Apoptosis Regulatory Proteins. Bone Marrow Cells / metabolism. Culture Media, Conditioned / pharmacology. Culture Media, Serum-Free / metabolism. Enzyme-Linked Immunosorbent Assay. Erythrocytes / metabolism. Female. Fetal Blood / metabolism. Flow Cytometry. Glycophorin / metabolism. Humans. Immunohistochemistry. Leukemia, Myeloid, Acute / blood. Leukocytes, Mononuclear / metabolism. Ligands. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand. Time Factors

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  • (PMID = 15681838.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Apoptosis Regulatory Proteins; 0 / Culture Media, Conditioned; 0 / Culture Media, Serum-Free; 0 / Glycophorin; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1602326
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43. Abe T, Furukawa T, Masuko M, Sugimoto A, Okazuka K, Honma K, Fujimura T, Iguchi S, Nishi S, Ueno M, Nagahashi M, Watanabe G, Ajioka Y, Isahai N, Nagai K, Kazuyama Y, Aizawa Y: Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation. Int J Hematol; 2009 Oct;90(3):421-5
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  • We report a case of a 29-year-old male patient with a generalized adenovirus (AdV) infection after cord blood transplantation (CBT) for acute myelocytic leukemia with maturation at 2nd complete remission.
  • [MeSH-major] Adenovirus Infections, Human / etiology. Cord Blood Stem Cell Transplantation / adverse effects. Cystitis / etiology. Hemorrhage / etiology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Fatal Outcome. Humans. Male. Urinary Bladder / pathology

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  • (PMID = 19763745.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Samorapoompichit P, Schernthaner GH, Worda C, Wimazal F, Krauth MT, Sperr WR, Valent P: Evaluation of neoplastic human mast cells by tryptase-immunoelectron microscopy. Histopathology; 2006 Feb;48(3):247-57

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  • METHODS: We have examined the ultrastructure and cytomorphological features of MC derived from cord blood cells, neoplastic bone marrow MC in patients with systemic mastocytosis (SM, n = 4), myelomastocytic leukaemia (MML, n = 2), mast cell leukaemia (MCL, n = 2) and tryptase-positive acute myeloid leukaemia (AML, n = 4).
  • In all samples examined, the identity of MC could be reconfirmed by immunoelectron microscopy, irrespective of the stage of cell maturation or the disease variant, all types of MC contained tryptase in their cytoplasmic granules.
  • CONCLUSION: Immunoelectron microscopy may be a helpful approach in confirming the identity of neoplastic MC in myeloid neoplasms.
  • [MeSH-major] Leukemia, Myeloid / pathology. Leukemia, Myelomonocytic, Acute / pathology. Mast Cells / enzymology. Mast Cells / ultrastructure. Mastocytosis, Systemic / pathology. Serine Endopeptidases / analysis
  • [MeSH-minor] Adult. Aged. Cell Nucleus / ultrastructure. Cytoplasm / enzymology. Cytoplasm / ultrastructure. Female. Fetal Blood / cytology. Humans. Leukemia, Mast-Cell / enzymology. Leukemia, Mast-Cell / pathology. Male. Microscopy, Electron. Microscopy, Immunoelectron. Middle Aged. Tryptases

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  • (PMID = 16430471.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
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45. Jegalian AG, Facchetti F, Jaffe ES: Plasmacytoid dendritic cells: physiologic roles and pathologic states. Adv Anat Pathol; 2009 Nov;16(6):392-404
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  • Demonstrating potential for neoplastic transformation reflective of varying stages of maturation, clonal proliferations range from PDC nodules most commonly associated with chronic myelomonocytic leukemia to the rare but highly aggressive malignancy now known as blastic plasmacytoid dendritic cell neoplasm (BPDCN).
  • Acute leukemia therapy regimens may lead to sustained clinical remission of BPDCN, with bone marrow transplantation in first complete remission potentially curative in adult patients.
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / pathology. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Male. Toll-Like Receptors / immunology

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  • (PMID = 19851130.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Toll-Like Receptors
  • [Number-of-references] 151
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46. Bennett CL, Evens AM, Andritsos LA, Balasubramanian L, Mai M, Fisher MJ, Kuzel TM, Angelotta C, McKoy JM, Vose JM, Bierman PJ, Kuter DJ, Trifilio SM, Devine SM, Tallman MS: Haematological malignancies developing in previously healthy individuals who received haematopoietic growth factors: report from the Research on Adverse Drug Events and Reports (RADAR) project. Br J Haematol; 2006 Dec;135(5):642-50
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  • Pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) and granulocyte colony-stimulating factor (G-CSF) promote haematopoietic progenitor cell maturation.
  • Acute myeloid leukaemia was diagnosed 4 and 5 years after G-CSF mobilisation in two donors who underwent peripheral blood stem cell donation for sibling allogeneic haematopoietic stem cell transplantation.
  • Following intensive chemotherapy, one died from acute leukaemia and the second is in complete remission.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autoantibodies / immunology. Clinical Trials as Topic. Female. Granulocyte Colony-Stimulating Factor / adverse effects. Humans. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / etiology. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / etiology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / etiology. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Polyethylene Glycols / adverse effects. Recombinant Proteins / adverse effects. Thrombopoietin / adverse effects. Thrombopoietin / immunology

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  • [CommentIn] Br J Haematol. 2007 Apr;137(1):77-8; author reply 79-80 [17359373.001]
  • [CommentIn] Br J Haematol. 2007 Apr;137(1):78-9; author reply 79-80 [17359374.001]
  • [CommentIn] Br J Haematol. 2006 Dec;135(5):651-2 [17054429.001]
  • (PMID = 17054431.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA 102713-01; United States / NCI NIH HHS / CA / K23 CA109613-A1; United States / NCI NIH HHS / CA / P 30 CA60553
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Hematopoietic Cell Growth Factors; 0 / Recombinant Proteins; 0 / polyethylene glycol-recombinant human megakaryocyte growth and development factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 30IQX730WE / Polyethylene Glycols; 9014-42-0 / Thrombopoietin
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47. Yamagata T, Maki K, Mitani K: Runx1/AML1 in normal and abnormal hematopoiesis. Int J Hematol; 2005 Jul;82(1):1-8
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  • Runx1 not only is critical for definitive hematopoiesis in the fetus but also is required for normal megakaryocytic maturation and T-lymphocyte and B-lymphocyte development in adult mice.
  • Runx1 has been identified in leukemia-associated chromosomal translocations, including t(8;21) (Runx1-ETO/MTG8), t(16;21) (Runx1-MTG16), t(3;21) (Runx1-Evi1), t(12;21) (TEL-Runx1), and t(X;21) (Runx1-Fog2).
  • However, expression of the fusion protein is not sufficient by itself to cause leukemia and likely requires additional events for leukemogenesis.
  • Point mutations in a Runx1 allele cause haploinsufficiency and a biallelic null for Runx1, which are associated with familial platelet disorder with a propensity for acute myeloid leukemia (FPD/AML) and AML-M0, respectively.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. Hematopoiesis / genetics. Hematopoiesis / physiology. Leukemia / genetics. Leukemia / physiopathology

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  • (PMID = 16105753.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
  • [Number-of-references] 81
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48. Veltroni M, Sainati L, Zecca M, Fenu S, Tridello G, Testi AM, Merlone AD, Buldini B, Leszl A, Lo Nigro L, Longoni D, Bernini G, Basso G, AIEOP-MDS Study Group: Advanced pediatric myelodysplastic syndromes: can immunophenotypic characterization of blast cells be a diagnostic and prognostic tool? Pediatr Blood Cancer; 2009 Mar;52(3):357-63
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  • These studies have focused on the identification of abnormalities in the maturation pathway of antigen expression of myelo-monocytic cells, and characterization of blast populations.
  • Therefore, phenotype has been proposed as a diagnostic and prognostic criterion tool for adult MDS.
  • PROCEDURE: We evaluated by multiparameter flow cytometry 26 MDS pediatric patients with more than 2% of blast cells at bone marrow morphological examination (17 de novo MDS and 9 secondary MDS) and 145 pediatric de novo acute myeloid leukemia (AML) cases (M3 excluded).
  • As control group, 12 healthy age-matched donors for allogenic bone marrow transplantation (BMD) and 6 regenerating bone marrow samples, collected from children with acute lymphoblastic leukemia (ALL) in remission after induction chemotherapy, were studied.

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  • (PMID = 19061215.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7
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49. Nguyen S, Beziat V, Dhedin N, Kuentz M, Vernant JP, Debre P, Vieillard V: HLA-E upregulation on IFN-gamma-activated AML blasts impairs CD94/NKG2A-dependent NK cytolysis after haplo-mismatched hematopoietic SCT. Bone Marrow Transplant; 2009 May;43(9):693-9
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  • This implies that maturation of NK cells is the key to improved immune responses and transplantation outcome.
  • [MeSH-major] HLA Antigens / genetics. Hematopoietic Stem Cell Transplantation. Histocompatibility Antigens Class I / genetics. Interferon-gamma / pharmacology. Interferon-gamma / physiology. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / pathology. NK Cell Lectin-Like Receptor Subfamily C / immunology. NK Cell Lectin-Like Receptor Subfamily D / immunology
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Cytotoxicity, Immunologic. Female. Haplotypes. Hematopoiesis. Histocompatibility / immunology. Humans. Immune System / immunology. Immune System / pathology. Male. Treatment Outcome. Up-Regulation / genetics. Young Adult

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  • (PMID = 19011664.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-E antigen; 0 / Histocompatibility Antigens Class I; 0 / KLRC1 protein, human; 0 / KLRD1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily C; 0 / NK Cell Lectin-Like Receptor Subfamily D; 82115-62-6 / Interferon-gamma
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50. Dupret C, Asnafi V, Leboeuf D, Millien C, Ben Abdelali R, Preudhomme C, Beldjord K, Delabesse E, Macintyre E: IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner. Leukemia; 2005 Dec;19(12):2337-8

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  • [Title] IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. B-Lymphocytes / pathology. Gene Rearrangement. Genes, T-Cell Receptor. Humans. Immunoglobulin Heavy Chains / genetics. Myeloid Cells / pathology. T-Lymphocytes / pathology

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  • (PMID = 16304577.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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