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1. Silva FP, Almeida I, Morolli B, Brouwer-Mandema G, Wessels H, Vossen R, Vrieling H, Marijt EW, Valk PJ, Kluin-Nelemans HC, Sperr WR, Ludwig WD, Giphart-Gassler M: Genome wide molecular analysis of minimally differentiated acute myeloid leukemia. Haematologica; 2009 Nov;94(11):1546-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome wide molecular analysis of minimally differentiated acute myeloid leukemia.
  • BACKGROUND: Minimally differentiated acute myeloid leukemia is heterogeneous in karyotype and is defined by immature morphological and molecular characteristics.
  • This originally French-American-British classification is still used in the new World Health Organization classification when other criteria are not met.
  • DESIGN AND METHODS: We performed whole genome single nucleotide polymorphism analysis and extensive molecular analysis in a cohort of 52 patients with minimally differentiated acute myeloid leukemia.
  • These point towards a variety of candidate genes that could contribute to the pathogenesis of minimally differentiated acute myeloid leukemia, including the tumor suppressor genes TP53 and NF1, and reinforced the importance of RUNX1 in this leukemia.
  • Furthermore, for the first time in this minimally differentiated form of leukemia we detected mutations in the transactivation domain of RUNX1.
  • Mutations in other acute myeloid leukemia associated transcriptions factors were infrequent.
  • Irrespective of the RUNX1 mutation status, our results show that RAS signaling is the most important pathway for proliferation in minimally differentiated acute myeloid leukemia.
  • CONCLUSIONS: Our results suggest that in patients without RUNX1 mutation, several other molecular aberrations, separately or in combination, contribute to a common minimally differentiated phenotype.
  • [MeSH-major] Genome, Human. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Differentiation. Child. Child, Preschool. Cohort Studies. Core Binding Factor Alpha 2 Subunit / genetics. Humans. Karyotyping. Middle Aged. Polymorphism, Single Nucleotide. Young Adult

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  • (PMID = 19773259.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
  • [Other-IDs] NLM/ PMC2770965
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2. Barbaric D, Alonzo TA, Gerbing RB, Meshinchi S, Heerema NA, Barnard DR, Lange BJ, Woods WG, Arceci RJ, Smith FO: Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961. Blood; 2007 Mar 15;109(6):2314-21
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  • [Title] Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961.
  • To assess the impact of minimally differentiated acute myeloid leukemia (AML-M0) morphology in children, we analyzed 2 sequential Children's Cancer Group AML clinical trials.
  • We compared presenting characteristics and outcomes of 82 CCG-2891 and CCG-2961 patients with de novo, non-Down syndrome (DS) AML-M0 with those of 1620 patients with non-M0 AML, and of 10 CCG-2891 patients with DS-associated AML-M0 with those of 179 with DS-associated non-M0 AML.
  • The non-DS AML-M0 children had a lower white blood cell (WBC) count (P = .001) than their non-M0 counterparts and a higher incidence of chromosome 5 deletions (P = .002), nonconstitutional trisomy 21 (P = .027), and hypodiploidy (P = .002).
  • Outcome analyses considering all children with non-DS AML demonstrated no significant differences between M0 and non-M0 patients.
  • Analyses restricted to intensive-timing CCG-2891 and CCG-2961 demonstrated comparable complete response (CR) rates (79% and 78%) between non-DS M0 and non-M0 patients.
  • OS from end of induction (45% +/- 17% versus 63% +/- 3%; P = .038), event-free survival (EFS; 23% +/- 11% versus 41% +/- 3%; P = .018), and disease-free survival (DFS; 31% +/- 14% versus 52% +/- 3%; P = .009) were inferior in the M0 group.
  • There was no significant outcome difference between DS-associated AML-M0 and non-M0 children.
  • This study suggests that intensively treated non-DS-associated AML-M0 children have an inferior outcome compared with children with non-M0 AML.

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  • (PMID = 17158236.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 98413; United States / NCI NIH HHS / CA / CA 98543
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1852193
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3. Silva FP, Swagemakers SM, Erpelinck-Verschueren C, Wouters BJ, Delwel R, Vrieling H, van der Spek P, Valk PJ, Giphart-Gassler M: Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status. Blood; 2009 Oct 1;114(14):3001-7
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  • [Title] Gene expression profiling of minimally differentiated acute myeloid leukemia: M0 is a distinct entity subdivided by RUNX1 mutation status.
  • Minimally differentiated acute myeloid leukemia (AML-M0) is defined by immature morphology and expression of early hematologic markers.
  • By gene expression profiling (GEP) and subsequent unsupervised analysis of 35 AML-M0 samples and 253 previously reported AML cases, we demonstrate that AML-M0 cases express a unique signature that is largely separated from other molecular subtypes.
  • Hematologic transcription regulators such as CEBPA, CEBPD, and ETV6, and the differentiation associated gene MPO appeared strongly down-regulated, in line with the primitive state of this leukemia.
  • AML-M0 frequently carries loss-of-function RUNX1 mutation.
  • Unsupervised analyses revealed a subdivision between AML-M0 cases with and without RUNX1 mutations.
  • RUNX1 mutant AML-M0 samples showed a distinct up-regulation of B cell-related genes such as members of the B-cell receptor complex, transcription regulators RUNX3, ETS2, IRF8, or PRDM1, and major histocompatibility complex class II genes.
  • Importantly, prediction with high accuracy of the AML-M0 subtype and prediction of patients carrying RUNX1 mutation within this subtype were possible based on the expression level of only a few transcripts.
  • We propose that RUNX1 mutations in this AML subgroup cause lineage infidelity, leading to aberrant coexpression of myeloid and B-lymphoid genes.
  • Furthermore, our results imply that AML-M0, although originally determined by morphology, constitutes a leukemia subgroup.
  • [MeSH-major] Biomarkers, Tumor / genetics. Cell Differentiation. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Mutation / genetics

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  • (PMID = 19666867.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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4. Auewarakul CU, Leecharendkeat A, Thongnoppakhun W, Limwongse C, Tocharoentanaphol C: Mutations of AML1 in non-M0 acute myeloid leukemia: six novel mutations and a high incidence of cooperative events in a South-east Asian population. Haematologica; 2006 May;91(5):675-8
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  • [Title] Mutations of AML1 in non-M0 acute myeloid leukemia: six novel mutations and a high incidence of cooperative events in a South-east Asian population.
  • Point mutations of AML1 are uncommon and predominantly reported in a rare minimally differentiated acute myeloid leukemia (M0 AML).
  • Few data exist regarding the frequency of AML1 mutations in non-M0 cases.
  • We screened 284 consecutive adult Thai patients with de novo AML and found that 3.9% had AML1 mutations.
  • Six novel mutations were uniquely identified in non-M0 cases.
  • Sixty-four percent of the non-M0 patients with AML1 mutations had coexisting genetic abnormalities including FLT3 mutation in 36%.
  • Our study provides evidence to support the model of multiple co-operating events, which could also be critical in the development of leukemia in non-M0 AML patients with mutated AML1.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Asia, Southeastern / epidemiology. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Humans. Introns / genetics. Male. Middle Aged. Mutagenesis, Insertional. Phenotype. Protein Folding. Protein Structure, Tertiary. RNA Splice Sites / genetics. Thailand / epidemiology

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  • (PMID = 16627249.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / RNA Splice Sites; 0 / RUNX1 protein, human
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5. Mantadakis E, Danilatou V, Stiakaki E, Paterakis G, Papadhimitriou S, Kalmanti M: T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia. Pediatr Blood Cancer; 2007 Mar;48(3):354-7
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  • [Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.
  • We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.
  • Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.
  • This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.
  • [MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16206214.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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6. Lin LI, Chen CY, Lin DT, Tsay W, Tang JL, Yeh YC, Shen HL, Su FH, Yao M, Huang SY, Tien HF: Characterization of CEBPA mutations in acute myeloid leukemia: most patients with CEBPA mutations have biallelic mutations and show a distinct immunophenotype of the leukemic cells. Clin Cancer Res; 2005 Feb 15;11(4):1372-9
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  • [Title] Characterization of CEBPA mutations in acute myeloid leukemia: most patients with CEBPA mutations have biallelic mutations and show a distinct immunophenotype of the leukemic cells.
  • PURPOSE: The transcription factor CCAAT/enhancer binding protein alpha, encoded by the CEBPA, is crucial for the differentiation of immature granulocytes.
  • We sought to characterize the CEBPA mutation in acute myeloid leukemia (AML) and to clarify if there is a distinct immunophenotype for leukemic cells with the mutation.
  • EXPERIMENT DESIGN: One hundred and four patients with de novo AML were evaluated for the CEBPA mutation and immunophenotype of the leukemic cells.
  • RESULTS: Twenty-two distinct mutations were identified in 16 (15%) of 104 AML patients.
  • CONCLUSION: These data revealed that most AML with CEBPA mutations were associated with an immunophenotype of HLA-DR(+)CD7(+)CD13(+)CD14(-)CD15(+)CD33(+)CD34(+).
  • The close relationship of CEBPA mutations with the leukemia status of the patients and the concordance of mutation in presenting and relapse samples implicate the CEBPA mutation as a potential marker for monitoring minimal residue disease.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Alleles. Amino Acid Sequence. Antigens, CD / analysis. Base Sequence. Child. Child, Preschool. DNA Mutational Analysis. Female. Gene Duplication. HLA-DR Antigens / analysis. Humans. Immunophenotyping. Infant. Male. Middle Aged. Neoplasm Recurrence, Local. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. fms-Like Tyrosine Kinase 3

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  • (PMID = 15746035.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / HLA-DR Antigens; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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7. Jung SI, Cho HS, Lee CH, Kim KD, Ha JO, Kim MK, Lee KH, Hyun MS: Two cases of trisomy 19 as a sole chromosomal abnormality in myeloid disorders. Korean J Lab Med; 2008 Jun;28(3):174-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two cases of trisomy 19 as a sole chromosomal abnormality in myeloid disorders.
  • Trisomy 19 is frequently encountered in cases of chronic myeloid leukemia (CML) as a secondary abnormality: however, trisomy 19 rarely occurs as a sole chromosomal abnormality and, to date, it has only been reported in 48 hematopoietic malignancies, 1 case of adenocarcinoma and 1 case of astrocytic tumor.
  • Here, we report two additional cases of trisomy 19 as a sole karyotypic aberration in myeloid malignancies.
  • One of these cases involved a 6-month-old male who was diagnosed with acute myeloid leukemia minimally differentiated.
  • Based on a review of the existing literature and the results of this report, trisomy 19 not only as a secondary abnormality but also as a sole karyotypic aberration is strongly associated with myeloid disorder; however, it is not preferentially found in specific FAB subgroups of myelodysplasic syndrome or acute myeloid leukemia.
  • [MeSH-major] Anemia, Refractory / diagnosis. Anemia, Refractory / genetics. Chromosomes, Human, Pair 19. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Trisomy
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Female. Humans. Infant. Karyotyping. Male

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  • (PMID = 18594167.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
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8. Galili N, Devemy E, Raza A: Isolation of specific and biologically active peptides that bind cells from patients with acute myeloid leukemia (AML). J Hematol Oncol; 2008;1:8
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  • [Title] Isolation of specific and biologically active peptides that bind cells from patients with acute myeloid leukemia (AML).
  • PURPOSE: In a departure from conventional strategies to improve treatment outcome for myeloid malignancies, we report the isolation of leukemia-specific peptides using a phage display library screened with freshly obtained human myeloid leukemia cells.
  • RESULTS: A phage display library was screened by 5 rounds of biopanning with freshly isolated human AML cells.
  • Individual colonies were randomly picked and after purification, biologic activity (growth and differentiation) on fresh AML cells was profiled.
  • Multiple peptides were found to selectively bind to acute myeloid leukemia (AML) cells.
  • The peptides bound to leukemia cells, were internalized and could induce proliferation and/or differentiation in the target patient cells.
  • Two of the peptides, HP-A2 and HP-G7, appeared to have a novel mechanism of inducing differentiation since they did not cause G1 arrest in cycling cells even as the expression of the differentiation marker CD11b increased.
  • CONCLUSION: Peptide induced differentiation of leukemia cells offers a novel treatment strategy for myeloid malignancies, whereas their ability to induce proliferation could be harnessed to make cells more sensitive to chemotherapy.
  • Conceptually, these leukemia specific peptides can also be used to refine diagnosis, document minimal residual disease, and selectively deliver toxins to malignant cells.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Myeloid Cells / cytology. Peptides / metabolism
  • [MeSH-minor] Amino Acid Sequence. Cell Differentiation. Cell Line, Tumor. Cell Proliferation. Cells, Cultured. Humans. Peptide Library. Protein Binding


9. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI: Immunocytochemical markers in acute leukaemias diagnosis. Exp Oncol; 2010 Sep;32(3):195-9
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  • [Title] Immunocytochemical markers in acute leukaemias diagnosis.
  • The study included 1742 patients with acute myeloblastic leukaemias (AML) and acute lymphoblastic leukaemias (ALL), Kyiv city residents and patients from 20 regions of Ukraine.
  • Immunocytochemical techniques (APAAP, LSAB) and broad panel of monoclonal antibodies (MoAbs) against lineage specific and differentiation antigens of leukocytes were employed for immunophenotyping of leukemic blast cells directly in blood and bone marrow smears.
  • Different types of AML were defined by the expression of the cell surface and cytoplasmic antigens.
  • Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation, acute megakaryoblastic leukaemia, acute erythroid leukaemia and acute leukaemias of ambiguous lineage.
  • Acute lymphoblastic leukaemias was broadly classified into B-lineage and T-lineage ALL.
  • According to the degree of B-lymphoid differentiation of the blast cells four subtypes of B-lineage ALL were established.
  • Immunocytochemical examination was required to diagnose AL of ambiguous lineage with no clear evidence of lineage differentiation (acute undifferentiated leukaemia) or those with blasts that express markers of more than one lineage (mixed phenotype acute leukaemias).
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology

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  • (PMID = 21403617.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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10. Chen S, Xue Y, Zhu X, Wu Y, Pan J: Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins. Acta Haematol; 2007;118(1):38-41
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  • [Title] Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins.
  • Here we report a rare chromosomal translocation, t(12;22)(p13;q11), which was detected in a 53-year-old female patient diagnosed as having minimally differentiated acute myeloid leukemia (AML-M0) according to the French-American-British classification criteria.
  • As far as we know, this is the first report of t(12;22)(p13;q11) translocation involving TEL and MN1 genes in an AML-M0 patient.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / analysis. Translocation, Genetic

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17476096.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
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11. Horikoshi A, Takei K, Iriyama N, Uenogawa K, Ishizuka H, Shiraiwa H, Hosokawa Y, Sawada S, Kitoh T: Effect of L-asparaginase combined with vincristine and prednisolone on acute myeloblastic leukemia (M0) associated with non-Hodgkin lymphoma. Acta Haematol; 2009;122(1):54-7
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  • [Title] Effect of L-asparaginase combined with vincristine and prednisolone on acute myeloblastic leukemia (M0) associated with non-Hodgkin lymphoma.
  • She was eventually diagnosed as having acute myeloblastic leukemia (AML;.
  • M0) with non-Hodgkin lymphoma (NHL).
  • We investigated the therapeutic efficacy of L-asparaginase (L-Asp), vincristine and prednisolone for both her AML and NHL.
  • Asparagine synthetase (AS) activity in her AML blast cells was undetectable.
  • Complete remission (CR) of AML and NHL was achieved.
  • CR of the AML lasted for 18 months without further consolidation therapy.
  • We conclude that L-Asp can be an effective drug for the treatment of AML in which blasts are negative for AS.
  • [MeSH-major] Asparaginase / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Prednisolone / therapeutic use. Vincristine / therapeutic use

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  • [Copyright] 2009 S. Karger AG, Basel
  • (PMID = 19816010.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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12. Jurcic JG: Immunotherapy for acute myeloid leukemia. Curr Oncol Rep; 2005 Sep;7(5):339-46
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  • [Title] Immunotherapy for acute myeloid leukemia.
  • Although the humanized anti-CD33 antibody HuM195 has only modest activity against overt acute myeloid leukemia (AML), it can eliminate minimal residual disease in acute promyelocytic leukemia.
  • Targeted chemotherapy with the anti-CD33- calicheamicin construct gemtuzumab ozogamicin has produced remissions in relapsed AML and appears promising when used in combination with standard chemotherapy for newly diagnosed AML.
  • T-cell recognition of peptide antigens presented on the cell surface in combination with major histocompatibility complex antigen provides another potentially promising approach for the treatment of AML.
  • [MeSH-major] Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / chemistry. Antigens, CD45 / chemistry. Antigens, Differentiation, Myelomonocytic / chemistry. Bismuth / chemistry. Cell Adhesion Molecules / chemistry. Humans. Immunotoxins / chemistry. Radioimmunotherapy. Radioisotopes / chemistry. Recurrence. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. T-Lymphocytes / metabolism

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  • (PMID = 16091194.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Immunotoxins; 0 / Radioisotopes; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; EC 3.1.3.48 / Antigens, CD45; U015TT5I8H / Bismuth
  • [Number-of-references] 51
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13. Zeleznikova T, Stevulova L, Kovarikova A, Babusikova O: Increased myeloid precursors in regenerating bone marrow; implications for detection of minimal residual disease in acute myeloid leukemia. Neoplasma; 2007;54(6):471-7
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  • [Title] Increased myeloid precursors in regenerating bone marrow; implications for detection of minimal residual disease in acute myeloid leukemia.
  • Presented study is focused on exact immunophenotypic definition of myeloid precursors and their following stages in regenerating bone marrow during treatment of ALL/AML for correct interpretation of the immunophenotype results and proper distinction from minimal residual disease (MRD) by multiparameter flow cytometry.
  • This study includes bone marrow samples from 36 controls, 27 patients with AML, 39 patients with B-ALL undergoing therapy who remained in complete remission after treatment and also 30 B-ALL patients one year after the end of therapy.
  • Myeloid precursors were significantly increased after cessation of induction therapy cycle of B-ALL (1.27+/-2.04%, p=0.0064) and also AML patients (0.87+/-0.77%, p=0.001), but also during follow-up of B-ALL patients (1.42+/-2.36%, p=0.0001) when compared with non-treated controls (0.38+/-0.29%).
  • Some cases where their frequencies achieved up to 12% reflect the massive regeneration of myeloid lineage in bone marrow after chemotherapy cycles.
  • Especially in these cases accurate interpretation of such a high frequency of immature myeloid cells as myeloid precursors was very important to exclude incoming relapse or secondary leukemia.
  • The myeloid precursors represented by CD34+ in regenerating bone marrow expressed CD45 (94.8+/-5.5%), CD117 (38.3+/-26.2%), CD38 (91.4+/-5.7%), HLA-DR (90.6+/-7.6%), CD13 (73.0+/-20.8%) and CD33 (85.2+/-15.6%), while CD90 (2.7+/-2.5%), CD133 (10.0+/-8.2%) and T or B lymphocyte markers were negative.
  • In addition, according to expression of these markers three different subsets of myeloid precursor cells were identified in regenerating bone marrow samples: CD34+ CD117- HLA-DR+, CD34+ CD117+ HLA-DR+ and CD34- CD117+ HLA-DR-/+ without aberrant marker expression.
  • In conclusion for the correct discrimination of MRD in acute leukemia it is indispensable to define the range of normality in myeloid differentiation by extensive studies of bone marrows not only from healthy donors but also from regenerating bone marrow of patients undergoing therapy.
  • [MeSH-major] Bone Marrow Cells / cytology. Hematopoietic Stem Cells / cytology. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 17949229.001).
  • [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 / Antineoplastic Agents
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14. Zhao Y, Yu L, Wang QS, Li HH, Bo J, Wang SH, Jin HJ, Lou FD: [Id4 gene methylation for detection of minimal residual disease in acute leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):298-301
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  • [Title] [Id4 gene methylation for detection of minimal residual disease in acute leukemia].
  • OBJECTIVE: To evaluate the possibility of Id4 gene promoter methylation as a biomarker for minimal residual disease (MRD) detection in acute leukemia.
  • METHODS: Methylation specific-PCR technique was used to detect Id4 gene methylation in samples with different percentages of leukemia cells from leukemia cell line and bone marrows from leukemia patients in complete remission (CR).
  • RESULTS: Id4 gene methylation could be detected in samples containing 1% or lower leukemia cells.
  • Frequency of Id4 gene methylation in acute lymphoblastic leukemia (ALL) patients in CR was 64.3% being higher than that in acute myeloid leukemia (AML) patients in CR.
  • In 8 AML patients with Id4 gene methylation, 5 relapsed in 12 months, while two relapsed in 20 AML patients with Id4 gene methylation.
  • CONCLUSION: Id4 gene promoter methylation is a candidate of biomarker for MRD detection in acute leukemias.
  • [MeSH-major] DNA Methylation. Inhibitor of Differentiation Proteins / genetics. Leukemia / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Line. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. Promoter Regions, Genetic / genetics. Young Adult

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  • (PMID = 16875575.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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15. Popov AM, Verzhbitskaia TIu, Tsaur GA, Shorikov EV, Savel'ev LI, Tsvirenko SV, Fechina LG: [Minimal residual disease monitoring by flow cytometry in children with acute lymphoblastic leukemia]. Klin Lab Diagn; 2010 Aug;(8):36-41
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  • [Title] [Minimal residual disease monitoring by flow cytometry in children with acute lymphoblastic leukemia].
  • A combination of these cells is given the name minimal residual disease (MRD).
  • This technique is based on the detection of the so-called leukemia-associated immunophenotype (LAIP), i.e., a tumor-specific combination of the expression of membrane and cytoplasmic markers.
  • Flow cytometry may be successfully used to monitor MRD in 90-95% cases of acute lymphoblastic leukemia (ALL) and in 80-85% of patients with acute myelocytic leukemia.
  • The monoclonal antibody panels recommended by different groups of investigators for MRD monitoring in B-lineage ALL include antibodies to the pan-B-cell antigen CD19, markers of different stages of differentiation of B-lineage precursors of CD10, CD34, and CD20 and leukemia-associated markers different for each panel, such as CD22, CD38, CD58, CD45, TdT, CD13, CD33.
  • The hyperexpression of CD10, CD34, CD19, TdT, the decreased expression of CD38, CD45, CD22, CD19, the simultaneous expression of markers of different stages of differentiation of B lymphocytes, such as CD10 and CD20, and the lymphoblast coexpression of myeloid markers of CD13, CD33, CDS15 are the most frequently described immunophenotype aberrations in B-lineage ALL.
  • The selection of combinations of markers for MRD monitoring in children with T-ALL is based on the simultaneous expression of combinations of the antigens characteristic for early stages of differentiation of normal T lymphocytes, namely TdT and cytoplasmic CD3.
  • [MeSH-major] Flow Cytometry / methods. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 20886718.001).
  • [ISSN] 0869-2084
  • [Journal-full-title] Klinicheskaia laboratornaia diagnostika
  • [ISO-abbreviation] Klin. Lab. Diagn.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD
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16. Amadori S, Stasi R: Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia. Curr Opin Hematol; 2008 Mar;15(2):95-100
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  • [Title] Integration of monoclonal antibodies and immunoconjugates into the treatment of acute myeloid leukemia.
  • PURPOSE OF REVIEW: This review addresses use of monoclonal antibodies and immunoconjugates to treat acute myeloid leukemia.
  • RECENT FINDINGS: Monoclonal antibodies used in acute myeloid leukemia have been directed against the antigens CD33, CD45, and CD66.
  • Unconjugated monoclonal antibodies such as lintuzumab have modest activity against overt acute myeloid leukemia but can eliminate minimal residual disease in acute promyelocytic leukemia.
  • Gemtuzumab ozogamicin has shown activity both singly, particularly in acute promyelocytic leukemia, and combined with conventional cytotoxic chemotherapy.
  • Antibodies reactive with CD66 have been used to deliver targeted radiation to hematopoietic tissues in patients with advanced myeloid malignancies.
  • SUMMARY: Both unlabeled monoclonal antibodies and immunoconjugates appear to have a limited role if used as single agents to treat acute myeloid leukemia.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunoconjugates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Antigens, Differentiation, Myelomonocytic / drug effects. Antigens, Differentiation, Myelomonocytic / immunology. Clinical Trials as Topic. Humans

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  • (PMID = 18300754.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Immunoconjugates
  • [Number-of-references] 49
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17. Fajtova M, Babusikova O: Immunophenotype characterization of hematopoietic stem cells, progenitor cells restricted to myeloid lineage and their leukemia counterparts. Neoplasma; 2010;57(5):392-400
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  • [Title] Immunophenotype characterization of hematopoietic stem cells, progenitor cells restricted to myeloid lineage and their leukemia counterparts.
  • The aim of this review is to evaluate recent immunophenotype knowledge of hematopoietic stem cells and their restricted progenies committed to myeloid lineage - common myeloid progenitors, myelo-monocytic progenitors, megakaryo-erythroid progenitors and granulocyte progenitors up to mature neutrophil granulocyte.
  • This study evaluates also recent knowledge of immunophenotype of leukemic stem cells and their more differentiated progeny committed to myeloid lineage - acute myeloid leukemia blast cells with regard to their phenotypic similarity to normal stem and granulocyte committed progenitor cells.
  • Improved knowledge of normal stem and progenitor cells phenotypes, identifying new leukemia-specific markers, searching for aberrant marker expression and evaluation of aberrant intensity or combination of various marker expressions is important for distinguishing normal cells from their malignant counterpart in view of the diagnostics of leukemias or follow-up of minimal residual disease.
  • [MeSH-major] Hematopoietic Stem Cells / immunology. Leukemia / immunology. Myeloid Cells / immunology. Neoplastic Stem Cells / immunology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Lineage. Humans. Immunophenotyping

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  • (PMID = 20568892.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Slovakia
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18. Thol F, Ganser A: Molecular pathogenesis of acute myeloid leukemia: a diverse disease with new perspectives. Front Med China; 2010 Dec;4(4):356-62
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  • [Title] Molecular pathogenesis of acute myeloid leukemia: a diverse disease with new perspectives.
  • Acute myeloid leukemia (AML) is a very heterogeneous neoplasm of the hematopoietic stem cell.
  • Despite important achievements in the treatment of AML, the long term survival of patients with the disease remains poor.
  • Understanding the pathogenesis of AML better is crucial for finding new treatment approaches.
  • During AML development, hematopoietic precursor cells undergo clonal transformation in a multistep process through acquisition of chromosomal rearrangements and/or different gene mutations.
  • Over recent years, novel gene mutations have been found in patients with AML.
  • These mutations can be divided into two important categories, class I mutations that confer a proliferation advantage and class II mutations that inhibit myeloid differentiation.
  • Screening for some of these mutations is now part of the initial diagnostic workup in newly diagnosed AML patients.
  • Information about the mutation status of specific genes is useful for risk-stratification, minimal residual disease (MRD) monitoring and increasingly also for targeted therapy, especially for patients with cytogenetically normal AML (CN-AML).
  • This article reviews some of the most common mutations in CN-AML and gives a perspective of the translation of these discoveries from bench to bedside.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 21125345.001).
  • [ISSN] 1673-7458
  • [Journal-full-title] Frontiers of medicine in China
  • [ISO-abbreviation] Front Med China
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
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19. Grimwade D, Mistry AR, Solomon E, Guidez F: Acute promyelocytic leukemia: a paradigm for differentiation therapy. Cancer Treat Res; 2010;145:219-35
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  • [Title] Acute promyelocytic leukemia: a paradigm for differentiation therapy.
  • Acute promyelocytic leukemia(APL) is characterized by the t(15;17) chromosomal translocation leading to the formation of the PML-RARalpha oncoprotein.
  • This leukemia has attracted considerable interest in recent years, being the first in which therapies that specifically target the underlying molecular lesion, i.e., all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), leading to induction of differentiation and apoptosis have been successfully used in clinical practice.
  • The advent of ATRA therapy has transformed APL from being a disease with a poor outlook to one of the most prognostically favorable subsets of acute myeloid leukemia.
  • This raises the possibility that some patients can be cured using differentiation therapies alone, without the need for chemotherapy, thereby potentially reducing treatment-related toxicity.
  • It is clear that the success of such an approach is critically dependent upon molecular diagnostics and monitoring for minimal residual disease (MRD) to distinguish those patients who can potentially be cured with differentiation therapy from those requiring additional myelosuppressive agents.
  • This represents an exciting new phase in the treatment of acute leukemia, highlighting the potential of molecularly targeted and MRD-directed therapies to achieve an individualized approach to patient management.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Cell Differentiation / drug effects. Dyspnea / chemically induced. Fever / chemically induced. Gene Expression Regulation, Leukemic. Humans. Leukocytosis / chemically induced. Models, Biological. Neoplasm, Residual. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Transcription, Genetic. Treatment Outcome

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  • (PMID = 20306254.001).
  • [ISSN] 0927-3042
  • [Journal-full-title] Cancer treatment and research
  • [ISO-abbreviation] Cancer Treat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 77
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20. Rausei-Mills V, Chang KL, Gaal KK, Weiss LM, Huang Q: Aberrant expression of CD7 in myeloblasts is highly associated with de novo acute myeloid leukemias with FLT3/ITD mutation. Am J Clin Pathol; 2008 Apr;129(4):624-9
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  • [Title] Aberrant expression of CD7 in myeloblasts is highly associated with de novo acute myeloid leukemias with FLT3/ITD mutation.
  • Acute myeloid leukemia (AML) with normal cytogenetics represents approximately 40% to 50% of de novo AML.
  • This heterogeneous AML subgroup constitutes the single largest cytogenetic group with an intermediate prognosis.
  • Previous studies have suggested that the Fms-like tyrosine kinase-3 internal tandem duplication (FLT3/ITD) mutation-positive de novo AML may represent a distinctive subgroup of AML.
  • We analyzed the clinical and pathologic features of 15 cases of de novo AML with normal cytogenetics and with the FLT3/ITD mutation.
  • In comparison with patients with AML without the FLT3/ITD mutation, patients with FLT3/ITD+ AML are relatively younger, more often have marked peripheral leukocytosis with a higher number of circulating blasts at initial examination, more often have minimal differentiation morphologic features, more frequently have abnormal CD7 coexpression, and have poorer outcome.
  • Close association of aberrant CD7 expression and FLT3/ITD mutation in the myeloblasts of FLT3/ITD+ AML suggests that FLT3/ITD- mediated leukemic transformation occurs in the more early stage of myeloid progenitor cells.
  • [MeSH-major] Antigens, CD7 / metabolism. Granulocyte Precursor Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [CommentIn] Am J Clin Pathol. 2008 Oct;130(4):644; author reply 645 [18825844.001]
  • (PMID = 18343790.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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21. Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama JW, Orfao A, European Working Group of Clinical Cell Analysis: Discriminant function analysis as decision support system for the diagnosis of acute leukemia with a minimal four color screening panel and multiparameter flow cytometry immunophenotyping. Leukemia; 2007 Jun;21(6):1204-11
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  • [Title] Discriminant function analysis as decision support system for the diagnosis of acute leukemia with a minimal four color screening panel and multiparameter flow cytometry immunophenotyping.
  • Despite several recommendations for standardization of multiparameter flow cytometry (MFC) the number, specificity and combinations of reagents used by diagnostic laboratories for the diagnosis and classification of acute leukemias (AL) are still very diverse.
  • We determined the potential value of a minimal four-color combination panel of 13 monoclonal antibodies (mAbs) with a CD45/sideward light scatter-gating strategy for a standardized MFC immunophenotyping of the clinically most relevant subgroups of AL.
  • Bone marrow samples from 155 patients with acute myeloid leukemia (AML, n=79), B-cell precursor acute lymphoblastic leukemia (BCP-ALL, n=29), T-cell precursor acute lymphoblastic leukemia (T-ALL, n=12) and normal bone marrow donors (NBMD, n=35) were analyzed.
  • A knowledge-based learning algorithm was generated by comparing the results of the minimal panel with the actual diagnosis, using discriminative function analysis.
  • Correct classification of the test sample according to lineage, that is, BCP-ALL, T-ALL, AML and differentiation of NBMD was achieved in 97.2% of all cases with only six of the originally applied 13 mAbs of the panel.
  • [MeSH-major] Diagnosis, Computer-Assisted / methods. Flow Cytometry / methods. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Algorithms. Antibodies, Monoclonal. Bone Marrow / pathology. Cell Lineage. Color. Humans. Immunophenotyping. Reference Standards

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  • (PMID = 17410192.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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22. Rahmani M, Mayo M, Dash R, Sokhi UK, Dmitriev IP, Sarkar D, Dent P, Curiel DT, Fisher PB, Grant S: Melanoma differentiation associated gene-7/interleukin-24 potently induces apoptosis in human myeloid leukemia cells through a process regulated by endoplasmic reticulum stress. Mol Pharmacol; 2010 Dec;78(6):1096-104
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  • [Title] Melanoma differentiation associated gene-7/interleukin-24 potently induces apoptosis in human myeloid leukemia cells through a process regulated by endoplasmic reticulum stress.
  • Melanoma differentiation associated gene-7 (mda-7)/interleukin-24 (IL-24), a member of the IL-10 cytokine gene family, preferentially induces cell death in neoplastic epithelial cells types while sparing their normal counterparts.
  • The effects of mda-7/IL-24 in acute myeloid leukemia (AML) cells have not been extensively characterized.
  • Treatment with recombinant GST-MDA-7/IL-24 potently induced apoptosis in diverse myeloid leukemia cell types including U937, HL60, MV4-11, EOL-1, and MLL/ENL cells.
  • MDA-7/IL-24 also markedly induced apoptosis in and suppressed the colony-forming capacity of primary AML blasts but exerted minimal toxicity toward normal CD34(+) hematopoietic progenitor cells.
  • MDA-7/IL-24 lethality was associated with pronounced endoplasmic reticulum (ER) stress induction in leukemia cell lines and primary AML blasts, manifested by the accumulation of growth arrest and DNA damage-inducible protein 34 (GADD34), 78-kDa glucose-regulated protein (GRP78)/BiP, inositol-requiring enzyme 1α (IRE1α), and eukaryotic initiation factor 2α phosphorylation.
  • Ectopic Mcl-1 expression or shRNA knockdown of Bim or Noxa significantly attenuated MDA-7/IL-24-mediated leukemia cell death.
  • Together, these findings indicate that MDA-7/IL-24 potently induces apoptosis in human myeloid leukemia cells through a process regulated by ER stress induction, Mcl-1 down-regulation, and Bim and Noxa up-regulation.
  • They also suggest that MDA-7/IL-24 warrants further investigation in myeloid leukemia.

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  • (PMID = 20858700.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01-CA104177; United States / NCI NIH HHS / CA / R01 CA93738-05; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / R01 CA141703; United States / NCI NIH HHS / CA / P01 CA104177; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / R01 CA150214
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukins; 0 / interleukin-24
  • [Other-IDs] NLM/ PMC2993469
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23. Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS: Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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  • [Title] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
  • PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.
  • Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with AML.
  • Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.
  • Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+ AML.
  • EXPERIMENTAL DESIGN: Eight patients with CD33+ AML received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.
  • CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk AML is feasible and well tolerated with minimal toxicity.
  • The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+ AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods

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  • (PMID = 16203817.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL07968
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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24. Chen P, Wang J, Hope K, Jin L, Dick J, Cameron R, Brandwein J, Minden M, Reilly RM: Nuclear localizing sequences promote nuclear translocation and enhance the radiotoxicity of the anti-CD33 monoclonal antibody HuM195 labeled with 111In in human myeloid leukemia cells. J Nucl Med; 2006 May;47(5):827-36
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  • [Title] Nuclear localizing sequences promote nuclear translocation and enhance the radiotoxicity of the anti-CD33 monoclonal antibody HuM195 labeled with 111In in human myeloid leukemia cells.
  • Our objective was to evaluate the toxicity of the anti-CD33 monoclonal antibody HuM195 modified with peptides (CGYGPKKKRKVGG) harboring the nuclear localizing sequence (NLS; underlined) of simian virus 40 large T antigen and labeled with (111)In against acute myeloid leukemia (AML) cells.
  • The immunoreactivity of NLS-HuM195 was evaluated by its ability to displace the binding of (111)In-HuM195 to HL-60 leukemia cells.
  • The antiproliferative effects of (111)In-NLS-HuM195 and (111)In-HuM195 on HL-60, U937, or K562 cells with high, intermediate, or minimal CD33 expression, respectively, were studied.
  • The survival of HL-60 cells or patient AML specimens treated with (111)In-NLS-HuM195 or (111)In-HuM195 was studied.
  • The surviving fraction decreased >2-fold in 7 of 9 AML specimens treated with an excess of (111)In-NLS-HuM195 and >10-fold in 2 of these specimens.
  • There was no morphologic damage to the liver or kidneys.
  • CONCLUSION: We conclude that NLS-peptides routed (111)In-HuM195 to the nucleus of AML cells, where the emitted Auger electrons were lethal. (111)In-NLS-HuM195 is a promising targeted radiotherapeutic agent for AML.
  • [MeSH-major] Active Transport, Cell Nucleus. Antibodies, Monoclonal / chemistry. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Indium Radioisotopes / therapeutic use. Leukemia, Myeloid / radionuclide imaging. Leukemia, Myeloid / radiotherapy. Nuclear Localization Signals

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  • [CommentIn] J Nucl Med. 2006 May;47(5):738-9 [16644741.001]
  • (PMID = 16644753.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Indium Radioisotopes; 0 / Nuclear Localization Signals; 0 / Peptides; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / monoclonal antibody M195
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25. Wong KF, Lam SC, Leung JN: Isochromosome 7q in Down syndrome. Cancer Genet Cytogenet; 2006 Jan 15;164(2):152-4
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  • Isochromosome 7q is not an uncommon chromosomal abnormality.
  • A notable example is its association with t(4;11)(q21;q23) in acute lymphoblastic leukemia.
  • It has rarely been described in myelodysplastic syndrome and acute myeloid leukemia.
  • We report the occurrence of i(7q) as the primary abnormality in a 2-year-old boy with Down syndrome and minimally differentiated acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 7. Down Syndrome / genetics. Isochromosomes. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16434320.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. Lo-Coco F, Ammatuna E, Montesinos P, Sanz MA: Acute promyelocytic leukemia: recent advances in diagnosis and management. Semin Oncol; 2008 Aug;35(4):401-9
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  • [Title] Acute promyelocytic leukemia: recent advances in diagnosis and management.
  • Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia (AML) characterized by a specific genetic alteration, affecting the retinoic acid receptor-alpha (RARalpha), and leading to a blockage in the differentiation of the granulocytic cells.
  • The body of available biological information on APL establishes this leukemia as a unique entity that has to be promptly recognized and clearly distinguished from all other acute leukemias, especially in light of its striking response to treatment with anthracyclines and differentiating agents such as all-trans retinoic acid (ATRA) or arsenic trioxide (ATO).
  • Current state-of-the-art treatments, which include simultaneous administration of ATRA and anthracycline-based chemotherapy for induction and consolidation, as well as ATRA-based maintenance, have dramatically transformed APL into the most curable acute leukemia in adults, with approximately 80% of long-term survivors.
  • We also highlight other aspects that can be crucial for the outcome of individual patients, including supportive care, recognition and treatment of life-threatening complications, management of ATRA- and ATO-associated adverse events, and the role of minimal residual disease (MRD) monitoring.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / therapy

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  • (PMID = 18692690.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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27. Shin S, Kahng J, Kim M, Lim J, Kim Y, Han K: [Distribution of antigenic aberration in the bone marrow of acute leukemia in complete remission]. Korean J Lab Med; 2008 Feb;28(1):1-7
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  • [Title] [Distribution of antigenic aberration in the bone marrow of acute leukemia in complete remission].
  • BACKGROUND: The aberrant, leukemia-associated antigen expression patterns allow us to discriminate leukemic blasts from normal precursor cells.
  • Our major goal was to determine a guideline for the detection of minimal residual disease using CD20+/CD34+ and myeloid Ag+/CD19+ combination in the bone marrow of acute leukemia in complete remission (CR) after chemotherapy.
  • METHODS: Bone marrow samples from 117 patients with acute leukemia in complete remission after chemotherapy and from 22 healthy controls were immunophenotyped by triple staining and measured by flow cytometry.
  • % (0.8plusmn;0.82%, P=0.000) in CD20+/CD34+ B-lineage ALL CR (N=31), from 0.03% to 4.2% (0.7plusmn;0.83%, P=0.000) in CD20-/CD34- B-lineage ALL CR (N=66), from 0.1% to 0.96% (0.45plusmn;0.32%, P=0.016) in T-ALL CR (N=10), and from 0.02% to 0.48% (0.18plusmn;0.15%, P=0.776) in AML CR (N=10).
  • The CD13,33+/CD19+ cells in R1 gate ranged from 0% to 2.69% (0.37plusmn;0.48%, P<0.001) in CD13,33+/CD19+ B-lineage ALL CR (N=31), from 0% to 1.8% (0.31plusmn;0.28%, P<0.001) in CD13,33-/CD19+B-lineage ALL CR (N=65), from 0.02% to 0.64% (0.29plusmn;0.22%, P=0.071) in T-ALL CR (N=9), and from 0% to 0.17% (0.07plusmn;0.09%, P=0.341) in AML CR (N=3).
  • CONCLUSIONS: Using an immunophenotypic method for the detection of early relapse or minimal residual disease of B-lineage ALL bone marrow in CR after chemotherapy, different cutoff values should be applied according to antigen combination and gating.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow Cells / classification. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD19 / metabolism. Antigens, CD20 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / analysis. Antigens, Differentiation, Myelomonocytic / metabolism. Biomarkers, Tumor / immunology. Flow Cytometry. Hematopoietic Stem Cells / classification. Hematopoietic Stem Cells / metabolism. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Neoplasm, Residual. Remission Induction

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  • (PMID = 18309249.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor
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28. Tallman MS: The expanding role of arsenic in acute promyelocytic leukemia. Semin Hematol; 2008 Jul;45(3 Suppl 2):S25-9
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  • [Title] The expanding role of arsenic in acute promyelocytic leukemia.
  • Ten percent to 15% of adults in the United States with acute myeloid leukemia (AML) are diagnosed with acute promyelocytic leukemia (APL) each year, which amounts to approximately 1,200 newly diagnosed patients.
  • In almost all APL patients, the retinoic acid receptor-alpha (RARalpha) gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, denoted as t(15;17)(q22;q12).
  • Identification of this fusion transcript is important for both diagnosis and for detection of minimal residual disease.
  • All-trans retinoic acid (ATRA) causes cells to differentiate and arsenic trioxide (ATO) induces both differentiation and apoptosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18760708.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 32
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29. Riedt T, Ebinger M, Salih HR, Tomiuk J, Handgretinger R, Kanz L, Grünebach F, Lengerke C: Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia. Blood; 2009 Apr 23;113(17):4049-51
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  • [Title] Aberrant expression of the homeobox gene CDX2 in pediatric acute lymphoblastic leukemia.
  • Previously, we reported that the murine homologues (Cdx1, Cdx2, and Cdx4) affect formation and differentiation of embryonic stem cell (ESC)-derived hematopoietic progenitor cells.
  • Consistent with the notion that embryonic pathways can reactivate during adult oncogenesis, recent studies suggest involvement of CDX2 in human acute myeloid leukemia (AML).
  • Analysis of a cohort of 37 childhood acute lymphoblastic leukemia (ALL) patients treated in our hospital reveals that high CDX2 expression levels at diagnosis correlate with persistence of minimal residual disease (MRD) during the course of treatment.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Homeodomain Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 19218548.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
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30. Sidhom I, Shaaban K, Soliman S, Ezzat S, El-Anwar W, Hamdy N, Yassin D, Salem S, Hassanein H, Mansour MT: Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia. J Egypt Natl Canc Inst; 2008 Jun;20(2):111-20
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  • [Title] Clinical significance of immunophenotypic markers in pediatric T-cell acute lymphoblastic leukemia.
  • AIM: To investigate the prevalence of the expression of CD34, CD10 and myeloid associated antigens (CD13/ CD33) in childhood T-ALL and to relate their presence to initial clinical and biologic features and early response to therapy.
  • Immunophenotypic markers and minimal residual disease (MRD) were studied by five-color flow cytometry.
  • No significant association was encountered between CD34, CD10 or myeloid antigen positivity and the presenting clinical features as age, sex, TLC and CNS leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Neoplasm, Residual / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Antigens, CD13 / metabolism. Antigens, CD34 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Differentiation. Child. Child, Preschool. Egypt. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Neprilysin / metabolism. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 20029466.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13; EC 3.4.24.11 / Neprilysin
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31. Neudenberger J, Hotfilder M, Rosemann A, Langebrake C, Reinhardt D, Pieters R, Schrauder A, Schrappe M, Röttgers S, Harbott J, Vormoor J: Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11). Br J Haematol; 2006 May;133(3):337-44
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  • [Title] Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11).
  • Therefore, these leukaemic stem cells should be the target cells for therapy and for minimal residual disease (MRD) detection.
  • Six acute myeloid leukaemia (AML)/abn(11q23) and three acute lymphoblastic leukaemia (ALL)/t(4;11) samples were analysed by four-colour flow cytometry for NG2 expression on primitive cell populations.
  • Candidate leukaemic cell populations were defined by the antigen profiles CD34+CD38- in AML and CD34+CD19-CD117+ in ALL.
  • Instead, a correlation between the expression of the myeloid differentiation marker CD33 and increasing levels of NG2 on maturing cells could be demonstrated.
  • Thus, NG2 appears to be upregulated with differentiation and not to be expressed on primitive disease-maintaining cells.
  • [MeSH-major] Antigens / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Neoplastic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteoglycans / metabolism
  • [MeSH-minor] Acute Disease. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Flow Cytometry / methods. Humans. Neoplasm Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Sialic Acid Binding Ig-like Lectin 3. Translocation, Genetic

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  • (PMID = 16643437.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / chondroitin sulfate proteoglycan 4
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32. Song JH, Kim HJ, Lee CH, Kim SJ, Hwang SY, Kim TS: Identification of gene expression signatures for molecular classification in human leukemia cells. Int J Oncol; 2006 Jul;29(1):57-64
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  • [Title] Identification of gene expression signatures for molecular classification in human leukemia cells.
  • Although the methods by which leukemia is classified have been improved for effective therapies, leukemia patients occasionally exhibit diverse, sometimes unpredictable, responses to treatment.
  • Consequently, these patients also evidence individually different clinical courses when administered with anti-leukemia drugs.
  • In order to find new, more precise molecular markers for leukemia classification, we have analyzed the gene expression profiles from 65 diagnostic bone marrow specimens of adult patients with AML, ALL, CML or CLL by using high-throughput DNA microarrays harboring approximately 8,300 unique human genes or expression sequence tags.
  • In the present study, we identified a group of leukemia-specific genes, which manifest gene expression profiles distinctly representative of normal bone marrow samples, as determined by a significance analysis of microarray (SAM) and GeneSpring 6.1 programs.
  • We also determined the minimal number of genes showing a difference between acute and chronic leukemia patient groups.
  • Furthermore, the unsupervised cluster analysis revealed a gene subset which can be used to distinguish between AML, ALL, CML and CLL patient groups, based on expression signatures.
  • Our results may provide a novel set of molecular criteria for the classification of leukemia patients, and may also facilitate effects to discovery new targets, allowing for more effective treatment of leukemia patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. Bone Marrow Cells / metabolism. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, Differentiation, T-Lymphocyte / genetics. Antigens, Differentiation, T-Lymphocyte / metabolism. Biopsy. Cluster Analysis. Female. Genetic Markers. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Lectins, C-Type. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16773185.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / CD69 antigen; 0 / Genetic Markers; 0 / HHEX protein, human; 0 / Homeodomain Proteins; 0 / Lectins, C-Type; 0 / Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human
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33. Lee J, Lu X, Shin ES, Kern WF, Mulvihill JJ, Li S: A novel subtelomeric translocation t(5;9) and a deletion of the RB1 gene in a patient with acute myeloid leukemia (AML-M0). Cancer Genet Cytogenet; 2008 Feb;181(1):36-9
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  • [Title] A novel subtelomeric translocation t(5;9) and a deletion of the RB1 gene in a patient with acute myeloid leukemia (AML-M0).
  • No chromosomal rearrangements have been identified as specifically associated with minimally differentiated acute myeloid leukemia (AML-M0).
  • Several research groups studied the cytogenetic features of AML-M0 and found that as much as 81% of patients with AML-M0 had chromosomal rearrangements; primarily -5/5q- and/or -7/7q- deletions or translocations involving 12p.
  • A patient, who was diagnosed with AML-M0 eighteen months ago, was referred for cytogenetic evaluation for possible AML relapse.
  • To rule out the possibility that these chromosomal changes were related to the relapse of AML in this case, we repeated the same FISH test on the specimen at initial diagnosis before any treatment.
  • To our knowledge, this is the first case reported with subtelomeric t(5;9)(q35.3;q34.3) and the deletion of the RB1 gene in a patient with AML-M0.
  • Whether the t(5;9) combined with the deletion of the RB1 gene plays an important role in the development of AML-M0 warrants further investigation.
  • [MeSH-major] Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / genetics. Retinoblastoma Protein / genetics. Telomere / genetics. Translocation, Genetic


34. Tsimberidou AM, Giles FJ, Estey E, O'Brien S, Keating MJ, Kantarjian HM: The role of gemtuzumab ozogamicin in acute leukaemia therapy. Br J Haematol; 2006 Feb;132(4):398-409
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  • [Title] The role of gemtuzumab ozogamicin in acute leukaemia therapy.
  • Gemtuzumab ozogamicin (GO) is an immunoconjugate that binds to CD33 on the surface of acute myeloid leukaemia (AML) blasts and, after internalisation, releases a cytotoxic drug, calicheamicin.
  • GO is approved by the US Food and Drug Administration for the treatment of CD33-positive AML at first relapse in patients 60 years and older who are not candidates for other cytotoxic therapy.
  • GO is probably most active in acute promyelocytic leukaemia (APL).
  • It is used for induction regimens in high-risk APL and for the elimination of minimal residual APL.
  • Case reports suggest that GO also has activity in CD33-positive acute lymphoblastic leukaemia.
  • In conclusion, single agent GO can induce responses in patients with CD33-positive AML in first recurrence.
  • Ongoing clinical trials may better define the role of GO combinations, particularly in untreated AML.
  • [MeSH-major] Aminoglycosides / administration & dosage. Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / administration & dosage. Antibodies, Monoclonal / therapeutic use. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance. Enediynes. Humans. Protein Binding. Randomized Controlled Trials as Topic. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16412015.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 82
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35. Sholl LM, Longtine J: Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms. Curr Protoc Hum Genet; 2010 Oct;Chapter 10:Unit 10.4
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  • [Title] Molecular analysis of gene rearrangements and mutations in acute leukemias and myeloproliferative neoplasms.
  • A large subset of acute leukemias and other myeloproliferative neoplasms contain specific genetic alterations, many of which are associated with unique clinical and pathologic features.
  • These alterations include chromosomal translocations leading to oncogenic fusion genes, as well as mutations leading to aberrant activation of a variety of proteins critical to hematopoietic progenitor cell proliferation and differentiation.
  • Molecular analysis is central to diagnosis and clinical management of leukemias, permitting genetic confirmation of a clinical and histologic impression, providing prognostic and predictive information, and facilitating detection of minimal residual disease.
  • This unit will outline approaches to the molecular diagnosis of the most frequent and clinically relevant genetic alterations in acute leukemias and myeloproliferative neoplasms.

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  • (PMID = 20891029.001).
  • [ISSN] 1934-8258
  • [Journal-full-title] Current protocols in human genetics
  • [ISO-abbreviation] Curr Protoc Hum Genet
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Candoni A, Martinelli G, Toffoletti E, Chiarvesio A, Tiribelli M, Malagola M, Piccaluga PP, Michelutti A, Simeone E, Damiani D, Russo D, Fanin R: Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years. Leuk Res; 2008 Dec;32(12):1800-8
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  • [Title] Gemtuzumab-ozogamicin in combination with fludarabine, cytarabine, idarubicin (FLAI-GO) as induction therapy in CD33-positive AML patients younger than 65 years.
  • INTRODUCTION: The addition of gemtuzumab-ozogamicin (GO) to an induction regimen including synergistic drugs, such as intermediate dose of cytarabine (Ara-C), idarubicin and fludarabine (FLAI), could reduce treatment failure in acute myeloid leukemia (AML) patients.
  • Thirty consecutive AML patients were included.
  • Hematopoietic stem cell transplant (HSCT) was planned for all high risk AML patients in first complete remission (CR) after consolidation with intermediate doses of Ara-C and idarubicin (IDAC-IDA).
  • WT1 expression and cytogenetic (in positive cases) analyses were performed after induction to detect and follow minimal residual disease.
  • CONCLUSIONS: These preliminary results suggest that FLAI-GO is an effective and well tolerated induction regimen for CD33 positive AML patients younger than 65 years, with a high complete response rate, favourable safety profile, low DDI.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18621416.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Recombinant Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; PVI5M0M1GW / Filgrastim; ZRP63D75JW / Idarubicin
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37. Geletu M, Balkhi MY, Peer Zada AA, Christopeit M, Pulikkan JA, Trivedi AK, Tenen DG, Behre G: Target proteins of C/EBPalphap30 in AML: C/EBPalphap30 enhances sumoylation of C/EBPalphap42 via up-regulation of Ubc9. Blood; 2007 Nov 1;110(9):3301-9
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  • [Title] Target proteins of C/EBPalphap30 in AML: C/EBPalphap30 enhances sumoylation of C/EBPalphap42 via up-regulation of Ubc9.
  • CCAAT/enhancer-binding protein alpha (C/EBPalpha) is a critical regulator for early myeloid differentiation.
  • Mutations in C/EBPalpha occur in 10% of patients with acute myeloid leukemia (AML), leading to the expression of a 30-kDa dominant-negative isoform (C/EBPalphap30).
  • We confirmed the increased expression of Ubc9 in patients with AML with C/EBPalphap30 mutations compared with other subtypes.
  • Furthermore, we show that Ubc9-mediated enhanced sumoylation of C/EBPalphap42 decreases the transactivation capacity on a minimal C/EBPalpha promoter.
  • Importantly, overexpression of C/EBPalphap30 in granulocyte colony-stimulating factor (G-CSF)-stimulated human CD34(+) cells leads to a differentiation block, which was overcome by the siRNA-mediated silencing of Ubc9.
  • In summary, our data indicate that Ubc9 is an important C/EBPalphap30 target through which C/EBPalphap30 enhances the sumoylation of C/EBPalphap42 to inhibit granulocytic differentiation.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / metabolism. CCAAT-Enhancer-Binding Proteins / physiology. Leukemia, Myeloid, Acute / genetics. Mutant Proteins / physiology. Protein Processing, Post-Translational / genetics. SUMO-1 Protein / metabolism. Ubiquitin-Conjugating Enzymes / genetics. Up-Regulation
  • [MeSH-minor] Cell Differentiation / genetics. Gene Expression Regulation, Leukemic. Gene Silencing. Genes, Dominant / physiology. Granulocytes / cytology. Humans. K562 Cells. Lysine / metabolism. Models, Biological. Protein Isoforms / genetics. Protein Isoforms / metabolism. Receptors, Estrogen / genetics. Transcriptional Activation

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  • (PMID = 17671234.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Mutant Proteins; 0 / Protein Isoforms; 0 / Receptors, Estrogen; 0 / SUMO-1 Protein; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes; EC 6.3.2.19 / ubiquitin-conjugating enzyme UBC9; K3Z4F929H6 / Lysine
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38. Zada AA, Pulikkan JA, Bararia D, Geletu M, Trivedi AK, Balkhi MY, Hiddemann WD, Tenen DG, Behre HM, Behre G: Proteomic discovery of Max as a novel interacting partner of C/EBPalpha: a Myc/Max/Mad link. Leukemia; 2006 Dec;20(12):2137-46

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  • The transcription factor CCAAT/enhancer binding protein a (C/EBPalpha) is important in the regulation of granulopoiesis and is disrupted in human acute myeloid leukemia.
  • Endogenous C/EBPalpha and Max, but not Myc and Max, colocalize in intranuclear structures during granulocytic differentiation of myeloid U937 cells.
  • Max enhanced the transactivation capacity of C/EBPalpha on a minimal promoter.
  • A chromatin immunoprecipitation assay revealed occupancy of the human C/EBPalpha promoter in vivo by Max and Myc under cellular settings and by C/EBPalpha and Max under retinoic acid induced granulocytic differentiation.
  • Interestingly, enforced expression of Max and C/EBPalpha results in granulocytic differentiation of the human hematopoietic CD34(+) cells, as evidenced by CD11b, CD15 and granulocyte colony-stimulating factor receptor expression.
  • Silencing of Max by short hairpin RNA in CD34(+) and U937 cells strongly reduced the differentiation-inducing potential of C/EBPalpha, indicating the importance of C/EBPalpha-Max in myeloid progenitor differentiation.
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Dimerization. Hematopoietic Stem Cells / cytology. Humans. Promoter Regions, Genetic. RNA, Small Interfering / pharmacology. Thymidine Kinase / genetics

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  • (PMID = 17082780.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / MAX protein, human; 0 / MXD1 protein, human; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Small Interfering; 0 / Repressor Proteins; EC 2.7.1.21 / Thymidine Kinase
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39. Corpora T, Roudaia L, Oo ZM, Chen W, Manuylova E, Cai X, Chen MJ, Cierpicki T, Speck NA, Bushweller JH: Structure of the AML1-ETO NHR3-PKA(RIIα) complex and its contribution to AML1-ETO activity. J Mol Biol; 2010 Sep 24;402(3):560-77
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  • AML1-ETO is the chimeric protein product of t(8;21) in acute myeloid leukemia.
  • This mutation did not disrupt AML1-ETO's ability to enhance the clonogenic capacity of primary mouse bone marrow cells or its ability to repress proliferation or granulocyte differentiation.
  • Introduction of the mutation into AML1-ETO had minimal impact on in vivo leukemogenesis.
  • Therefore, the NHR3-PKA(RIIα) protein interaction does not appear to significantly contribute to AML1-ETO's ability to induce leukemia.

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20708017.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 2KYG
  • [Grant] United States / NCI NIH HHS / CA / CA108056-05; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01 CA108056; United States / NCI NIH HHS / CA / R01 CA108056-05
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclic AMP-Dependent Protein Kinase RIIalpha Subunit; 0 / Oncogene Proteins, Fusion; 0 / PRKAR2A protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS229086; NLM/ PMC2945414
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40. Jurcic JG: Ab therapy of AML: native anti-CD33 Ab and drug conjugates. Cytotherapy; 2008;10(1):7-12
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  • [Title] Ab therapy of AML: native anti-CD33 Ab and drug conjugates.
  • While the humanized anti-CD33MAb lintuzumab has only modest single-agent activity against overt AML, it can eliminate minimal residual disease detectable by reverse transcription-PCR in acute promyelocytic leukemia.
  • Targeted chemotherapy with the anti−CD33−calicheamicin construct gemtuzumab ozogamicin has produced remissions in patients with relapsed AML and appears promising when used in combination with standard chemotherapy in the treatment of newly diagnosed AML.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD / therapeutic use. Antigens, Differentiation, Myelomonocytic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17917880.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 0 / lintuzumab
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41. Cruse JM, Lewis RE, Pierce S, Lam J, Tadros Y: Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias. Exp Mol Pathol; 2005 Aug;79(1):39-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias.
  • CD7 and CD56 expression at diagnosis has been associated with low remission rates and biological aggressiveness in a significant proportion of acute leukemias.
  • Among 46 patients with acute myeloid leukemia, we found CD7 expression in 15 cases (32.6%) and CD56 positivity in 10 patients (21.7%).
  • Six of these myeloid leukemia cases (13%) showed expression of both CD7 and CD56.
  • Among the 10 that were acute myeloblastic leukemia, 8 expressed CD7, 4 expressed CD56, and 4 were positive for CD79a.
  • Thus, these markers were expressed early in hemopoietic ontogeny in the lesser-differentiated acute myeloid leukemia subtypes, including FAB M0, M1, and M2.
  • Whereas CD7 and CD56 were each positive in 4 cases of acute myelomonocytic leukemia (FAB M4 subtype), there was no CD79a expression in the M4 cases.
  • CD7 is expressed by mature T cells, NK cells, and an immature myeloid cell subset.
  • By contrast, CD79a is a B cell marker that is assigned a high score of 2.0 in the differentiation of acute leukemias of ambiguous lineage in the WHO classification.
  • The aberrant expression of CD7, CD56, and CD79a, representing the capacity of these leukemias for trilineal expression of leukocyte differentiation antigens, portends a poor prognosis.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD56 / biosynthesis. Antigens, CD7 / biosynthesis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Receptors, Antigen, B-Cell / biosynthesis

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  • (PMID = 16005710.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Biomarkers, Tumor; 0 / CD79A protein, human; 0 / Receptors, Antigen, B-Cell
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42. Roberson JR, Onciu M, Pounds S, Rubnitz JE, Pui CH, Razzouk BI: Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):542-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.
  • BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.
  • PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).
  • Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.
  • RESULTS: Median MPO expression was higher in FAB M2 subtype than in other subtypes (P < 0.0001) and differed significantly across cytogenetic risk groups (P = 0.002) with highest MPO expression among those with favorable karyotypes.
  • The percentage of MPO-positive blasts was not significantly associated with the probability of complete remission (P = 0.97), event-free survival (P = 0.72), or survival (P = 0.76) in multivariate analyses that accounted for age, FAB subtype, presenting WBC count, cytogenetic and protocol treatment risk group.
  • CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.
  • [MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763467.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.11.1.7 / Peroxidase
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43. Schumann M, Kiewe P, Hartlieb S, Neumann M, Schilling A, Koch HC, Thiel E, Korfel A: Diffuse leukoencephalopathy and brain edema: unusual presentations of CNS relapse of acute myeloid leukemia. J Neuroimaging; 2010 Apr;20(2):198-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse leukoencephalopathy and brain edema: unusual presentations of CNS relapse of acute myeloid leukemia.
  • An isolated CNS relapse is rarely seen in acute myeloid leukemia.
  • With the one-year-old history of an initially successfully treated FAB-M0 acute myeloid leukemia (AML) in mind, a lumbar puncture was carried out that showed a vast number of myeloid blasts in the morphologic analysis of the cerebrospinal fluid.
  • In conjunction with normal findings in the peripheral blood-count with differential and the bone marrow examination a diagnosis of an isolated CNS relapse of the AML was made.
  • [MeSH-major] Brain Edema / diagnosis. Brain Edema / etiology. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / diagnosis. Leukoencephalopathies / diagnosis. Leukoencephalopathies / etiology. Magnetic Resonance Imaging


44. Gozzetti A, Crupi R, Tozzuoli D, Calabrese S, Bocchia M, Pirrotta MT, Raspadori D, Lauria F: Trisomy 13 in a patient with acute myeloid leukemia M0 and unusual durable remission. Cancer Genet Cytogenet; 2006 Jun;167(2):182
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  • [Title] Trisomy 13 in a patient with acute myeloid leukemia M0 and unusual durable remission.
  • [MeSH-major] Chromosomes, Human, Pair 13. Leukemia, Myeloid / genetics. Trisomy
  • [MeSH-minor] Acute Disease. Aged. Disease-Free Survival. Humans. Male. Remission Induction. Treatment Outcome

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  • (PMID = 16737922.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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