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17. Ho PA, Alonzo TA, Gerbing RB, Pollard J, Stirewalt DL, Hurwitz C, Heerema NA, Hirsch B, Raimondi SC, Lange B, Franklin JL, Radich JP, Meshinchi S: Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group. Blood; 2009 Jun 25;113(26):6558-66
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  • [Title] Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
  • CEBPA mutations have been associated with improved outcome in adult acute myeloid leukemia (AML).
  • We evaluated the prevalence and prognostic significance of CEBPA mutations in 847 children with AML treated on 3 consecutive pediatric trials.
  • CEBPA mutations were significantly more common in older patients, patients with FAB M1 or M2, and patients with normal karyotype.
  • As CEBPA mutations are associated with lower relapse rate and improved survival, CEBPA mutation analysis needs to be incorporated into initial screening for risk identification and therapy allocation at diagnosis.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Clinical Trials as Topic / statistics & numerical data. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Polymorphism, Genetic. Prevalence. Prognosis. Protein Structure, Tertiary. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19304957.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009351; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2943755
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18. Nikolaievs'kyĭ VV: [Distribution of Mycobacterium tuberculosis strains in the south of Ukraine based on genotyping data]. Mikrobiol Z; 2006 Sep-Oct;68(5):52-61
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  • Other epidemiological groups were represented by the family strains T1, LAM1, LAM4, LAM5, S and Haarlem.

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  • (PMID = 17388120.001).
  • [ISSN] 1028-0987
  • [Journal-full-title] Mikrobiolohichnyĭ zhurnal (Kiev, Ukraine : 1993)
  • [ISO-abbreviation] Mikrobiol. Z.
  • [Language] ukr
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / DNA, Bacterial
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19. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • Therefore, the simultaneous presence of MLL amplification and del(5q) appears to be a nonrandom association that could be the signature of AML in elderly patients with a poor prognosis.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Aged. Cytogenetic Analysis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Pipobroman / therapeutic use. Prognosis. Sensitivity and Specificity. Thrombocytosis / diagnosis. Thrombocytosis / drug therapy

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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20. Tapinassi C, Gerbino E, Malazzi O, Micucci C, Gasparini P, Najera MJ, Calasanz MJ, Odero MD, Pelicci PG, Belloni E: A new dic(7;12)(p12.21;p12.2) chromosome aberration in a case of acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Sep;185(2):102-5
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  • [Title] A new dic(7;12)(p12.21;p12.2) chromosome aberration in a case of acute myeloid leukemia.
  • A new dic(7;12)(p12.21;p12.2) chromosome aberration was identified in an acute myeloid leukemia with FAB-M1 morphology and was cloned.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Leukemia, Myeloid, Acute / genetics


21. Boxx GM, Nishiya CT, Kozel TR, Zhang MX: Characteristics of Fc-independent human antimannan antibody-mediated alternative pathway initiation of C3 deposition to Candida albicans. Mol Immunol; 2009 Jan;46(3):473-80
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  • This study characterized antibody-dependent initiation of the alternative pathway using the recombinant human monoclonal antimannan Fab fragment M1 and its full-length IgG1 antibody M1g1.
  • Kinetic analysis of C3b deposition onto C. albicans with flow cytometry demonstrated the ability of M1g1 to restore the activity of either the classical or alternative pathway to the yeast-absorbed normal human serum, but the Fc-free M1 Fab restored only the activity of the alternative pathway.
  • This Fc-independent, antimannan Fab-mediated C3 deposition through the alternative pathway was also observed in a serum-free assay containing the six alternative pathway proteins and in C1q- or C2-depleted serum but not in factor B-depleted serum.
  • M1- or M1g1-dependent alternative pathway initiation of C3b deposition occurred in an asynchronous manner at discrete sites that expanded to cover the entire cell surface over time as revealed with immunofluorescence microscopy, in contrast to a uniform appearance of initial C3 deposition through the classical pathway.
  • Furthermore, antimannan Fab M1 promoted the assembly of the alternative pathway convertase on the cell surface seen as colocalization of C3 and factor B with immunofluorescence microscopy.

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  • (PMID = 19038459.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / S06 GM063119; United States / NIGMS NIH HHS / GM / S06 GM063119-05; United States / NIAID NIH HHS / AI / AI037194-050004; United States / NIAID NIH HHS / AI / R01 AI044786; United States / NIAID NIH HHS / AI / AI44786; United States / NIAID NIH HHS / AI / R01 AI014209-30; United States / NIAID NIH HHS / AI / P01 AI037194-050004; United States / NIGMS NIH HHS / GM / GM63119; United States / NIAID NIH HHS / AI / R15 AI052139-01; United States / NIAID NIH HHS / AI / AI014209-30; United States / NIAID NIH HHS / AI / R37 AI014209; United States / NIAID NIH HHS / AI / R15 AI052139; United States / NIAID NIH HHS / AI / P01 AI037194; United States / NIAID NIH HHS / AI / R01 AI044786-01A1; United States / NIAID NIH HHS / AI / AI52139; United States / NIAID NIH HHS / AI / AI052139-01; United States / NIAID NIH HHS / AI / R01 AI014209; United States / NIAID NIH HHS / AI / AI37194; United States / NIGMS NIH HHS / GM / GM063119-05; United States / NIAID NIH HHS / AI / AI14209; United States / NIAID NIH HHS / AI / AI044786-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Complement C3; 0 / Immunoglobulin Fab Fragments; 0 / Immunoglobulin G; 0 / Mannans; 0 / Receptors, Fc; 0 / Recombinant Proteins; EC 3.4.21.- / Complement C3-C5 Convertases
  • [Other-IDs] NLM/ NIHMS93796; NLM/ PMC2670400
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22. Tempescul A, Guillerm G, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jan 1;172(1):74-6
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  • [Title] Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia.
  • We report here two cases of patients with acute myeloblastic leukemia, type M1 (FAB classification), associated with a t(10;17)(p15;q21).
  • Four other patients with this translocation have been reported, three of them having acute undifferentiated or poorly differentiated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17175384.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human
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23. Øyan AM, Bø TH, Jonassen I, Gjertsen BT, Bruserud Ø, Kalland KH: cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation. Int J Oncol; 2006 May;28(5):1065-80
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  • [Title] cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to biology and clinical course.
  • In an attempt to address this question, we performed cDNA microarray analysis on peripheral blood samples of 25 patients with newly diagnosed AML with high blast counts.
  • Leave-one-out crossvalidation (LOOCV) showed with high accuracy that gene expression classifiers could predict if leukaemia samples belonged to the FAB AML-M1 or to the FAB AML-M2 groups.
  • Except for an accumulation of samples classified as FAB M1 and M2 in cluster 3, there was no evident relationship between the clusters and the FAB classification.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


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4. Hubeek I, Stam RW, Peters GJ, Broekhuizen R, Meijerink JP, van Wering ER, Gibson BE, Creutzig U, Zwaan CM, Cloos J, Kuik DJ, Pieters R, Kaspers GJ: The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia. Br J Cancer; 2005 Dec 12;93(12):1388-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The human equilibrative nucleoside transporter 1 mediates in vitro cytarabine sensitivity in childhood acute myeloid leukaemia.
  • Cytarabine (ara-C) is the most effective agent for the treatment of acute myeloid leukaemia (AML).
  • We determined mRNA expression of these factors using quantitative-real-time-PCR in leukemic blasts from children diagnosed with de novo AML.
  • Expression of the inactivating enzyme pyrimidine nucleotidase-I (PN-I) was 1.8-fold lower in FAB-M5 as compared to FAB-M1/2 (P=0.007).
  • In conclusion, decreased expression of hENT1, which transports ara-C across the cell membrane, appears to be a major factor in ara-C resistance in childhood AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytarabine / pharmacology. Equilibrative Nucleoside Transporter 1 / physiology. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Cell Membrane. Child. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 16333246.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Equilibrative Nucleoside Transporter 1; 0 / RNA, Messenger; 0 / SLC29A1 protein, human; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ PMC2361532
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25. Villa O, Salido M, Pérez-Vila ME, Ferrer A, Arenillas L, Pedro C, Espinet B, Corzo C, Serrano S, Woessner S, Florensa L, Solé F: Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):32-6
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  • [Title] Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia.
  • We report three cases of acute myeloid leukemia without maturation [AML-M1 subtype according to the French-American-British classification (FAB)] with the presence of MYC oncogene amplification in form of double minutes (dmin) or homogeneously staining region (hsr).
  • [MeSH-major] Cell Nucleus / pathology. Genes, myc. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 18656691.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
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26. Braham Jmili N, Omri H, Senana Sendi H, Fekih S, Hizem S, Sriha B, Khelif A, Saad A, Kortas M: Identification of the translocation t(15;17) in acute myeloid leukemia (AML) initially classified as FAB M1: case report and review of the literature. Clin Lab; 2006;52(3-4):125-30
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  • [Title] Identification of the translocation t(15;17) in acute myeloid leukemia (AML) initially classified as FAB M1: case report and review of the literature.
  • Immunophenotyping showed myeloid typical markers of granulocytic lineage (MP0+, CD13+, CD33+, CD117+, CD34-).
  • The diagnosis of acute myeloid leukaemia (AML) was then evoked initially.
  • The cytological features corresponded closely to the M1 subtype as defined in the FAB classification.
  • From the biological findings the patient was retrospectively diagnosed as having promyelocytic leukemia (hyperbasophilic form).
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic


27. Yang G, Tang SQ, Huang DS, Wang JW, Liu Y, Wang JY: [Aplastic anemia transformed into acute myeloblastic leukemia M1 8 years later: a case report]. Zhonghua Er Ke Za Zhi; 2005 Mar;43(3):221
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  • [Title] [Aplastic anemia transformed into acute myeloblastic leukemia M1 8 years later: a case report].
  • [MeSH-major] Anemia, Aplastic / complications. Leukemia, Myeloid, Acute / etiology


28. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In spite of intensive chemotherapy, the patient died within a year of diagnosis.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology


29. Hidaka H, Yagasaki H, Takahashi Y, Hama A, Nishio N, Tanaka M, Yoshida N, Villalobos IB, Wang Y, Xu Y, Horibe K, Chen S, Kadomatsu K, Kojima S: Increased midkine gene expression in childhood B-precursor acute lymphoblastic leukemia. Leuk Res; 2007 Aug;31(8):1045-51
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  • [Title] Increased midkine gene expression in childhood B-precursor acute lymphoblastic leukemia.
  • However, expression in acute leukemia has not been clarified.
  • We examined MK gene expression using real-time PCR in 94 children with acute leukemia.
  • MK gene was also overexpressed in more than half of patients with FAB M1 and M2 types of AML.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, B-Cell / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics. Nerve Growth Factors / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


30. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F: Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation. Pediatr Hematol Oncol; 2008 Apr-May;25(3):165-70
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  • [Title] Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation.
  • The authors report a rare case of acute myeloid leukemia (AML) M1 with faggot formation in mature neutrophils and metamyelocytes.
  • Although Auer rods in mature neutrophils are occasionally experienced, they are usually found in AML M2, M3, or M4 cases, but not in M1 cases.
  • In addition, faggot formation in mature neutrophils, as seen in this case, is considered to be particularly unusual because most previously reported cases tended to show simple Auer rods except for AML M3 cases.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neutrophils / pathology. Trisomy / pathology

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  • (PMID = 18432498.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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31. Graf M, Reif S, Kröll T, Hecht K, Nuessler V, Schmetzer H: Expression of MAC-1 (CD11b) in acute myeloid leukemia (AML) is associated with an unfavorable prognosis. Am J Hematol; 2006 Apr;81(4):227-35
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  • [Title] Expression of MAC-1 (CD11b) in acute myeloid leukemia (AML) is associated with an unfavorable prognosis.
  • There is evidence to suggest, that cellular adhesion molecules and receptors could play a role in leukemia, e.g., through altered adhesive qualities of leukemic blasts.
  • We have studied the expression of the beta2-integrin Mac-1 (CD11b) on mononuclear cells in 48 patients with AML at first diagnosis by flow cytometry using a direct fluorescein-conjugated antibody.
  • Within the FAB types, we observed a high expression rate in cases with M5 (100% MAC-1+ cases, 73% MAC-1+ cells), M4 (75% MAC-1+ cases, 48% MAC-1+ cells) and in cases with FAB-M1 with 71% MAC-1+ cases and 29% MAC-1+ cells.
  • For clinical evaluations only patients treated according to the protocols of the German AML Cooperative Group (AML-CG) were included (n = 29, cases with AML-M3 were excluded).
  • We can conclude that AML cases with high MAC-1 expression are characterized by a worse prognosis.
  • Evaluation of MAC-1 expression in AML might therefore contribute clinically important data with respect to develop new therapies that influence the interactions between integrins like MAC-1 on leukemic cells and endothelial or immunoreactive cells.
  • [MeSH-major] Antigens, CD11b / blood. Biomarkers, Tumor / blood. Blast Crisis / blood. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16550517.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Biomarkers, Tumor; 0 / Macrophage-1 Antigen
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