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1. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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2. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
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  • [Title] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • Therefore, we screened the AmL patients for known specific genetic abnormalities that could lead to more definitive prognoses.
  • METHODS: A total of 113 AML patients were evaluated at diagnosis based on routine morphology and cytochemistry and classified according to the WHO criteria.
  • The distribution of AML subtypes was M1(1), M2(32), M3(57), M4(14), M5(1), M6(1) and seven cases where morphological subtype could not be classified.
  • FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other AML subtypes (17.5 vs. 8.9%), the frequency greater in patients with bcr3 isoform (70%) than in those with in bcr1 isoform (30%).
  • AML1-ETO fusion transcript was detected in 16 of 56 patients with no correlation with clinical or haematological parameters.
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • Therefore, rapid identification of specific translocations at diagnosis is important for prognostic purposes and their detection should be incorporated into routine assessment.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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3. Secchiero P, Zerbinati C, di Iasio MG, Melloni E, Tiribelli M, Grill V, Zauli G: Synergistic cytotoxic activity of recombinant TRAIL plus the non-genotoxic activator of the p53 pathway nutlin-3 in acute myeloid leukemia cells. Curr Drug Metab; 2007 May;8(4):395-403
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  • [Title] Synergistic cytotoxic activity of recombinant TRAIL plus the non-genotoxic activator of the p53 pathway nutlin-3 in acute myeloid leukemia cells.
  • To potentiate the response of acute myeloid leukemia (AML) to TRAIL cytotoxicity, we have adopted a strategy of combining nutlin-3, a potent non-genotoxic activator of the p53 pathway, with recombinant TRAIL.
  • The rationale for using such a combination was that deletions and/or mutations of the p53 gene occur in only 5-10% of AML and that TRAIL and nutlin-3 activate the extrinsic and intrinsic pathways of apoptosis, respectively.
  • TRAIL induced a rapid increase of apoptosis when added to OCI M4-type and MOLM M5-type AML cells, carrying a wild-type p53, as well as to NB4 M3-type AML, carrying a mutated p53.
  • Of note, nutlin-3 up-regulated the surface expression of TRAIL-R2 and synergized with TRAIL in inducing apoptosis in OCI and MOLM as well as in primary M4-type and M5-type AML blasts, but not in NB4 cells.
  • The relevance of p21 down-regulation for sensitizing AML cells to apoptosis was underscored in knocking-down experiments with small interfering RNAs.
  • Our data suggest that the combined treatment of nutlin-3 plus TRAIL might offer a novel therapeutic strategy for AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Imidazoles / pharmacology. Leukemia, Myeloid, Acute / pathology. Piperazines / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17504227.001).
  • [ISSN] 1389-2002
  • [Journal-full-title] Current drug metabolism
  • [ISO-abbreviation] Curr. Drug Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Imidazoles; 0 / Piperazines; 0 / RNA, Small Interfering; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 3.4.22.- / Caspases
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4. Lightfoot T: Aetiology of childhood leukemia. Bioelectromagnetics; 2005;Suppl 7:S5-S11
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  • [Title] Aetiology of childhood leukemia.
  • Leukemia is the most common cancer to affect children, accounting for approximately a third of all childhood cancers.
  • The major morphological subtypes of leukemia, acute lymphoblastic leukemia (ALL), and acute myeloblastic leukemia (AML), are characterized by chromosomal translocations involving over 200 genes including mixed lineage leukemia (MLL), TEL, and AML1.
  • Chromosomal translocations involving the MLL gene at 11q23 are a common feature of infant acute leukemia, found in up to 80% of all cases, and there is strong evidence that rearrangements involving the MLL gene or the TEL-AML1 gene fusion can originate in utero.
  • As with most other cancers, the mechanism by which leukemia arises is likely to involve gene-environment interactions.
  • Accordingly, it is important to identify exposures that cause DNA damage and induce chromosome breaks which are inadequately repaired, ultimately leading to the initiation and disease progression.
  • Exposures acting before birth and early in life has long been thought to be important determinants of leukemia, and the list of suspected chemical, physical, and biological agents continues to increase.
  • Unfortunately, the evidence regarding the majority of suggested exposures is limited and often contradictory, and there are areas, which clearly warrant further investigation in order to further our understanding of the aetiology of childhood leukemia.
  • [MeSH-major] Electromagnetic Fields / adverse effects. Environmental Exposure / adverse effects. Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / physiopathology. Prenatal Exposure Delayed Effects / etiology. Prenatal Exposure Delayed Effects / physiopathology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16059922.001).
  • [ISSN] 0197-8462
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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5. Dăscălescu A, Zlei M, Grigore G, Dănăila C, Jitaru D, Carasevici E: [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients]. Rev Med Chir Soc Med Nat Iasi; 2009 Oct-Dec;113(4):1176-81
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  • [Title] [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients].
  • Leukemic cells have unique aberrant phenotypes, which permit identification of this cells at diagnose and in evolution of the disease.
  • The main aim of the current study is to identify correlation between recognized prognostic factors in acute myeloid leukemia (AML) patients and other phenotypic markers.
  • MATERIAL AND METHOD: Imunophenotypic analysis (BDFACS CantoII, FACSDiva Software) was performed on peripheral blood/bone marrow aspirate samples of 56 patients diagnosed with AML (9 M0, 3 M1, 10 M2, 4 M3, 28 M4/M5, 1 M6, 1 M7) between 2007-2009 in Hematology Department of "Sf.
  • RESULTS: In our study, IL7R expression on AML blasts was significant correlate with low WBC count at diagnosis (p = 0.04) and with multilinear displasia (p = 0.01), high CXCR4 expression was correlate (p = 0.05) with lack of response at first induction therapy and CD123 (IL3Ra) expression was correlate with M4 FAB phenotype.
  • Survival was negative influenced by presence of IL3R on AML blasts, but flt3 mutations, CXCR4, IL7R expression on leukemic cells, other phenotypic aberrancies did not influenced treatment response and survival in our patients population.
  • CONCLUSION: Complete investigation of leukemic cells phenotype extended with cytokines/chemokines receptors at diagnostic is useful for correct characterization of the disease, for discover new prognostic categories and for better identification of minimal residual disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid, Acute / immunology. Receptors, Chemokine / blood. Receptors, Cytokine / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Male. Middle Aged. Phenotype. Predictive Value of Tests. Prognosis. Receptors, CCR5 / blood. Receptors, CXCR4 / blood. Receptors, Interleukin-3 / blood. Receptors, Interleukin-7 / blood. Retrospective Studies. Survival Analysis

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  • (PMID = 20191895.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, CCR5; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Receptors, Interleukin-3; 0 / Receptors, Interleukin-7
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6. Turhan N, Yürür-Kutlay N, Topcuoglu P, Sayki M, Yüksel M, Gürman G, Tükün A: Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4. Leuk Res; 2006 Jul;30(7):903-5
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  • [Title] Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4.
  • We report a case of AML-M4 in which G-band karyotyping revealed a previously unreported t(13;17)(q14;q25) in metaphase preparations.
  • This report of AML-M4 harboring t(13;17)(q14;q25) as a unique cytogenetic abnormality provides more data on the leukomogenesis with rearrangements related with 13q14 and 17q25.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myelomonocytic, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16469377.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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7. Togashi Y, Sakoda H, Sugahara H, Asagoe K, Matsuzawa Y: [Loeys-Dietz syndrome with acute myeloid leukemia]. Rinsho Ketsueki; 2008 Aug;49(8):664-7
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  • [Title] [Loeys-Dietz syndrome with acute myeloid leukemia].
  • A 54-year-old man, who had been diagnosed with Loeys-Dietz syndrome based on his past history, family history, clinical findings, and the presence of a gene mutation, was referred to our hospital because of easy fatigability.
  • Furthermore, karyotype analysis of bone marrow cells showed t(11;19)(q23;p13.1) and MLL abnormality was detected on RT-PCR A diagnosis of acute myeloid leukemia (M4) with 11q23 (MLL) abnormality was made.
  • Loeys-Dietz syndrome is a Marfan-like congenital connective tissue disorder caused by a heterozygous missense mutation of a TGF-beta receptor I or II gene.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Marfan Syndrome / complications. Marfan Syndrome / genetics


8. Muramatsu T, Ueki T, Ohashi K, Negishi K, Suzuki T, Shitara M, Honma M, Ito T, Sakai M, Yamashita T, Akiyama H, Sakamaki H: [Successful treatment with voriconazole for disseminated cutaneous and visceral infection by Fusarium solani in a patient with acute myeloid leukemia]. Rinsho Ketsueki; 2006 Aug;47(8):753-7
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  • [Title] [Successful treatment with voriconazole for disseminated cutaneous and visceral infection by Fusarium solani in a patient with acute myeloid leukemia].
  • A 51-year-old man with acute myeloblastic leukemia (M4) underwent two courses of remission induction therapy with cytarabine and daunorubicin.
  • Although the patient was treated with amphotericin B (AMPH-B), the clinical symptoms worsened.
  • [MeSH-major] Antifungal Agents / therapeutic use. Dermatomycoses / complications. Dermatomycoses / drug therapy. Fusarium. Leukemia, Myeloid, Acute / complications. Mycoses / complications. Mycoses / drug therapy. Opportunistic Infections / complications. Opportunistic Infections / drug therapy. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 16986714.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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9. Shen M, Yen A: Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells. Oncology; 2009;76(2):91-100
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  • [Title] Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells.
  • Nicotinamide, the amide derivative of vitamin B(3), cooperates with retinoic acid (RA), a form of vitamin A, and 1,25-dihydroxyvitamin D(3) (D3), to regulate cell differentiation and proliferation of human myeloblastic leukemia cells.
  • In human myeloblastic leukemia cells, RA or D3 are known to cause MAPK signaling leading to myeloid or monocytic differentiation and G0 cell cycle arrest.
  • [MeSH-major] Calcitriol / metabolism. Leukemia, Myelomonocytic, Acute / drug therapy. Niacinamide / administration & dosage. Tretinoin / administration & dosage

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  • (PMID = 19127080.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD14; 25X51I8RD4 / Niacinamide; 5688UTC01R / Tretinoin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.2.2.5 / Antigens, CD38; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2826433
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10. Chan WK, Cheung CC, Law HK, Lau YL, Chan GC: Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function. J Hematol Oncol; 2008;1:9
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  • [Title] Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function.
  • The question of how leukemic cells especially in monocytic lineage respond to GL-PS stimuli remains unclear.
  • RESULTS: In this study, we used in vitro culture model with leukemic monocytic cell-lines THP-1 and U937 as monocytic effectors cells for proliferation responses and DCs induction.
  • CONCLUSION: Our findings suggested that GL-PS could induce selected monocytic leukemic cell differentiation into DCs with immuno-stimulatory function.
  • The possible clinical impact of using this commonly used medicinal mushroom in patients with monocytic leukemia (AML-M4 and M5) deserved further investigation.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Dendritic Cells / immunology. Leukemia / immunology. Monocytes / immunology. Polysaccharides / immunology. Reishi / chemistry

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  • (PMID = 18644156.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Polysaccharides; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2517069
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11. Cuiffo B, Ren R: Palmitoylation of oncogenic NRAS is essential for leukemogenesis. Blood; 2010 Apr 29;115(17):3598-605
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  • Activating mutations of NRAS are common in acute myeloid leukemia, chronic myelomonocytic leukemia, and myelodysplastic syndrome.
  • We have previously shown that expression of oncogenic NRAS using a bone marrow transduction and transplantation model efficiently induces a chronic myelomonocytic leukemia- or acute myeloid leukemia-like disease in mice.

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  • (PMID = 20200357.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL083515; United States / NHLBI NIH HHS / HL / R01HL083515
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 2V16EO95H1 / Palmitic Acid; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2867268
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12. Stahnke B, Thepen T, Stöcker M, Rosinke R, Jost E, Fischer R, Tur MK, Barth S: Granzyme B-H22(scFv), a human immunotoxin targeting CD64 in acute myeloid leukemia of monocytic subtypes. Mol Cancer Ther; 2008 Sep;7(9):2924-32
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  • [Title] Granzyme B-H22(scFv), a human immunotoxin targeting CD64 in acute myeloid leukemia of monocytic subtypes.
  • Acute myeloid leukemia (AML) cells of subtypes M4 and M5 show enhanced expression of CD64 (FcgammaRI), the high-affinity receptor for IgG, which is normally expressed at high levels only on activated cells of the myeloid lineage.
  • After evaluating the sensitivity of the AML-related cell line U937 toward cytosolic granzyme B, we genetically fused granzyme B to H22, a humanized single-chain antibody fragment (scFv) specific for CD64, to obtain Gb-H22(scFv), a fusion protein lacking the immunogenic properties of nonhuman immunofusions.
  • Finally, apoptosis was observed in primary CD64+ AML cells, whereas CD64(-) AML cells were unaffected.
  • This is the first report of a completely human granzyme B-based immunotoxin directed against CD64, with activity against an AML-related cell line and primary AML cells.
  • [MeSH-major] Granzymes / pharmacology. Immunoglobulin Variable Region / pharmacology. Immunotoxins / pharmacology. Leukemia, Monocytic, Acute / metabolism. Receptors, IgG / antagonists & inhibitors. Recombinant Fusion Proteins / pharmacology

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  • (PMID = 18790773.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Immunotoxins; 0 / Receptors, IgG; 0 / Recombinant Fusion Proteins; EC 3.4.21.- / Granzymes; EC 3.4.22.- / Caspase 3
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13. Kufner S, Fleischer RP, Kroell T, Schmid C, Zitzelsberger H, Salih H, de Valle F, Treder W, Schmetzer HM: Serum-free generation and quantification of functionally active Leukemia-derived DC is possible from malignant blasts in acute myeloid leukemia and myelodysplastic syndromes. Cancer Immunol Immunother; 2005 Oct;54(10):953-70
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  • [Title] Serum-free generation and quantification of functionally active Leukemia-derived DC is possible from malignant blasts in acute myeloid leukemia and myelodysplastic syndromes.
  • Functional dendritic cells (DC) are professional antigen presenting cells (APC) and can be generated in vitro from leukemic cells from acute myeloid leukemia AML patients, giving rise to APC of leukemic origin presenting leukemic antigens (DC(leu)).
  • We have already shown that DC can be successfully generated from AML and myeloplastic syndromes (MDS) cells in serum-free 'standard' medium (X-vivo + GM-CSF + IL-4 +TNFalpha + FL) in 10-14 days.
  • In this study, we present that DC counts generated from mononuclear cells (MNC) varied between 20% (from 55 MDS samples), 34% (from 100 AML samples) and 25% (from 38 healthy MNC samples) medium.
  • DC harvests were highest in monocytoid FAB types (AML-M4/M5, MDS-CMML) and independent from cytogenetic risk groups, demonstrating that DC-based strategies can be applied for patients with all cytogenetic risk groups.
  • Proof of the clonal derivation of DC generated was obtained in five AML and four MDS cases with a combined FISH/immunophenotype analysis (FISH-IPA): The clonal numerical chromosome aberrations of the diseases were regularly codetectable with DC markers; however, not with all clonal cells being convertible to leukemia-derived DC(leu) (on average, 53% of blasts in AML or MDS).
  • In 41 AML and 13 MDS cases with a suitable antigen expression, we could confirm FISH-IPA data by Flow cytometry: although DC(leu) are regularly detectable, on average only 57% of blasts in AML and 64% of blasts in MDS were converted to DC(leu).
  • After coculture with DC in mixed lymphocyte reactions (MLR), autologous T cells from AML and MDS patients proliferate and upregulate costimulatory receptors.
  • The specific lysis of leukemic cells by autologous T cells could be demonstrated in three cases with AML in a Fluorolysis assay.
  • (1) the generation of DC is regularly possible in AML and also in MDS under serum-free conditions. (2) Clonal/leukemia-derived DC(leu) can be regularly generated from MDS and AML-MNC; however, not with all blasts being converted to DC(leu) and not all DC generated carrying leukemic markers.
  • We recommend to select DC(leu) for vaccinations or ex vivo T-cell activations to avoid contaminations with non-converted blasts and non-leukemia-derived DC and to improve the harvest of specific, anti-leukemic T cells.
  • DC and DC-primed T cells could provide a practical strategy for the immunotherapy of AML and MDS.
  • [MeSH-major] Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology. Myelodysplastic Syndromes / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigen-Presenting Cells. Antigens, CD. Antigens, CD80 / immunology. Antigens, CD80 / metabolism. Blast Crisis. Cell Culture Techniques. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Immunoglobulins / immunology. Immunoglobulins / metabolism. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Membrane Glycoproteins / immunology. Membrane Glycoproteins / metabolism. Middle Aged. T-Lymphocytes / immunology. T-Lymphocytes, Cytotoxic. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 15789235.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD80; 0 / CD83 antigen; 0 / Culture Media, Serum-Free; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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14. Wonsettler DM, Chang WW, Wenger SL: Extra copy of 20q deletion, acute myelomonocytic leukemia (M4) and Niemann-Pick disease. J Assoc Genet Technol; 2005;31(2):55-8
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  • [Title] Extra copy of 20q deletion, acute myelomonocytic leukemia (M4) and Niemann-Pick disease.
  • A 59-year-old hypertensive white male was diagnosed with acute myelogenous leukemia (AML), M4.
  • The majority of cases with 20q deletion are associated with myeloid disorders; however, an extra copy of the 20q deletion has rarely been reported.
  • Many foamy macrophages with bubbling cytoplasm in the spleen, liver, bone marrow and lymph nodes were suggestive of Niemann-Pick disease, type E.
  • AML has not previously been reported with Niemann-Pick disease.

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  • (PMID = 16027483.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Draper NL, Conley C, Smith C, Benson K: Dispermic chimerism identified during HLA typing for stem cell transplantation. Transfusion; 2008 Jul;48(7):1398-402
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  • CASE REPORT: A 32-year-old man was diagnosed with acute myelomonocytic leukemia.
  • Molecular HLA typing may increase the accurate identification of phenotypically normal chimeras and aid in selecting proper donors for transplantation to reduce graft-versus-host disease and transplant rejection in these patients.
  • [MeSH-minor] Adult. HLA-B Antigens / genetics. HLA-C Antigens / genetics. Haplotypes / genetics. Humans. Leukemia, Myelomonocytic, Acute / surgery. Male. Microsatellite Repeats / genetics. Sequence Analysis, DNA

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  • (PMID = 18422842.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-B Antigens; 0 / HLA-C Antigens
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16. Mayayo E, Landeyro J, Stchigel AM, Gazzoni A, Capilla J: [Perineural spread by fungal cells. Case report and literature review]. Rev Iberoam Micol; 2010 Jun 30;27(2):94-7
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  • [Transliterated title] Infiltración perineural por células fúngicas. Presentación de un caso y revisión de la literatura.
  • We present a clinical case of a 73-year-old male, with diabetes and acute myelomonocytic leukaemia that began with tumefaction on the left side of his face, spreading to the sinus with invasion of the soft tissues and fistulae in the oral cavity.
  • Clinical examination showed cerebral involvement.
  • [MeSH-minor] Aged. Blast Crisis / complications. Diabetes Mellitus, Type 2 / complications. Disease Progression. Fatal Outcome. Humans. Immunocompromised Host. Leukemia, Myelomonocytic, Chronic / complications. Lung Diseases, Fungal / microbiology. Male

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  • [Copyright] Copyright 2009 Revista Iberoamericana de Micología. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20347372.001).
  • [ISSN] 1130-1406
  • [Journal-full-title] Revista iberoamericana de micología
  • [ISO-abbreviation] Rev Iberoam Micol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 18
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17. Graf M, Reif S, Hecht K, Pelka-Fleischer R, Kroell T, Pfister K, Schmetzer H: High expression of costimulatory molecules correlates with low relapse-free survival probability in acute myeloid leukemia (AML). Ann Hematol; 2005 May;84(5):287-97
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  • [Title] High expression of costimulatory molecules correlates with low relapse-free survival probability in acute myeloid leukemia (AML).
  • Costimulatory molecules such as lymphocyte function-associated antigen (LFA)-1 (CD11a), LFA-3 (CD58), intercellular adhesion molecule (ICAM)-1 (CD54), neuronal cell adhesion molecule (NCAM) (CD56), B7-1 (CD80), or B7-2 (CD86) are important regulatory elements in healthy immunological cascades, but their role in acute myeloid leukemia (AML) has only been rarely investigated.
  • We studied their expression on mononuclear bone marrow (BM) cells from 105 patients with AML at initial diagnosis and evaluated their prognostic significance.
  • The expression of these markers in different French-American-British (FAB) classification types (M0-M5) was heterogeneous, except for CD56, which showed a higher proportion of positive cells in monocytic subtypes of AML.
  • In addition, cases with a "poor risk" karyotype as well as patients succumbing to "early death" after double induction therapy according to the AML Cooperative Group (CG) protocol were characterized by a high expression of CD56.
  • CD54 was preferentially expressed in AML M4(eo) and in addition in "favorable" cytogenetic risk groups and in cases that had responded to AML-CG therapy.
  • CD80 and CD86 expressions were similar in all FAB types.
  • Patients who had responded to AML-CG therapy showed higher CD80 proportions and lower CD86 proportions compared to the "nonresponder" group.
  • Expression profiles of CD11a and CD58 were not associated with specific FAB types or prognostically relevant groups.
  • (1) Expression of costimulatory molecules in AML is very variable.
  • This reflects the great diversity of immunophenotypes in AML. (2) CD56 is mainly expressed in monocytic subtypes of AML.
  • CD56(+) subtypes of AML seem to be a separate entity with a worse prognosis independent of the karyotype. (3) High expression of some costimulatory molecules correlates with a worse prognosis concerning relapse-free survival times.
  • [MeSH-major] Antigens, CD / blood. Biomarkers, Tumor / blood. Bone Marrow Cells / metabolism. Leukemia, Myeloid, Acute / blood
  • [MeSH-minor] Disease-Free Survival. Flow Cytometry. Humans. Predictive Value of Tests. Recurrence. Risk Factors


18. Mu QT, Chen ZM, Lou JY, Cheng YZ, Wang YG, Ni WM, Wang HP, Xu H, Yu YB, Jin J: [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2010 May;39(3):236-40
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  • [Title] [Cytogenetic analysis of 154 case of acute myeloid leukemia with t(8;21)].
  • OBJECTIVE: To investigate the cytogenetic features of acute myeloid leukemia (AML) with t(8;21).
  • METHODS: The clinical characteristics of 154 cases of acute myeloid leukemia with t(8;21) in our hospital were analyzed retrospectively.
  • According to the chromosome karyotype, all cases were divided into three groups: the group without additional chromosome abnormality, the group with single sex chromosome loss and the group with additional chromosome abnormalities other than sex chromosome loss.
  • RESULT: In this study, according to FAB classification, there were 127 cases of M2 (82.5%), 15 of M5 (9.7%), 6 of M4 (3.9%), 4 of M1(2.6%) and 2 of M0(1.3%).
  • Cytogenetically, 85 (55.2%) AML patients with t(8;21) had additional chromosome abnormalities.
  • In the group of t(8;21) with additional chromosome abnormalities, 11 cases (35.5%) were non-M2 AML, higher than that in single t(8;21) group (17.4%)(P<0.05); however, there was no significant difference between the group of single t(8;21) and the group of t(8;21) with single sex chromosome loss(P>0.05).
  • CONCLUSION: t(8;21) translocation is usually accompanied by additional chromosome abnormalities, particularly in M2; while t(8;21) with additional chromosome abnormalities other than sex chromosome loss is more frequently observed in non-M2 AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20544983.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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19. Gallegos-Castorena S, Medina-Sanson A, Gonzalez-Ramella O, Sanchez-Zubieta F, Martínez-Avalos A: Improved treatment results in Mexican children with acute myeloid leukemia using a Medical Research Council (MRC)-acute myeloid leukemia 10 modified protocol. Leuk Lymphoma; 2009 Jul;50(7):1132-7
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  • [Title] Improved treatment results in Mexican children with acute myeloid leukemia using a Medical Research Council (MRC)-acute myeloid leukemia 10 modified protocol.
  • Protocol III (2003-2005) on six cycles MRC AML 10 modified.
  • Patients with de novo acute myeloid leukemia 0 to 18 years were included.
  • Demographic and clinical characteristics were analysed.
  • Patients with >100,000 leukocytes, M4 or M5 and primary CNS disease were considered high risk.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Child. Disease-Free Survival. Female. Humans. Male. Medical Oncology / methods. Mexico. Recurrence. Remission Induction. Treatment Outcome

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  • (PMID = 19557634.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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20. Wang TY, Huang XO, Xu CG, Chen XC, Wang H: [Acute myelomonocytic leukemia occurred after multiple myeloma treated: a case report]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2007 Mar;38(2):347-9
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  • [Title] [Acute myelomonocytic leukemia occurred after multiple myeloma treated: a case report].
  • We reported a case of multiple myeloma, who suffered from the acute myelomonocytic leukemia (AML-M4) after the chemotherapy of alkylating agent.
  • Thus, the diagnosis of multiple myeloma in remission and secondary AML-M4 was established.
  • When the chemotherapy regimen to AML was being planned for this patient, she died of massive hemorrhage of gastrointestinal tract due to thrombocytopenia and ineffectiveness.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Multiple Myeloma / drug therapy


21. Zhou HF, Li JY, Wu YJ, Yang H, Qiu HR, Li L: [Immunophenotypic and cytogenetic features of acute myelomonocytic leukemia]. Ai Zheng; 2006 Oct;25(10):1252-5
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  • [Title] [Immunophenotypic and cytogenetic features of acute myelomonocytic leukemia].
  • BACKGROUND & OBJECTIVE: The expression of some antigens has been involved in cytogenetic abnormalities in leukemia.
  • This study was to explore the immunophenotypes of acute myelomonocytic leukemia (M4), analyze the correlation of M4 to cytogenetic abnormalities, and provide evidences for the diagnosis and therapy.
  • METHODS: Immunophenotypic analysis was performed using a panel of monoclonal antibodies and three-color immunofluorescent staining methods of flow cytometry in 81 patients with M4 leukemia.
  • RESULTS: Among the 81 M4 leukemia patients, CD33 (84.0%) was the most commonly expressed antigen, followed by CD13 (81.5%) and CD14 (24.7%).
  • CONCLUSIONS: Acute myelomonocytic leukemia mainly expresses myeloid lineage antigens.
  • Inv(16) exists in 40% of M4 patients and the expression of all the antigens has no correlation to inv(16).
  • [MeSH-major] Antigens, CD / metabolism. Immunophenotyping. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / immunology

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  • (PMID = 17059770.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD2; 0 / Antigens, CD34
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22. Sakagami H, Kishino K, Kobayashi M, Hashimoto K, Iida S, Shimetani A, Nakamura Y, Takahashi K, Ikarashi T, Fukamachi H, Satoh K, Nakashima H, Shimizu T, Takeda K, Watanabe S, Nakamura W: Selective antibacterial and apoptosis-modulating activities of mastic. In Vivo; 2009 Mar-Apr;23(2):215-23
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  • Among a total of thirteen human cell types, promyelocytic leukemia HL-60 was the most sensitive to the cytotoxicity of mastic, followed by myeloblastic leukemia (ML-1, KG-1), erythroleukemia (K-562), oral squamous cell carcinoma (HSC-2, HSC-3, HSC-4), hepatocellular carcinoma (HepG2), glioblastoma (T98G, U87MG) and normal oral cells (gingival fibroblast, pulp cell, periodontal ligament fibroblast, most resistant).

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  • (PMID = 19414406.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Resins, Plant; 61789-92-2 / gum mastic; EC 3.4.22.- / Caspase 3; V10TVZ52E4 / Putrescine
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23. Corazza F, Hermans C, D'Hondt S, Ferster A, Kentos A, Benoît Y, Sariban E: Circulating thrombopoietin as an in vivo growth factor for blast cells in acute myeloid leukemia. Blood; 2006 Mar 15;107(6):2525-30
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  • [Title] Circulating thrombopoietin as an in vivo growth factor for blast cells in acute myeloid leukemia.
  • We studied patients with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) and used TPO-induced c-fos protein up-regulation as a marker of c-mpl functionality and observed that c-mpl-presenting blast cells were present in 62% (37 of 60) of patients with ALL but that c-mpl was nonfunctional in 0 of 28 patients and that they were present in 56% (22 of 39) of patients with AML and were functional in 43% (12 of 28).
  • Adequate increases in serum TPO level in response to thrombocytopenia were seen in patients with ALL and with c-mpl-deficient (c-mpl-) AML.
  • In contrast, in patients with c-mpl-proficient (c-mpl+) AML, TPO levels were found to be inappropriately low but increased to expected values during induction chemotherapy as blasts disappeared.
  • In vitro significant TPO-associated blast cell proliferation or decreased apoptosis was observed only in patients with c-mpl+ AML compared with ALL or c-mpl- AML and was highly correlated with low in vivo TPO levels (P < .001).
  • These data suggest that, in patients with AML, inadequate TPO levels are secondary to TPO clearing by functional c-mpl receptor myeloid blast cells and that TPO may serve as an in vivo myeloid leukemic growth factor in a significant number of patients.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Thrombopoietin / blood
  • [MeSH-minor] Acute Disease. Apoptosis. Cell Proliferation. Growth Substances / blood. Humans. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / physiology. Receptors, Cytokine / analysis. Receptors, Cytokine / physiology. Receptors, Thrombopoietin. Thrombocytopenia / blood

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  • (PMID = 16317100.001).
  • [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 / Growth Substances; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytokine; 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; 9014-42-0 / Thrombopoietin
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24. Pogoda JM, Katz J, McKean-Cowdin R, Nichols PW, Ross RK, Preston-Martin S: Prescription drug use and risk of acute myeloid leukemia by French-American-British subtype: results from a Los Angeles County case-control study. Int J Cancer; 2005 Apr 20;114(4):634-8
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  • [Title] Prescription drug use and risk of acute myeloid leukemia by French-American-British subtype: results from a Los Angeles County case-control study.
  • Chemotherapy is a well-established risk factor for acute myeloid leukemia (AML) but little is known about other prescription drugs and AML risk.
  • We report data from a population-based Los Angeles County study in which 299 matched case-control pairs had complete data on prescription drug use and 88% of cases were subtyped according to the French-American-British (FAB) criteria.
  • Prescription nonsteroidal anti-inflammatory drug (NSAID) use for at least 4 weeks in the 2 to 10 years before diagnosis was associated with decreased risk (odds ratio = 0.5, 95% confidence interval=0.3, 1.0; p=0.04) with dose-response most evident for FAB subtype M2 (OR = 0.6, CI: 0.1, 2.9 for duration < or =6 months; OR = 0.2, CI: 0.0, 1.6 for >6 months).
  • For subtype M4, ORs increased with increasing duration of benzodiazepine use in the 2 to 10 years before diagnosis (OR = 1.5, CI: 0.3, 9.0 for < or =6 months vs. OR = 5.0, CI: 0.6, 42.8 for >6 months).
  • These results suggest that prescription drugs other than chemotherapy may have FAB subtype-specific effects on AML risk.
  • [MeSH-major] Drug Prescriptions. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / etiology

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  • (PMID = 15609330.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 5 P30 ES07048-06; United States / NCI NIH HHS / CA / CA17054; United States / NCI NIH HHS / CN / N01-CN-25403
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 12794-10-4 / Benzodiazepines
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25. Kappelmayer J, Simon A, Katona E, Szanto A, Nagy L, Kiss A, Kiss C, Muszbek L: Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias. Thromb Haemost; 2005 Aug;94(2):454-9
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  • [Title] Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias.
  • This study was designed to study the sensitivity and specificity of factor XIII subunit A (FXIII-A) labelling in cultured myeloblastic and monoblastic cell lines and to investigate the intracytoplasmic expression of FXIII-A in de novo acute myeloid leukemia (AML) samples.
  • Myeloblastic and a monoblastic cell lines were cultured and investigated for lineage specific maturation markers and FXIII-A expression.
  • Furthermore, FXIII-A expression was investigated in 12 normal samples (7 bone marrow and 5 peripheral blood), 86 de novo AML samples and 6 chronic myelomonocytic leukemia (CMML) samples.
  • In the monoblastic MonoMac6 cell line the appearance of FXIII-A preceded that of CD14 while it remained negative in the myeloblastic PLB-985 cell line throughout its maturation period.
  • Among the AML samples the average frequency of FXIII-A positive cells in myeloblastic leukemia samples was below 10%, while in M4 and M5AML samples it was above 50% and was significantly higher than the generally used CD14 marker (p < 0.0001).
  • In the AML M4 and M5 cases, FXIII-A proved sensitive for the identification of monoblasts.
  • FXIII-A can be considered as a reliable intracytoplasmic marker for the monocytic and megakaryocytic series and its presence is highly predictive for mono- and megakaryocytic AML and for CMML.
  • [MeSH-major] Factor XIIIa / metabolism. Factor XIIIa / physiology. Flow Cytometry / methods. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / metabolism. Antigens, CD14 / biosynthesis. Cell Line. Cell Line, Tumor. Cell Lineage. Cells, Cultured. Cytoplasm / metabolism. Granulocytes / cytology. Humans. Leukocytes / metabolism. Megakaryocytes / cytology. Monocytes / cytology. Monocytes / metabolism. Myeloid Cells / cytology. Sensitivity and Specificity

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  • (PMID = 16113839.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD14; EC 2.3.2.13 / Factor XIIIa
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26. Liu LB, Li WM, He W, Zhang M, Xiao J, Zhong ZD, Li L, Zou P: [Blocking the escape of leukemic cells from killing of T cell by combining anti-Fas ribozyme and CD80-IgG fusion protein]. Zhonghua Yi Xue Za Zhi; 2005 Dec 28;85(49):3469-74
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  • OBJECTIVE: To study Fas expression regulation of cytotoxic T lymphocyte(CTL)via anti-Fas ribozyme, increasing of CD80 epitope on the surface of acute myelomonocytic leukemia cells by CD80-IgG fusion protein and their effects on the apoptosis and killing ability against acute myelomonocytic leukemia cells of CTL.
  • Then allogeneic mixed lymphocytes culture between the mouse spleen T cells transfected with pEGFP-RZ596 and WEHI-3 cells (mouse acute myelomonocyte leukemia cell line) incubated with CD80-IgG fusion protein was performed.
  • [MeSH-minor] Animals. Antigens, CD80 / genetics. Antigens, CD80 / immunology. Antigens, CD80 / metabolism. Antigens, CD95 / genetics. Antigens, CD95 / immunology. Antigens, CD95 / metabolism. Blotting, Western. CHO Cells. Cell Line, Tumor. Coculture Techniques. Cricetinae. Cricetulus. Female. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Immunoglobulin G / genetics. Immunoglobulin G / immunology. Immunoglobulin G / metabolism. Leukemia, Myelomonocytic, Acute / immunology. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Mice. Mice, Inbred BALB C. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Escape

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  • (PMID = 16686062.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD95; 0 / Immunoglobulin G; 0 / RNA, Catalytic; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins
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27. Villiers E, Baines S, Law AM, Mallows V: Identification of acute myeloid leukemia in dogs using flow cytometry with myeloperoxidase, MAC387, and a canine neutrophil-specific antibody. Vet Clin Pathol; 2006 Mar;35(1):55-71
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  • [Title] Identification of acute myeloid leukemia in dogs using flow cytometry with myeloperoxidase, MAC387, and a canine neutrophil-specific antibody.
  • BACKGROUND: Flow cytometry may be used to determine immunophenotype or lineage of leukemic cells, but few antibodies are available that are specific for cells of monocytic and granulocytic lineage.
  • OBJECTIVE: The purpose of this study was to evaluate the flow cytometric staining patterns of 3 commercial monoclonal antibodies for monocytes and granulocytes in clinically healthy dogs and in dogs with acute myeloid leukemia (AML).
  • METHODS: Mouse antihuman macrophage antibody (MAC387), mouse anti-human myeloperoxidase (MPO), and a canine neutrophil-specific antibody (NSA) were evaluated using flow cytometry on blood from 6 clinically healthy control dogs, and on blood (n = 7) and/or bone marrow (n = 2) from 8 dogs with AML.
  • A diagnosis of acute leukemia was confirmed by >30% blasts in bone marrow or >30% blasts in peripheral blood, together with bi- or pancytopenia, circulating CD34-positive blast cells, and clinical signs of disease.
  • One case was classified as AML of granulocytic lineage (AML-M1), 6 cases were classified as acute monocytic leukemia (AML-M5), and 1 case was classified as acute myelomonocytic leukemia (AML-M4).
  • Neoplastic myeloblasts in the dog with granulocytic AML were positive for MPO, NSA, MAC387, and CD4.
  • All monoblasts from the dogs with AML-M5 were positive for CD14, 5 of 6 were positive for MAC387, and 2 were positive for MPO.
  • NSA staining was negative in the 2 dogs with AML-M5 in which it was evaluated.
  • In the dog with AML-M4 variable percentages of blast cells were positive for CD14, MPO, MAC387, CD4, and NSA.
  • These 3 antibodies may be useful as part of a wider panel for immunophenotyping AML in dogs.

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  • (PMID = 16511792.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; EC 1.11.1.7 / Peroxidase
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28. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • The deletion was identified at initial diagnosis in one patient and at relapse in the other two.
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • These cases often show features of myelomonocytic or monocytic differentiation.
  • The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

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  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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29. Freycon F, Trombert-Paviot B, Casagranda L, Bertrand Y, Plantaz D, Marec-Bérard P: Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA). Pediatr Blood Cancer; 2008 Jun;50(6):1213-20
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  • [Title] Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA).
  • No difference was observed in treatment- and transplantation-related deaths in patients with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but OS was better in patients with AML (P = 0.02).
  • Severe graft-versus-host disease was also observed among patients with ALL (P = 0.036).
  • CONCLUSION: Although mortality declined, improved adherence to therapeutic guidelines and more restricted indications of allograft are needed to preclude further treatment- and transplantation-related deaths, particularly among those with leukemia.
  • [MeSH-minor] Central Nervous System Neoplasms / mortality. Central Nervous System Neoplasms / therapy. Child. Cohort Studies. Female. France / epidemiology. Guideline Adherence. Hematopoietic Stem Cell Transplantation / mortality. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Practice Guidelines as Topic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Registries

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18300318.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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30. Numakura K, Tsuchiya N, Habuchi T, Takahashi N: [Therapy related leukemia with 11q23 abnormality induced by chemotherapy consisted of docetaxel for advanced prostatic carcinoma: case report]. Nihon Hinyokika Gakkai Zasshi; 2009 Jul;100(5):580-5
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  • [Title] [Therapy related leukemia with 11q23 abnormality induced by chemotherapy consisted of docetaxel for advanced prostatic carcinoma: case report].
  • A balanced translocation involving 11q23 (MLL gene) could be observed in therapy related leukemia (TRL) patients generally treated with topoisomerase II inhibitors.
  • Herein, we report a patient who developed acute myelomonocytic leukemia (AMMoL) with t (9;. 11) (p22;.
  • Although, no disease progression of the prostatic carcinoma was observed, AMMoL with t (9;. 11) (p22;.
  • q23) translocation and clinical course.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carcinoma / therapy. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myelomonocytic, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / genetics. Neoplasms, Second Primary. Prostatic Neoplasms / therapy. Taxoids / adverse effects. Translocation, Genetic

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  • (PMID = 19663246.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 23
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31. Benesch M, Sovinz P, Lackner H, Schwinger W, Dornbusch HJ, Urban C: Five-month marrow aplasia in a child with refractory acute myeloid leukemia: successful management with continuous granulocyte support and reduced-intensity conditioning followed by matched unrelated bone marrow transplantation. J Pediatr Hematol Oncol; 2005 Apr;27(4):236-8
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  • [Title] Five-month marrow aplasia in a child with refractory acute myeloid leukemia: successful management with continuous granulocyte support and reduced-intensity conditioning followed by matched unrelated bone marrow transplantation.
  • A 10-year-old girl diagnosed with acute myeloid leukemia FAB M4 failed to achieve remission following several courses of induction chemotherapy.
  • Graft-versus-host disease did not occur.
  • [MeSH-major] Anemia, Aplastic / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Graft vs Host Disease / prevention & control. Leukemia, Myelomonocytic, Acute / therapy. Neoplasm Recurrence, Local / therapy. Transplantation Conditioning. Vidarabine / analogs & derivatives

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  • (PMID = 15838401.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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32. Callera F, Mulin CC, Rosa ES, Melo DB, Melo CM: High prevalence of morphological subtype FAB M1 in adults with de novo acute myeloid leukemia in São José dos Campos, São Paulo. Sao Paulo Med J; 2006 Jan 5;124(1):45-7
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  • [Title] High prevalence of morphological subtype FAB M1 in adults with de novo acute myeloid leukemia in São José dos Campos, São Paulo.
  • CONTEXT AND OBJECTIVE: Geographical variations have been described in acute myelogenous leukemia (AML).
  • The aim of this study was to demonstrate the high prevalence of French-American-British (FAB) M1 subtype in adults with de novo AML in São José dos Campos, State of São Paulo, Brazil.
  • METHODS: Records from 39 consecutive adult patients with de novo AML referred to Hospital Pio XII between January 2002 and September 2004 were reviewed.
  • Peripheral blood and blood marrow smears were reviewed blindly by five hematologists and classified according to FAB criteria.
  • The rates of remission, relapse, mortality according treatment phase, survival and leukemia-free survival were calculated.
  • RESULTS: The prevalence of each category as determined via a consensus among five observers was M0: 0%; M1: 43.6%; M2: 30.7%; M3: 12.8%; M4: 5.1%; M5: 2.6%: M6: 2.6%; and M7: 2.6%.
  • The survival rate was 30% and leukemia-free survival was 33%.
  • CONCLUSIONS: The study demonstrated a high prevalence of FAB M1 subtype in adults with de novo AML in São José dos Campos.
  • Our data suggest the occurrence of different regional prevalences of FAB AML categories in Brazil.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology

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  • (PMID = 16612463.001).
  • [ISSN] 1516-3180
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
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33. Bacher U, Kern W, Schnittger S, Hiddemann W, Schoch C, Haferlach T: Further correlations of morphology according to FAB and WHO classification to cytogenetics in de novo acute myeloid leukemia: a study on 2,235 patients. Ann Hematol; 2005 Nov;84(12):785-91
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  • [Title] Further correlations of morphology according to FAB and WHO classification to cytogenetics in de novo acute myeloid leukemia: a study on 2,235 patients.
  • In routine diagnostic procedures of acute myeloid leukemia (AML), the French-American-British (FAB) and World Health Organization (WHO) classifications both play a central role.
  • Some morphologic subtypes are specifically associated to distinct cytogenetic and molecular aberrations; however, such close correlations do not exist for the majority of entities.
  • We evaluated cytogenetics in 2,235 patients at diagnosis of AML with the FAB subtypes M0-2, M4, and M5-7.
  • Thus, cytomorphology of AML may be helpful to support or even initiate other diagnostic procedures, e.g., interphase fluorescence in situ hybridization and polymerase chain reaction.
  • In conclusion, the central role of morphology as defined by the FAB and WHO classification in AML at diagnosis is still justified in combination with other techniques.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 11 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Retrospective Studies. World Health Organization

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  • (PMID = 16132906.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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34. Patel BB, Mohamed AN, Schiffer CA: "Acute myelogenous leukemia like" translocations in CML blast crisis: two new cases of inv(16)/t(16;16) and a review of the literature. Leuk Res; 2006 Feb;30(2):225-32
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  • [Title] "Acute myelogenous leukemia like" translocations in CML blast crisis: two new cases of inv(16)/t(16;16) and a review of the literature.
  • We describe two patients with CML blast crisis with clonal evolution affecting 16q22 (t(16;16)(p13;q22) and inv(16)(p13;q22), abnormalities of core binding factor, usually found in de novo acute myeloid leukemia (AML)).
  • The bone marrow of both cases showed myelomonocytic (M4) differentiation and eosinophilia.
  • Both patients had prominent extramedullary disease and had poor response to treatment.
  • A literature search focused on patients with CML and additional chromosome changes more typical of AML, revealed that the morphology of the blasts correlated with the finding typical of the underlying "AML" cytogenetic abnormality and an overall very poor clinical outcome, even in the groups with "favorable" AML type translocations.
  • [MeSH-major] Blast Crisis / genetics. Chromosome Inversion. Chromosomes, Human, Pair 16. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid, Acute / genetics


35. Woo KS, Kim KE, Kim KH, Kim SH, Park JI, Shaffer LG, Han JY: Deletions of chromosome arms 7p and 7q in adult acute myeloid leukemia: a marker chromosome confirmed by array comparative genomic hybridization. Cancer Genet Cytogenet; 2009 Oct 15;194(2):71-4
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  • [Title] Deletions of chromosome arms 7p and 7q in adult acute myeloid leukemia: a marker chromosome confirmed by array comparative genomic hybridization.
  • Acute myeloid leukemia (AML) cases with monosomy 7 (-7) and del(7q) comprise a heterogeneous subgroup.
  • The association of losses in 7q with myeloid leukemia suggests that this region contains a tumor suppressor gene or genes whose loss of function contributes to leukemic transformation or tumor progression.
  • In the present case, we identified a rare abnormality involving deletion of both arms of chromosome 7 presenting with a marker chromosome-like appearance in an AML patient.
  • Bone marrow aspiration and biopsy revealed acute myelomonocytic leukemia.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Deletion. Chromosomes, Human, Pair 7. Leukemia, Myeloid, Acute / genetics


36. Gutierrez JA, Pan YX, Koroniak L, Hiratake J, Kilberg MS, Richards NG: An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line. Chem Biol; 2006 Dec;13(12):1339-47
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  • [Title] An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line.
  • Drug resistance in lymphoblastic and myeloblastic leukemia cells is poorly understood, with several lines of evidence suggesting that resistance can be correlated with upregulation of human asparagine synthetase (hASNS) expression, although this hypothesis is controversial.
  • These observations represent direct evidence that potent hASNS inhibitors may prove to be effective agents for the clinical treatment of acute lymphoblastic leukemia.

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  • (PMID = 17185229.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052064; United States / NIDDK NIH HHS / DK / R01 DK059315; United States / NIDDK NIH HHS / DK / DK52064; United States / NIDDK NIH HHS / DK / DK59315
  • [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 / Amino Acids, Sulfur; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
  • [Other-IDs] NLM/ NIHMS447417; NLM/ PMC3608209
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37. Ng KP, Soo-Hoo TS, Na SL, Tay ST, Hamimah H, Lim PC, Chong PP, Seow HF, Chavez AJ, Messer SA: The mycological and molecular study of Hortaea werneckii isolated from blood and splenic abscess. Mycopathologia; 2005 Jun;159(4):495-500
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  • We report the isolation of H. werneckii from blood and splenic abscess of two patients with acute myelomonocytic leukaemia. H. werneckii grew at room temperature but not at 37 degrees C, it was identified by biochemical tests, growth characteristics and the presence of conspicuous collarette intercalary on dividing yeast cells.
  • [MeSH-major] Fungemia / microbiology. Leukemia, Myelomonocytic, Acute / microbiology. Mitosporic Fungi / genetics. Mitosporic Fungi / isolation & purification. Splenic Diseases / microbiology

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  • (PMID = 15983734.001).
  • [ISSN] 0301-486X
  • [Journal-full-title] Mycopathologia
  • [ISO-abbreviation] Mycopathologia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA, Fungal
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38. Sun X, Zhang W, Ramdas L, Stivers DN, Jones DM, Kantarjian HM, Estey EH, Vadhan-Raj S, Medeiros LJ, Bueso-Ramos CE: Comparative analysis of genes regulated in acute myelomonocytic leukemia with and without inv(16)(p13q22) using microarray techniques, real-time PCR, immunohistochemistry, and flow cytometry immunophenotyping. Mod Pathol; 2007 Aug;20(8):811-20
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  • [Title] Comparative analysis of genes regulated in acute myelomonocytic leukemia with and without inv(16)(p13q22) using microarray techniques, real-time PCR, immunohistochemistry, and flow cytometry immunophenotyping.
  • Acute myeloid leukemia with inv(16)(p13q22), also known as M4Eo, is a distinct type of leukemia with characteristic clinicopathologic and cytogenetic features.
  • Cases of acute myelomonocytic leukemia without CBFbeta-MYH11 (M4) acted as our control.
  • We found that in the gene expression profile of M4Eo, NF-kappaB activators and inhibitors were upregulated and downregulated, respectively, suggesting that the NF-kappaB signaling pathway is activated at a higher level in M4Eo than in acute myelomonocytic leukemia M4.
  • These findings most likely represent the functional consequences of the abnormal chimeric protein CBFbeta-MYH11, which is unique to this disease, and suggest that NF-kappaB is a potential therapeutic target for treating M4Eo patients.
  • [MeSH-major] Chromosomes, Human, Pair 16. Flow Cytometry. Gene Expression Profiling / methods. Immunohistochemistry. Immunophenotyping / methods. Leukemia, Myelomonocytic, Acute / genetics. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction

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  • (PMID = 17571080.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30 CA016672-28
  • [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 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factor RelA
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39. Tarkun P, Hacıhanefioğlu A, Demirbağ E, Turgut T: Development of autoimmune hemolytic anemia during the treatment of a patient with acute myelomonocytic leukemia. Turk J Haematol; 2005 Jun 5;22(2):95-9
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  • [Title] Development of autoimmune hemolytic anemia during the treatment of a patient with acute myelomonocytic leukemia.
  • [Transliterated title] Akut miyelomonositik lösemili bir hastanın tedavisi srasında ortaya çıkan otoimmün hemolitik anemi.

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  • (PMID = 27264668.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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40. Mozziconacci MJ, Carbuccia N, Prebet T, Charbonnier A, Murati A, Vey N, Chaffanet M, Birnbaum D: Common features of myeloproliferative disorders with t(8;9)(p12;q33) and CEP110-FGFR1 fusion: report of a new case and review of the literature. Leuk Res; 2008 Aug;32(8):1304-8
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  • The 8p12 myeloproliferative syndrome is a rare, generally aggressive chronic myeloproliferative disorder (MPD).
  • We report here the tenth case of translocation (8;9)(p12;q33) in an acute myelomonocytic leukemia and provide a review of the literature that points to common syndrome features: the t(8;9)(p11;q33) MPD transforms rapidly, and always in myelomonocytic leukemia, with a possible B- or T-lymphoid involvement, which may include tonsil invasion.
  • [MeSH-major] Chromosomes, Human, Pair 8. Chromosomes, Human, Pair 9. Leukemia, Myelomonocytic, Acute / genetics. Myeloproliferative Disorders / genetics. Oncogene Proteins, Fusion / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism. Translocation, Genetic

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  • (PMID = 18096225.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.- / CEP110-FGFR1 fusion protein, human
  • [Number-of-references] 14
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41. Lin HR, Wang YZ, Wang DX, Chang Y, Hao L, Qin YZ, Li JL, Li LD, Huang XJ, Liu YR: [Quantitative analysis of dendritic cell subsets in bone marrow of patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1249-54
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  • [Title] [Quantitative analysis of dendritic cell subsets in bone marrow of patients with acute myeloid leukemia].
  • In order to study the quantity of dendritic cell (DC) subsets of bone marrow in patients with acute myeloid leukemia (AML), the bone marrow aspirate were collected from 77 newly diagnosed AML patients and from 30 healthy persons.
  • The quantity of DC subsets (myeloid dendritic cells, mDC and plasmacytoid dendritic cells, pDC) were detected by flow cytometry and analysed by 3-color and 4-color cytometric gate.
  • In subtypes of AML-M2, AML-M3 or AML-M4/5, 81.4%, 100% and 42.1% patients showed mDC decrease and 88.4%, 100% and 89.5% patients showed pDC decrease respectively by 4-color cytometric analysis.
  • It is concluded that the 4-color cytometric gate is better method for detection of mDC and pDC from bone marrow of newly diagnosed AML patients as compared with 3-color cytometric gate, the majority of AML patients showed reduction of mDC and pDC.
  • The percentages of patients with mDC normal or mDC increase in AML-M4/5 subtypes are more than that in AML-M2/3 subtypes, while the pDC does not show difference between AML subtypes.

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  • (PMID = 19840461.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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42. Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF: Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation. Blood; 2010 Apr 8;115(14):2749-54
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  • [Title] Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.
  • Recent genome-wide screening also revealed IDH1 mutation as a recurrent event in acute myeloid leukemia (AML), but its clinical implications in AML are largely unknown.
  • We analyzed 493 adult Chinese AML patients in Taiwan and found 27 patients (5.5%) harboring this mutation.
  • IDH1 mutation was strongly associated with normal karyotype (8.4%, P = .002), isolated monosomy 8 (P = .043), NPM1 mutation (P < .001), and French-American-British M1 subtype (P < .001), but inversely associated with French-American-British M4 subtype (P = .030) and expression of HLA-DR, CD13, and CD14 (P = .002, .003, and .038, respectively).
  • None of the 112 patients without IDH1 mutation at diagnosis acquired this mutation at relapse.
  • We conclude that IDH1 is associated with distinct clinical and biologic characteristics and seems to be very stable during disease evolution.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics

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  • [CommentIn] Blood. 2010 Jul 22;116(3):495-6 [20651083.001]
  • (PMID = 20097881.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13
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43. Eliashar R, Resnick IB, Goldfarb A, Wohlgelernter J, Gross M: Endoscopic surgery for sinonasal invasive aspergillosis in bone marrow transplantation patients. Laryngoscope; 2007 Jan;117(1):78-81
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  • Demographic data, primary disease, comorbidities, signs and symptoms, blood test results, preparation for surgery, surgical technique, and outcome were recorded.
  • The primary disease was acute myelogenous leukemia in 6, acute lymphoblastic leukemia in 3, chronic myeloblastic leukemia in one, severe combined immunodeficiency disease in 2, and myelodysplastic syndrome in 2 patients.
  • Diagnosis was made by physical examination, biopsy, culture, and computed tomography scan.
  • Six patients died of the primary illness or of comorbidities with no evidence of residual disease.
  • CONCLUSION: Early detection of IA in BMT patients enables aggressive treatment before the disease spreads into the orbit or brain.
  • [MeSH-major] Aspergillosis / surgery. Bone Marrow Transplantation / adverse effects. Endoscopy / methods. Leukemia / complications. Opportunistic Infections / surgery. Paranasal Sinus Diseases / surgery


44. Eljaafari A, Van Snick J, Voisin A, Cormont F, Farre A, Bienvenu J, Bernaud J, Rigal D, Thomas X: Alloreaction increases or restores CD40, CD54, and/or HLA molecule expression in acute myelogenous leukemia blasts, through secretion of inflammatory cytokines: Dominant role for TNFbeta, in concert with IFNgamma. Leukemia; 2006 Nov;20(11):1992-2001
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  • [Title] Alloreaction increases or restores CD40, CD54, and/or HLA molecule expression in acute myelogenous leukemia blasts, through secretion of inflammatory cytokines: Dominant role for TNFbeta, in concert with IFNgamma.
  • Here, we addressed whether alloreaction-derived cytokines may also lead to acute myelogenous leukemia (AML) blast differentiation.
  • With this aim, supernatant (sn) harvested from major or minor histocompatibility antigen-mismatched mixed lymphocyte reaction (MLR) were used to culture French American Bristish (FAB) type M4 or M5 AML blasts.
  • Our results showed that the secreted factors induced upregulation of CD40, CD54, and/or HLA molecules in AML blasts.
  • But, in line of its much higher levels of secretion, TNFbeta, rather than TNFalpha, was likely to play a preponderant role in AML blast differentiation.
  • Moreover TNFbeta and IFNgamma were also likely to be involved in the AML blast differentiation-mediated by HLA-identical donor T-cell alloresponse against recipient AML blasts.
  • In conclusion, we show herein that upon allogeneic reaction, TNFbeta secretion contributes, in concert with IFNgamma, to increase or restore surface molecules involved in AML blast interaction with T cells.
  • [MeSH-major] Antigens, CD40 / metabolism. Histocompatibility Antigens Class II / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / metabolism. Leukemia, Myeloid, Acute / metabolism. Lymphotoxin-alpha / metabolism

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  • (PMID = 16990783.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD40; 0 / Blood Proteins; 0 / Culture Media, Serum-Free; 0 / Histocompatibility Antigens Class II; 0 / Interleukin-1; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma
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45. Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K: KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells. Leuk Res; 2008 Sep;32(9):1358-65
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  • [Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
  • We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in leukemia cells.
  • We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
  • Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
  • This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.
  • [MeSH-major] Cell Cycle / physiology. Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology

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  • (PMID = 18384876.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
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46. Vora HH, Shukla SN, Brahambhatt BV, Mehta SH, Patel NA, Parikh SK, Shah KN, Shah PM: Clinical relevance of FLT3 receptor protein expression in Indian patients with acute leukemia. Asia Pac J Clin Oncol; 2010 Dec;6(4):306-19
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  • [Title] Clinical relevance of FLT3 receptor protein expression in Indian patients with acute leukemia.
  • AIM: FLT3 is a receptor tyrosine kinase that plays an important role in the pathogenesis of leukemia.
  • The present study aimed to evaluate the role of FLT3 protein in patients with acute leukemia.
  • METHOD: FLT3 protein was quantified by flow cytometry on leukemic blasts using CD135 antibody in 160 patients with acute leukemia.
  • RESULTS: We demonstrated FLT3 protein expression (>20%) in 82% of acute myeloid leukemia (AML), 60% of B-lineage acute lymphoblastic leukemia (B-ALL), 23% of T-lineage acute lymphoblastic leukemia (T-ALL) and 80% of biphenotypic leukemia.
  • Further, FLT3 expression was seen to be significantly higher in AMLM2, M4, and M5 than in AMLM3.
  • When correlated with disease status, all patients in the relapsed AML group had FLT3 > 20% at diagnosis.
  • Unlike AML, the relapsed group of B-ALL showed a lower incidence of FLT3 than the remission group.
  • CONCLUSION: In summary, our data imply that there is frequent overexpression of the FLT3 protein in AML and B-ALL patients of Indian origin.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. fms-Like Tyrosine Kinase 3 / metabolism

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  • [Copyright] © 2010 Blackwell Publishing Asia Pty Ltd.
  • (PMID = 21114781.001).
  • [ISSN] 1743-7563
  • [Journal-full-title] Asia-Pacific journal of clinical oncology
  • [ISO-abbreviation] Asia Pac J Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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47. Shimizu T, Kuromi A, Takeda K: Synergistic induction of gene expression during the differentiation into mature macrophage in human myeloblastic leukemia cells treated with TPA and KH1060. Leuk Res; 2009 Jun;33(6):803-9
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  • [Title] Synergistic induction of gene expression during the differentiation into mature macrophage in human myeloblastic leukemia cells treated with TPA and KH1060.
  • Treatment of human myeloblastic leukemia ML-1 cells with the phorbol ester TPA in combination with the vitamin D(3) analogue KH1060 will induce a synergistic differentiation to mature macrophage with multinuclei.
  • [MeSH-major] Calcitriol / analogs & derivatives. Cell Differentiation. Gene Expression Regulation / drug effects. Leukemia, Myeloid, Acute / pathology. Macrophages / cytology. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 19144406.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 131875-08-6 / KH 1060; FXC9231JVH / Calcitriol; NI40JAQ945 / Tetradecanoylphorbol Acetate
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48. Blatt J, Greenwood R, Weig S, Rao K, Fedoriw GD, Dent G: Isolated central nervous system relapse in an adolescent with acute myelomonocytic leukemia, Charcot Marie Tooth syndrome, and paraneoplastic autoantibody. J Pediatr Hematol Oncol; 2010 Oct;32(7):571-3
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  • [Title] Isolated central nervous system relapse in an adolescent with acute myelomonocytic leukemia, Charcot Marie Tooth syndrome, and paraneoplastic autoantibody.
  • A 17-year-old boy, with acute myelomonocytic leukemia and inversion 16(p13q22) developed polyneuropathy and isolated central nervous system relapse.
  • Scoliosis and high-arched feet suggested a diagnosis of Charcot Marie Tooth (CMT) syndrome and genetic testing confirmed duplication at the PMP22 locus at chromosome 17p11.12.
  • This case extends the clinical spectrum of cancer with CMT, and of paraneoplastic disorders.
  • [MeSH-major] Autoantibodies / blood. Charcot-Marie-Tooth Disease / immunology. Leukemia, Myelomonocytic, Acute / immunology. Paraneoplastic Syndromes, Nervous System / immunology

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  • (PMID = 20724950.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Myelin Proteins; 0 / PMP22 protein, human
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49. Otsubo K, Kanegane H, Eguchi M, Eguchi-Ishimae M, Tamura K, Nomura K, Abe A, Ishii E, Miyawaki T: ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 Oct 1;202(1):22-6
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  • [Title] ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia.
  • Leukemia with t(1;12)(q21;p13) was previously described in a 5-year-old boy with acute myeloblastic leukemia (AML-M2) who exhibited a novel ETV6-aryl hydrocarbon receptor nuclear translocator (ARNT) fusion protein.
  • We herein report the case of a 2-year-old boy with T-cell lymphoblastic leukemia (T-ALL) harboring t(1;12)(q21;p13).
  • The ETV6-ARNT fusion is associated not only with AML but also with T-ALL.
  • [MeSH-major] ARNTL Transcription Factors / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804916.001).
  • [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 / ARNTL Transcription Factors; 0 / DNA Primers; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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50. Park TS, Lee ST, Song J, Lee KA, Lee JH, Kim J, Lee HJ, Han JH, Kim JK, Cho SR, Choi JR: Detection of a novel CBFB/MYH11 variant fusion transcript (K-type) showing partial insertion of exon 6 of CBFB gene using two commercially available multiplex RT-PCR kits. Cancer Genet Cytogenet; 2009 Mar;189(2):87-92
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  • [Title] Detection of a novel CBFB/MYH11 variant fusion transcript (K-type) showing partial insertion of exon 6 of CBFB gene using two commercially available multiplex RT-PCR kits.
  • We report on a 20-year-old man with acute myeloid leukemia (AML) showing a distinct novel CBFB/MYH11 variant fusion transcript.
  • Initial results of bone marrow, chromosome, and flow cytometric analyses were not in accordance with the diagnosis of acute myelomonocytic leukemia with eosinophilia (AML-M4Eo) or AML with a CBFB/MYH11 rearrangement.
  • Not only does this case show a partial insertion of exon 6 of the CBFB (ENSG00000067955) gene, but it also involves novel breakpoints within both exon 6 of the CBFB gene and exon 28 (previously exon 7) of the MYH11 (ENSG00000133392) gene, which is regarded as a previously non-reported, new type (K-type) of CBFB/MYH11 fusion transcript.
  • Therefore, multiplex RT-PCR and sequence analysis of these atypical products should be performed to diagnose atypical AML with CBFB/MYH11 rearrangement, to predict prognosis of these patients as well as to elucidate the molecular mechanism.
  • [MeSH-major] Core Binding Factor beta Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutagenesis, Insertional. Myosin Heavy Chains / genetics. Reagent Kits, Diagnostic. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19215788.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; 0 / Reagent Kits, Diagnostic; 0 / Recombinant Fusion Proteins; EC 3.6.4.1 / Myosin Heavy Chains
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51. Chou CY, Chien CH, Han YS, Prebanda MT, Hsieh HP, Turk B, Chang GG, Chen X: Thiopurine analogues inhibit papain-like protease of severe acute respiratory syndrome coronavirus. Biochem Pharmacol; 2008 Apr 15;75(8):1601-9
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  • [Title] Thiopurine analogues inhibit papain-like protease of severe acute respiratory syndrome coronavirus.
  • The papain-like protease of severe acute respiratory syndrome coronavirus (PLpro) (EC 3.4.22.46) is essential for the viral life cycle and therefore represents an important antiviral target.
  • Both 6MP and 6TG are still used extensively in clinics, especially for children with acute lymphoblastic or myeloblastic leukemia.

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  • (PMID = 18313035.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protease Inhibitors; 0 / Viral Proteins; E7WED276I5 / 6-Mercaptopurine; EC 3.4.22.- / 3C-like protease, SARS coronavirus; EC 3.4.22.- / Cysteine Endopeptidases; FTK8U1GZNX / Thioguanine
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52. Astashkin EI, Suvorov NI, Mikhailova AA, Grachev SV: Change in the Ca2+ response to formyl peptide in HL-60 myeloblastic leukemia cells after the induction of their differentiation by MP-4 myelogenic peptide. Dokl Biol Sci; 2006 May-Jun;408:265-8
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  • [Title] Change in the Ca2+ response to formyl peptide in HL-60 myeloblastic leukemia cells after the induction of their differentiation by MP-4 myelogenic peptide.
  • [MeSH-major] Calcium / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Oligopeptides / therapeutic use

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53. Shen M, Yen A: c-Cbl tyrosine kinase-binding domain mutant G306E abolishes the interaction of c-Cbl with CD38 and fails to promote retinoic acid-induced cell differentiation and G0 arrest. J Biol Chem; 2009 Sep 18;284(38):25664-77
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  • Retinoic acid (RA) causes HL-60 human myeloblastic leukemia cell myeloid differentiation that is dependent on MAPK signaling.
  • Unlike wild-type (WT) c-Cbl, the G306E mutant c-Cbl fails to propel RA-induced differentiation, and disrupts the normal association with CD38.

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  • (PMID = 19635790.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / Membrane Glycoproteins; 0 / Multiprotein Complexes; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins c-vav; 0 / SLP-76 signal Transducing adaptor proteins; 5688UTC01R / Tretinoin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC2757968
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54. Pan JL, Xue YQ, Jiang HY, He J, Wang W, Wu YF: [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Aug;22(4):444-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5].
  • OBJECTIVE: To explore the value of reverse transcription-multiplex nested PCR in detecting MLL rearrangement in lzAML-M4/M5.
  • Five common MLL fusion genes and MLL partial tandem duplication in 40 AML cases, including 12 M4 and 28 M5 were detected by reverse transcription(RT)-multiplex nested PCR.
  • CONCLUSION: RT-multiplex nested PCR is a powerful technique in the detection of MLL rearrangement for tentativelly diagnosed AML-M4/M5.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic

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  • (PMID = 16086288.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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55. Zhu YL, Liu J, Zhu P, DU JW, Zhang Y, Gu JY: [Expression of PRAME gene in acute leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1144-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of PRAME gene in acute leukemia and its clinical significance].
  • This study was aimed to detect the expression levels of preferentially expressed antigen of melanoma (PRAME) gene in acute leukemia (AL) and to evaluate the clinical significance of PRAME gene.
  • The quantitative detection method was established by SYBR Green I real-time quantitative RT-PCR, then PRAME mRNA was measured by this method in 55 cases of acute leukemia, out of which 43 cases were acute myeloid leukemia (AML), 9 cases were acute lymphocytic leukemia (ALL) and other types leukemia were 3 cases.
  • The results showed that the expression of PRAME gene was found in 35 cases of acute leukemia, the positive percentage was 64%.
  • In 35 PRAME positive cases, 28 cases were AML, which mainly belonged to M3, M4 and M2 subtypes, and 5 cases was ALL.
  • No significant relationship was found between PRAME expression level and clinical characteristics (age, sex, WBC count, blast cells in BM).
  • It is concluded that the PRAME gene expresses in 64% AML patients, which mainly belonged to M3, M4 and M2 subtypes, no expression could be detected in any of the non-malignant hematological diseases and healthy volunteers.
  • These results suggest that PRAME expression in acute leukemia may be a useful marker to detect the minimal resi-dual disease (MRD) and to determine the response to therapy in AL patients.

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  • (PMID = 18088454.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
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56. Lemez P, Gáliková J, Michalová K, Dvoráková D, MacWhannell A, Zemanová Z, Stejskal J: [Patients older than 80 years with de novo acute myeloid leukemias without erythroblastic and/or megakaryocytic dysplasia achieve complete remission and longer survival after classical chemotherapy 3 + 7]. Vnitr Lek; 2010 Jan;56(1):37-43
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  • [Title] [Patients older than 80 years with de novo acute myeloid leukemias without erythroblastic and/or megakaryocytic dysplasia achieve complete remission and longer survival after classical chemotherapy 3 + 7].
  • [Transliterated title] Nemocní starsí 80 let s de novo akutními myeloidními leukemiemi bez dysplazie v erytroblastické 8/nebo megakaryocytární radĕ dosahují kompletní remise a delsího prezlití po klasické chemoterapii 3+7.
  • Chemotherapy in most patients with AML over 80 years of age is not recommended because their median survival is about 1 month.
  • We report 9 consecutive patients with de novo AML diagnosed and treated in 1992-2008.
  • All bone marrow samples were hypercellular, classified as FAB types M2 in 2 cases, M4 in 6, and M5 in one case.
  • Two patients with a normal karyotype had resistant AML and survived 1.0 and 2.7 months; one patient with a complex karyotype died of septic shock on the 10th day of therapy.
  • Three remaining patients with AML M4, a normal karyotype but without EMD, achieved complete remission in spite of co-morbidities and a poor performance status.
  • Very elderly AML patients without EMD appear to represent a favorable prognostic biological category (single-lineage AML) that show a good response to standard dose chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20184110.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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57. Zhu YL, Zhang Y, Zhu P, Yang Y, Du JW, Liu J: [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):236-9
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  • [Title] [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia].
  • OBJECTIVE: To assess the value of common fusion genes analysis in the diagnosis and classification of leukemia by multiplex RT-PCR.
  • METHODS: The multiplex RT-PCR, including 8 parallel PCR reactions, could screen 86 mRNA breakpoints or splice variants at the same time, which was important for the diagnosis and prognosis of leukemia.
  • Bone marrow samples from 161 cases of leukemia and 8 cases of myelodysplastic syndrome (MDS) were involved in the study.
  • The distribution of common fusion genes in leukemia was analyzed by the method mentioned above in combination with clinical and morphological features.
  • RESULTS: Ten fusion genes were detected in 115 cases of leukemia, including AML1/ETO, PML/RAR alpha, PLZF/RAR alpha, dupMLL, MLL/AF6, MLL/AF10, CBFbeta/MYH11, BCR/ABL, Hox11, and EVI1 BCR/ABL was positive in all the 52 cases of chronic myeloid leukemia; PML/RAR alpha was found in 21 of 25 acute promyelocytic leukemia (APL), and PLZF/RAR alpha was detected in one case of APL.
  • Sixteen cases of 17 AML1/ETO-positive acute leukemia (AL) belonged to FAB-M2 subtype, and one case was mixed leukemia.
  • Three of 4 AL cases carrying CBFbeta/MYH11 were M4 subtype, and one was M5 subtype.
  • Furthermore, BCR/ABL was detected in 5 acute lymphoblastic leukemia (ALL) cases.
  • Fusion genes were also found in 2 MDS cases, of which AML1/ETO positive-MDS-RAEB progressed to AML rapidly.
  • CONCLUSION: Screening of common fusion genes by multiplex RT-PCR is an important tool which could provide useful and reliable molecular genetic information for the diagnosis and treatment of leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 15968309.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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58. Steinherz PG, Shukla N, Kobos R, Steinherz L: Remission re-induction chemotherapy with clofarabine, topotecan, thiotepa, and vinorelbine for patients with relapsed or refractory leukemia. Pediatr Blood Cancer; 2010 May;54(5):687-93
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  • [Title] Remission re-induction chemotherapy with clofarabine, topotecan, thiotepa, and vinorelbine for patients with relapsed or refractory leukemia.
  • BACKGROUND: We determined the maximum tolerated dose (MTD) of clofarabine when administered with topotecan, vinorelbine, thiotepa, and dexamethasone (TVTC) for children with relapsed or refractory acute leukemia, and observed the efficacy and toxicities of this therapy.
  • PROCEDURE: Twelve patients with acute lymphoblastic or myeloblastic leukemia were given a 14-day remission induction therapy.
  • Three patients had progressive disease.
  • One patient died on day 45 with marrow hypoplasia without evidence of leukemia.
  • CONCLUSION: TVTC has significant anti-leukemic activity in both acute lymphoblastic and myeloblastic leukemia.
  • This is the recommended dose for the phase II study in patients with refractory or relapsed leukemia, a population which has limited therapeutic options.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy

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  • (PMID = 20205253.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 5V9KLZ54CY / Vinblastine; 762RDY0Y2H / clofarabine; 7M7YKX2N15 / Topotecan; 905Z5W3GKH / Thiotepa; Q6C979R91Y / vinorelbine
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59. Yen A, Varvayanis S, Smith JL, Lamkin TJ: Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Eur J Cell Biol; 2006 Feb;85(2):117-32
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  • Retinoic acid (RA) is known to cause MAPK signaling which propels G0 arrest and myeloid differentiation of HL-60 human myeloblastic leukemia cells.
  • A triple Y to F mutant SLP-76 known to be a dominant negative in T-cell receptor signaling failed to enhance RA-induced paxillin expression, but enhanced RA-induced ERK activation, differentiation and G0 arrest essentially as well as wild-type SLP-76.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Blotting, Western. Enzyme Activation. HL-60 Cells. Humans. Immunoprecipitation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / physiopathology. Mutation. Paxillin / genetics. Paxillin / physiology. Phosphorylation. Receptors, Antigen, T-Cell / physiology. Signal Transduction. Superoxides / metabolism. Transfection. Up-Regulation / drug effects

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  • (PMID = 16439309.001).
  • [ISSN] 0171-9335
  • [Journal-full-title] European journal of cell biology
  • [ISO-abbreviation] Eur. J. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Paxillin; 0 / Phosphoproteins; 0 / Receptors, Antigen, T-Cell; 0 / SLP-76 signal Transducing adaptor proteins; 11062-77-4 / Superoxides; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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60. Lamkin TJ, Chin V, Varvayanis S, Smith JL, Sramkoski RM, Jacobberger JW, Yen A: Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels. J Cell Biochem; 2006 Apr 15;97(6):1328-38
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  • [Title] Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels.
  • Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell.
  • Expression of CD38 enhanced retinoic acid-induced myeloid differentiation and G0 cell cycle arrest, but at higher expression levels, induced differentiation was blocked and retinoic acid induced a loss of cell viability instead.
  • In the case of 1,25-dihydroxyvitamin D3, induced monocytic differentiation was also enhanced by CD38 and not enhanced by higher expression levels, but without induced loss of viability.
  • [MeSH-major] Antigens, CD38 / metabolism. Cell Differentiation / drug effects. Cell Survival / drug effects. Leukemia, Myeloid, Acute / metabolism. Tretinoin / pharmacology

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16329108.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / T32 ES007052
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin; EC 3.2.2.5 / Antigens, CD38
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61. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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  • [Title] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In this study, we investigated the cellular and molecular function of FOXM1 in AML cells.
  • The FOXM1 messenger RNA (mRNA) expressed in AML cell lines was predominantly the FOXM1B isoform, and its levels were significantly higher than in normal high aldehyde dehydrogenase activity (ALDH(hi)) cells.
  • Reduction of FOXM1 expression in AML cells inhibited cell proliferation compared with control cells, through induction of G(2)/M cell cycle arrest, a decrease in the protein expression of Aurora kinase B, Survivin, Cyclin B1, S-phase kinase-associated protein 2 and Cdc25B and an increase in the protein expression of p21(Cip1) and p27(Kip1).
  • FOXM1 messenger RNA (mRNA) was overexpressed in all 127 AML clinical specimens tested (n = 21, 56, 32 and 18 for M1, M2, M4 and M5 subtypes, respectively).
  • Compared with normal ALDH(hi) cells, FOXM1 gene expression was 1.65- to 2.26-fold higher in AML cells.
  • Moreover, the FOXM1 protein was more strongly expressed in AML-derived ALDH(hi) cells compared with normal ALDH(hi) cells.
  • In addition, depletion of FOXM1 reduced colony formation of AML-derived ALDH(hi) cells due to inhibition of Cdc25B and Cyclin B1 expression.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • Thus, inhibition of FOXM1 expression represents an attractive target for AML therapy.
  • [MeSH-major] Cell Cycle. Cell Cycle Proteins / metabolism. Cell Proliferation. Forkhead Transcription Factors / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Aged. Aldehyde Dehydrogenase / genetics. Aldehyde Dehydrogenase / metabolism. Apoptosis. Aurora Kinase B. Aurora Kinases. Blotting, Western. Cells, Cultured. Cyclin B1 / genetics. Cyclin B1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Fluorescent Antibody Technique. Humans. Inhibitor of Apoptosis Proteins. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocytes / metabolism. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Middle Aged. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / metabolism

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  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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62. Bowen DT, Frew ME, Hills R, Gale RE, Wheatley K, Groves MJ, Langabeer SE, Kottaridis PD, Moorman AV, Burnett AK, Linch DC: RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years. Blood; 2005 Sep 15;106(6):2113-9
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  • [Title] RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years.
  • The pathogenesis of acute myeloid leukemia (AML) involves the cooperation of mutations promoting proliferation/survival and those impairing differentiation.
  • The RAS pathway has been implicated as a key component of the proliferative drive in AML.
  • We have screened AML patients, predominantly younger than 60 years and treated within 2 clinical trials, for NRAS (n = 1106), KRAS (n = 739), and HRAS (n = 200) hot-spot mutations using denaturing high-performance liquid chromatography or restriction fragment length polymorphism (RFLP) analysis.
  • KRAS mutations were relatively overrepresented in French-American-British (FAB) type M4 (P < .001).
  • RAS mutation did not influence clinical outcome (overall/disease-free survival, complete remission, relapse rate) either for the entire cohort or within cytogenetic risk groups.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. ras Proteins / genetics
  • [MeSH-minor] Acute Disease. Age Factors. Cytogenetic Analysis. DNA Mutational Analysis. Genes, ras. Humans. Middle Aged. Molecular Epidemiology. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Survival Analysis. Treatment Outcome. fms-Like Tyrosine Kinase 3

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  • (PMID = 15951308.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
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63. Bacher U, Haferlach C, Kern W, Haferlach T, Schnittger S: Prognostic relevance of FLT3-TKD mutations in AML: the combination matters--an analysis of 3082 patients. Blood; 2008 Mar 1;111(5):2527-37
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  • [Title] Prognostic relevance of FLT3-TKD mutations in AML: the combination matters--an analysis of 3082 patients.
  • We characterized the mutational status of the FLT3 tyrosine kinase domain (FLT3-TLD) in 3082 patients with newly diagnosed AML.
  • FLT3-TKD mutations were most frequent in the AML FAB subtypes M5b (15 of 114; 13.2%), M3v (6 of 51; 11.8%), and M4 (39 of 484; 8.1%).
  • Similar to FLT3-LM, the FLT3-TKD mutations show elevated peripheral leukocytes compared with FLT3wt AML.
  • In contrast, we found an additional favorable impact of FLT3-TKD on EFS in prognostically favorable AML with NPM1- or CEBPA mutations.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / chemistry. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17965322.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Neoplasm Proteins; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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64. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Cohort Studies. Comorbidity. Cytogenetic Analysis / methods. Down Syndrome / diagnosis. Down Syndrome / epidemiology. Down Syndrome / genetics. Female. Humans. Incidence. Infant. Infant, Newborn. Karyotyping. Male. Ploidies. Recurrence. Registries / statistics & numerical data. Risk Factors. Scandinavian and Nordic Countries / epidemiology

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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65. Patnaik MM, Gangat N, Knudson RA, Keefe JG, Hanson CA, Pardanani A, Ketterling RP, Tefferi A: Chromosome 8p11.2 translocations: prevalence, FISH analysis for FGFR1 and MYST3, and clinicopathologic correlates in a consecutive cohort of 13 cases from a single institution. Am J Hematol; 2010 Apr;85(4):238-42
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  • FISH analysis was performed in 13 patients (12 had myeloid neoplasms) and revealed abnormalities of MYST3 (n = 4) or FGFR1 (n = 4) in eight patients.
  • MYST3 abnormalities were associated with acute myeloid leukemia (AML), M4 in three and M6 in one.
  • Three of the four FGFR1-rearranged cases were associated with myeloproliferative neoplasms but none, including the two with sole 8p11.2, displayed the typical phenotype for stem cell leukemia/lymphoma (SCLL) and only one had eosinophilia; the fourth case had AML-M4.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Hematologic Neoplasms / genetics. Histone Acetyltransferases / genetics. In Situ Hybridization, Fluorescence / methods. Myeloproliferative Disorders / genetics. Oncogene Fusion. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cohort Studies. Eosinophilia / genetics. Female. Genetic Predisposition to Disease. Genetic Testing. Humans. Karyotyping. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Retrospective Studies

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  • (PMID = 20143402.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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66. Abdelkefi A, Torjman L, Ladeb S, Sghaïer Z, Jeddi R, Lakhal A, Ramzu A, Gamoudi A, Othman TB: Isolated extramedullary relapse in the breast of a patient with acute myeloid leukemia following allogeneic stem cell transplantation: case report and review of the literature. Int J Hematol; 2007 Feb;85(2):149-53
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  • [Title] Isolated extramedullary relapse in the breast of a patient with acute myeloid leukemia following allogeneic stem cell transplantation: case report and review of the literature.
  • We report an unsual case of a woman with acute myeloid leukemia who showed an isolated extramedullary relapse (IEMR) in the breast following allogeneic stem cell transplantation and review the related literature.
  • The review suggests that an M2 or M4 phenotype in the French-American-British classification and a favorable cytogenetic risk group are more frequently associated with the occurrence of IEMR.
  • [MeSH-major] Breast Neoplasms. Leukemia, Myeloid, Acute. Stem Cell Transplantation

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  • (PMID = 17321994.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 32
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67. Mylonakis ME, Petanides TA, Valli VE, Vernau W, Koytinas AF, Michael RS: Acute myelomonocytic leukaemia with short-term spontaneous remission in a cat. Aust Vet J; 2008 Jun;86(6):224-8
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  • [Title] Acute myelomonocytic leukaemia with short-term spontaneous remission in a cat.
  • A complete blood count (CBC) and a biochemistry profile showed leukocytosis, numerous blast cells in the peripheral blood, thrombocytopenia, hyperglobulinaemia and a positive test for feline leukaemia virus antigen.
  • A diagnosis of acute myelomonocytic leukaemia was made on the basis of the results of bone marrow cytology, histopathology, and immunochemistry (CD3, CD79a, lysozyme, and myeloperoxidase) tests.
  • Following an unexpected 1-month period of clinical and clinicopathological remission without chemotherapy, the cat relapsed and died 1 week later.
  • [MeSH-major] Cat Diseases / diagnosis. Leukemia, Myelomonocytic, Acute / veterinary. Neoplasm Regression, Spontaneous

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  • (PMID = 18498558.001).
  • [ISSN] 0005-0423
  • [Journal-full-title] Australian veterinary journal
  • [ISO-abbreviation] Aust. Vet. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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68. Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia. Leuk Res; 2005 May;29(5):557-64
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  • [Title] p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
  • Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with acute leukemia.
  • To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-cell acute lymphoblastic leukemia (PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
  • Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
  • Among 108 AML patients, p15 mRNA expression was significantly lower in the myeloid lineage (M1, M2, M3) than the monocytic lineage (M4, M5) (P = 0.0019).
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Lineage. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured

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  • (PMID = 15755508.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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69. Koga Y, Matsuzaki A, Suminoe A, Washitoh N, Hara T, Hara T, Tajiri T, Taguchi T: Treatment-related acute myelomonocytic leukemia with t(11;19) in a child following chemotherapy for hepatoblastoma. Pediatr Blood Cancer; 2008 Apr;50(4):943-4
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  • [Title] Treatment-related acute myelomonocytic leukemia with t(11;19) in a child following chemotherapy for hepatoblastoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hepatoblastoma / drug therapy. Leukemia, Myelomonocytic, Acute / chemically induced. Liver Neoplasms / drug therapy. Neoplasms, Second Primary / chemically induced. Translocation, Genetic


70. Shahin D, Aly R, Ebrahim MA: Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics. Egypt J Immunol; 2010;17(2):23-32
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  • [Title] Prognostic significance of FLT3 internal tandem duplication in egyptian patients with acute myeloid leukemia with normal or favorable risk cytogenetics.
  • Internal tandem duplication (ITD) of the FLT3 gene (FLT3/ITD) has been linked to poor outcome in acute myeloid leukemia (AML).
  • The aim of this study was to evaluate the prognostic significance of FLT3/ITD in patients with de novo AML and normal or favorable risk cytogenetics (NFC-AML).
  • Blood samples from 39 patients with AML were subjected to PCR of exons 14 and 15 of the FLT3 gene.
  • Patients were M1 3/13, M2 2/12, M3 1/9, M4 0/4 and M5 0/1.
  • Interestingly, disease free survival (DFS) at 3 years was significantly different in studied patients: DFS was 5% in patients with FLT3/ITD+ vs 30% of patients with FLT3/ITD- (P = 0.001).

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  • (PMID = 23082484.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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71. Yan Q, Jiang Z, Yang S, Deng W, Han L: A novel homodimeric lectin from Astragalus mongholicus with antifungal activity. Arch Biochem Biophys; 2005 Oct 1;442(1):72-81
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  • A novel lectin (AMML) was isolated from a Chinese herb, i.e., the roots of Astragalus mongholicus, using a combination of ammonium sulfate fraction and ion exchange chromatographies.
  • The molecular mass of intact AMML was determined to be 66,396 Da by MALDI-TOF mass spectrometry and 61.8 kDa by gel filtration, respectively.
  • AMML was a dimeric protein composed of two identical subunits each with a molecular mass of 29.6 kDa.
  • N-terminal amino acid sequence of AMML was determined as ESGINLQGDATLANN.

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  • (PMID = 16140255.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Blood Group Antigens; 0 / Glycoproteins; 0 / Lectins; SU46BAM238 / Ammonium Sulfate; X2RN3Q8DNE / Galactose
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72. Struhal W, Oberndorfer S, Lahrmann H, Lindeck-Pozza E, Hess B, Nussgruber V, Pöhnl R, Dobner T, Grisold W: Myeloid sarcoma in the central nervous system: case report and review of the literature. Acta Clin Croat; 2008 Mar;47(1):19-24
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  • [Title] Myeloid sarcoma in the central nervous system: case report and review of the literature.
  • Myeloid sarcomas are rare manifestations of mainly myeloblastic leukemia.
  • A case is added herewith and a review was performed to investigate clinical characteristics and treatment options of central nervous system myeloid sarcoma.
  • A 61-year-old female with acute myeloblastic leukemia (FAB M5) and progressive left sided hemiparesis showed a right parieto-occipital epidural lesion mimicking meningioma.
  • Partial resection was performed to reveal a myeloid sarcoma.
  • Reviewing the literature we identified 44 cases with sufficient description of the diagnosis, treatment and follow up to one year.
  • [MeSH-major] Brain Neoplasms / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary. Occipital Lobe. Parietal Lobe. Sarcoma, Myeloid / diagnosis

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  • (PMID = 18714643.001).
  • [ISSN] 0353-9466
  • [Journal-full-title] Acta clinica Croatica
  • [ISO-abbreviation] Acta Clin Croat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 20
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73. Kiss F, Simon A, Csáthy L, Hevessy Z, Katona E, Kiss C, Kappelmayer J: A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII. Cytometry A; 2008 Mar;73(3):194-201
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  • [Title] A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII.
  • By using 3- and 4-color flow cytometry FXIII expression was investigated in normal peripheral blood and bone marrow samples and in acute myeloblastic (AML) and lymphoblastic (ALL) leukemia cases.
  • In samples derived from patients with AML M4 and M5, FXIII-A sensitively identified blast cells.
  • These data provide evidence that FXIII-A is a sufficiently sensitive marker in differentiating myeloblasts and monoblasts and is suitable for identifying leukemia-associated phenotypes in ALL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Factor XIII / chemistry. Factor XIII / physiology. Leukemia / blood. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Animals. Blood Platelets / chemistry. Blood Platelets / metabolism. Blood Platelets / pathology. Flow Cytometry / methods. Humans. Monocytes / chemistry. Monocytes / metabolism. Monocytes / pathology

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  • [Copyright] Copyright 2007 International Society for Analytical Cytology.
  • (PMID = 18000871.001).
  • [ISSN] 1552-4930
  • [Journal-full-title] Cytometry. Part A : the journal of the International Society for Analytical Cytology
  • [ISO-abbreviation] Cytometry A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9013-56-3 / Factor XIII
  • [Number-of-references] 56
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74. Monreal MB, Pardo ML, Pavlovsky MA, Fernandez I, Corrado CS, Giere I, Sapia S, Pavlovsky S: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia. Cytometry B Clin Cytom; 2006 Mar;70(2):63-70
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  • METHODS: We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19).
  • RESULTS: Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7).
  • De novo AML showed decreased immature HPC.
  • High numbers of immature HPC correlated with higher IPSS risk groups (P = 0.05) and showed significant impact on disease progression (P = 0.03).
  • Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Disease Progression. Female. Flow Cytometry. HLA-DR Antigens / immunology. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / immunology. Male. Middle Aged. Multiple Myeloma / diagnosis. Multiple Myeloma / immunology. Observer Variation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Reproducibility of Results. Risk Factors

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  • [Copyright] Copyright 2005 International Society for Analytical Cytology.
  • (PMID = 16470534.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; EC 3.2.2.5 / Antigens, CD38
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75. Reikvam H, Hatfield KJ, Oyan AM, Kalland KH, Kittang AO, Bruserud O: Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation. Eur J Haematol; 2010 Mar;84(3):239-51
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  • [Title] Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation.
  • OBJECTIVES: Angiogenesis seems important for both leukemogenesis and chemosensitivity in acute myelogenous leukemia (AML).
  • We investigated the constitutive release of MMPs and TIMPs for a large group of consecutive AML patients.
  • METHODS: AML cells were cultured in vitro either alone or together with microvascular endothelial cells, and levels of MMPs and TIMPs were determined in culture supernatants.
  • RESULTS: AML cells showed constitutive release of several MMPs and TIMPs.
  • MMP-9 release was higher for AML cells with monocytic differentiation corresponding to the FAB-subtype M4/M5 AML; it was mainly released in its inactive form, but endogenously active MMP-9 could be detected even in the presence of the constitutively released TIMP-1/2.
  • Endothelial cells released relatively high levels of MMP-10, and these levels were further increased by coculture with AML cells.
  • CONCLUSION: We conclude that primary human AML cells show constitutive release of both MMPs and TIMPs, and this release may be important for leukemogenesis and possibly also for chemosensitivity.
  • [MeSH-major] Leukemia, Myeloid / pathology. Matrix Metalloproteinases / secretion. Neoplasm Proteins / secretion. Tissue Inhibitor of Metalloproteinases / secretion
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Angiopoietin-2 / pharmacology. Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Boronic Acids / pharmacology. Bortezomib. Cells, Cultured / cytology. Chemokines / secretion. Coculture Techniques. Culture Media, Serum-Free / pharmacology. Cytarabine / administration & dosage. Diterpenes / pharmacology. Endothelial Cells / cytology. Female. Humans. Imidazoles / pharmacology. Male. Matrix Metalloproteinase Inhibitors. Middle Aged. NF-kappa B / antagonists & inhibitors. Protease Inhibitors / pharmacology. Pyrazines / pharmacology. Quinoxalines / pharmacology. Receptor, TIE-2 / antagonists & inhibitors. Receptor, TIE-2 / physiology. Recombinant Proteins / pharmacology. Tumor Cells, Cultured / enzymology. Tumor Cells, Cultured / secretion

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  • (PMID = 19922462.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 3-ingenyl angelate; 0 / 4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline; 0 / Angiopoietin-2; 0 / Anthracyclines; 0 / Boronic Acids; 0 / Chemokines; 0 / Culture Media, Serum-Free; 0 / Diterpenes; 0 / Imidazoles; 0 / Matrix Metalloproteinase Inhibitors; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; 0 / Pyrazines; 0 / Quinoxalines; 0 / Recombinant Proteins; 0 / Tissue Inhibitor of Metalloproteinases; 04079A1RDZ / Cytarabine; 69G8BD63PP / Bortezomib; EC 2.7.10.1 / Receptor, TIE-2; EC 3.4.24.- / Matrix Metalloproteinases
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76. Tong H, Lu C, Zhang J, Liu Z, Ma Y: Immunophenotypic, cytogenetic and clinical features of 192 AML patients in China. Clin Exp Med; 2009 Jun;9(2):149-55
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  • [Title] Immunophenotypic, cytogenetic and clinical features of 192 AML patients in China.
  • Immunophenotypic characterization of the leukemic cells has been widely used as a tool for diagnosis, classification and prognosis of leukaemia.
  • A total of 192 Chinese patients with acute myeloid leukemia (AML) were immunophenotyped by flow cytometry using a panel of monoclonal antibodies.
  • We found that CD33, CD13, MPO and CD117 were the most commonly expressed antigens in AML.
  • A combination of intensive autofluorescence, both CD34(-) and HLA-DR(-), and high expression of CD13, CD33 and MPO had significant value for M3 diagnosis.
  • CD14 was expressed only in M4 and M5, and both intensive positivity of CD64 and CD15 with high expression of HLA-DR may suggest great possibility for diagnosis of M5.
  • Lymphoid markers expression was documented in 47.9% of the 192 AML cases analyzed.
  • CD56 (26.0%) and CD7 (20.8%) were the most commonly expressed lymphoid markers in AML patients.
  • Our results indicate that immunophenotype analysis was useful for AML diagnosis and classification and the immunophenotype did have relevance to the abnormal cytogenetic changes and clinical features in AML.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 19205620.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD19; 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / HLA-DR Antigens
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77. Graf M, Reif S, Hecht K, Kroell T, Nuessler V, Schmetzer H: Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies. Eur J Haematol; 2005 Dec;75(6):477-84
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  • [Title] Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies.
  • There is evidence to suggest, that those receptors could have a role in leukemia.
  • We have studied the expression of PRR molecules PRR1 and PRR2 on mononuclear bone marrow (BM) cells of 55 patients with acute myeloid leukemia (AML) at first diagnosis by FACS-analysis using directly Phycoerythrin-labeled markers (PRR1 clone R1.302.12; PRR2 clone R2.477.1) in combination with other Fluorescein conjugated antibodies to evaluate the blast phenotype in AML.
  • We could demonstrate, that on average 35% PRR1(+) or 45% PRR2(+) cells in AML were found.
  • Within FAB-types we observed a high PRR1 expression in cases with M3 and M4 and lowest expressions in M0 and M5; a high PRR2 expression was found in cases with M3, M4, M5 and M1 and lowest expressions in M0 and M2.
  • Qui-square analyses showed, that 3 of 4 cases with FAB-type M3 (P = 0.03) or a favorable karyotype (P = 0.04) were found in the group with >7% PRR1(+) cells, due to only few cases available a similar correlation, however, could not be found in cases with >78% PRR2(+) cells.
  • We can conclude, that blasts in AML regularly express PRR1 and PRR2.
  • [MeSH-major] Biomarkers, Tumor. Cell Adhesion Molecules. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Membrane Glycoproteins
  • [MeSH-minor] Antigens, CD34 / metabolism. Bone Marrow Cells / metabolism. Cohort Studies. Disease-Free Survival. Endothelial Cells / metabolism. Female. Hematopoietic Stem Cells / metabolism. Humans. Male. Phenotype. Predictive Value of Tests. Prognosis. Recurrence

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  • (PMID = 16313259.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / Membrane Glycoproteins; 0 / nectins
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78. Takahashi W, Arai Y, Tadokoro J, Takeuchi K, Yamagata T, Mitani K: [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia]. Rinsho Ketsueki; 2006 Feb;47(2):111-4
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  • [Title] [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia].
  • A 63-year-old female was diagnosed as having Philadelphia chromosome-positive acute myelomonocytic leukemia in June 2002.
  • The patient received monotherapy with imatinib mesylate or combination therapy with DCM and idarubicin/cytarabine, both of which failed in attaining disease remission.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. Leukemia, Myelomonocytic, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16529013.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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79. Italia KY, Colah R, Mohanty D: Evaluation of F cells in sickle cell disorders by flow cytometry -- comparison with the Kleihauer-Betke's slide method. Int J Lab Hematol; 2007 Dec;29(6):409-14
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  • Adult F cell numbers are raised in inherited haemoglobin disorders, such as beta-thalassaemia and sickle cell anaemia, hereditary persistence of foetal haemoglobin, and some acquired conditions, such as juvenile myelomonocytic leukaemia, during acute erythropoietic stress and pregnancy.
  • [MeSH-minor] Adult. Erythropoiesis. Female. Fetomaternal Transfusion / blood. Fetomaternal Transfusion / pathology. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / pathology. Male. Pregnancy. Sensitivity and Specificity

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  • (PMID = 17988294.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9034-63-3 / Fetal Hemoglobin
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80. Ali R, Ozkalemkas F, Ozkocaman V, Ozcelik T, Akalin H, Ozkan A, Altundal Y, Tunali A: Hydatid disease in acute leukemia: effect of anticancer treatment on echinococcosis. Microbes Infect; 2005 Jul;7(9-10):1073-6
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  • [Title] Hydatid disease in acute leukemia: effect of anticancer treatment on echinococcosis.
  • Echinococcosis, also known as hydatid disease or hydatidosis, is a zoonotic illness caused by the larval form of Echinococcus spp.
  • We treated and followed approximately 1200 patients with different hematologic neoplastic diseases between 1985 and 2003, and only one of these individuals had concomitant acute leukemia and liver hydatidosis.
  • This report describes the case of a 19-year-old man who had both primary refractoriness of acute leukemia (AML-M4) and liver hydatidosis.
  • The patient underwent 3 months of treatment with agents that targeted the leukemia (daunorubicin, idarubicin, cytarabine, fludarabine) and its complications (amphotericin B, amphotericin B lipid complex, liposomal amphotericin B).

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  • (PMID = 15996888.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
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81. Helbling D, Mueller BU, Timchenko NA, Schardt J, Eyer M, Betts DR, Jotterand M, Meyer-Monard S, Fey MF, Pabst T: CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16). Blood; 2005 Aug 15;106(4):1369-75
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  • [Title] CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16).
  • The pericentric inversion of chromosome 16, inv(16)(p13q22), is associated with acute myeloid leukemia (AML) subtype M4Eo that is characterized by the presence of myelomonocytic blasts and atypical eosinophils.
  • The myeloid transcription factor CCAAT/enhancer-binding protein alpha (CEBPA) is crucial for normal granulopoiesis.
  • Alterations of structure and expression of CEBPA have been implicated in particular subtypes of AML.
  • No differences were detected in CEBPA mRNA levels in patients with inv(16) AML-M4Eo (n = 12) compared to patients with AML with a normal karyotype and M4 subtype (n = 6), whereas CEBPA protein and binding activity were significantly reduced in patients with CBFB-SMMHC.
  • Furthermore, calreticulin, an inhibitor of CEBPA translation, was induced on mRNA and protein level in CBFB-SMMHC patients with AML and after expression of CBFB-SMMHC in the U937-cell system.
  • Our results suggest that modulation of CEBPA by calreticulin represents a novel mechanism involved in the differentiation block in CBFB-SMMHC AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Calreticulin / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. RNA, Neoplasm / analysis. RNA, Small Interfering / pharmacology. Translocation, Genetic

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  • (PMID = 15855281.001).
  • [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 / CBFbeta-MYH11 fusion protein; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Calreticulin; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / inv(16) fusion protein, human
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82. Matsuo Y, Drexler HG, Harashima A, Okochi A, Kojima K, Asakura S, Tanimoto M, Orita K: Acute myeloid leukemia cell lines MOLM-17 and MOLM-18 derived from patient with advanced myelodysplastic syndromes. Leuk Res; 2005 Jun;29(6):701-10
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  • [Title] Acute myeloid leukemia cell lines MOLM-17 and MOLM-18 derived from patient with advanced myelodysplastic syndromes.
  • The two acute myelomonocytic leukemia sister cell lines MOLM-17 and MOLM-18 and the Epstein-Barr-virus positive non-malignant B-lymphoblastoid cell lines (B-LCLs) B422 and B423 were established from the bone marrow sample of a 60-year-old Japanese male in the advanced leukemic phase of refractory anemia with excess of blasts, a subtype of myelodysplastic syndromes (MDS).
  • MOLM-17 and B422 were established at eight months after the initial diagnosis, while MOLM-18 and B423 were derived from a sample one month later.
  • Immunophenotyping of the first leukemia sample revealed a mixed lineage leukemia immunophenotype with positivity for terminal deoxynucleotidyl transferase (TdT), CD13 and CD19; the second sample revealed solely myeloid characteristics with positivity for CD13, CD41 and CD61, whereas TdT was negative.
  • MOLM-17/-18 showed immunomarker profiles typical of the myelomonocytic lineage.
  • [MeSH-major] Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / pathology


83. Naithani R, Mahapatra M: Parotid involvement in acute myelomonocytic leukemia. Indian J Pediatr; 2007 Oct;74(10):965-6
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  • [Title] Parotid involvement in acute myelomonocytic leukemia.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / pathology. Leukemic Infiltration / pathology. Parotid Gland / pathology
  • [MeSH-minor] Biopsy, Needle. Bone Marrow / pathology. Child. Diagnosis, Differential. Facial Paralysis / pathology. Female. Humans

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  • [CommentIn] Indian J Pediatr. 2009 Apr;76(4):438-9 [19412591.001]
  • (PMID = 17978464.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] India
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84. Inukai T, Zhang X, Goto M, Hirose K, Uno K, Akahane K, Nemoto A, Goi K, Sato H, Takahashi K, Honna H, Kagami K, Nakamoto K, Yagita H, Okumura K, Koyama-Okazaki T, Nakazawa S, Sugita K: Resistance of infant leukemia with MLL rearrangement to tumor necrosis factor-related apoptosis-inducing ligand: a possible mechanism for poor sensitivity to antitumor immunity. Leukemia; 2006 Dec;20(12):2119-29
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  • [Title] Resistance of infant leukemia with MLL rearrangement to tumor necrosis factor-related apoptosis-inducing ligand: a possible mechanism for poor sensitivity to antitumor immunity.
  • Immune escape mechanisms also contribute to the failure of graft-versus-leukemia (GVL) effect after allogeneic hematopoietic stem cell transplantation (allo-SCT).
  • Infant leukemias with mixed-lineage leukemia (MLL) rearrangement have a remarkably short latency, and GVL effect after allo-SCT has not been clearly evidenced in these leukemias.
  • We investigated the in vitro sensitivity of MLL-rearranged acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML) cells to TRAIL- and FasL-mediated cytotoxicity.
  • Most of cell lines and primary leukemia cells were highly resistant to TRAIL primarily owing to low cell-surface expression of death receptors in ALL and simultaneous expression of decoy receptors in AML.
  • Nearly half of cell lines and majority of primary leukemia cells showed low sensitivity to FasL.
  • These results suggest that resistance to death-inducing ligands, particularly to TRAIL, could be one of the mechanisms for a rapid clonal expansion and a poor sensitivity to the GVL effect in infant leukemias with MLL rearrangement.
  • [MeSH-major] Gene Rearrangement. Leukemia / immunology. Myeloid-Lymphoid Leukemia Protein / genetics. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tumor Escape
  • [MeSH-minor] Drug Resistance, Neoplasm. Graft vs Leukemia Effect. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / analysis

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  • (PMID = 17066095.001).
  • [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 / MLL protein, human; 0 / NF-kappa B; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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85. Kang LC, Dunphy CH: Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes. Arch Pathol Lab Med; 2006 Feb;130(2):153-7
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  • [Title] Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes.
  • CONTEXT: MIC2 ("thymus leukemia") antigen has been shown to be expressed by T cells and monocytes, as well as B cells and granulocyte-lineage cells.
  • It is most intensely expressed by the most immature thymus T-lineage cells and is more intensely expressed by CD34-positive/CD33-positive myeloid cells (compared to more mature myeloid cells) and the earliest CD34-positive/CD10-positive B-cell precursor cells (compared to cells of later B-cell precursor stages).
  • CD99 (MIC2) is characteristically expressed in precursor B- and T-cell lymphoblastic lymphomas/leukemias, as well as in Ewing sarcoma/primitive neuroectodermal tumors (ES/PNET).
  • It has also been shown to be expressed in a few terminal deoxynucleotidyl transferase (TdT)-positive myeloid processes, but has been uniformly negative in TdT-negative myeloid processes.
  • A more recent study showed that 43% of acute myeloid leukemias (AMLs) and 55% of chloromas express CD99, concluding that CD99 is commonly expressed in AML and rarely seen in myeloproliferative disorders, myelodysplastic syndromes, or normal bone marrow.
  • Although this study speculated that MIC2 expression was probably not limited to TdT-positive AML, there was no comparison with TdT reactivity in this study.
  • OBJECTIVE: Since AML and high-grade myelodysplastic syndrome may occasionally be difficult to distinguish morphologically from acute lymphoblastic leukemia and ES/ PNET, we undertook a study to analyze MIC2 expression in conjunction with TdT reactivity in distinguishing AML or high-grade myelodysplastic syndrome from acute lymphoblastic leukemia and ES/PNET.
  • DESIGN: We studied bone marrow core and clot paraffin specimens from AML (classified according to criteria of the World Health Organization; n = 49), myelodysplastic syndromes (n = 4), precursor B-cell acute lymphoblastic leukemia (n = 4), ES/PNET (n = 1), and normal bone marrow (n = 3) with MIC2 (CD99) and TdT immunohistochemistry.
  • RESULTS: Overall, CD99 was expressed in 24 (49%) of 49 AML cases, including all (11/11) TdT-positive cases.
  • CD99 was expressed in all subtypes of AML except M5.
  • Expression of TdT was limited to a subset of AML-M0, -M1, -M2, and -M4, and AML with multilineage dysplasia.
  • An M5 AML may likely be excluded based on a uniform TdT-negative/CD99-negative immunophenotype.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow / metabolism. Cell Adhesion Molecules / metabolism. DNA Nucleotidylexotransferase / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Neuroectodermal Tumors, Primitive / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retrospective Studies. Sarcoma, Ewing / diagnosis

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  • (PMID = 16454553.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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86. Karam A, Eveillard JR, Ianoto JC, Quinio D, Le Flohic AM, Le Roy JP, Misery L, Berthou C: [Disseminated cutaneous and visceral fusariosis in an aplastic patient: an unusual digestive entry]. Ann Dermatol Venereol; 2005 Mar;132(3):255-8
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  • We report a case of cutaneous and systemic fusariosis due to Fusarium moniliforme in a patient with acute lymphoblastic leukemia.
  • CASE-REPORT: A 20 year-old male student was suffering from acute type 6 myeloblastic leukemia.
  • Treatment with voriconazole in association with transfusions of leukocytes led to clinical and microbiological cure.
  • DISCUSSION: In our case report, the clinical pattern starting with digestive symptoms suggested dissemination from a digestive site, which is very unusual in Europe.
  • [MeSH-major] Fusarium / pathogenicity. Mycoses / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 15924050.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 00DPD30SOY / Amsacrine; 04079A1RDZ / Cytarabine; JFU09I87TR / Voriconazole
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87. Elouennass M, Doghmi K, Fagot T, Soler C, Mac Nab C, Foissaud V, De Revel T, Hervé V: [Hepatosplenic and kidneys candidasis complicating an acute myeloblastic leukemia. A case treated with voriconazole and caspofungin]. Ann Biol Clin (Paris); 2005 Jul-Aug;63(4):423-7
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  • [Title] [Hepatosplenic and kidneys candidasis complicating an acute myeloblastic leukemia. A case treated with voriconazole and caspofungin].
  • We report the observation of hepato-splenic and kidneys candidiasis complicating the chemotherapy of a myeloblastic leukemia (LAM5b).
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis / drug therapy. Kidney Diseases / microbiology. Leukemia, Myeloid, Acute / microbiology. Liver Diseases / microbiology. Peptides, Cyclic / therapeutic use. Pyrimidines / therapeutic use. Splenic Diseases / microbiology. Triazoles / therapeutic use


88. Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Morice P, Bourquard P, Banzakour S, Le Calvez G, Marion V, Berthou C, De Braekeleer M: Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations. Cancer Genet Cytogenet; 2005 Mar;157(2):169-74
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  • [Title] Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations.
  • We report here 2 male adults in whom a diagnosis of acute myelomonoblastic leukemia (FAB M4) and acute monoblastic leukemia (FAB M5) was made.
  • Fourteen and 24 patients, including ours, with acute myeloblastic leukemia associated with a t(1;11)(p32;q23) and a t(11;17)(q23;q21), respectively have been reported in the literature.
  • Several patients with the latter translocation have also been identified to have acute lymphoblastic leukemia (ALL).
  • Although both translocations are preferentially associated with monocytic differentiation, the t(11;17)(q23;q21) is more common in adults and has been reported in many patients with ALL, compared to the t(1;11)(p32;q23).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15721641.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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89. Christopeit M, Mueller LP, Hainz M, Holzhausen HJ, Behre G: Cytogenetics detects infiltrations of a primary cutaneous acute myeloid leukemia to the kidney. Ann Hematol; 2007 Apr;86(4):291-3
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  • [Title] Cytogenetics detects infiltrations of a primary cutaneous acute myeloid leukemia to the kidney.
  • Extramedullary manifestations of acute myeloid leukemia (AML) are rare and commonly involve one tissue.
  • We report of a cutaneous acute myelomonocytic leukemia infiltrating the kidney next to the skin.
  • A 61-year-old female patient with complex karyotype cutaneous AML FAB M4 underwent abdominal computed tomography scans.
  • However, fluorescence in situ hybridization cytogenetics revealed a chromosome 11q23 abnormality in the nephrectomy specimen, which also appeared in the leukemic blasts of skin and bone marrow.
  • Closer histomorphologic workup revealed an infiltration of the kidney with leukemia.
  • This case report illustrates how modern diagnostic procedures can help to reveal rare sites of disease.
  • [MeSH-major] Kidney / pathology. Leukemia, Myelomonocytic, Acute / pathology. Leukemic Infiltration / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 17206419.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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90. Wang C, Chen Z, Li Z, Cen J: The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells. Leuk Res; 2010 Aug;34(8):1083-90
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  • [Title] The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells.
  • The frequency of extramedullary infiltration (EMI) in acute myeloblastic leukemia (AML) is reported up to 40% and most prevalent in myelo-monoblastic and monoblastic subtypes of AML (M4 and M5 according to FAB classification).
  • To explore mechanism underlying EMI, we analyzed SHI-1 cells, a highly invasive human acute monocytic leukemia cell line, and found their strong expression of matrix metalloproteinase 2 (MMP-2), membrane type 1 MMP (MT1-MMP) and tissue inhibitor of metalloproteinase 2 (TIMP-2).
  • SHI-1 cells showed higher invasive ability to traverse reconstituted basement membranes (Matrigel) and stronger activation of proMMP-2 than other leukemia cell line such as NB4, K562, U937 and THP-1 cells.
  • Our study indicated that increasing TIMP-2 in AML patients with EMI may potentially cause adverse effects, particularly in patients containing high levels of MMP-2 and MT1-MMP.
  • [MeSH-major] Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Matrix Metalloproteinase 14 / metabolism. Matrix Metalloproteinase 2 / metabolism. Tissue Inhibitor of Metalloproteinase-2 / metabolism

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138666.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 119978-18-6 / matrigel; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 9007-34-5 / Collagen; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
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91. Pulsoni A, Iacobelli S, Bernardi M, Borgia M, Camera A, Cantore N, Di Raimondo F, Fazi P, Ferrara F, Leoni F, Liso V, Mancini M, Marmont F, Matturro A, Maurillo L, Melillo L, Meloni G, Mirto S, Specchia G, Valentini CG, Venditti A, Leone G, Foà R, Mandelli F, Pagano L: M4 acute myeloid leukemia: the role of eosinophilia and cytogenetics in treatment response and survival. The GIMEMA experience. Haematologica; 2008 Jul;93(7):1025-32
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  • [Title] M4 acute myeloid leukemia: the role of eosinophilia and cytogenetics in treatment response and survival. The GIMEMA experience.
  • BACKGROUND: Myelomonocytic acute myeloid leukemia (M4-AML) is frequently associated with the cytogenetic marker inv(16) and/or the presence of eosinophilia.
  • DESIGN AND METHODS: Adult patients with acute myeloid leukemia consecutively enrolled in the GIMEMA trials AML10 and LAM99p were retrospectively analyzed.
  • RESULTS: Among 1686 patients, 400 cases of M4-AML were identified; of these, 78% had neither eosinophilia nor inv(16), 6% had eosinophilia only, 8% had inv(16) only and 8% had both.
  • CONCLUSIONS: In a large series of patients with M4-AML we confirmed the favorable role of inv(16), but the weight of this factor among the whole M4 population was of limited relevance.
  • Based on the results of this large case population, overall and relapse-free survival rates of patients with M4-AML are not significantly better than those of patients with non-M4 AML, while the concomitant presence of both inv(16) and eosinophilia was associated with a significantly improved prognosis.
  • [MeSH-major] Cytogenetics / methods. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Age Factors. Chromosome Inversion. Combined Modality Therapy. Disease-Free Survival. Eosinophilia / diagnosis. Eosinophilia / genetics. Humans. Middle Aged. Prognosis. Remission Induction. Retrospective Studies. Treatment Outcome

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  • (PMID = 18508801.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
  • [Publication-country] Italy
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92. Bächli EB, Schaer DJ, Walter RB, Fehr J, Schoedon G: Functional expression of the CD163 scavenger receptor on acute myeloid leukemia cells of monocytic lineage. J Leukoc Biol; 2006 Feb;79(2):312-8
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  • [Title] Functional expression of the CD163 scavenger receptor on acute myeloid leukemia cells of monocytic lineage.
  • We have previously shown that CD163 is expressed by acute myeloid leukemia (AML) cells of monocytic lineage.
  • Herein, we expand this finding by demonstrating constitutive and glucocorticoid-enhanced CD163 expression on French-American-British M4/M5 AML cells, and leukemic blasts of other AML subtypes and normal hematopoietic progenitor cells do not express CD163.
  • We provide evidence that the functional characteristics of CD163 are preserved on malignant cells by showing the capability of types M4/M5 blast cells to internalize Hb-Hp by a CD163-mediated mechanism.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / biosynthesis. Antigens, Differentiation, Myelomonocytic / immunology. Hematopoietic Stem Cells / immunology. Leukemia, Myeloid / immunology. Monocytes / immunology. Receptors, Cell Surface / biosynthesis. Receptors, Cell Surface / immunology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Lineage / immunology. Glucocorticoids / pharmacology. Haptoglobins / immunology. Hemoglobins / immunology. Humans

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  • (PMID = 16368951.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD163 antigen; 0 / Glucocorticoids; 0 / Haptoglobins; 0 / Hemoglobins; 0 / Receptors, Cell Surface
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93. Niparuck P, Chuncharunee S, Ungkanont A, Udomtrupayakul U, Aungchaisuksiri P, Rerkamnuatchoke B, Jootar S, Atichartakarn V: Long-term outcomes of de novo acute myeloid leukemia in Thai patients. J Med Assoc Thai; 2009 Sep;92(9):1143-9
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  • [Title] Long-term outcomes of de novo acute myeloid leukemia in Thai patients.
  • BACKGROUND: Acute myeloid leukemia (AML) is the heterogeneous disease.
  • As per previous reports, there are some differences in clinical features and cytogenetic biomarkers of AML among different ethnic backgrounds.
  • Therefore, we conducted a retrospective study to analyze clinical outcomes and predictive factors of Thai AML patients receiving chemotherapy treatment.
  • MATERIAL AND METHOD: The authors performed a retrospective analysis of 106 adults with newly diagnosed de novo AML at Ramathibodi Hospital between 2003 and 2007.
  • Common subtypes were M4 (28.3%), M1 (26.4%) and M2 (20.8%).
  • AML with recurrent cytogenetic translocations, complex chromosome, trisomy 8, polyploidy, del 5q and del 7q were found in 16.8, 6.3, 5.3, 5.3, 2.1 and 3.2%, respectively.
  • CONCLUSION: The overall complete remission rate of Thai AML patients is in 60%.
  • Only a small proportion of the presented patients have long-term DFS and OS, the significant factor for predicting survival of Thai AML patients is the complete remission status.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Cohort Studies. Disease-Free Survival. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Thailand. Treatment Outcome. Young Adult

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  • (PMID = 19772172.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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94. Akimkin VG, Ledin EV, Skvortsov SV, Rukavitsyn OA: [Incidence of hepatitis B virus infection in patients with blood disease]. Ter Arkh; 2007;79(11):28-31
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  • [Title] [Incidence of hepatitis B virus infection in patients with blood disease].
  • AIM: To define incidence of HBV infection in patients with blood diseases caused by blood components transfusion; correlation between infection rate and blood disease nosological entity, intensity of hemoreplacement therapy, time of hepatitis B incubation period in patients with hematological malignancies after the diagnosis and initiation of polychemotherapy (PCT).
  • MATERIAL AND METHODS: In 2000-2007 a prospective clinicoepidemiological trial was made to detect markers of HBV infection among 303 patients 15 to 76 years of age treated in the department of acute leukemia chemotherapy of N.N.
  • Burdenko Military Hospital for acute lymphoid and myeloblastic leukemia, chronic myeloid leukemia in a blastic crisis, myelodysplastic syndrome in blast transformation, lymphoproliferative diseases with bone marrow affection.
  • Among the infected patients there were 16 (53.4%) patients with different variants of acute myeloblastic leukemia, 12 (40.0%) with different immunophenotypes of acute lymphoblastic leukemia, 1 (3.3%) patient with acute biphenotypical leukemia and 1 (3.3%) with lymphoma/leukemia.
  • Most of the patients - 23 (74%) of 30 - were infected with HBV within the first year after hematological diagnosis and PCT induction course.
  • [MeSH-major] Hepatitis B / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18219969.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Biomarkers
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95. Wojcik I, Szybka M, Golanska E, Rieske P, Blonski JZ, Robak T, Bartkowiak J: Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias. Neoplasma; 2005;52(4):318-24
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  • [Title] Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias.
  • Abnormalities of the P53 network have been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).
  • The purpose of this study was to define P53 gene mutations, to detect MDM2 gene amplification and to estimate mRNA expression of P53, MDM2, BCL2 and BAX genes in patients with ALL and AML.
  • Twenty-five patients with ALL and 65 patients with AML, both recently diagnosed, were included into this study.
  • Mutation of the P53 gene was found in one patient of the 25 with ALL and in five patients of the 65 with AML.
  • One mutation in intronic sequence in ALL and four missense mutations and one silent nucleotide substitution in AML were identified.
  • Amplification of MDM2 gene was detected by multiplex-PCR analysis in only one sample from patient with ALL, but was not observed in any case of AML.
  • To gain further insight into the role of P53 network in the evolution of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in portion samples from patients with ALL and AML were analyzed using multiplex RT-PCR.
  • A high frequency of BCL2 mRNA overexpression and a relatively low frequency of BAX mRNA overexpression detected in both analyzed leukemias in this study, indicate that altered transcription of these genes may be involved in leukemogenesis.
  • [MeSH-major] Gene Amplification. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16059649.001).
  • [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 / BAX protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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96. Pulte D, Gondos A, Brenner H: Trends in survival after diagnosis with hematologic malignancy in adolescence or young adulthood in the United States, 1981-2005. Cancer; 2009 Nov 1;115(21):4973-9
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  • [Title] Trends in survival after diagnosis with hematologic malignancy in adolescence or young adulthood in the United States, 1981-2005.
  • METHODS: : Period analysis was used to calculate 5- and 10-year relative survival for adolescents and young adults diagnosed with Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL), acute lymphoblastic leukemia (ALL), acute myeloblastic leukemia (AML), and chronic myelocytic leukemia (CML) for 5 5-year periods from 1981-1985 to 2001-2005, using data from the Surveillance, Epidemiology, and End Results database.
  • Increases in 10-year relative survival between 1981-1985 and 2001-2005 were as follows: HL, from 80.4% to 93.4%; NHL, from 55.6% to 76.2%; ALL, from 30.5% to 52.1%; AML, from 15.2% to 45.1%; CML, from 0 to 74.5% (P < .001 in all cases).
  • However, although survival improved steadily throughout the period examined for the lymphomas and CML, survival was stable during the late 1990s and early 21st century for the acute leukemias.
  • However, with the exception of HL, survival rates have not reached the levels observed for children diagnosed with these malignancies, and survival expectations for patients with acute leukemia have stabilized at relatively low levels.
  • [MeSH-minor] Adolescent. Hodgkin Disease / mortality. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myeloid, Acute / mortality. Lymphoma, Non-Hodgkin / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Survival Rate. Time Factors. United States / epidemiology. Young Adult

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  • (PMID = 19705347.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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97. Potenza L, Luppi M, Riva G, Morselli M, Ferrari A, Imovilli A, Giacobbi F, Temperani P, Donelli A, Narni F, Torelli G: Isolated extramedullary relapse after autologous bone marrow transplantation for acute myeloid leukemia: case report and review of the literature. Am J Hematol; 2006 Jan;81(1):45-50
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  • [Title] Isolated extramedullary relapse after autologous bone marrow transplantation for acute myeloid leukemia: case report and review of the literature.
  • Isolated extramedullary relapse (IEMR) is a pattern of acute myeloid leukemia (AML) relapse post-allogeneic bone marrow transplantation (alloBMT).
  • We report a case of a woman with M4 AML who experienced IEMR post-autoBMT and review the related literature.
  • The review suggests that an M2 or M4 French-American-British (FAB) phenotype, intermediate cytogenetic risk group, and chromosome 8 abnormalities are more frequently associated with the occurrence of IEMR.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy


98. Mo J, Lampkin B, Perentesis J, Poole L, Bao L: Translocation (8;18;16)(p11;q21;p13). A new variant of t(8;16)(p11;p13) in acute monoblastic leukemia: case report and review of the literature. Cancer Genet Cytogenet; 2006 Feb;165(1):75-8
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  • [Title] Translocation (8;18;16)(p11;q21;p13). A new variant of t(8;16)(p11;p13) in acute monoblastic leukemia: case report and review of the literature.
  • A complex three-way t(8;18;16)(p11;q21;p13) was detected in a 15-month-old patient with acute myeloid leukemia (AML).
  • The patient had typical clinical manifestation and bone marrow features of AML subtype M5b associated with t(8;16)(p11;p13).
  • Therefore, we believe that the t(8;18;16) is a new variant of t(8;16) related to AML M4/M5.
  • [MeSH-major] Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 8. Genetic Variation. Leukemia, Monocytic, Acute / genetics. Translocation, Genetic

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  • (PMID = 16490600.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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99. Koh G, Yamane T, Aoyama Y, Sakamoto C, Nakamae H, Hasegawa T, Terada Y, Hino M: [Acute myelomonocytic leukemia complicated with multiple lower intestinal ulcers induced by nonsteroidal anti-inflammatory drugs]. Gan To Kagaku Ryoho; 2005 Jan;32(1):111-3
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  • [Title] [Acute myelomonocytic leukemia complicated with multiple lower intestinal ulcers induced by nonsteroidal anti-inflammatory drugs].
  • We report an 18-year-old woman with acute myelomonocytic leukemia, who developed massive lower intestinal bleeding following induction chemotherapy.
  • Colonoscopy revealed multiple circular ulcers but no infectious colitis or infiltration of leukemia.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Colonic Diseases / chemically induced. Leukemia, Myelomonocytic, Acute / complications. Peptic Ulcer Hemorrhage / chemically induced

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  • (PMID = 15675595.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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100. Reiterer G, Yen A: Platelet-derived growth factor receptor regulates myeloid and monocytic differentiation of HL-60 cells. Cancer Res; 2007 Aug 15;67(16):7765-72
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  • [Title] Platelet-derived growth factor receptor regulates myeloid and monocytic differentiation of HL-60 cells.
  • Here, we show that the platelet-derived growth factor receptor (PDGFR) regulates myeloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid (RA) and vitamin D3 (D3), respectively.
  • In addition, we found calcium levels to be decreased by RA and D3 but increased when AG1296 was given in addition to RA or D3, suggesting that calcium levels decrease during myeloid or monocytic differentiation, and elevated calcium levels can disturb the expression of certain differentiation markers.
  • [MeSH-major] Monocytes / pathology. Myeloid Cells / pathology. Receptors, Platelet-Derived Growth Factor / metabolism

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  • (PMID = 17699781.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA33505; United States / NIDDK NIH HHS / DK / DK072105
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11b; 0 / Antigens, CD14; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / Fc(alpha) receptor; 0 / GPI-Linked Proteins; 0 / ITGAM protein, human; 0 / Membrane Glycoproteins; 0 / Receptors, Fc; 0 / Tyrphostins; 0 / Ubiquitin; 146535-11-7 / 6,7-dimethoxy-3-phenylquinoxaline; 1C6V77QF41 / Cholecalciferol; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; SY7Q814VUP / Calcium
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