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1. 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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2. Zhang L, Alsabeh R, Mecucci C, La Starza R, Gorello P, Lee S, Lill M, Schreck R: Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature. Cancer Genet Cytogenet; 2007 Oct 1;178(1):42-8
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  • [Title] Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature.
  • Balanced chromosome rearrangements are the hallmark of therapy-related leukemia that develops in patients treated with topoisomerase II inhibitors.
  • With time, the patient's disorder progressed to acute myelomonocytic leukemia with cytogenetic evidence of clonal evolution.
  • To our knowledge, this is the first report of a patient presenting with a myelodysplastic syndrome with isolated t(1;11) (q23;p15), which evolved into therapy-related acute myeloid leukemia (t-AML).
  • This patient is the third reported with this cytogenetic rearrangement and t-AML, and is compared with the other two reports of t(1;11)(q23;p15).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Myelomonocytic, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neutrophils / metabolism


3. Hubeek I, Peters GJ, Broekhuizen R, Zwaan CM, Kaaijk P, van Wering ES, Gibson BE, Creutzig U, Janka-Schaub GE, den Boer ML, Pieters R, Kaspers GJ: In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia. Haematologica; 2006 Jan;91(1):17-23
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  • [Title] In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia.
  • BACKGROUND AND OBJECTIVES: Cytarabine (ara-C) is a key drug in the treatment of acute leukemia.
  • DESIGN AND METHODS: Using the MTT assay, we determined in vitro sensitivity and cross-resistance to deoxynucleoside analogs in 362 acute leukemia samples from untreated children and 32 normal bone marrow mononuclear cell samples.
  • RESULTS: Normal bone marrow samples were significantly more resistant to ara-C, cladribine and fludarabine than were acute myeloid leukemia (AML) samples and significantly more resistant to ara-C and fludarabine than were acute lymphoblastic leukemia (ALL) samples.
  • The only drug to which AML samples were more sensitive in vitro than ALL was cladribine.
  • AML FAB M5 was significantly more sensitive in vitro to ara-C and cladribine than FAB M1/2 or FAB M4.
  • A paired analysis of 60 AML and 99 ALL samples demonstrated significant cross-resistance between all four deoxynucleoside analogs.
  • Cross-resistance was also observed between ara-C and etoposide (Rp=0.54, p<0.0001), and ara-C and daunorubicin (Rp=0.48, p<0.0001) in AML.
  • INTERPRETATION AND CONCLUSIONS: Cladribine appears to be a useful drug in AML, particularly in FAB M5.
  • We observed cross-resistance between ara-C and other deoxynucleoside analogs, as well as between ara-C and drugs with different modes of action in childhood acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple. Leukemia / drug therapy. Nucleosides / therapeutic use
  • [MeSH-minor] Acute Disease. Child. Cytarabine / therapeutic use. Drug Screening Assays, Antitumor. Humans

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  • (PMID = 16434366.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nucleosides; 04079A1RDZ / Cytarabine
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4. Liu M, Wei XD, Lü XD, Fan RH, Yin QS, Zhou J: [Expression of NF-kappaB mRNA in acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Apr;18(2):359-62
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  • [Title] [Expression of NF-kappaB mRNA in acute myeloid leukemia].
  • This study was aimed to investigate the expression level of NF-kappaB mRNA in acute myeloid leukemia (AML) using real time fluorescence quantitative polymerase chain reduction (qPCR) detection and to explore the effect of NF-kappaB mRNA in pathogenesis of AML.
  • The fresh bone marrow was collected from 60 newly diagnosed patients with AML, the total RNA was extracted by means of RTIzoL, the cDNA was synthesized, the expression of NF-kappaB mRNA was detected by qPCR using GAPDH as internal reference.
  • The results showed that the expression of NF-kappaB mRNA in patients with AML was higher than that in normal healthy persons with significant difference (p<0.05), the expression of NF-kappaB mRNA in patients with AML-M4 and -M5 were higher than that in patients with AML-M1, -M2 and -M3.
  • It is concluded that the expression of NF-kappaB mRNA is higher in patients with AML.
  • The up-regulation of NF-kappaB expression in patients with AML may play an important role in pathogenesis of AML.

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  • (PMID = 20416168.001).
  • [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 / NF-kappa B; 0 / RNA, Messenger
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5. Liu LB, Li WM, Zou P, He W, Zhang M: [Depressing the immune escape of acute myelomonocytic leukemia via an anti-Fas ribozyme]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Oct;14(5):862-6
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  • [Title] [Depressing the immune escape of acute myelomonocytic leukemia via an anti-Fas ribozyme].
  • In order to investigate the inhibition role of anti-Fas hammerhead ribozyme on Fas expression and Fas-mediated apoptosis in CTLL-2 cells (mouse CTL cell line), and to explore a new way for enhancing the ability of T cells against Leukemia in donor lymphocytes infusion, CTLL-2 cells were transfected with pEGFP-RZ596 and pEGFPC1 (mock-transfected) via electroporation.
  • The killing effect of CTL against WEHI-3 (mouse acute myelomonocytic leukemia cell line) highly expressing FasL in vitro was detected by MTT assay.
  • It is concluded that anti-Fas ribozyme can remarkably decrease Fas expression on CTLL-2 cells, so as to avoid Fas-mediated apoptosis by Fas ligand on WEHI-3 cells, and to enhance their killing activity against WEHI-3 cells, as a result, the immune escape of acute myelomonocytic leukemia was depressed.

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  • (PMID = 17096877.001).
  • [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] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Fas Ligand Protein; 0 / RNA, Catalytic; 0 / hammerhead ribozyme
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6. 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


7. Abe A, Kiyoi H, Ninomiya M, Yamazaki T, Murase T, Ozeki K, Suzuki M, Hayakawa F, Katsumi A, Emi N, Naoe T: Establishment of a stroma-dependent human acute myelomonocytic leukemia cell line, NAMO-2, with FLT3 tandem duplication. Int J Hematol; 2006 Nov;84(4):328-36
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  • [Title] Establishment of a stroma-dependent human acute myelomonocytic leukemia cell line, NAMO-2, with FLT3 tandem duplication.
  • We have established a stroma-dependent myelomonocytic cell line, NAMO-2, with FLT3 internal tandem duplication (FLT3/ITD).
  • Leukemia cells from a patient with acute myelomonocytic leukemia were administered to form subcutaneous tumors in nude mice, which were maintained successively, although we failed to establish continuously growing cells from the original leukemia cell culture.
  • The leukemia cells showed continuous growth dependent on this stroma, and this cell line was named NAMO-2.
  • NAMO-2 provides a useful tool to analyze adherence-dependent survival signaling of leukemia with FLT3/ITD and a model for the screening of FLT3 kinase inhibitors.
  • [MeSH-major] Cell Line, Tumor. Leukemia, Myelomonocytic, Acute / pathology. Stromal Cells / physiology. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics


8. Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS: Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up. Chang Gung Med J; 2006 Sep-Oct;29(5):532-7
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  • [Title] Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
  • Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.
  • AML with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.
  • It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).
  • This case illustrates a typical AMML Eo confirmed by a multi-modality diagnostic approach including morphology, cytochemistry, flow cytometry, immunohistochemistry, and conventional cytogenetic study.
  • [MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 17214400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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9. Dunphy CH, Tang W: The value of CD64 expression in distinguishing acute myeloid leukemia with monocytic differentiation from other subtypes of acute myeloid leukemia: a flow cytometric analysis of 64 cases. Arch Pathol Lab Med; 2007 May;131(5):748-54
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  • [Title] The value of CD64 expression in distinguishing acute myeloid leukemia with monocytic differentiation from other subtypes of acute myeloid leukemia: a flow cytometric analysis of 64 cases.
  • CONTEXT: Flow cytometric immunophenotyping is a useful ancillary tool in the diagnosis and subclassification of acute myeloid leukemias (AMLs).
  • A recent study concluded that CD64 is sensitive and specific for distinguishing AMLs with a monocytic component (ie, AML M4 and AML M5) from other AML subtypes.
  • However, in that study, the intensity of CD64 was not well defined and the number of non-M4/non-M5 AMLs was small.
  • OBJECTIVE: To evaluate the usefulness of CD64 by flow cytometric immunophenotyping in distinguishing AMLs with monocytic differentiation from other AML subtypes.
  • RESULTS: CD64 was expressed in AML subtypes M0 to M5 in varying intensities: heterogeneously expressed in 1 of 7 M0s; dimly expressed in 3 of 11 M1s; dimly and moderately expressed in 6 and 2 of 17 M2s, respectively; dimly and moderately expressed in 5 and 1 of 7 M3s, respectively; dimly expressed in 4 of 9 M4s; and heterogeneously, moderately, and strongly expressed in 1, 3, and 3 of 7 M5s, respectively.
  • CONCLUSIONS: Strong CD64 expression distinguishes AML M5; however, heterogeneous, dim, or moderate expression in itself does not distinguish M0 through M4 subtypes from M5 with dim to moderate CD64 expression.
  • However, any CD64 expression associated with strong CD15 expression distinguishes AML M4 or M5, from other AML subtypes.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Myeloid / diagnosis. Receptors, IgG / biosynthesis
  • [MeSH-minor] Acute Disease. Antigens, CD / analysis. Flow Cytometry. HLA-DR Antigens. Humans. Immunophenotyping. Monocytes / metabolism

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  • (PMID = 17488160.001).
  • [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 / Biomarkers, Tumor; 0 / HLA-DR Antigens; 0 / Receptors, IgG
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10. Liu Y, Chao X, Gu W, Hua X, Xu N: Acute thrombosis in superior mesenteric artery as first symptom in a AML patient. Int J Gen Med; 2008;1:7-9
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  • [Title] Acute thrombosis in superior mesenteric artery as first symptom in a AML patient.
  • It is well known that acute leukemia may accompany thromboembolic events; even severe thrombocytopenia does not prevent thrombosis.
  • Most thromboembolism is localized in venous vessels in acute leukemic patients and it happens rarely in the artery.
  • We report a case of acute thrombosis in the superior mesenteric artery as the first symptom in a patient suffering from acute myeloid leukemia (FAB M4).

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  • (PMID = 20428399.001).
  • [ISSN] 1178-7074
  • [Journal-full-title] International journal of general medicine
  • [ISO-abbreviation] Int J Gen Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2840534
  • [Keywords] NOTNLM ; acute leukemia / pathogenesis / thromboembolism
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11. Haase R, Merkel N, Diwan O, Elsner K, Kramm CM: Leukapheresis and exchange transfusion in children with acute leukemia and hyperleukocytosis. A single center experience. Klin Padiatr; 2009 Nov-Dec;221(6):374-8
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  • [Title] Leukapheresis and exchange transfusion in children with acute leukemia and hyperleukocytosis. A single center experience.
  • BACKGROUND: The risk of severe complications or death during the initial period of acute leukemia was markedly decreased due to the progress in pediatric oncology and use of simple measures like hyperhydration, forced diuresis, treatment of hyperuricemia, correction of electrolyte and coagulation disturbances and the careful use of antileukemic drugs.
  • The incidence of leukostasis and tumor lysis syndrome depends on absolute initial white blood cell counts and the underlying type of leukemia.
  • METHODS: Records of all pediatric patients who were newly diagnosed with acute leukemia between 1 / 1998 und 12 / 2008 were retrospectively reviewed for presence of hyperleukocytosis(white blood cell count > 100 GPT / l) at diagnosis and subsequent leukapheresis or exchange transfusion in regards to the clinical outcome.
  • RESULTS: At diagnosis 11 (14 % ) of 77 children with acute leukemia (7 acute lymphoblastic leukemia / ALL; 4 acute myeloblastic leukemia /AML) had hyperleukocytosis.
  • 4 patients (2 ALL, 2 AML) received exchange transfusion and 2 others (1 ALL, 1 AML) underwent leukapheresis.
  • The exact impact of leukapheresis or exchange transfusion on short and long term outcome in pediatric patients with acute leukemia and initial hyperleukocytosis has to be evaluated in future multicentre studies or by the formation of clinical registries.
  • [MeSH-major] Exchange Transfusion, Whole Blood. Leukapheresis. Leukemia, Myeloid, Acute / therapy. Leukocytosis / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Infant. Leukocyte Count. Male. Retrospective Studies

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 19890790.001).
  • [ISSN] 1439-3824
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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12. Bekou V, Franke I, Gollnick H, Leverkus M: [Livid polycyclic plaques of the lower extremities]. Hautarzt; 2008 Nov;59(11):942-5
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  • In 10%-55% of patients, leukemia cutis (LC) manifest as a symptom of acute myelomonocytic leukemia and is associated with a poor overall prognosis.
  • Disseminated bluish-violet or red-brownish papules and plaques, nodules and also hemorrhagic ulcers may dominate the initial clinical picture.
  • The role of the dermatologist is the rapid clinical and dermatohistopathological diagnosis in order to allow immediate, adequate treatment of the patient's underlying systemic disease.
  • [MeSH-major] Leg Dermatoses / pathology. Leukemia, Myelomonocytic, Acute / pathology. Lower Extremity / pathology

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  • (PMID = 18712322.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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13. Bonci D, Musumeci M, Coppola V, Addario A, Conticello C, Hahne M, Gulisano M, Grignani F, De Maria R: Blocking the APRIL circuit enhances acute myeloid leukemia cell chemosensitivity. Haematologica; 2008 Dec;93(12):1899-902
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  • [Title] Blocking the APRIL circuit enhances acute myeloid leukemia cell chemosensitivity.
  • Resistance to chemotherapy-induced cell death represents a major obstacle in the treatment of acute myeloid leukemia.
  • We investigated APRIL expression and activity in acute myeloid leukemia.
  • We found that APRIL mRNA and protein, including the secreted form, are expressed in leukemic cells of patients with M0, M2 and M4 acute myeloid leukemia subtypes but not in normal hematopoietic progenitors.
  • Conversely, blocking APRIL function by recombinant soluble APRIL receptors increased chemotherapeutic drugs-induced cell adeath in acute myeloid leukemia cells.
  • These results indicate that APRIL acts in an autocrine fashion to protect acute myeloid leukemia cells from drug-induced death and foresee a therapeutic potential of APRIL antagonists in the treatment of acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / pathology. Tumor Necrosis Factor Ligand Superfamily Member 13 / antagonists & inhibitors

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  • (PMID = 18838478.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor Ligand Superfamily Member 13
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14. Kar R, Rao S, Pati HP: Systemic mastocytosis with acute myelomonocytic leukemia: a case report. Indian J Hematol Blood Transfus; 2008 Dec;24(4):182-5
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  • [Title] Systemic mastocytosis with acute myelomonocytic leukemia: a case report.
  • Bone marrow mastocytosis may be associated with many clonal non mast cell hematological neoplasms and its association with acute myeloid leukemia especially with t (8;.
  • We describe an interesting case of coexistence of systemic mastocytosis with acute myelomonocytic leukemia in a young child.
  • Diagnosis of acute myelomonocytic leukemia was based on bone marrow aspirate findings coupled with cytochemistry.

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  • (PMID = 23100960.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3475428
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Systemic mastocytosis / Toluidine blue
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15. Kaufman DW, Anderson TE, Issaragrisil S: Risk factors for leukemia in Thailand. Ann Hematol; 2009 Nov;88(11):1079-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk factors for leukemia in Thailand.
  • A case-control study of adult-onset leukemia was conducted in Bangkok, Thailand to explore the contribution of cellular telephone use and other factors to the etiology of the disease; 180 cases (87 acute myeloblastic leukemia, 40 acute lymphoblastic leukemia, 44 chronic myelogenous leukemia, eight chronic lymphocytic leukemia, one unclassified acute leukemia) were compared with 756 age- and sex-matched hospital controls.
  • Myeloid leukemia (acute and chronic combined) was associated with benzene (OR, 3.9; 95% confidence interval, 1.3-11), a nonspecific group of other solvents (2.3; 1.1-4.9), occupational pesticides that were mostly unspecified (3.8; 2.1-7.1), and working with or near powerlines (4.3; 1.3-15).
  • [MeSH-major] Leukemia / epidemiology
  • [MeSH-minor] Adult. Aged. Benzene / adverse effects. Case-Control Studies. Cell Phones. Electromagnetic Fields / adverse effects. Female. Humans. Leukemia, Radiation-Induced / epidemiology. Leukemia, Radiation-Induced / etiology. Male. Middle Aged. Occupational Exposure. Pesticides / adverse effects. Radiography / adverse effects. Risk Factors. Smoking / epidemiology. Solvents / adverse effects. Thailand / epidemiology. Young Adult

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  • (PMID = 19294385.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Pesticides; 0 / Solvents; J64922108F / Benzene
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16. Chen YX, Zhang MY, Xiong S, Qian CW, Wang YF: [Analysis of the relationship between nm23-H1 gene and human chronic myeloblastic leukemia using siRNA]. Sheng Wu Gong Cheng Xue Bao; 2006 May;22(3):403-7
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  • [Title] [Analysis of the relationship between nm23-H1 gene and human chronic myeloblastic leukemia using siRNA].
  • To investigate the relationship between nm23-H1 gene and human chronic myeloblastic leukemia we designed siRNAs which target nm23-H1 gene.
  • Therefore nm23-H1 gene might be a potential target of leukemia treatment.
  • [MeSH-major] Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / pathology. NM23 Nucleoside Diphosphate Kinases / genetics. RNA, Small Interfering / genetics

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  • (PMID = 16755918.001).
  • [ISSN] 1000-3061
  • [Journal-full-title] Sheng wu gong cheng xue bao = Chinese journal of biotechnology
  • [ISO-abbreviation] Sheng Wu Gong Cheng Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / NM23 Nucleoside Diphosphate Kinases; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 2.7.4.6 / NME1 protein, human
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17. 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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18. 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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19. Novotny JR, Nückel H, Dührsen U: Correlation between expression of CD56/NCAM and severe leukostasis in hyperleukocytic acute myelomonocytic leukaemia. Eur J Haematol; 2006 Apr;76(4):299-308
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  • [Title] Correlation between expression of CD56/NCAM and severe leukostasis in hyperleukocytic acute myelomonocytic leukaemia.
  • OBJECTIVE: The possible contribution of surface molecules to the development of leukostasis syndrome in hyperleukocytic acute myeloid leukaemia (AML) was assessed by routine immunophenotyping and grading of the probability of clinical leukostasis.
  • METHODS: Fifty-three patients (23 women, 30 men, median age 59 yr) with hyperleukocytic AML [white blood count (WBC) above 50 x 10(9)/L] were graded for the probability of clinical leukostasis according to the severity of neurologic, pulmonary and other symptoms possibly caused by leukostasis using a recently published scoring system.
  • RESULTS: In patients with acute monocytic leukaemia (AML M4/M5) the absolute count of leukaemic blasts expressing CD56/NCAM was highly associated with the development of symptoms graded as highly probable leukostasis and all three patients succumbing to early death were CD56 positive.
  • This was not found in AML without monocytic involvement (AML M1, M2, M3v).
  • CONCLUSIONS: The expression of CD56/NCAM, a surface marker used in routine immunophenotyping of AML, may help to predict severe and potentially fatal leukostasis in hyperleukocytic acute myelomonocytic leukaemia.
  • These results emphasize the usefulness of this four-stage clinical grading scale for analysing the factors, which lead to severe leukostasis in hyperleukocytic patients.
  • We extend previous findings that the mechanisms of leukostasis are different depending on the involvement of the monocytic lineage.
  • [MeSH-major] Antigens, CD56 / blood. Gene Expression Regulation, Leukemic. Leukemia, Myelomonocytic, Acute / blood. Leukostasis / blood

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  • (PMID = 16519701.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD56
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20. 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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21. Elgendi HM, Mekawy MA, Abdel Wahab SE, Tawfik LM, Ismail EA, Adly AA: AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome. J Pediatr Hematol Oncol; 2010 May;32(4):286-93
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  • [Title] AC133 expression in egyptian children with acute leukemia: impact on treatment response and disease outcome.
  • Hence, it is expected to be a valuable prognostic marker in acute leukemia.
  • Sixty Egyptian children with acute leukemia were enrolled into this prospective study divided into 2 groups: 30 acute myeloblastic leukemia (AML) and 30 acute lymphoblastic leukemia (ALL) patients.
  • AC133 was expressed in 66.7% and 40% of AML and ALL patients, respectively.
  • In AML, 80% of patients with poor clinical outcome (relapse or death) were positive for AC133 expression, whereas, all ALL patients who developed resistance as well as those who displayed poor clinical outcome had AC133-positive expression (P<0.05).
  • Patients with positive AC133 expression had significantly shorter overall and disease-free survival times compared with AC133-negative patients in both ALL (P<0.001) and AML (P<0.05) groups.
  • AC133-positive expression is an independent poor prognostic factor in childhood acute leukemia and could characterize a group of patients with resistance to standard chemotherapy, as well as high incidence of relapse and death.
  • [MeSH-major] Antigens, CD / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Glycoproteins / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Peptides / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20224439.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Glycoproteins; 0 / Peptides
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22. Anuchapreeda S, Limtrakul P, Thanarattanakorn P, Sittipreechacharn S, Chanarat P: Inhibitory effect of curcumin on WT1 gene expression in patient leukemic cells. Arch Pharm Res; 2006 Jan;29(1):80-7
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  • Leukemias are common worldwide.
  • Wilms' tumor1 (WT1) protein is highly expressed in leukemic blast cells of myeloid and lymphoid origin.
  • Thus, WT1 mRNA serves as a tumor marker for leukemias detection and monitoring disease progression.
  • The leukemic cells were collected from 70 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period July 2003 to February 2005.
  • There were 58 cases of acute lymphoblastic leukemia (ALL), 10 cases of acute myeloblastic leukemia (AML), and 2 cases of chronic myelocytic leukemia (CML).
  • Thus, curcumin treatment may provide a lead for clinical treatment in leukemic patients in the future.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Genes, Wilms Tumor / drug effects. Leukemia / drug therapy. Leukemia / genetics

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  • (PMID = 16491848.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
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23. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • Rearrangements of the MLL gene are found in most cases of infant AML and regardless of age confer an intermediate risk.
  • The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and AML-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.
  • The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.
  • It may also prove to have a useful role in both diagnosis and prognosis.
  • This review considers recent advances in our understanding of the role of MLL gene rearrangements in pediatric clinical practice.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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24. Murati A, Gervais C, Carbuccia N, Finetti P, Cervera N, Adélaïde J, Struski S, Lippert E, Mugneret F, Tigaud I, Penther D, Bastard C, Poppe B, Speleman F, Baranger L, Luquet I, Cornillet-Lefebvre P, Nadal N, Nguyen-Khac F, Pérot C, Olschwang S, Bertucci F, Chaffanet M, Lessard M, Mozziconacci MJ, Birnbaum D, Groupe Francophone de Cytogénétique Hématologique: Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases. Leukemia; 2009 Jan;23(1):85-94
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  • [Title] Genome profiling of acute myelomonocytic leukemia: alteration of the MYB locus in MYST3-linked cases.
  • The t(8;16)(p11;p13) is a rare translocation involved in de novo and therapy-related myelomonocytic and monocytic acute leukemia.
  • MYST3-linked acute myeloid leukemias (AMLs) share specific clinical and biological features and a poor prognosis.
  • We have established the genome and gene expression profiles of a multicentric series of 61 M4/M5 AMLs including 18 MYST3-linked AMLs by using array comparative genome hybridization (aCGH) (n=52) and DNA microarrays (n=44), respectively.
  • We show that M4/5 AMLs have a variety of rare genomic alterations.
  • These features, reminiscent of T-cell acute lymphoid leukemia (ALL), suggest the targeting of a common T-myeloid progenitor.
  • [MeSH-major] Gene Expression Profiling / methods. Genes, myb / genetics. Histone Acetyltransferases / genetics. Leukemia, Myelomonocytic, Acute / genetics

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  • (PMID = 18818702.001).
  • [ISSN] 1476-5551
  • [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 / Antigens, CD4; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins c-myb; 157907-48-7 / HoxA protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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25. Caceres-Cortes JR: A potent anti-carcinoma and anti-acute myeloblastic leukemia agent, AG490. Anticancer Agents Med Chem; 2008 Oct;8(7):717-22
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  • [Title] A potent anti-carcinoma and anti-acute myeloblastic leukemia agent, AG490.
  • JAK-2, have emerged as essentials in cell survival for cervical carcinoma and acute myeloblastic leukemia, respectively.
  • [MeSH-major] Antineoplastic Agents. Leukemia, Myeloid, Acute / drug therapy. Tyrphostins

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  • (PMID = 18855573.001).
  • [ISSN] 1871-5206
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / STAT3 Transcription Factor; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 95
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26. Bauvois B, Nguyen J, Tang R, Billard C, Kolb JP: Types I and II interferons upregulate the costimulatory CD80 molecule in monocytes via interferon regulatory factor-1. Biochem Pharmacol; 2009 Sep 1;78(5):514-22
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  • Type I (alpha/beta) and type II (gamma) IFNs are widely administered as adjuvant therapy.
  • In monocytic U937 cells, IRF-1 is activated by IFN-gamma but not by IFN-alpha/beta, whereas it is the reverse for IRF-7; in the latter cells, only IFN-gamma is capable of stimulating CD80 transcription emphasizing the essential role of IRF-1.
  • In AML cells, IFNs upregulate CD40, CD80 and IRF-1 in the FAB-M4/M5 subtypes but not in the less differentiated M1/M2 subtypes.
  • Monitoring the expression of CD80 on AML cells and its modulation by IFNs could help to predict the patients more susceptible to benefit from therapeutic strategies aimed at eliciting specific T cell responses to leukemia-associated antigens.
  • [MeSH-major] Antigens, CD80 / physiology. Interferon Regulatory Factor-1 / physiology. Interferon Type I / physiology. Interferon-gamma / physiology. Monocytes / metabolism. Up-Regulation / physiology

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  • (PMID = 19433065.001).
  • [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 / Antigens, CD80; 0 / DNA Primers; 0 / IRF1 protein, human; 0 / Interferon Regulatory Factor-1; 0 / Interferon Type I; 82115-62-6 / Interferon-gamma
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27. Nikolaievs'kyĭ VV: [Distribution of Mycobacterium tuberculosis strains in the south of Ukraine based on genotyping data]. Mikrobiol Z; 2006 Sep-Oct;68(5):52-61
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  • Other epidemiological groups were represented by the family strains T1, LAM1, LAM4, LAM5, S and Haarlem.

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  • (PMID = 17388120.001).
  • [ISSN] 1028-0987
  • [Journal-full-title] Mikrobiolohichnyĭ zhurnal (Kiev, Ukraine : 1993)
  • [ISO-abbreviation] Mikrobiol. Z.
  • [Language] ukr
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / DNA, Bacterial
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28. 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


29. Leroy H, Roumier C, Huyghe P, Biggio V, Fenaux P, Preudhomme C: CEBPA point mutations in hematological malignancies. Leukemia; 2005 Mar;19(3):329-34
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  • The CCAAT/enhancer-binding protein-alpha (CEBPA) is a transcription factor strongly implicated in myelopoiesis through control of proliferation and differentiation of myeloid progenitors.
  • In this work, we analyzed characteristics of mutations and their correlation with disease characteristics described in previous studies.
  • CEBPA mutations were reported exclusively in acute myeloid leukemia (AML) (according to WHO classification criteria) and mutated patients preferentially belonged to M1, M2 and M4 FAB subtypes.
  • Systematic analysis of CEBPA mutations, in addition to that of alterations in master genes of hematopoiesis, may be useful to assess the prognosis of AML particularly in patients belonging to the 'intermediate' prognostic subgroup.

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  • (PMID = 15674366.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 39
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30. Chen HM, Yuan HY, Fan X, He HY, Chen B, Shi JY, Zhu YM: [Application of multiplex rt-PCR assay for screening rare or cryptic chromosome translocations in de novo patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1138-42
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  • [Title] [Application of multiplex rt-PCR assay for screening rare or cryptic chromosome translocations in de novo patients with acute myeloid leukemia].
  • This study was aimed to investigate the clinical feasibility of using multiplex PT-PCR assay for screening rare/cryptic chromosome translocations in patients with de novo acute myeloid leukemia.
  • For 126 patients with de novo AML-M4/M5 without common chromosome translocations including t(15;17), t(8;21) and t(16;16), 3 parallel multiplex RT-PCR assays were set up to detect 6 mll-related gene rearrangements (mll/af10, mll/af17, mll/ell, mll/af9, mll/af6 and mll/enl) with low detection rate and 4 rare fusion genes (dek/can, tls/erg, aml1/mds (evi1) and npm/mlf1).
  • Among them, 10 cases were AML-M5 (16.67%), 1 cases AML-M4 (1.51%).
  • It is concluded that multiplex RT-PCR designed in this study can quickly, effectively and accurately identify the rare/cryptic chromosome translocations and can be used in clinical detection.


31. Stip E, Langlois R, Thuot C, Mancini-Marïe A: Fatal agranulocytosis: the use of olanzapine in a patient with schizophrenia and myelodysplasia. Prog Neuropsychopharmacol Biol Psychiatry; 2007 Jan 30;31(1):297-300
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  • Bone marrow cytogenetic study confirmed the deletion of the long arm of chromosome 11, as reported in myeloid leukemia.
  • If this patient would have died suddenly without the laboratory investigations that lead to the diagnosis of myeloblastic leukemia, the cause would have been probably and wrongfully allotted to treatment with olanzapine.

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  • (PMID = 16978752.001).
  • [ISSN] 0278-5846
  • [Journal-full-title] Progress in neuro-psychopharmacology & biological psychiatry
  • [ISO-abbreviation] Prog. Neuropsychopharmacol. Biol. Psychiatry
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 12794-10-4 / Benzodiazepines; 132539-06-1 / olanzapine
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32. Pillay M, Sturm AW: Evolution of the extensively drug-resistant F15/LAM4/KZN strain of Mycobacterium tuberculosis in KwaZulu-Natal, South Africa. Clin Infect Dis; 2007 Dec 1;45(11):1409-14
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  • [Title] Evolution of the extensively drug-resistant F15/LAM4/KZN strain of Mycobacterium tuberculosis in KwaZulu-Natal, South Africa.
  • The majority of the patients involved were infected with the same strain of Mycobacterium tuberculosis (F15/LAM4/KZN).
  • METHODS: We searched databases for studies performed during the period 1994-2005 that involved the resistance patterns of isolates of M. tuberculosis with the F15/LAM4/KZN strain fingerprint.
  • RESULTS: As early as 1994, the F15/LAM4/KZN strain was responsible for a number of cases of multidrug-resistant tuberculosis, indicating the ability of the strain to cause cases of primary resistant tuberculosis.
  • It is postulated that the introduction of these programs in the absence of susceptibility testing or drug resistance surveillance has been instrumental in the development of XDR in this highly transmissible F15/LAM4/KZN strain.

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  • [CommentIn] Clin Infect Dis. 2007 Dec 1;45(11):1415-6 [17990221.001]
  • (PMID = 17990220.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antitubercular Agents
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33. Gallipoli P, Leach M: Gingival infiltration in acute monoblastic leukaemia. Br Dent J; 2007 Nov 10;203(9):507-9
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  • [Title] Gingival infiltration in acute monoblastic leukaemia.
  • Acute myeloid leukaemias (AML) are aggressive haematopoietic neoplasms that, if untreated, can lead to death within days.
  • Up to 40% of presenting patients show evidence of extramedullary involvement (EMI) at diagnosis.
  • EMI is reportedly most prevalent in myelo-monoblastic and monoblastic subtypes of AML (M4 and M5 according to FAB classification) and can present as leukaemic infiltrates in many sites including gingival enlargement and mucosal and skin nodules.
  • [MeSH-major] Gingiva / pathology. Gingival Overgrowth / etiology. Leukemia, Monocytic, Acute / pathology. Leukemic Infiltration

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  • (PMID = 17992229.001).
  • [ISSN] 1476-5373
  • [Journal-full-title] British dental journal
  • [ISO-abbreviation] Br Dent J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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34. Zhang JH, Zheng YC, Wang YX, Zhang JY, Liu ZG: Laboratory study on near-tetraploid acute myelogenous leukemia of childhood. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):263-6
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  • [Title] Laboratory study on near-tetraploid acute myelogenous leukemia of childhood.
  • Near-tetraploidy is a rare cytogenetic abnormality in myelocytic malignancies in children, and its significance is unknown.
  • To investigate the characteristics of near-tetraploidy in a child with acute myelogenous leukemia (AML-M4), bone marrow smears were prepared for morphological analysis.
  • Combined with morphological and immunophenotypic results, AML-M4 was confirmed.
  • The patient was given four cycles of chemotherapy, and finally achieved clinical remission.
  • However, the duration achieving the remission in the child was longer than AML children with normal karyotype.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Polyploidy
  • [MeSH-minor] Bone Marrow Cells / pathology. Child. DNA, Neoplasm / analysis. Female. Humans. Immunophenotyping. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19374808.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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35. 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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  • [Cites] Blood. 1999 Jun 15;93(12):4395-405 [10361138.001]
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  • (PMID = 16909995.001).
  • [ISSN] 0012-4966
  • [Journal-full-title] Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
  • [ISO-abbreviation] Dokl. Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / phenylalanyl-arginyl-prolyl-arginyl-isoleucyl-methionyl-threonyl-proline; 137833-32-0 / myelopeptides; 59880-97-6 / N-Formylmethionine Leucyl-Phenylalanine; SY7Q814VUP / Calcium
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36. Regasini LO, Castro-Gamboa I, Silva DH, Furlan M, Barreiro EJ, Ferreira PM, Pessoa C, Lotufo LV, de Moraes MO, Young MC, Bolzani Vda S: Cytotoxic guanidine alkaloids from Pterogyne nitens. J Nat Prod; 2009 Mar 27;72(3):473-6
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  • As part of a bioprospecting program aimed at the discovery of potential anticancer drugs, two new guanidine-type alkaloids, nitensidines D and E (1, 2), and the known pterogynine (3), pterogynidine (4), and galegine (5), were isolated from the leaves of Pterogyne nitens.
  • Compound 2 exhibited cytotoxicity for HL-60 (human myeloblastic leukemia) and SF-245 (human glioblastoma) cells.

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  • (PMID = 19159272.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents, Phytogenic; 0 / Guanidines; 0 / nitensidine D; 0 / nitensidine E
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37. González-Vela MC, Val-Bernal JF, Mayorga M, Cagigal ML, Fernández F, Mazorra F: Myeloid sarcoma of the extrahepatic bile ducts presenting as obstructive jaundice. APMIS; 2006 Sep;114(9):666-8
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  • [Title] Myeloid sarcoma of the extrahepatic bile ducts presenting as obstructive jaundice.
  • We report a rare case of myeloid sarcoma (MS) of the extrahepatic bile ducts presenting as obstructive jaundice in a patient without leukemia at time of diagnosis.
  • Eight months following surgery the patient presented with multiple cutaneous nodules and bone marrow trephine biopsy showed acute myelomonocytic leukemia.
  • MS should be taken into consideration in the differential diagnosis of a patient with obstructive jaundice.
  • Immunohistochemistry is essential for a correct diagnosis.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Ducts, Extrahepatic. Cholestasis, Extrahepatic / pathology. Jaundice, Obstructive / pathology. Sarcoma, Myeloid / pathology

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  • (PMID = 16948823.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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38. Pillay M, Sturm AW: Nosocomial transmission of the F15/LAM4/KZN genotype of Mycobacterium tuberculosis in patients on tuberculosis treatment. Int J Tuberc Lung Dis; 2010 Feb;14(2):223-30
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  • [Title] Nosocomial transmission of the F15/LAM4/KZN genotype of Mycobacterium tuberculosis in patients on tuberculosis treatment.
  • Four of them acquired a F15/LAM4/KZN genotype, while two acquired fully susceptible Beijing strains.
  • Three of the four F15/LAM4/KZN strains were multidrug-resistant with identical fingerprint patterns, while the fourth was fully susceptible.
  • Both HIV-infected and non-infected patients are at risk of infection with the F15/LAM4/KZN strain in health care facilities and within the community.

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  • (PMID = 20074415.001).
  • [ISSN] 1815-7920
  • [Journal-full-title] The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease
  • [ISO-abbreviation] Int. J. Tuberc. Lung Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antitubercular Agents
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39. Cogulu O, Kosova B, Gunduz C, Karaca E, Aksoylar S, Erbay A, Karapinar D, Vergin C, Vural F, Tombuloglu M, Cetingul N, Ozkinay F: The evaluation of hTERT mRNA expression in acute leukemia children and 2 years follow-up of 40 cases. Int J Hematol; 2008 Apr;87(3):276-83
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  • [Title] The evaluation of hTERT mRNA expression in acute leukemia children and 2 years follow-up of 40 cases.
  • The aim of this study is to evaluate (1) the human telomerase-specific reverse transcriptase (hTERT) mRNA expression in childhood acute leukemia, (2) the association between the hTERT mRNA expression with the patients' characteristics and the known prognostic factors and (3) the correlation of the patients' survival with the initial hTERT mRNA value at diagnosis.
  • A total of 40 newly diagnosed patients consist of children [31 cases with acute lymphoblastic leukemia (ALL) and 9 cases with acute myeloblastic leukemia (AML)] were prospectively included into the study.
  • All cases were re-evaluated for their survival after 2 years.
  • The highest hTERT mRNA value was observed in Pre B-cell ALL patients followed by B-cell ALL, T-cell ALL and AML.
  • The hTERT mRNA relative ratio difference between the ALL and AML groups was significant.
  • Patients who had higher initial hTERT mRNA values showed significantly longer disease-free survival (DFS) and overall survival (OS) in ALL (P = 0.000 and 0.01, respectively).
  • Although DFS and OS was longer in AML patients with lower initial hTERT mRNA, the difference was not significant.
  • In conclusion, the hTERT mRNA expression values were not significantly associated with the known prognostic factors in children both with ALL and AML. hTERT mRNA value is a significant factor for childhood ALL at diagnosis in relation to the estimated survival.
  • [MeSH-major] Biomarkers, Tumor / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Telomerase / metabolism
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Infant. Male. Prospective Studies

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  • (PMID = 18293058.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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40. Maitta RW, Cannizzaro LA, Ramesh KH: Association of MLL amplification with poor outcome in acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):40-3
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  • [Title] Association of MLL amplification with poor outcome in acute myeloid leukemia.
  • Chromosomal rearrangements and amplification of the MLL gene at 11q23 are common abnormalities found in patients with severe myelodysplastic disorders and lymphoid and acute myeloid leukemias.
  • MLL rearrangements are associated with aggressive disease in both children and adults, with current evidence suggesting that MLL alterations are associated with a poor prognosis.
  • We report the clinical, cytogenetic and histologic findings of a patient who presented with a de novo diagnosis of AML-M4 and who fits the profile of patients presenting with MLL alterations, such as old age at presentation, rapid progression, therapeutic refractoriness, and poor outcome.
  • [MeSH-major] Gene Amplification / physiology. Leukemia, Myeloid, Acute / diagnosis. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19480936.001).
  • [ISSN] 1873-4456
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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41. Musil D, Krc I: Migrating venous thrombosis in acute leukemia. Blood Coagul Fibrinolysis; 2010 Jun;21(4):365-7
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  • [Title] Migrating venous thrombosis in acute leukemia.
  • We present a 55-year-old man with acute migrating thrombophlebitis and deep vein thrombosis of muscle veins in both calves indicating occurrence of acute myelomonocytic leukemia.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / complications. Venous Thrombosis / complications

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  • (PMID = 20305540.001).
  • [ISSN] 1473-5733
  • [Journal-full-title] Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
  • [ISO-abbreviation] Blood Coagul. Fibrinolysis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticoagulants; 5Q7ZVV76EI / Warfarin
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42. Tang YM, Guo L, Yang SL, Shen HQ, Qian BQ, Zhang Y, Zhang HZ: [Reactivity of a novel monoclonal antibody ZCH-2B8a on normal hematopoietic cells and malignant cell lines and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Oct;14(5):990-4
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  • ZCH-2B8a (IgG2a) is a novel monoclonal antibody (McAb) generated in laboratory of Children Hospital of Medical College, Zhejiang University recently using human myeloblastic leukemia cell line KG1a as immunogen.
  • The aim of this study was to investigate the reactivity of this antibody on normal blood cells and malignant cell lines and to explore its possible application in clinical practice.
  • Cell line analysis showed that the antibody notably reacted to three out of 4 cell lines (Raji, SMS-SB, Nalm-6 and Nall-1) with the positive rates of 98.78%, 98.61%, 94.93% respectively and weakly to one of them with 5.68% in B lineage cell lines and monoblastic cell line (U937, 67.78%) while it was only weakly positive or negative for other myeloid leukemia cell lines including Meg01 (33.40%), HL-60 (29.70%), K562 (28.19%), KG1a (16.23%) and HEL92.1.7 (8.02%).
  • Among 4 T lineage leukemia, 5 neuroblastoma and 1 colon cancer cell lines tested, only Molt-3 was found weakly positive (31.40%) for 2B8a, while the remaining 3 T cell lines (Molt4, JM and CCRF-CEM), 5 neuroblastoma cell lines (LA-N1, KCNR, BE, SK-N-SH, SK-N-AS) and the colon cancer cell line (HR8348) tested were negative.
  • It is concluded that 2B8a antibody primarily reacts to B lineage and monocytic lineage cells which may bear the diagnostic and therapeutic applications among different types of hematopoietic malignancies.

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  • (PMID = 17096904.001).
  • [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 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / HLA Antigens
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43. Uçar C, Calýskan U, Martini S, Heinritz W: Acute myelomonocytic leukemia in a boy with LEOPARD syndrome (PTPN11 gene mutation positive). J Pediatr Hematol Oncol; 2006 Mar;28(3):123-5
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  • [Title] Acute myelomonocytic leukemia in a boy with LEOPARD syndrome (PTPN11 gene mutation positive).
  • Leukemia has not previously been reported in patients with LEOPARD syndrome.
  • The authors describe a 13-year-old boy diagnosed with both LEOPARD syndrome and acute myelomonocytic leukemia (AML-M4).
  • [MeSH-major] LEOPARD Syndrome / complications. LEOPARD Syndrome / genetics. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / genetics
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Female. Humans. Intracellular Signaling Peptides and Proteins / genetics. Male. Middle Aged. Mutation, Missense. Pedigree. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Protein Tyrosine Phosphatases / genetics

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  • (PMID = 16679933.001).
  • [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 / Intracellular Signaling Peptides and Proteins; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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44. Basa J, Wolska-Smoleń T, Walter Z, Skotnicki AB: [Granulocytic sarcoma with late transformation into acute myeloblastic leukemia--case report]. Przegl Lek; 2006;63(8):706-10
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  • [Title] [Granulocytic sarcoma with late transformation into acute myeloblastic leukemia--case report].
  • Case presentation of a 28-year-old patient with acute myeloblastic leukemia (FAB AML-M4), who underwent surgery of an inguinal tumor a year before the diagnosis of leukemia was made.
  • In retrospective assessment a diagnosis of granulocytic sarcoma was made.
  • [MeSH-major] Brain Neoplasms / secondary. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology. Sarcoma, Myeloid / complications. Sarcoma, Myeloid / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Cell Transformation, Neoplastic / pathology. Disease-Free Survival. Fatal Outcome. Groin. Humans. Male. Neoplasm Recurrence, Local / diagnosis. Remission Induction / methods. Tomography, X-Ray Computed

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  • (PMID = 17441389.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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45. 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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46. Lu XG, Zhu L, Wang WQ, Zhang XH, Zhao XY, Xu GB, Xu Z: Morphological study on the megakaryocytes with nuclear extrusion and nucleocytoplasmic separation in four cases. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):1082-5
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  • To investigate the morphological changes of megakaryocytes with nuclear extrusion and nucleocytoplasmic separation, the morphological characteristics of megakaryocytes in peripheral blood films, bone marrow smears, and bone marrow biopsies from 4 newly diagnosed patients with primary myelofibrosis (PMF), myelodysplastic syndrome (MDS), myeloblastic leukemia with maturation (M(2)) and erythroleukemia (M(6)) were studied by using light microscope.

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  • (PMID = 16403285.001).
  • [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] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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47. 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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48. 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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49. Shen M, Yen A: c-Cbl interacts with CD38 and promotes retinoic acid-induced differentiation and G0 arrest of human myeloblastic leukemia cells. Cancer Res; 2008 Nov 1;68(21):8761-9
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  • [Title] c-Cbl interacts with CD38 and promotes retinoic acid-induced differentiation and G0 arrest of human myeloblastic leukemia cells.
  • In HL-60 human myeloblastic leukemia cells, it causes mitogen-activated protein kinase (MAPK) signaling leading to myeloid differentiation and G(0) cell cycle arrest.
  • Stable transfectants ectopically expressing c-Cbl underwent myeloid differentiation faster than wild-type (wt) cells when treated with RA.

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  • (PMID = 18974118.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [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] United States
  • [Chemical-registry-number] 0 / DNA Primers; 5688UTC01R / Tretinoin; EC 3.2.2.5 / Antigens, CD38; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ NIHMS790262; NLM/ PMC4896297
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50. Lulli V, Romania P, Riccioni R, Boe A, Lo-Coco F, Testa U, Marziali G: Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation. Haematologica; 2010 Oct;95(10):1633-41
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  • [Title] Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation.
  • This study focuses on the role of Ets-1 during granulocytic differentiation of NB4 promyelocytic and HL60 myeloblastic leukemia cell lines induced by all-trans retinoic acid.
  • Expression of Ets-1 was also reduced during dimethylsulfoxide-induced differentiation and during granulocytic differentiation of human CD34(+) hematopoietic progenitor cells but not in NB4.R2 and HL60R cells resistant to all-trans retinoic acid.
  • In line with these observations, transduction of a transdominant negative molecule of Ets-1, which inhibited DNA binding and transcriptional activity of the wild-type Ets-1, significantly increased chemical-induced differentiation.
  • Interestingly, p51 Ets-1 over-expression was frequently observed in CD34(+) hematopoietic progenitor cells derived from patients with acute myeloid leukemia, as compared to its expression in normal CD34(+) cells.
  • CONCLUSIONS: Our results indicated that a decreased expression of Ets-1 protein generalizes to granulocytic differentiation and may represent a crucial event for granulocytic maturation.
  • [MeSH-minor] Cell Line, Tumor. HL-60 Cells. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Leukemia / pathology. Leukemia, Promyelocytic, Acute. RNA, Small Interfering / pharmacology


51. Kauss MA, Reiterer G, Bunaciu RP, Yen A: Human myeloblastic leukemia cells (HL-60) express a membrane receptor for estrogen that signals and modulates retinoic acid-induced cell differentiation. Exp Cell Res; 2008 Oct 1;314(16):2999-3006
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  • [Title] Human myeloblastic leukemia cells (HL-60) express a membrane receptor for estrogen that signals and modulates retinoic acid-induced cell differentiation.
  • An estrogen receptor has now been found localized to the plasma membrane of human myeloblastic leukemia cells (HL-60).
  • They also modulated the effect of retinoic acid, an inducer of MAPK dependent terminal differentiation along the myeloid lineage in these cells.
  • In particular the ligands inhibited retinoic acid-induced inducible oxidative metabolism, a functional marker of terminal myeloid cell differentiation.
  • There is thus a membrane localized estrogen receptor in HL-60 myeloblastic leukemia cells that can cause ERK activation and modulates the response of these cells to retinoic acid, indicating crosstalk between the membrane estrogen and retinoic acid evoked pathways relevant to propulsion of cell differentiation.

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  • (PMID = 18692045.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA033505; United States / NCI NIH HHS / CA / CA033505-24S1; United States / NCI NIH HHS / CA / R01 CA033505-24S1; United States / NCI NIH HHS / CA / R01 CA033505; United States / NCI NIH HHS / CA / CA033505-24; United States / NCI NIH HHS / CA / R01 CA033505-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Estrogen Antagonists; 0 / Estrogens; 0 / ITGAM protein, human; 0 / Membrane Glycoproteins; 0 / Reactive Oxygen Species; 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen; 5688UTC01R / Tretinoin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
  • [Other-IDs] NLM/ NIHMS72606; NLM/ PMC2580735
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52. Karasawa M, Yamane A, Mitsui T, Irisawa H, Sakura T, Matsushima T, Tsukamoto N, Nojima Y, Miyawaki S: Long-term persistence of host cells detected by X-chromosome gene-based assay in patients undergoing gender-mismatched hematopoietic stem cell transplantation. Am J Hematol; 2005 Oct;80(2):101-5
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  • Chimerism was examined in four patients with myeloid malignancies: two patients with acute myeloid leukemia (AML) from myelodysplastic syndrome (MDS), and one patient each with AML M3 and AML M4.
  • All patients underwent myeloablative conditioning regimens and exhibited good clinical results during a median follow-up period of 6.6 years (range, 3.4-7.5 years).
  • [MeSH-minor] Adult. Chromosomes, Human, X. Female. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myeloid / therapy. Longitudinal Studies. Middle Aged. Receptors, Androgen / genetics. Sensitivity and Specificity. Sex Factors

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16184584.001).
  • [ISSN] 0361-8609
  • [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] 0 / AR protein, human; 0 / Receptors, Androgen
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53. Olaniyi JA: An Acute Leukaemia Masquerading as Immune Thrombocytopaenic Purpura (ITP)? A Case Report. Clin Med Case Rep; 2009;2:31-4
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  • [Title] An Acute Leukaemia Masquerading as Immune Thrombocytopaenic Purpura (ITP)? A Case Report.
  • This is a case report of a 35 year old female with diagnosed Immune Thrombocytopaenic Purpura (ITP) that was strangely followed by acute myeloid leukaemia at 10 months post diagnosis of ITP.
  • Shortly after delivery, she represented with gingival bleeding and peripheral film review and subsequent bone marrow cytology was in keeping with AML-M4 subtype.
  • She died shortly after diagnosis without being able to receive chemotherapy.

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  • (PMID = 24179370.001).
  • [ISSN] 1178-6450
  • [Journal-full-title] Clinical medicine. Case reports
  • [ISO-abbreviation] Clin Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3785378
  • [Keywords] NOTNLM ; M4 subtype / acute myeloid leukaemia / bleeding / immune thrombocytopaenic purpura / pregnancy
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54. 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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55. Levine RL, Loriaux M, Huntly BJ, Loh ML, Beran M, Stoffregen E, Berger R, Clark JJ, Willis SG, Nguyen KT, Flores NJ, Estey E, Gattermann N, Armstrong S, Look AT, Griffin JD, Bernard OA, Heinrich MC, Gilliland DG, Druker B, Deininger MW: The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood; 2005 Nov 15;106(10):3377-9
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  • [Title] The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.
  • Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
  • We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B-lineage acute lymphoblastic leukemia (ALL), T-cell ALL, and chronic lymphocytic leukemia (CLL).
  • Analysis of 222 patients with AML identified JAK2V617F mutations in 4 patients with AML, 3 of whom had a preceding MPD.
  • We did not identify the JAK2V617F disease allele in B-lineage ALL (n = 83), T-cell ALL (n = 93), or CLL (n = 45).
  • These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies.


56. 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


57. Shih LY, Huang CF, Lin TL, Wu JH, Wang PN, Dunn P, Kuo MC, Tang TC: Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia. Clin Cancer Res; 2005 Mar 1;11(5):1821-6
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  • [Title] Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia.
  • PURPOSE: We aimed to assess the role of CEBPalpha mutations in the progression of myelodysplastic syndrome (MDS) to acute myelogenous leukemia (AML) and their cooperating mutations.
  • EXPERIMENTAL DESIGN: Mutational analysis of CEBPalpha with direct sequencing for each PCR product was done on matched bone marrow samples obtained from 50 adult patients with MDS at diagnosis and at AML transformation.
  • RESULTS: CEBPalpha mutations were identified in four patients at diagnosis of MDS, including one with refractory anemia with excess blasts and three with chronic myelomonocytic leukemia.
  • At AML transformation, three patients retained the identical mutant clones as their initial diagnosis, three acquired the mutations, and one lost CEBPalpha mutation when she gained FLT3/ITD mutation.
  • Together, seven patients had CEBPalpha mutations throughout the disease course; four patients had NH(2)-terminal mutations resulting in a frameshift and truncation of the protein, three of them had two different mutations either on the same alleles or on different alleles, two had missense mutations, and one had a deletion in the basic region leucine zipper domain.
  • CEBPalpha mutations had no influence on the time to AML progression or overall survival.
  • CONCLUSIONS: Our results show that CEBPalpha mutations play a role in a subset of patients with MDS, especially in chronic myelomonocytic leukemia.
  • The mutation status was heterogeneous, exhibiting identical clone, clonal change, or clonal evolution during the progression to AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Cell Transformation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Alleles. DNA Mutational Analysis. Disease Progression. Female. Humans. Leucine Zippers. Male. Middle Aged


58. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


59. El-Mahdy MA, Zhu Q, Wang QE, Wani G, Wani AA: Thymoquinone induces apoptosis through activation of caspase-8 and mitochondrial events in p53-null myeloblastic leukemia HL-60 cells. Int J Cancer; 2005 Nov 10;117(3):409-17
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  • [Title] Thymoquinone induces apoptosis through activation of caspase-8 and mitochondrial events in p53-null myeloblastic leukemia HL-60 cells.
  • Here, we report that TQ exhibits antiproliferative effect, induces apoptosis, disrupts mitochondrial membrane potential and triggers the activation of caspases 8, 9 and 3 in myeloblastic leukemia HL-60 cells.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15906362.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES6074; United States / NIEHS NIH HHS / ES / R01 ES012991; United States / NIEHS NIH HHS / ES / R01 ES002388; United States / NIEHS NIH HHS / ES / ES12991; United States / NCI NIH HHS / CA / CA93413
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Tumor Suppressor Protein p53; 490-91-5 / thymoquinone; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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60. Mneimneh WS, Bonte H, Bernheim A, Martin A: Myeloid sarcoma of the prostate revealed by urinary retention: a case report. BMJ Case Rep; 2009;2009
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  • [Title] Myeloid sarcoma of the prostate revealed by urinary retention: a case report.
  • Myeloid sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.
  • Here, a singular case of a MS of the prostate discovered through investigations for urinary retention and revealing an acute leukaemia classified as an acute myeloid leukaemia (AML) with inversion 16 (inv16) according to the World Health Organization (WHO) classification (AML-M4 with inv16 in the French-American-British (FAB) classification) in a 65-year-old man is presented.
  • None of the previously reported and reviewed cases of prostatic MS were of AML-M4 type.
  • Such a translocation was recently described in some acute myeloid processes.
  • Radiation therapy could be beneficial for the localised disease of the prostate.

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  • [Cites] Haematologica. 1953;37(8):827-34 [13128526.001]
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  • (PMID = 21686890.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3029613
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61. 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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62. Asou N, Yanagida M, Huang L, Yamamoto M, Shigesada K, Mitsuya H, Ito Y, Osato M: Concurrent transcriptional deregulation of AML1/RUNX1 and GATA factors by the AML1-TRPS1 chimeric gene in t(8;21)(q24;q22) acute myeloid leukemia. Blood; 2007 May 1;109(9):4023-7
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  • [Title] Concurrent transcriptional deregulation of AML1/RUNX1 and GATA factors by the AML1-TRPS1 chimeric gene in t(8;21)(q24;q22) acute myeloid leukemia.
  • The Runt domain transcription factor AML1/RUNX1 is essential for the generation of hematopoietic stem cells and is the most frequent target of chromosomal translocations associated with leukemia.
  • Here, we present a new AML1 translocation found in a patient with acute myeloid leukemia M4 with t(8;21)(q24;q22) at the time of relapse.
  • TRPS1 encodes a putative multitype zinc finger (ZF) protein containing 9 C2H2 type ZFs and 1 GATA type ZF.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Core Binding Factor Alpha 2 Subunit / biosynthesis. DNA-Binding Proteins / biosynthesis. GATA Transcription Factors / metabolism. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion / biosynthesis. Transcription Factors / biosynthesis

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  • (PMID = 17244685.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / GATA Transcription Factors; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / TRPS1 protein, human; 0 / Transcription Factors
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63. Kim M, Lee JW, Lee JK, Hong YJ, Hong SI, Kang HJ, Cho EH, Chang YH: [A case of del(16)(q22) in a patient with acute myeloid leukemia with complex karyotype]. Korean J Lab Med; 2010 Aug;30(4):329-33
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  • [Title] [A case of del(16)(q22) in a patient with acute myeloid leukemia with complex karyotype].
  • Inversion of chromosome 16 [inv(16)(p13.1q22)] and t(16;16)(p13.1;q22) are associated with acute myelomonocytic leukemia (AMML) with eosinophilia and a favorable prognosis.
  • On the other hand, patients with del(16)(q22) usually present with MDS or chronic myelomonocytic leukemia (CMML), which can evolve to AMML without eosinophilia, and this chromosomal aberration is associated with older age, a complex karyotype, and a poor prognosis.
  • We report a case of AML with del(16)(q22) which showed a complex karyotype, absence of eosinophilia in bone marrow study and a poor response to chemotherapy.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 16. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20805702.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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64. Yu RX, Zhou YH, Lin SY: [Effects of combined therapy of human leucocyte antigen haploidentical related bone marrow transplantation and Chinese medicine in treating leukaemia]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2006 Jul;26(7):600-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of combined therapy of human leucocyte antigen haploidentical related bone marrow transplantation and Chinese medicine in treating leukaemia].
  • OBJECTIVE: To explore the feasibility of human leucocyte antigen (HLA) haploidentical related T-cell undepleted allogeneic bone marrow transplantation (Allo-BMT) combined with Chinese medicine for the treatment of leukaemia.
  • METHODS: Four patients with chronic myeloblastic leukemia (CML) and 4 with acute myeloid leukemia (AML) received allo-BMT with graft from 1 - 3 HLA-mismatched related donors.
  • The median follow-up duration was 18 (range 2-32) months, during this period six patients were alive in a disease-free situation.
  • CONCLUSION: Combined therapy of HLA haploidentical related T-cell undepleted Allo-BMT and Chinese medicine plus immunosuppressants with pre-harvest G-CSF application in doner could effectively reduce the incidence of acute severe GVHD and raise the disease-free survival rate in treating leukaemia.


65. Diermayr S, Himmelreich H, Durovic B, Mathys-Schneeberger A, Siegler U, Langenkamp U, Hofsteenge J, Gratwohl A, Tichelli A, Paluszewska M, Wiktor-Jedrzejczak W, Kalberer CP, Wodnar-Filipowicz A: NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities. Blood; 2008 Feb 1;111(3):1428-36
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  • [Title] NKG2D ligand expression in AML increases in response to HDAC inhibitor valproic acid and contributes to allorecognition by NK-cell lines with single KIR-HLA class I specificities.
  • This study exploited alloreactivity of natural killer (NK) cells for augmenting the recognition of human acute myeloid leukemia (AML).
  • We demonstrated efficient cytolysis of KIR-HLA class I-mismatched primary AML blasts even at low effector-to-target ratios.
  • To define the impact of tumor-associated activating NKG2D-ligands (NKG2D-L), 66 AML patients at diagnosis were analyzed.
  • NKG2D-L were selectively expressed on monoblastic cells in AML M4 and M5 yet absent or weakly expressed on myeloblastic cells in all AML subtypes.
  • Paucity of cell-surface NKG2D-L was not the result of shedding because levels of soluble ULBP1 ligand measured in AML plasma were in the normal range.
  • Notably, purified NKG2D-L(+) monoblastic cells were more susceptible to NK-mediated killing than NKG2D-L(-) myeloblastic cells.
  • These data suggest that adoptive transfer of selected populations of alloreactive HLA class I-mismatched NK cells in combination with pharmacologic induction of NKG2D-L merits clinical evaluation as novel approaches to immunotherapy of human AML.
  • [MeSH-major] HLA Antigens / immunology. Histone Deacetylase Inhibitors. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / metabolism. Receptors, Immunologic / metabolism. Valproic Acid / analogs & derivatives

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  • (PMID = 17993609.001).
  • [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 / Enzyme Inhibitors; 0 / GPI-Linked Proteins; 0 / HLA Antigens; 0 / Histocompatibility Antigens Class I; 0 / Histone Deacetylase Inhibitors; 0 / Intracellular Signaling Peptides and Proteins; 0 / KLRK1 protein, human; 0 / Ligands; 0 / MHC class I-related chain A; 0 / Membrane Proteins; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell; 0 / ULBP1 protein, human; 0 / valpronic acid; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Histone Deacetylases
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66. Dalamaga M, Nikolaidou A, Karmaniolas K, Hsi A, Chamberland J, Dionyssiou-Asteriou A, Mantzoros CS: Circulating adiponectin and leptin in relation to myelodysplastic syndrome: a case-control study. Oncology; 2007;73(1-2):26-32
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  • OBJECTIVE: Adiponectin plays a protective role in several malignancies, including myeloblastic leukemia, whereas leptin may increase the proliferation of progenitor cells and may stimulate leukemic cell growth in vitro.
  • [MeSH-minor] Aged. Biomarkers / blood. Biomarkers, Tumor / blood. Case-Control Studies. Female. Humans. Leukemia / blood. Leukemia / etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis


67. Shin HJ, Chung JS, Choi YJ, Cho GJ: A pilot study of priming with granulocyte macrophage colony-stimulating factor plus all-trans retinoic acid combined with remission induction chemotherapy in patients with acute myeloid leukemia. Am J Clin Oncol; 2009 Jun;32(3):227-32
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  • [Title] A pilot study of priming with granulocyte macrophage colony-stimulating factor plus all-trans retinoic acid combined with remission induction chemotherapy in patients with acute myeloid leukemia.
  • OBJECTIVES: Priming with granulocyte macrophage colony-stimulating factor (GM-CSF) plus all-trans retinoic acid (ATRA) during induction chemotherapy may enhance response rates and survival in patients with acute myeloid leukemia (AML) due to the differentiation of human myeloblastic leukemia cells into granulocytes.
  • Two-year probabilities were 45.5% (study group) and 47.4% (control group) for disease-free survival and 38.5% (study group) and 36.2% (control group) for overall survival.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 19433969.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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68. Chang WR, Park IJ, Lee HW, Park JS, Kim HC, Kim HJ, Han JH, Cho SR: [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts]. Korean J Lab Med; 2009 Oct;29(5):390-5
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  • [Title] [Two cases of acute myeloid leukemia with t(16;21)(p11;q22) and TLS/FUS-ERG fusion transcripts].
  • Many AML-associated chromosomal abnormalities, such as t(8;21), t(15;17), inv(16), t(9;11), t(9;22) and t(6;9) are well known.
  • The chromosomal aberration of t(16;21)(p11;q22) in AML is rare and it is known to be associated with poor prognosis, young age (median age, 22 yr), and involvement of various subtypes of the French-American-British classification.
  • We report here 2 AML patients with t(16;21)(p11;q22), proved by conventional cytogenetics and/or reverse transcription (RT)-PCR.
  • One patient was a 24 yr-old male with acute myelomonocytic leukemia.
  • Although he received allogeneic peripheral blood stem cell transplantation after the first remission, he died 9 months after the initial diagnosis due to relapse of the disease and graft-versus-host disease.
  • The other patient was a 72 yr-old male with acute myeloid leukemia without maturation.
  • We suggest that the presence of t(16;21)(p11;q22) and/or TLS/FUS-ERG fusion transcripts has to be considered in cases of AML with erythrophagocytosis.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Graft vs Host Disease / diagnosis. Humans. Karyotyping. Male. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • (PMID = 19893346.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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69. Nagel S, Kaufmann M, Scherr M, Drexler HG, MacLeod RA: Activation of HLXB9 by juxtaposition with MYB via formation of t(6;7)(q23;q36) in an AML-M4 cell line (GDM-1). Genes Chromosomes Cancer; 2005 Feb;42(2):170-8
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  • [Title] Activation of HLXB9 by juxtaposition with MYB via formation of t(6;7)(q23;q36) in an AML-M4 cell line (GDM-1).
  • Mutation or dysregulation of related homeobox genes occurs in leukemia.
  • Using RT-PCR, we screened members of the EHG family of homeobox genes, comprising EN1 (at 2q14), GBX2 (at 2q36), and EN2, GBX1, and HLXB9 (at 7q36), for dysregulation in acute myeloid leukemia (AML) cell lines indicated by chromosomal breakpoints at these sites.
  • Only one EHG-family gene was expressed, HLXB9, in cell line GDM-1 (AML-M4).
  • Fluorescence in situ hybridization analysis showed chromosomal breakpoints close to the region upstream of HLXB9, at 7q36, a region rearranged in certain AML patients, and at 6q23 upstream of MYB, a gene activated in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Expression Regulation, Neoplastic / genetics. Genes, myb / physiology. Homeodomain Proteins / genetics. Leukemia, Myelomonocytic, Acute / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15540222.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Proto-Oncogene Proteins c-myb; 0 / Transcription Factors
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70. Saito M, Mori A, Irie T, Tanaka M, Morioka M: [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer]. Rinsho Ketsueki; 2009 Mar;50(3):192-6
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  • [Title] [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer].
  • Among cases of therapy-related acute myeloid leukemia (t-AML) due to DNA topoisomerase II inhibitors, 11q23 abnormality is often detected.
  • Few studies have reported t-AML due to paclitaxel.
  • In this study, we report a patient who developed t-AML with 11q23 abnormality and bone marrow metastasis after breast cancer treatment with paclitaxel.
  • Bone marrow aspiration suggested AML (M4) with (11;19)(q23;p13) chromosome abnormalities.
  • Based on the clinical course, t-AML may have developed after paclitaxel therapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Bone Marrow Neoplasms / secondary. Breast Neoplasms / pathology. Chromosome Aberrations / drug effects. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Neoplasms, Second Primary. Paclitaxel / adverse effects


71. Yan Q, Li Y, Jiang Z, Sun Y, Zhu L, Ding Z: Antiproliferation and apoptosis of human tumor cell lines by a lectin (AMML) of Astragalus mongholicus. Phytomedicine; 2009 Jun;16(6-7):586-93
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  • [Title] Antiproliferation and apoptosis of human tumor cell lines by a lectin (AMML) of Astragalus mongholicus.
  • A lectin (AMML) from the roots of Astragalus mongholicus was extracted and purified by affinity chromatographic technique.
  • Human cervical carcinoma cell line (HeLa), human osteoblast-like cell line (MG63) and human leukemia cell line (K562) were used to check the effects of AMML on cell proliferation, apoptosis and cell cycle.
  • Morphological observation showed that AMML-treated HeLa cells displayed outstanding apoptosis characteristics, such as nuclear fragmentation and appearance of membrane-enclosed apoptotic bodies.
  • For the first time we also report a significant cell cycle arrest at S phase of HeLa cells by AMML.

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  • (PMID = 19403285.001).
  • [ISSN] 1618-095X
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Lectins
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72. Anuchapreeda S, Thanarattanakorn P, Sittipreechacharn S, Tima S, Chanarat P, Limtrakul P: Inhibitory effect of curcumin on MDR1 gene expression in patient leukemic cells. Arch Pharm Res; 2006 Oct;29(10):866-73
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  • The leukemic cells were collected from 78 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period from July 2003 to February 2005.
  • There were 61 cases of acute lymphoblastic leukemia (ALL), 14 cases of acute myeloblastic leukemia (AML), and 3 cases of chronic myelocytic leukemia (CML).
  • Thus, curcumin treatment may provide a lead for clinical treatment of leukemia patients in the future.
  • [MeSH-minor] Acute Disease. Adolescent. Age Factors. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Bone Marrow / drug effects. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Survival / drug effects. Child, Preschool. Female. Humans. Infant. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / genetics. RNA, Messenger / isolation & purification. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured

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  • (PMID = 17121181.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; IT942ZTH98 / Curcumin
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73. Slavcheva V, Lukanov T, Balatsenko G, Angelova S, Antonov A, Bogdanov L, Tsvetkov N: Clinical case of acute myeloblastic leukemia with t(8;21)(q22;q22) in a patient with Klinefelter's syndrome. Hematol Rep; 2010 Jan 26;2(1):e11
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  • [Title] Clinical case of acute myeloblastic leukemia with t(8;21)(q22;q22) in a patient with Klinefelter's syndrome.
  • Often the disease can be diagnosed accidentally, when carrying out cytogenetic analysis in cases of a malignant blood disease.
  • We present the clinical case of a patient diagnosed with acute myelomonoblastic leukemia-M4 Eo (AML- M4), where by means of classic cytogenetics a karyotype was found corresponding to Klinefelter's syndrome.
  • Three induction courses of polychemotherapy wermade, which led to remission of the disease, documented both flowcytometrically and cytogenetically.

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  • (PMID = 22184514.001).
  • [ISSN] 2038-8330
  • [Journal-full-title] Hematology reports
  • [ISO-abbreviation] Hematol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3222265
  • [Keywords] NOTNLM ; Klinefelter's syndrome / genetics / leukemia / remission.
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74. Ahmad F, Mandava S, Das BR: Mutations of NPM1 gene in de novo acute myeloid leukaemia: determination of incidence, distribution pattern and identification of two novel mutations in Indian population. Hematol Oncol; 2009 Jun;27(2):90-7
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  • [Title] Mutations of NPM1 gene in de novo acute myeloid leukaemia: determination of incidence, distribution pattern and identification of two novel mutations in Indian population.
  • Mutations in the nucleophosmin (NPM1) gene have been recently described to occur in about one-third of acute myeloid leukaemias (AMLs) and represent the most frequent genetic alteration currently known in this subset, specially in those with normal karyotype.
  • This study explored the prevalence and clinical profile of NPM1 mutations in a cohort of 200 Indian adult and children with AML.
  • NPM1 mutations were significantly associated with normal karyotype (p = 0.001), high WBC count (p = 0.034), AML-M4 subtype (p = 0.039) and a gradient increase of mutation rate with the increase in age groups.
  • Majority of the patients had mutation type A (69.2%), followed by B (5.1%), D (15.3%), H* (2.5%) and Nm (2.5%) all involving COOH terminal of the NPM1 protein.
  • More ongoing larger studies are warranted to elucidate the molecular pathogenesis of AML that arises in this part of the world.
  • Furthermore, we believe that in light of its high prevalence worldwide, inclusion of NPM1 mutation detection assay in diagnostic evaluations of AML may improve the efficacy of routine genetic characterization and allow assignment of patients to better-defined risk categories.
  • [MeSH-major] Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. DNA Mutational Analysis. DNA, Neoplasm / genetics. Exons / genetics. Female. Gene Frequency. Global Health. Humans. In Situ Hybridization, Fluorescence. India / epidemiology. Infant. Karyotyping. Male. Middle Aged. Mutagenesis, Insertional. Young Adult

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  • (PMID = 19365794.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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75. Rao S, Kar R, Saxena R: Pseudo Chediak-Higashi anomaly in acute myelomonocytic leukemia. Indian J Pathol Microbiol; 2009 Apr-Jun;52(2):255-6
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  • [Title] Pseudo Chediak-Higashi anomaly in acute myelomonocytic leukemia.
  • Pseudo Chediak-Higashi anomaly in acute leukemia is a rarely described entity.
  • The significance of this intriguing morphological finding largely remains unknown, although some authors have predicted a poorer outcome in such cases because of a higher susceptibility to fulminant infections.
  • [MeSH-major] Chediak-Higashi Syndrome / pathology. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 19332932.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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76. Reiterer G, Chen L, Tassef R, Varner JD, Chen CY, Yen A: RAF associates with phosphorylated nuclear BubR1 during endoreduplication induced by JAK inhibition. Cell Cycle; 2010 Aug 15;9(16):3297-304
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  • The role of JAK signaling in cell cycle transit and maintenance of genomic stability was determined in HL-60 human myeloblastic leukemia cells.
  • In the current study we find that JAK inhibition caused nuclear re-localization of RAF-1 which could be inhibited by RAF inhibitor GW5074.
  • In this hypothetical model JAK suppresses RAF/MEK phosphorylation and nuclear re-localization, but JAK inhibition induces the phosphorylations and relocalization with association of RAF and phosphorylated BubR1 in the nucleus leading to endoreduplication.

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  • (PMID = 20703093.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033505; United States / NCI NIH HHS / CA / R01 CA100498; United States / NCI NIH HHS / CA / CA100498; United States / NCI NIH HHS / CA / CA33505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-iodo-3-((3,5-dibromo-4-hydroxyphenyl)methylene)-2-indolinone; 0 / Indoles; 0 / Phenols; 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Janus Kinases; EC 2.7.11.1 / BUB1 protein, human; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 2.7.12.2 / MAP Kinase Kinase 1
  • [Other-IDs] NLM/ PMC3230478
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77. Kuliszkiewicz-Janus M, Tuz MA, Kiełbiński M, Baczyński S, Jaźwiec B, Sladowska H: Platelet-activating factor changes in phospholipid extracts from the plasma, peripheral blood mononuclear cells and bone marrow mononuclear cells of patients with acute leukemia--a 31P MRS in vitro study. Cell Mol Biol Lett; 2008;13(1):58-66
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  • [Title] Platelet-activating factor changes in phospholipid extracts from the plasma, peripheral blood mononuclear cells and bone marrow mononuclear cells of patients with acute leukemia--a 31P MRS in vitro study.
  • The aim of this investigation was to evaluate the changes in PAF concentrations in the plasma, PBMC and BMMC of patients with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).
  • The plasma was from 23 healthy volunteers (HV) and 44 patients with AL (16 ALL, 28 AML).
  • The PBMC were from 15 HV and 55 patients with AL (18 ALL, 37 AML), and the BMMC from 40 patients with AL (11 ALL, 29 AML).
  • The PAF concentration in the plasma of the patients with ALL or AML was lower than that for the healthy volunteers.
  • The PAF concentration in the plasma of the patients with ALL did not differ significantly from that of the patients with AML.
  • In the case of both the PBMC and BMMC, the PAF concentration was significantly diminished in patients with ALL relative to the concentration for those with AML and for the healthy volunteers.
  • No differences were observed in the PAF concentrations for the AML patients and the healthy volunteers.
  • [MeSH-major] Bone Marrow Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Magnetic Resonance Spectroscopy. Phospholipids / blood. Platelet Activating Factor / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 17952375.001).
  • [ISSN] 1689-1392
  • [Journal-full-title] Cellular & molecular biology letters
  • [ISO-abbreviation] Cell. Mol. Biol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Phospholipids; 0 / Phosphorus Isotopes; 0 / Platelet Activating Factor
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78. Reiterer G, Yen A: Inhibition of the janus kinase family increases extracellular signal-regulated kinase 1/2 phosphorylation and causes endoreduplication. Cancer Res; 2006 Sep 15;66(18):9083-9
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  • The role of Janus-activated kinase (JAK) signaling in cell cycle transit and maintenance of genomic stability was determined in HL-60 myeloblastic leukemia cells.

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  • (PMID = 16982750.001).
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / Flavonoids; 0 / MAD2L1 protein, human; 0 / Mad2 Proteins; 0 / Protein Kinase Inhibitors; 0 / Repressor Proteins; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / Janus Kinase 3; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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79. Grüllich C, Ziegler C, Finke J: Rabbit anti T-lymphocyte globulin induces apoptosis in peripheral blood mononuclear cell compartments and leukemia cells, while hematopoetic stem cells are apoptosis resistant. Biol Blood Marrow Transplant; 2009 Feb;15(2):173-82
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  • [Title] Rabbit anti T-lymphocyte globulin induces apoptosis in peripheral blood mononuclear cell compartments and leukemia cells, while hematopoetic stem cells are apoptosis resistant.
  • Polyclonal anti-T-lymphocyte globulins (ATG) are used in allogeneic stem cell transplantation (SCT) for the prophylaxis of graft versus host disease (GVHD) by in vivo T cell depletion.
  • We also detected antileukemic activity of ATG by measuring apoptosis in myeloid and lymphatic leukemia cell lines and primary leukemia cells.
  • The human leukemia cell lines Jurkat, Daudi, DG-75 (lymphoblastic), and K562, HL-60, KG1, and U937 (myeloblastic) underwent ATG-induced apoptosis, whereas the NK-cell line YT was resistant.
  • Primary leukemia cells from 6 investigated patients with acute lymphoblastic leukemia, 9 of 10 patients with chronic lymphocytic leukemia, and 4 of 8 patients with acute myeloblastic leukemia underwent ATG-induced apoptosis.
  • [MeSH-major] Antilymphocyte Serum / pharmacology. Apoptosis / drug effects. Graft vs Host Disease / prevention & control. Hematopoietic Stem Cells / cytology. Leukemia / pathology. Leukocytes, Mononuclear / cytology
  • [MeSH-minor] Animals. B-Lymphocytes. Cells, Cultured. Humans. Leukemia, Lymphocytic, Chronic, B-Cell. Leukemia, Myeloid, Acute. Monocytes. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Rabbits. T-Lymphocytes

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  • (PMID = 19167677.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum
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80. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • Both cases were thought to represent therapy-related AML because the patients had previously received combination chemotherapy including epipodophyllotoxin, anthracycline, and alkylating agents for the ATL.
  • The cases were diagnosed as AML M4 with eosinophilia and AML M2, with the chromosomal abnormalities inv(16)(p13q22) and t(8;21)(q22;q22), respectively.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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81. Tong HX, Wang HH, Zhang JH, Liu ZG, Zheng YC, Wang YX: [Immunophenotypes, cytogenetics and clinical features of 192 patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1174-8
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  • [Title] [Immunophenotypes, cytogenetics and clinical features of 192 patients with acute myeloid leukemia].
  • The objective of this study was to investigate the immunophenotypic subtype profiles of 192 patients with acute myeloid leukemia (AML) and its association to cytogenetics and clinical features.
  • The results showed that CD33, CD13, myeloperoxidase (MPO) and CD117 were the most commonly expressed antigens in AML.
  • CD117 expressed in 84.6% of AML-M3 cases.
  • A combination of intensive autofluorescence, both CD34- and HLA-DR-, and high expression of CD13, CD33 and MPO had significant value for AML-M3 diagnosis.
  • CD14 expressed only in AML-M4 and AML-M5, and both intensive positivity of CD64 and CD15 with high expression of HLA-DR may suggest great possibility for diagnosis of AML-M5.
  • Lymphoid marker expression was documented in 47.9% of the 192 AML cases.
  • CD56 (26.0%) and CD7 (20.8%) were the most commonly expressed lymphoid markers in AML patients, followed by CD19 (9.9%) and CD2 (7.3%).
  • Correlation test showed that t(8;21) was found only in 17 cases of AML-M2 and strongly associated with the individual or combinational expressions of CD15/CD19/CD56.
  • And 28 cases of t(15;17) were found in AML-M3; 2 cases of inv(16) were found in AML-M4EO.
  • It is concluded that immunophenotype analysis is useful for AML diagnosis and classification, and the immunophenotype has close relevance to the abnormal cytogenetic changes and clinical features in AML.
  • The results suggested that a new prognostic scoring system that integrated the morphology, cytogenetic abnormalities and immunophenotype parameters would benefit the diagnosis, classification, and estimation of prognosis in AML patients.

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  • (PMID = 19840445.001).
  • [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
  • [Publication-country] China
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82. Kadkol SS, Bruno A, Oh S, Schmidt ML, Lindgren V: MLL-SEPT6 fusion transcript with a novel sequence in an infant with acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Jul 15;168(2):162-7
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  • [Title] MLL-SEPT6 fusion transcript with a novel sequence in an infant with acute myeloid leukemia.
  • The MLL gene at 11q23 is a site of frequent rearrangement in acute leukemia with multiple fusion partners.
  • A relatively uncommon rearrangement, associated with infant AML-M4, fuses the MLL and SEPT6 genes.
  • We describe the case of an infant with acute myelogenous leukemia who showed cytogenetic evidence of rearrangement between 11q23 and Xq24 regions.
  • The findings emphasize the importance of combined cytogenetic and molecular analyses in the workup of acute leukemia, especially in those leukemias that occur infrequently.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics


83. Yildirim I, Aytac S, Ceyhan M, Cetin M, Tuncer M, Cengiz AB, Secmeer G, Yetgin S: Piperacillin/tazobactam plus amikacin versus carbapenem monotherapy as empirical treatment of febrile neutropenia in childhood hematological malignancies. Pediatr Hematol Oncol; 2008 Jun;25(4):291-9
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  • A prospective, randomized clinical trial was conducted to compare the efficacy of piperacillin/tazobactam and amikacin combination with carbapenem monotherapy for the empirical treatment of febrile neutropenic episodes of children with acute lymphoblastic leukemia or acute myeloblastic leukemia.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Bacterial Infections / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18484473.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Carbapenems; 0 / Enzyme Inhibitors; 157044-21-8 / piperacillin, tazobactam drug combination; 84319SGC3C / Amikacin; 87-53-6 / Penicillanic Acid; X00B0D5O0E / Piperacillin
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84. 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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85. Fu L, Katsube K, Tohda S: Transition of cleaved Notch1 and gene expression changes in myeloblastic leukemia cells stimulated with notch ligands. Anticancer Res; 2009 Oct;29(10):3967-70
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  • [Title] Transition of cleaved Notch1 and gene expression changes in myeloblastic leukemia cells stimulated with notch ligands.
  • BACKGROUND: Notch activation by ligand stimulation regulates the growth of acute myeloid leukemia (AML) cells.
  • MATERIALS AND METHODS: Two AML cell lines, THP-1 and TMD7, and three Notch ligands, Jagged1, Dll1 and Dll4, were used.
  • [MeSH-major] Calcium-Binding Proteins / pharmacology. Intercellular Signaling Peptides and Proteins / pharmacology. Leukemia, Myeloid, Acute / metabolism. Membrane Proteins / pharmacology. Receptor, Notch1 / metabolism

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  • (PMID = 19846937.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Dlk1 protein, mouse; 0 / Intercellular Signaling Peptides and Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Recombinant Proteins; 0 / delta protein; 134324-36-0 / Serrate proteins
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86. Hamilton JA, Whitty G, Masendycz P, Wilson NJ, Jackson J, De Nardo D, Scholz GM: The critical role of the colony-stimulating factor-1 receptor in the differentiation of myeloblastic leukemia cells. Mol Cancer Res; 2008 Mar;6(3):458-67
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  • [Title] The critical role of the colony-stimulating factor-1 receptor in the differentiation of myeloblastic leukemia cells.
  • An early event during induction of macrophage differentiation in the myeloblastic leukemia M1 cell line by different stimuli, such as leukemia inhibitory factor (LIF) and interleukin-6 (IL-6), is expression of the colony-stimulating factor-1 receptor (CSF-1R).
  • We also propose that expression and activation of the CSF-1R explain much prior literature on macrophage lineage commitment in M1 leukemic cells and may be important in controlling the progression of certain myeloid leukemias.
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Interleukin-6 / pharmacology. Leukemia Inhibitory Factor / pharmacology. Leukemia, Myeloid, Acute / pathology. Macrophages / cytology. Macrophages / drug effects. Mice. Receptors, OSM-LIF / drug effects. Receptors, OSM-LIF / physiology

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  • (PMID = 18337452.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Leukemia Inhibitory Factor; 0 / Receptors, OSM-LIF; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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87. Gibbs JD, Liebermann DA, Hoffman B: Egr-1 abrogates the E2F-1 block in terminal myeloid differentiation and suppresses leukemia. Oncogene; 2008 Jan 3;27(1):98-106
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  • [Title] Egr-1 abrogates the E2F-1 block in terminal myeloid differentiation and suppresses leukemia.
  • Previously, we have shown that ectopic expression of the zinc finger transcription factor Egr-1 in M1 myeloblastic leukemia cells promotes terminal differentiation with interleukin-6 (IL-6).
  • In addition, we have shown that deregulated expression of the oncogene E2F-1 blocks the myeloid terminal differentiation program, resulting in proliferation of immature cells in the presence of IL-6.
  • Here it is shown that the positive regulator of differentiation Egr-1 abrogates the E2F-1-driven block in myeloid terminal differentiation.
  • Furthermore, Egr-1 diminished the aggressiveness of M1E2F-1 leukemias and abrogated the leukemic potential of IL-6-treated M1E2F-1 cells.
  • Previously, we reported that Egr-1 abrogated the block in terminal myeloid differentiation imparted by deregulated c-myc, which blocks differentiation at a later stage than E2F-1, resulting in cells that have the characteristics of functionally mature macrophages that did not undergo G(0)/G(1) arrest.
  • Taken together, this work extends and highlights the tumor suppressor role of Egr-1, with Egr-1 behaving as a tumor suppressor against two oncogenes, each blocking myeloid differentiation by a different mechanism.
  • [MeSH-major] Cell Differentiation / physiology. Early Growth Response Protein 1 / physiology. Growth Inhibitors / physiology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / prevention & control. Myeloid Cells / metabolism. Myeloid Cells / pathology. Tumor Suppressor Proteins / physiology

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  • (PMID = 17599039.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA081168
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / E2f1 protein, mouse; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Growth Inhibitors; 0 / Interleukin-6; 0 / Tumor Suppressor Proteins
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88. Liu LB, Li WM, He W, Zou P: [Expression of immune response molecules and function of fas ligand on surface of AML WEHI-3 cells]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):535-8
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  • [Title] [Expression of immune response molecules and function of fas ligand on surface of AML WEHI-3 cells].
  • The purpose of this study was to investigate the expression of Fas, Fas ligand (FasL) and CD80 and function of FasL on the surface of acute myelomonocytic leukemia cells from WEHI-3 line.

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  • (PMID = 16800937.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD95; 0 / Fas Ligand Protein
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89. Hasanbegović E: [Acute lymphoblastic leukaemia as a secondary malignoma after treatment of acute myeloic leukaemia (AML/M4)]. Med Arh; 2006;60(5):315-6
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  • [Title] [Acute lymphoblastic leukaemia as a secondary malignoma after treatment of acute myeloic leukaemia (AML/M4)].
  • [Transliterated title] Akutna limfoblastana leukemija kao sekundarni malignom poslije tretmana akutne mijeloicne leukemije (AML/M4).
  • We report about very rare case of ten years old boy with diagnose of acute myeloic leukaemia which was diagnosed in his age of five (March of 2000) at Pediatric Clinic in Sarajevo.
  • Just 7 months after transplantation boy had relaps of illness in the form of acute lymphoblastic leukaemia (ALL/L2).
  • Complete therapeutic protocol for acute lymphoblastic leukaemia was done and now boy is in complete clinical and hematologic remission.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16944736.001).
  • [Journal-full-title] Medicinski arhiv
  • [ISO-abbreviation] Med Arh
  • [Language] bos
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Bosnia and Herzegovina
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90. Ortuño FJ, Castilla C, Moreno MJ, del Mar Osma M, Gonzalez M, Vicente V: Erythrophagocytosis in de novo-philadelphia-positive acute leukemia of ambiguous lineage. Haematologica; 2006 Aug;91(8 Suppl):ECR43
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  • [Title] Erythrophagocytosis in de novo-philadelphia-positive acute leukemia of ambiguous lineage.
  • Erythrophagocytosis by neoplastic cells in acute leukemia has been most frequently associated with FAB M4 and M5 subtypes, with the t(8;16) and with C-MOZ rearrangements, however it is exceptional in acute lymphoblastic leukemia and has not been previously reported in Philadelphia-positive (Ph+) acute leukemia.
  • We herein present a case of Ph+ acute leukemia of ambiguous lineage in which erythrophagocytosis is an outstanding feature.
  • [MeSH-major] Erythrocytes / pathology. Leukemia / pathology. Philadelphia Chromosome

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  • (PMID = 16923527.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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91. Chung HJ, Park CJ, Jang S, Chi HS, Seo EJ, Seo JJ: A case of lineage switch from acute lymphoblastic leukemia to acute myeloid leukemia. Korean J Lab Med; 2007 Apr;27(2):102-5
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  • [Title] A case of lineage switch from acute lymphoblastic leukemia to acute myeloid leukemia.
  • Lineage switch from acute lymphoblastic leukemia (ALL) to acute myeloid leukemia (AML) is very rare.
  • We report a case of a 9 yr-old ALL patient relapsed as acute myelomonocytic leukemia.
  • At the initial diagnosis, the blast cell morphology and immunophenotype were consistent with the diagnosis of typical ALL (L1 subtype according to FAB classification).
  • Nine months, which is a very short time compared with other cases in the literatures, after the diagnosis of ALL, she relapsed with completely different blasts (typical AML, M4 according to FAB classification) in morphology, cytochemistry, and immunophenotyping.
  • The karyotype has changed from 56,XY,+X,+Y,+Y,+4,+8,+10, +14,+17,-20,+21,+21,+21[6]/57,idem,+Y[19] to 46,XY,t(8;16)(p11.2;p13.1)[19]/46,XY[1], showing unrelated chromosomal abnormality to the karyotype at the initial diagnosis.
  • Moreover, both findings were quite specific for each common cell ALL and acute myelomonocytic leukemia.
  • The treatment with AML 2000 protocol chemotherapy failed, and he underwent the chemotherapy with the combination of high dose cytarabine and mitoxantrone and has been in CR state for 21 months, until now.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


92. Shafarenko M, Liebermann DA, Hoffman B: Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation. Blood; 2005 Aug 1;106(3):871-8
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  • [Title] Egr-1 abrogates the block imparted by c-Myc on terminal M1 myeloid differentiation.
  • Thus, understanding functional interactions between genes that regulate normal blood cell development, including cell growth and differentiation, and how their altered expression contributes to leukemia, is important for rational drug design.
  • Previously, we have shown that the zinc finger transcription factor Egr-1 plays a role in monocytic differentiation.
  • Ectopic expression of Egr-1 in M1 myeloblastic leukemia cells was observed to activate the macrophage differentiation program in the absence of the differentiation inducer interleukin 6 (IL-6) and to promote terminal differentiation in its presence.
  • In addition, we have shown that deregulated expression of the proto-oncogene c-myc blocks the myeloid terminal differentiation program.

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  • (PMID = 15840692.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1 RO1 CA59774; United States / NCI NIH HHS / CA / 1 RO1 CA81168; United States / NCI NIH HHS / CA / CA88261-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Immediate-Early Proteins; 0 / Myc protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1895156
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93. Guo TB, Lu J, Li T, Lu Z, Xu G, Xu M, Lu L, Dai W: Insulin-activated, K+-channel-sensitive Akt pathway is primary mediator of ML-1 cell proliferation. Am J Physiol Cell Physiol; 2005 Aug;289(2):C257-63
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  • Here we report that suppression of a voltage-gated K(+) channel with 4-aminopyridine (4-AP), barium, and tetraethylammonium inhibited both EGF- and insulin-stimulated myeloblastic leukemia ML-1 cell proliferation in a concentration-dependent manner.

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  • (PMID = 15800056.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Potassium Channel Blockers; 0 / Potassium Channels; 0 / Proto-Oncogene Proteins; 24GP945V5T / Barium; 62229-50-9 / Epidermal Growth Factor; 66-40-0 / Tetraethylammonium; BH3B64OKL9 / 4-Aminopyridine; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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94. Ashiru OT, Pillay M, Sturm AW: Adhesion to and invasion of pulmonary epithelial cells by the F15/LAM4/KZN and Beijing strains of Mycobacterium tuberculosis. J Med Microbiol; 2010 May;59(Pt 5):528-33
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  • [Title] Adhesion to and invasion of pulmonary epithelial cells by the F15/LAM4/KZN and Beijing strains of Mycobacterium tuberculosis.
  • One such genotype, the F15/LAM4/KZN (KZN) family of M. tuberculosis, has predominated in KwaZulu-Natal, South Africa, since the early 1990s.

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  • (PMID = 20110390.001).
  • [ISSN] 1473-5644
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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95. Zangrando A, Dell'orto MC, Te Kronnie G, Basso G: MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures. BMC Med Genomics; 2009;2:36
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  • [Title] MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures.
  • BACKGROUND: The presence of MLL rearrangements in acute leukemia results in a complex number of biological modifications that still remain largely unexplained.
  • Armstrong et al. proposed MLL rearrangement positive ALL as a distinct subgroup, separated from acute lymphoblastic (ALL) and myeloblastic leukemia (AML), with a specific gene expression profile.
  • Here we show that MLL, from both ALL and AML origin, share a signature identified by a small set of genes suggesting a common genetic disregulation that could be at the basis of mixed lineage leukemia in both phenotypes.
  • METHODS: Using Affymetrix(R) HG-U133 Plus 2.0 platform, gene expression data from 140 (training set) + 78 (test set) ALL and AML patients with (24+13) and without (116+65) MLL rearrangements have been investigated performing class comparison (SAM) and class prediction (PAM) analyses.
  • A final subset of 14 genes grants the characterization of acute leukemia patients with and without MLL rearrangements.
  • CONCLUSION: Our study demonstrated that a small subset of genes identifies MLL-specific rearrangements and clearly separates acute leukemia samples according to lineage origin.
  • The subset included well-known genes and newly discovered markers that identified ALL and AML subgroups, with and without MLL rearrangements.

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  • (PMID = 19549311.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2709660
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96. Kenne E, Soehnlein O, Genové G, Rotzius P, Eriksson EE, Lindbom L: Immune cell recruitment to inflammatory loci is impaired in mice deficient in basement membrane protein laminin alpha4. J Leukoc Biol; 2010 Sep;88(3):523-8
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  • We used several recruitment models in Lam4(-/-) and WT mice to determine whether lack of laminin-411 in the perivascular BM influences extravasation of inflammatory cells.
  • Recruitment of all major leukocyte subsets (neutrophils, monocytes, and lymphocytes) was reduced in Lam4(-/-) mice compared with WT.
  • With the use of intravital microscopy, we concluded that this decrease was a result of impaired diapedesis through the vessel wall, as neither leukocyte adhesion to the endothelial lining nor migration in extravascular tissue was hampered in Lam4(-/-) mice.

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  • (PMID = 20483922.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lama4 protein, mouse; 0 / Laminin; 0 / Protein Isoforms; 0 / laminin alpha5
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97. Gra OA, Glotov AS, Kozhekbaeva Zhm, Makarova OV, Nasedkina TV: [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia]. Mol Biol (Mosk); 2008 Mar-Apr;42(2):214-25
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  • [Title] [Genetic polymorphism in GST, NAT2, and MTRR and susceptibility to childhood acute leukemia].
  • In the present work the frequencies of xenobiotic-metabolizing gene polymorphisms in 332 children with the diagnosis acute lymphoblastic leukemia (ALL), 71 children with the diagnosis acute myeloblastic leukemia (AML) and 490 healthy donors have been determined using allele-specific hybridization on the biochip.
  • Statistically significant increase in the frequency of GSTT1 "null" genotype (OR = 1.9, p = 4.7E-5) and GSTT1/GSTM1 double "null" genotype (OR = 3.1, p = 2.5E-8) in children with acute leukemia relative to healthy donors group has been revealed.
  • Also 1.8-fold increase in the frequency of NAT2 genotype 341T/T, 481C/C, 590G/G in children with acute leukemia relative to healthy donors group (p = 0.026) has been recognized.
  • Analysis of gene-gene interactions has showed that in patients with acute leukemia genotype NAT2 341T/T, 481C/C, 590G/G in combination with GSTT1 "null" and/or GSTM1 "null" genotype is significantly more frequent than in population control.
  • Besides the reduction of MTRR genotype 66G/G frequency in girls with acute leukemia relative to female healthy donors has been found (OR = 0.50, p = 0.0015).
  • Analysis of gene-gene interactions has shown that the presence of GSTT1 "null" and/or GSTM1 "null" genotype in combination with MTRR genotype 66A/- may consider as risk factor of acute leukemia in girls.
  • Thus, the studied polymorphic variants of genes GSTT1, GSTM1, NAT2 and MTRR can modulate the risk of childhood acute leukemia, residents of European part of Russia.
  • [MeSH-major] Arylamine N-Acetyltransferase / genetics. Ferredoxin-NADP Reductase / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18610829.001).
  • [ISSN] 0026-8984
  • [Journal-full-title] Molekuliarnaia biologiia
  • [ISO-abbreviation] Mol. Biol. (Mosk.)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 1.18.1.- / methionine synthase reductase; EC 1.18.1.2 / Ferredoxin-NADP Reductase; EC 2.3.1.5 / Arylamine N-Acetyltransferase; EC 2.3.1.5 / NAT2 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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98. Charafeddine KM, Mahfouz RA, Zaatari GS, Ibrahim GY, Muwakkit SA, Najm ND, Farra CG: Essential thrombocythemia with myelofibrosis transformed into acute myeloid leukemia with der(1;15)(q10;q10): case report and literature review. Cancer Genet Cytogenet; 2010 Jul 1;200(1):28-33
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  • [Title] Essential thrombocythemia with myelofibrosis transformed into acute myeloid leukemia with der(1;15)(q10;q10): case report and literature review.
  • We herein report the first case in the literature, to our knowledge, of a 44-year-old female with essential thrombocythemia and severe myelofibrosis who developed acute myeloid leukemia (AML-M4) with der(1;15)(q10;q10) after 13 years of treatment.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Primary Myelofibrosis / genetics. Thrombocythemia, Essential / genetics


99. 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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100. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • The clinical evidence was derived from an open-label randomised controlled trial referred to as study AZA-001.
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy






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