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Items 1 to 100 of about 284
1. Han JS, Oh SY, Kim SH, Kwon HC, Hong SH, Han JY, Park KJ, Kim HJ: A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2. Yonsei Med J; 2010 Jan;51(1):138-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2.
  • A splenic rupture as the initial manifestation of acute myeloid leukemia is extremely rare.
  • In this study, we described a rare case of acute myeloid leukemia presenting principally as an acute abdomen due to a pathologic splenic rupture in a 35-year old male patient.
  • The oncologist should be aware of this rare initial presentation of acute myeloid leukemia (AML) M2, as the condition generally necessitates a prompt splenectomy.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Splenic Rupture / diagnosis

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  • (PMID = 20046528.001).
  • [ISSN] 1976-2437
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2799964
  • [Keywords] NOTNLM ; Acute myeloid leukemia M2 / pathologic / splenic rupture
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2. Vundinti BR, Kerketta L, Madkaikar M, Jijina F, Ghosh K: Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22. Indian J Cancer; 2008 Jan-Mar;45(1):30-2
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  • [Title] Three way translocation in a new variant of t(8;21) acute myeloid leukemia involving Xp22.
  • The t(8;21)(q22;q22) is one of the most frequent chromosomal abnormality associated with acute myeloid leukemia (AML) M2 sub type.
  • We report a case of AML-M2 with t(X;8;21)(p22;q22;q22) associated with loss of Y chromosome.
  • The patient did not respond to therapy and follow-up of cytogenetics revealed same chromosome abnormality.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18453738.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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3. Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Isolated extramedullary relapse presenting as autologous lymphocyte response. Am J Hematol; 2008 Jun;83(6):512-4
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  • Isolated EMR in the CNS is a relatively rare form of recurrent leukemia.
  • We report here a case of a 38-year-old man with inv(16) acute myeloid leukemia (AML, M2) who suffered a central nervous system (CNS) relapse after allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor.
  • His leukemia relapsed in the CNS 2.5 years after the allogeneic BMT.
  • Lumbar puncture revealed 780/muL white blood cells with 67.3% leukemia cells and 32.7% mature lymphocytes.
  • Fluorescent in situ hybridization (FISH) using a probe for the Y chromosome demonstrated that both leukemia cells and lymphocytes in the cerebrospinal fluid (CSF) were derived from the recipient, although the bone marrow cells were from the donor.
  • No leukemia cells with inv(16) were detected by FISH in the bone marrow.
  • This observation suggests that the CNS is a "sanctuary" site not only from chemotherapy but also from the graft-versus-leukemia effect.
  • The present case contributes to our understanding of the possibility of immunological escape phenomenon of recurrent leukemia cells in extramedullary sites.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Bone Marrow Transplantation / methods. Humans. Male. Recurrence. Sarcoma, Myeloid. Transplantation Chimera

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18306363.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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4. Udayakumar AM, Alkindi S, Pathare AV, Raeburn JA: Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2). Arch Med Res; 2008 Feb;39(2):252-6
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  • [Title] Complex t(8;13;21)(q22;q14;q22)--a novel variant of t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for about 3% of all t(8;21)(q22;q22) in acute myeloid leukemia (AML) patients.
  • We report a case of AML-M2 with t(8;13;21)(q22;q14;q22), not reported earlier.
  • Involvement of chromosome region 13q14 has never been reported earlier, although region 13q12 as a variant in AML with t(8;21) has been reported earlier.
  • [MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18164974.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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5. de Oliveira FM, Tone LG, Simões BP, Falcão RP, Brassesco MS, Sakamoto-Hojo ET, dos Santos GA, Marinato AF, Jácomo RH, Rego EM: Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1. Cancer Genet Cytogenet; 2007 Jan 15;172(2):154-7
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  • [Title] Acute myeloid leukemia (AML-M2) with t(5;11)(q35;q13) and normal expression of cyclin D1.
  • We report a case of acute myeloid leukemia (AML) subtype M2, with t(5;11)(q35;q13), in a 30-year-old man.
  • Conventional cytogenetic, spectral karyotyping, and fluorescence in situ hybridization (FISH) studies on bone marrow sample obtained at diagnosis revealed an abnormal karyotype in all cells examined.
  • Similar to the 11q23 region, 11q13 changes can be found in both myeloid and lymphoid neoplasias with different chromosomes serving as donors in translocations.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Cyclin D1 / biosynthesis. Cyclin D1 / genetics. Gene Expression Regulation, Neoplastic / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Humans. Leukemia, Myelomonocytic, Acute. Male


6. Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z: Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jan 15;188(2):95-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Acute myeloid leukemia with maturation (AML-M2 based on the French-American-British classification) is often accompanied by typical chromosomal changes such as t (8;21)(q22;q22).
  • We report a case of a 31-year-old female with a positive RUNX1/CBFA2T1 (alias AML1/ETO) fusion gene and a karyotype with a t(2;21;8)(p12;q22;q22).
  • The role of this complex variant translocation, as well as the possible formation mechanism, prognostic factors, and morphologic changes are discussed.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • [RetractionIn] Cancer Genet Cytogenet. 2009 Jul;192(1):54 [19489159.001]
  • (PMID = 19100512.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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7. Balamurugan S, Sugapriya D, Shanthi P, Thilaka V, Venkatadesilalu S, Pushpa V, Madhavan M: Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias. Indian J Hematol Blood Transfus; 2007 Dec;23(3-4):73-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multidrug resistance 1 gene expression and AgNOR in childhood acute leukemias.
  • We have studied MDR1 expression and AgNORS in 41 cases of acute leukemia in children.
  • In this study, AgNOR counts in patients with acute lymphoblastic leukemia (ALL) L2 subtype (FAB classification) were significantly higher as compared to the ALL L1 subtype.
  • Similarly, mean AgNOR count in the acute myeloid Leukemia (AML) M2 subtype was significantly higher as compared to the ALL L1 subtype.
  • However, there was no correlation between AgNOR and treatment outcome or between AgNOR counts and MDR1 expression in any of the subtypes of acute leukemia included in this series.
  • In AML, MDR1 gene expression was found to be related to reduced remission induction rates and hence poorer prognosis.

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  • (PMID = 23100919.001).
  • [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/ PMC3453125
  • [Keywords] NOTNLM ; Acute leukemia / AgNOR / Multidrug Resistance 1 / P-glycoprotein
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8. Studzinski GP, Wang X, Ji Y, Wang Q, Zhang Y, Kutner A, Harrison JS: The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway. J Steroid Biochem Mol Biol; 2005 Oct;97(1-2):47-55
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  • [Title] The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway.
  • The evidence for the promising potential for derivatives of Vitamin D (deltanoids) in the treatment of myeloid leukemias is increasing, but currently is not matched by the understanding of the precise mechanisms by which these anti-neoplastic effects are achieved.
  • Unlike solid tumors in which growth retardation by deltanoids appears to result from inhibition of cell proliferation and the promotion of cell death by apoptosis, control of myeloid leukemia proliferation by deltanoids results from the induction of differentiation of the immature myelo-monocytic cells towards functional monocytic cells.
  • We present here the accumulating evidence that a pathway that is initiated by deltanoid activation of Vitamin D receptor (VDR) and leads to monocytic differentiation of human myeloblastic HL60 cells, includes the MEK-ERK and JNK mitogen-activated protein kinases (MAPKs), their positive and negative regulators and a downstream effector C/EBPbeta.
  • Importantly, in freshly obtained acute myeloid leukemia (AML)-M2 cells exposed to PRI-2191, a novel deltanoid with a modified side chain, upregulation of C/EBPbeta paralleled the induction of monocytic differentiation.
  • These data provide a basis for the hypothesis that deltanoid-induced upregulation of C/EBPbeta bypasses the block to granulocytic differentiation in myeloid leukemia cells by redirecting the cells to monocytic differentiation.

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  • (PMID = 16046262.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-15; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-15; United States / NCI NIH HHS / CA / R01 CA44722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Retinoblastoma Protein; 1406-16-2 / Vitamin D; EC 2.7.- / Protein Kinases; EC 2.7.1.- / KSR-1 protein kinase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS169830; NLM/ PMC2814418
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9. Bae SY, Kim JS, Ryeu BJ, Lee KN, Lee CK, Kim YK, Lim CS, Cho Y, Choi CW, Ryu SW, Yoon SY: Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases. Cancer Genet Cytogenet; 2010 May;199(1):31-7
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  • [Title] Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases.
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for approximately 3% of all t(8;21)(q22;q22) found in patients with acute myeloid leukemia (AML).
  • The clinicopathologic features of AML with the variant t(8;21) have not been well established.
  • We report three cases of AML with variants of t(8;21) characterized, respectively, by derivative 8 with the interstitial inverted insertion of 21q and concurrent monosomy 21, t(8;18;21)(p22;q11.3;q22), and t(2;21;8)(q11.2;q22;q22).
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20417866.001).
  • [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
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10. Shah N, Leaker MT, Teshima I, Baruchel S, Abdelhaleem M, Ye CC: Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 May;50(5):1052-3
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  • [Title] Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia.
  • A 3-year-old female was diagnosed with acute myeloid leukemia (AML-M2).
  • Cytogenetic analysis revealed a clone with trisomy 8 at diagnosis that was replaced by a clone containing a t(11;15) and del(20q) by the end of the second induction.
  • A new clone, characterized by a Philadelphia chromosome, with the minor BCR/ABL p190 transcript, emerged 14 months after diagnosis and remained to the end of disease course.
  • The late occurrence of the Philadelphia chromosome in AML has been documented rarely in adults.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18213712.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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11. Liu X, Zhang Q, Zhang DE, Zhou C, Xing H, Tian Z, Rao Q, Wang M, Wang J: Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis. Leukemia; 2009 Apr;23(4):739-45
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  • [Title] Overexpression of an isoform of AML1 in acute leukemia and its potential role in leukemogenesis.
  • In this study, we found a higher expression level of AML1a in acute lymphoblastic leukemia and acute myeloid leukemia (AML)-M2 patients in comparison to the controls.
  • To investigate the role of AML1a in hematopoiesis and leukemogenesis in vivo, murine bone marrow mononuclear cells were transduced with AML1a and then transplanted into lethally irradiated mice, which developed lymphoblastic leukemia after transplantation.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Animals. Bone Marrow Cells / metabolism. Bone Marrow Transplantation. Case-Control Studies. Hematopoiesis. Humans. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic. Protein Isoforms / genetics. Receptor, Macrophage Colony-Stimulating Factor / genetics. Transcription, Genetic. Transduction, Genetic

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  • (PMID = 19151769.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Protein Isoforms; 0 / RUNX1 protein, human; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
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12. Adhya AK, Varma N, Varma S: Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases. Indian J Pathol Microbiol; 2007 Jul;50(3):655-8
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  • [Title] Acute myeloid leukemia (AML-M2) with mast cell hyperplasia of bone marrow: a report of three cases.
  • Bone marrow mastocytosis, though infrequently documented in Indian patients, may be observed in association with many non mast cell hematological neoplasms, including acute myeloblastic leukemia (AML) and myelodysplastic syndromes (MDS).
  • We report three cases of acute myeloid leukemia with excess of mast cells in the bone marrow (BM) samples.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Mast Cells / pathology. Mastocytosis, Systemic / pathology


13. Miao YQ, Chen ZX, He J, Cen JN, Bao XJ, Qiu QC, Zhang DE, Yan M: [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jan;28(1):27-9
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  • [Title] [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype].
  • OBJECTIVE: To investigate the expression of AML1/ETO9a isoform in the acute myeloid leukemia (AML)-M2 patients.
  • METHODS: Expressions of AML1/ETO fusion gene and AML1/ETO9a isoform were detected by using reverse transcriptase-polymerase chain reaction (RT-PCR) in leukemia patients, MDS patients, leukemia cell lines and healthy subjects.
  • RESULT: In 30 newly diagnosed AML-M2 patients 15 were found to express AML1/ETO9a isoform, while the rest including 20 AML-M2CR, 18 other subtypes of AML, 5 chronic myelogenous leukemia (CML), 3 myelodysplastic syndromes (MDS), 3 leukemia cell lines (NB4, KG-1, K562) and 5 healthy subjects were AML1/ETO9a negative.
  • Among the 15 AML/ETO9a isoform expressing cases, 13 were demonstrated t(8;21) translocation and AML1/ETO expression.
  • CONCLUSION: Isoform AML1/ETO9a was correlated to AML/M2, and it may promote the development of leukemia in combination with the AML1/ETO fusion gene.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 17649722.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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14. Bacher U, Schnittger S, Kern W, Trenn G, Weisser M, Haferlach T, Schoch C: Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22). Cancer Genet Cytogenet; 2006 Jul 15;168(2):172-4
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  • [Title] Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22).
  • We here report on an 48-year-old male patient with a primary diagnosis of acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22), who developed complete hematologic and molecular remission after induction chemotherapy.
  • Thirteen months later, he relapsed and showed an AML-M2 with t(3;21)(q26;q22).
  • Retrospectively, polymerase chain reaction (PCR) for AML1-EVI1 and EVI1 overexpression was performed on bone marrow and peripheral blood samples taken at diagnosis and during the first year after the first manifestation of AML to quantify the AML1-EVI1-positive clone.
  • In a bone marrow sample taken 25 days from diagnosis, PCR for AML1-EVI1 was negative, and EVI1 expression, as assessed by quantitative real-time PCR, was within the same range as that of healthy controls.
  • These data suggest that this patient developed a secondary therapy-related AML rather than a relapse.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843110.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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15. Medeiros BC, Gotlib JR, Coutre SE, Jones C, Khan SA, Rajwanshi R, Rajwanshi R, Zehnder J, Zehnder J: Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7052

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  • [Title] Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia.
  • : 7052 Background: High treatment-related mortality and low response rates often discourage elderly patients with acute myeloid leukemia from receiving treatment.
  • METHODS: Phase II clinical trial of tailored temozolomide therapy to high-risk AML patients according to AGAT methylation promoter status.
  • Patients demonstrating evidence of AGAT promoter methylation were stratified to conventional doses of temozolomide at 200 mg/m2 orally x 7 days.
  • Patients demonstrating lack of AGAT promoter methylation (unmethylated) received protracted doses of temozolomide (100 mg/m2 orally x 14 days) followed by conventional doses of temozolomide.
  • De novo AML was diagnosed in eight patients and five patients had s-AML.
  • Three patients remain in CR with a median duration of 22 weeks (14-36 weeks).
  • With a median follow-up of 38 weeks (10-48), the median overall survival for the entire population is 12 weeks (3.5 - 38) weeks (responders 26.5 weeks).
  • CONCLUSIONS: These preliminary results suggest that temozolomide therapy may be individually tailored to elderly patients with AML according to AGAT promoter status.

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  • (PMID = 27961417.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Schwind S, Marcucci G, Maharry K, Radmacher MD, Whitman SP, Paschka P, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML). J Clin Oncol; 2009 May 20;27(15_suppl):7001

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  • [Title] MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML).
  • : 7001 Background: We showed recently that CEBPA mutations (mut) in CN AML are associated with better outcome and a unique microRNA expression profile, including miR-181a upregulation.
  • METHODS: We analyzed 187 de novo CN AML adult patients (pts) aged <60 years (y; median 45) similarly treated on CALGB 9621 and 19808.
  • Of these, 122 had molecular high risk [FLT3-ITD or NPM1 wild type (wt)] and 65 low risk (no FLT3-ITD, NPM1 mut) CN AML.
  • RESULTS: Higher miR-181a levels (miR-181a↑) were associated with CEBPA mut, NPM1 wt, no FLT3-TKD, lower ERG expression, higher %FAB M1/M2, lower WBC and age, higher blood blasts, and lower % gum hypertrophy. miR-181a↑ tended to associate with more complete remissions (CRs; p = .07) and significantly associated with longer disease-free (DFS; p = .05) and overall (OS; p = .01) survival (median follow-up 6.5 y for pts alive).
  • CONCLUSIONS: miR-181a expression is a prognostic marker in CN AML, mainly in the molecular high risk group, where it predicts outcome independently of other variables including CEBPA mutations.
  • As miR-181a↑ confer better treatment response, novel approaches increasing miR-181a levels might benefit not only CN but also other AML pts.

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  • (PMID = 27961373.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Sawant RB, Rajadhyaksha SB: Plasma exchange for thrombotic thrombocytopenic purpura following hematopoietic stem cell transplantation. J Assoc Physicians India; 2005 Nov;53:981-3
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  • A 17 years old female diagnosed with acute myeloid leukemia (AML)-M2 received an allogeneic haematopoietic stem cell transplant (HSCT) and was given graft versus host disease (GVHD) prophylaxis with methotrexate, cyclosporin-A (CsA) and methyl prednisolone.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / surgery. Plasma Exchange. Purpura, Thrombotic Thrombocytopenic / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Female. Humans

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  • (PMID = 16515239.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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18. Nishizawa M, Hirayama F, Matsuyama N, Tada K, Kaneko H, Watanabe M, Miura Y, Tsudo M: [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate]. Rinsho Ketsueki; 2009 Jan;50(1):16-22
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  • [Title] [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate].
  • We report a fatal case of transfusion-related acute lung injury (TRALI) with anti-leukocyte antibodies detected both in the patient's serum and in the causative red cell concentrate (RC-M.A.P).
  • A 41-year-old Japanese woman diagnosed as having acute myeloid leukemia (AML, M2) developed TRALI caused by RC-M.A.P 15 days after the start of induction therapy for AML.
  • [MeSH-major] Acute Lung Injury / etiology. Autoantibodies / blood. Erythrocyte Transfusion / adverse effects. HLA Antigens / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes / immunology

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  • (PMID = 19225224.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / HLA Antigens
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19. Retraction. Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jul;192(1):54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retraction. Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).

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  • [RetractionOf] Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z. Cancer Genet Cytogenet. 2009 Jan 15;188(2):95-8 [19100512.001]
  • (PMID = 19489159.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Retraction of Publication
  • [Publication-country] United States
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20. Lahortiga I, Belloni E, Vázquez I, Agirre X, Larrayoz MJ, Vizmanos JL, Valgañón M, Zudaire I, Sáez B, Mateos MC, Di Fiore PP, Calasanz MJ, Odero MD: NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2. Cancer Genet Cytogenet; 2005 Mar;157(2):151-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2.
  • This translocation has been associated with myeloid leukemias, predominantly acute myeloid leukemia (AML) M2 subtype with trilineage myelodysplastic features, and with a poor prognosis.
  • ;p1?2) in a patient with AML-M2 and poor prognosis.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 7. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Translocation, Genetic

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  • [ErratumIn] Cancer Genet Cytogenet. 2005 Jun;159(2):194
  • (PMID = 15721637.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NUP98-HOXA9 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9
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21. Khalil SH: Molecular hematology. Qualitative to quantitative techniques. Saudi Med J; 2005 Oct;26(10):1516-22
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  • The Section of Hematology, Department of Pathology and Laboratory Medicine at King Faisal Specialist Hospital and Research Center has shared this experience during the last 10 years with more than 6,546 samples submitted for the analysis of different gene rearrangements, fusion gene transcripts and gene mutations including Ig heavy chain gene rearrangement for B-cell malignancies, T-cell receptor gamma chain gene rearrangement for T-cell malignancies, BCR/ABL-P210 and P190 fusion gene transcripts, for chronic myeloid leukemia and Philadelphia positive acute lymphoblastic leukemia, PML/RARalpha fusion gene for promyelocytic leukemia, AML1/ETO for acute myeloid leukemia AML-M2 with t8;21, CBFB/MYH11 for AML M4E0 with inv 16, BCL-2 for follicular lymphoma, and BCL-1 for mantle cell lymphoma.
  • Hence, most molecular assays are qualitative in nature, quantitative assays are deemed necessary in the monitoring and follow-up of minimal residual disease in leukemia and lymphoma, and proved in our experience to serve as an essential tool to confirm complete remission CR post-chemotherapy and bone marrow transplantation, and to detect signs of early relapse for proper clinical intervention.
  • [MeSH-major] Hematologic Neoplasms / diagnosis. Molecular Biology / methods

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  • (PMID = 16228048.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Saudi Arabia
  • [Number-of-references] 36
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22. Anand M, Ghara N, Kumar R, Singh S, Sengar M, Panikar N, Raina V, Sharma A: Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia. Ann Hematol; 2005 Nov;84(12):767-70
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  • [Title] Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.
  • Myeloperoxidase (MPO) cytochemical activity, recognized as a very important hallmark of myeloblasts, is generally negative in chronic myeloid leukemia (CML) blast crisis (BC).
  • Myeloperoxidase cytochemistry of peripheral blood blasts in 161 cases of CML, including 103 in chronic phase (CP) and 29 each in accelerated phase (AP) and BC, was assessed and compared with that of 30 cases of acute myeloid leukemia, AML-M2.
  • Compared with the strong MPO positivity, both in terms of intensity and proportion, in the AML-M2 cases, the positivity in the CML cases was generally weak and was seen in a small number of blasts (5-15%), except in one case of BC with 20% positive blasts.
  • This also explains why MPO cytochemistry, despite its high reputation as a myeloid-lineage marker, generally does not help in CML BC.
  • CML BC should therefore be considered as a possible diagnosis along with acute lymphoblastic leukemia, AML-M0, AML-M7, etc., in the setting of MPO-negative blasts.
  • Similarity between MPO expression pattern in CML, i.e., negative in blasts and positive in the more mature cells, and that during maturation of normal myeloid series of cells shows the deranged myelopoiesis of CML to be undisturbed at least with respect to MPO expression.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / biosynthesis. Peroxidase / biosynthesis
  • [MeSH-minor] Female. Gene Expression Regulation, Enzymologic. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukocytes / enzymology. Leukocytes / pathology. Male. Predictive Value of Tests

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  • (PMID = 15990995.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase
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23. Zhou J, Meng R, Sui XH, Meng L, Yang BF: Effects of arsenic trioxide administration styles on leukocytosis. Chin Med Sci J; 2006 Jun;21(2):111-4
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  • METHODS: Three kinds of leukemia cells, NB4, K562, and acute promyelocytic leukemia (APL) cells, were cultured in the media with constant concentration and varying concentrations of As2O3 respectively for 24 hours.
  • RESULTS: The apoptosis rates of NB4, K562, and APL leukemia cells in the media with constant As2O3 concentration were 56.6% +/- 2.4%, 27.6% +/- 3.1%, and 52.2% +/- 2.8%, respectively, which were significantly higher than those with changing As2O3 concentration (23.2% +/- 2.1%, 11.0% +/- 2.5%, and 21.0% +/- 2.5%, respectively, P < 0.01).
  • The apoptosis rates of APL, M2 type acute myeloid leukemia (AML-M2), and chronic myeloid leukemia (CML) patients in the trial group (28.5% +/- 1.9%, 9.5% +/- 0.6%, and 12.5% +/- 1.8%) were also significantly higher than those in control group (8.5% +/- 2.2%, 2.

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  • (PMID = 16845799.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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24. Ritchie EK, Roboz G, Hinchcliff K, Curcio T, Scandura J, Feldman E: Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7054

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  • [Title] Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS.
  • : 7054 Background: Laromustine is a novel sulfonylhydrazine-alkylating agent with activity in acute myeloid leukemia (AML).
  • Laromustine in phase I and II trials shows activity in patients with relapsed/refractory leukemia (1) and elderly patients with new AML (2).
  • Based on this data, a phase I study to evaluate the safety and efficacy of combining escalating doses of laromustine with infusional ara-C in AML and MDS patients over 60.
  • METHODS: Laromustine 300 mg/m2 (cohort 1, n = 6), 400 mg/m2 (cohort 2, n = 5) and 500 mg/m2 (cohort 3) was administered by IV infusion over 1 hour on day 1 in combination with ara-C 100 mg/m2/day as a continuous infusion for 7 days.
  • Patients achieving CR after induction therapy were offered up to 2 cycles of consolidation therapy for a maximum cumulative laromustine dose of 1,000 mg/m2.
  • One patient had grade 2 dyspnea possibly related to drug and improved with a short course of steroids.

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  • (PMID = 27961420.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F: Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation. Pediatr Hematol Oncol; 2008 Apr-May;25(3):165-70
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  • [Title] Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation.
  • The authors report a rare case of acute myeloid leukemia (AML) M1 with faggot formation in mature neutrophils and metamyelocytes.
  • Although Auer rods in mature neutrophils are occasionally experienced, they are usually found in AML M2, M3, or M4 cases, but not in M1 cases.
  • In addition, faggot formation in mature neutrophils, as seen in this case, is considered to be particularly unusual because most previously reported cases tended to show simple Auer rods except for AML M3 cases.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neutrophils / pathology. Trisomy / pathology

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  • (PMID = 18432498.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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26. Tirado CA, Chena W, Valdez FJ, Henderson S, Smart RL, Doolittle J, Garcia R, Patel S, Holdridge S, Chastain C, Auchus M, Collins RH: A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation. J Assoc Genet Technol; 2009;35(3):88-92
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  • [Title] A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation.
  • The t(8;21)/RUNX1-RUNX1T1 is found in ~5 percent of cases of acute myeloid leukemia (AML) and in 10 percent of the prior AML with maturation (M2) category of the French-American-British (FAB) classification.
  • While AML with t(8;21) is considered a distinct entity with a favorable prognosis, the clinical consequence of variant translocations is less well defined.
  • In this report we described a 45 year-old male patient having a diagnosis of AML-M2 with morphologic and immunophenotypic features suggestive of t(8;21).

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  • (PMID = 19738329.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
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  • [Title] Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The pancytopenia progressed rapidly, and he died 2 months after the diagnosis of MDS.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


28. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • A 2-year-old domestic shorthair cat was presented to us with decreased activity and anorexia.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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29. Guo C, Inghirami G, Ibrahim S, Sen F: Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia. Arch Pathol Lab Med; 2006 Jul;130(7):1075-6
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  • [Title] Epistaxis and severe weakness in a patient with multiple myeloma. Therapy-related acute myeloid leukemia, pure erythroid leukemia.
  • Therapy-related acute myeloid leukemias arise as a result of cytotoxic chemotherapy and/or radiation therapy.
  • The most common types of acute myeloid leukemia arising in this setting are acute myeloid leukemia with maturation, and lesser numbers of acute myelomonocytic leukemia, acute monocytic leukemia, acute erythroleukemia, or acute megakaryocytic leukemia.
  • We present a patient with multiple myeloma who was treated with melphalan and 4 years later developed acute erythroid leukemia.
  • The morphologic diagnosis of pure erythroid leukemia developing in the setting of multiple myeloma may be challenging.
  • [MeSH-major] Epistaxis / complications. Leukemia, Erythroblastic, Acute / complications. Multiple Myeloma / complications. Muscle Weakness / complications
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Humans. Leukemia, Myeloid. Male. Melphalan / adverse effects

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  • (PMID = 16831041.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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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31. Kim H, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ: [A Case of Acute Myeloid Leukemia with Masked t(8;21).]. Korean J Lab Med; 2006 Oct;26(5):338-42

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  • [Title] [A Case of Acute Myeloid Leukemia with Masked t(8;21).].
  • We report a case that revealed the characteristics of acute myeloblastic leukemia with maturation (AML-M2) on the morphology of the bone marrow biopsy and 45,X,-Y in conventional cytogenetic study, but was confirmed to have a typical AML1/ETO translocation by molecular studies using reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization.
  • In case typical morphologic features compatible with recurrent cytogenetic abnormalities are shown, molecular studies in addition to conventional cytogenetic study might be required to confirm the diagnosis.

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  • (PMID = 18156748.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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32. Wong KF, Yuen HL, Siu LL, Pang A, Kwong YL: t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia. Hum Pathol; 2008 Nov;39(11):1702-7
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  • [Title] t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia.
  • A Chinese girl presented with generalized papular rash and monocytic leukemia 19 days after birth.
  • Cytogenetic analysis showed t(8;16)(p11.2;p13.3) as the sole chromosomal abnormality.
  • Spontaneous regression of the leukemia was observed after 2 months, although the t(8;16) translocation persisted cytogenetically.
  • This was followed 7 months later by the development of acute myeloid leukemia with maturation and cytogenetic evolution with extra chromosomes 4 and 8.
  • Molecular study showed that the reciprocal MYST3 and CREBBP gene fusion characteristic of t(8;16) translocation persisted throughout the clinical course, even during spontaneous regression of the neonatal leukemia, and after chemotherapy-induced remission of the subsequent acute myeloid leukemia.
  • The possible role of MYST3 and CREBBP gene fusion in the pathogenesis of the leukemia is discussed.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18657848.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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33. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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

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

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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35. Abe T, Furukawa T, Masuko M, Sugimoto A, Okazuka K, Honma K, Fujimura T, Iguchi S, Nishi S, Ueno M, Nagahashi M, Watanabe G, Ajioka Y, Isahai N, Nagai K, Kazuyama Y, Aizawa Y: Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation. Int J Hematol; 2009 Oct;90(3):421-5
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  • [Title] Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation.
  • We report a case of a 29-year-old male patient with a generalized adenovirus (AdV) infection after cord blood transplantation (CBT) for acute myelocytic leukemia with maturation at 2nd complete remission.
  • Molecular diagnosis using PCR-restriction fragment length polymorphism analysis demonstrated that AdV with the serotype 14 caused the cystitis.
  • [MeSH-major] Adenovirus Infections, Human / etiology. Cord Blood Stem Cell Transplantation / adverse effects. Cystitis / etiology. Hemorrhage / etiology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19763745.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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36. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
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  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • However, APL and AML with maturation expressed comparable AQP9 levels, suggesting that AQP9 expression was related to granulocytic maturation.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

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  • (PMID = 16968895.001).
  • [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 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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37. Shen YM, Chao HY, Zhang R, Li WY, Feng YF, Zhu ZL, Xue YQ: [Detection of JAK2V617F mutation and its clinical significance in 80 patients with M2 acute myelogenous leukemia]. Zhonghua Zhong Liu Za Zhi; 2009 May;31(5):366-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Detection of JAK2V617F mutation and its clinical significance in 80 patients with M2 acute myelogenous leukemia].
  • OBJECTIVE: To explore the prevalence and prognostic significance of JAK2V617F gene mutation in acute myelogenous leukemia M2 (AML-M2) patients.
  • RESULTS: Of 80 de novo AML-M2 patients, 6 at the time of first diagnosis and 1 at relapse were found to have JAK2V617F gene mutation (8.8%, 7/80).
  • Morphologically, the whole blood and bone marrow of the 7 AML-M2 patients with JAK2V617F gene mutation presented a picture of acute leukemia instead of myeloproliferative disorders.
  • Immunophenotypically, bone marrow samples showed myelogenous linage expression.
  • Complete remission was obtained in 4 of 5 AML-M2 patients with JAK2V617F mutation who received treatment, while one patient had no response to the treatment.
  • Follow-up was performed in all the 5 patients, with a median survival of 18.5 months in 4 patients.
  • CONCLUSION: JAK2V617F gene mutation, as a type-1 mutation, might not be an initial event in the pathogenesis of acute myelogenous leukemia, and its presentation does not mean a poor prognosis in de novo AML patients.
  • [MeSH-major] Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 19799086.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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38. Villa O, Salido M, Pérez-Vila ME, Ferrer A, Arenillas L, Pedro C, Espinet B, Corzo C, Serrano S, Woessner S, Florensa L, Solé F: Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):32-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia.
  • We report three cases of acute myeloid leukemia without maturation [AML-M1 subtype according to the French-American-British classification (FAB)] with the presence of MYC oncogene amplification in form of double minutes (dmin) or homogeneously staining region (hsr).
  • [MeSH-major] Cell Nucleus / pathology. Genes, myc. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 18656691.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
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39. Saudemont A, Corm S, Wickham T, Hetuin D, Quesnel B: Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha. Mol Ther; 2005 Jun;11(6):950-9
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  • [Title] Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha.
  • Acute myeloid leukemia (AML) cells can be differentiated into dendritic cells (DCs) using appropriate combinations of cytokines but generation of autologous antileukemic cytotoxic T cells using leukemic DCs remains difficult.
  • Transduction by adenoviral vectors has been reported to induce efficient maturation of monocyte-derived DCs but AML cells are generally resistant to adenoviral gene transfer.
  • In this study we tested the effects of adenoviral TNF-alpha gene transfer on maturation of AML cells using the fiber-modified AdTNF.F(pK7) adenovirus.
  • AdTNF.F(pK7) induced significantly greater maturation of AML cells into antigen-presenting cells (APC) than did recombinant TNF-alpha or control adenoviral vector.
  • Maturation of leukemic cells into APCs was mediated at least partially via a PI3K/mTOR pathway, as the inhibitors LY294002, wortmannin, and rapamycin inhibited the maturation effect induced by the AdTNF.F(pK7) adenovirus.
  • In addition, CD8+ T cells expanded with AdTNF.F(pK7)-transduced AML cells showed greater expansion and specific CD8+ CTL activity against autologous AML cells than T cells expanded by other means.
  • Thus, fiber-modified adenoviral vectors encoding TNF-alpha are able to maturate AML cells into APCs with high efficacy and reproducibility, providing a useful tool to generate efficiently specific CD8+ CTLs against leukemic disease.
  • [MeSH-major] Adenoviridae / genetics. Cytotoxicity, Immunologic / immunology. Leukemia, Myeloid / immunology. T-Lymphocytes, Cytotoxic / immunology. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Acute Disease. Antigen-Presenting Cells / immunology. Capsid Proteins / genetics. Cell Differentiation. Coculture Techniques. Humans. Phenotype. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / physiology. Signal Transduction. TOR Serine-Threonine Kinases. Transduction, Genetic

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  • (PMID = 15922966.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 0 / hexon capsid protein, Adenovirus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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40. Jiao B, Wu CF, Liang Y, Chen HM, Xiong SM, Chen B, Shi JY, Wang YY, Wang JH, Chen Y, Li JM, Gu LJ, Tang JY, Shen ZX, Gu BW, Zhao WL, Chen Z, Chen SJ: AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2. Leukemia; 2009 Sep;23(9):1598-604
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  • [Title] AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2.
  • AML1-ETO fusion gene is generated from chromosomal translocation t(8;21) mainly in acute myeloid leukemia M2 subtype (AML-M2).
  • Its spliced variant transcript, AML1-ETO9a, rapidly induces leukemia in murine model.
  • To evaluate its clinical significance, AML1-ETO9a expression was assessed in 118 patients with t(8;21) AML-M2, using qualitative and nested quantitative reverse transcriptase (RT)-PCR methods.
  • Taken together, these data suggest that AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic

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  • (PMID = 19458628.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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41. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.

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  • [Cites] Blood. 1986 May;67(5):1328-32 [3697508.001]
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  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
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42. Vardiman JW: The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):16-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms.
  • The World Health Organization (WHO) classification of myeloid and lymphoid neoplasms utilizes morphology, immunophenotype, genetics and clinical features to define disease entities of clinical significance.
  • In general, the classification stratifies neoplasms according to their lineage (myeloid, lymphoid, histiocytic/dendritic) and distinguishes neoplasms of precursor cells from those comprised of functionally mature cells.
  • Five major subgroups of myeloid neoplasms are recognized based mainly on their degree of maturation and biologic properties: myeloproliferative neoplasms (MPNs) which are comprised primarily of mature cells with effective proliferation; myeloid (and lymphoid) neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB and FGFR1, defined largely by the finding of significant eosinophilia and specific genetic abnormalities; myelodysplastic/myeloproliferative neoplasms (MDS/MPN), comprised mainly of mature cells with both effective and ineffective proliferation of various lineages; myelodysplastic syndromes (MDS), in which immature and mature cells are found with abnormal, dysplastic and ineffective maturation, and acute myeloid leukemia (AML), comprised of precursor cells with impaired maturation.
  • Genetic abnormalities play an important role as diagnostic criteria for further sub-classification of some myeloid neoplasms, particularly of AML.
  • Although therapy-related MDS and AML (t-MDS/AML) often have genetic defects identical to those found in de novo AML and de novo MDS, they are classified separately from de novo AML and MDS in order to emphasize their unique clinical and biologic properties.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Lymphoma / classification. Myelodysplastic Syndromes / classification. Myelodysplastic-Myeloproliferative Diseases / classification. Myeloproliferative Disorders / classification


43. Ressel A, Trümper L, Bäsecke J: [Occlusion of the femoral arteries in de novo AML]. Med Klin (Munich); 2007 May 15;102(5):388-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Occlusion of the femoral arteries in de novo AML].
  • [Transliterated title] Femoralarterienverschluss bei De-novo-AML.
  • BACKGROUND: Leukemic emboli in acute (AML) and chronic myelocytic leukemia (CML) are associated with hyperleukocytosis (>100,000/microl leukocytes) and most frequently detected at autopsy.
  • CASE REPORT: A 53-year-old woman was admitted with hyperleukocytosis and acute pain in her right leg.
  • An occlusion of the right femoral arteries as the presenting symptom of a de novo AML (FAB M1/WHO: AML without maturation) with hyperleukocytosis was diagnosed.
  • CONCLUSION: Leukemic emboli of large vessels are uncommon in leukemia with hyperleukocytosis.
  • Leukemic emboli mainly occur in AML and CML in blast crisis and are rare in acute (ALL) and chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Arterial Occlusive Diseases / etiology. Femoral Artery. Leukemia, Myeloid, Acute / diagnosis. Neoplastic Cells, Circulating
  • [MeSH-minor] Angiography. Blood Coagulation Tests. Diagnosis, Differential. Female. Granulocyte Precursor Cells / pathology. Humans. Leukocyte Count. Leukocytosis / diagnosis. Leukocytosis / pathology. Middle Aged

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  • (PMID = 17497090.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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44. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In spite of intensive chemotherapy, the patient died within a year of diagnosis.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology

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  • (PMID = 20698144.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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45. Chen W, Konoplev S, Medeiros LJ, Koeppen H, Leventaki V, Vadhan-Raj S, Jones D, Kantarjian HM, Falini B, Bueso-Ramos CE: Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation. Cancer; 2009 Dec 1;115(23):5481-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cuplike nuclei (prominent nuclear invaginations) in acute myeloid leukemia are highly associated with FLT3 internal tandem duplication and NPM1 mutation.
  • BACKGROUND: A small subset of patients with acute myeloid leukemia (AML) have cuplike nuclei.
  • METHODS: The authors searched for patients who had AML with cuplike nuclei at their institution over a 10-year interval.
  • The relevant data were reviewed, and the results were compared with a control group of patients who had AML without cuplike nuclei.
  • RESULTS: In total, 22 patients who had AML with cuplike nuclei were identified and were classified as AML without maturation (French-American-British classification M1) (AML M1).
  • Compared with the control group (AML M1), patients who had AML with cuplike nuclei were associated significantly with fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication (ITD) (86% vs 38%, respectively; P = .002); nucleophosmin 1 (NPM1) mutations (86% vs 19%; P < .0001); both mutations (77% vs 14%; P < .0001); normal karyotype (86% vs 40%; P = .003); bone marrow blast count (90% vs 84%; P = .016); myeloperoxidase positivity (95% vs 30% blasts; P = .001); higher D-dimer levels (>5000 ng/mL vs 569 ng/mL; P = .001); and the absence of CD7 (91% vs 52%; P = .007), CD34 (82% vs 5%; P < .0001), and human leukocyte antigen, D-related (59% vs 10%; P = .001).
  • The positive predictive value of recognizing AML with cuplike nuclei for FLT3-ITD, NPM1, and both mutations was 81%, 86%, and 77%, respectively.
  • CONCLUSIONS: Cuplike nuclei in AML were highly associated with the presence of NPM1 and FLT3-ITD mutations and with several clinicopathologic and immunophenotypic features.
  • Recognition of the distinctive morphologic features of AML with cuplike nuclei may be helpful in streamlining the workup of these neoplasms.

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  • [Copyright] (c) 2009 American Cancer Society.
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  • (PMID = 19672946.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA 100632-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS140671; NLM/ PMC3378048
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46. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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47. Patroglu T, Torun YA, Karakukcu M, Gorozen F: A case of Turner syndrome associated with acute myeloid leukemia (M2). J Pediatr Hematol Oncol; 2006 Oct;28(10):682-3
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  • [Title] A case of Turner syndrome associated with acute myeloid leukemia (M2).
  • A 9-year-old girl was diagnosed as acute myeloid leukemia-M2 according to the French-American-British classification.
  • In addition, a diagnosis of Turner syndrome (TS) was made, on the basis of the presence of the chromosomal abnormality, ovarian failure, and abnormal physical features.
  • In particular, children with Down syndrome have increased risk of developing acute myeloblastic leukemia especially M7.
  • On the other hand, cases of myeloid leukemia that are complicated with TS are extremely rare.
  • This is the first report of TS with acute myeloid leukemia of M2 subtype and t (8;.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Turner Syndrome / genetics


48. Obara H, Nishimura S, Hayashi N, Numagami Y, Inoue T, Kubo K, Kaimori M, Nishijima M: [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia]. No To Shinkei; 2006 Sep;58(9):797-801
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia].
  • Granulocytic sarcoma (GS) is extramedullary tumor composed of immature leukemic cells.
  • GS is presenting usually as a complication during the course of hematologic neoplasm, such as acute myeloblastic leukemia as well as myeloproliferative and myelodysplastic syndrome.
  • We report a 41-year-old man with acute leukemia type M7, who developed GS in the right occipital lobe after complete remission was achieved.
  • The majority of reported cases of GS in acute myeloid leukemia were M2 FAB classification and have chromosome translocation.
  • Our patient was M7 FAB classification, not have specific chromosome translocation.
  • GS occurrence in AML: M7 patient was extremely rare.
  • This is the first case report of AML: M7 with GS in the central nervous system.
  • [MeSH-major] Brain Neoplasms / complications. Leukemia, Myeloid, Acute / complications. Neoplasms, Multiple Primary / pathology. Occipital Lobe. Sarcoma, Myeloid / complications


49. Bedekovics J, Rejto L, Telek B, Udvardy M, Ujfalusi A, Oláh E, Hevessy Z, Kappelmayer J, Kajtár B, Méhes G: [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression]. Orv Hetil; 2009 May 31;150(22):1031-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].
  • [Transliterated title] Mutáns nucleophosmin fehérje kimutatása akut myeloid leukaemiában: az NPMc+ AML biológiai és klinikai jellemzôi.
  • The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in acute myeloid leukemia (AML).
  • Due to the high frequency and the obvious impact on disease outcome, the current WHO classification also defines the new (tentative) entity of "AML with NPM mutation".
  • The present study focused on further biological and clinical characterization of NPMc+ AML determined by histological and cytological preparations of the bone marrow.
  • 41 adult AML cases were investigated in our center between 2005 and 2008, 6/41 cases were presented with cytoplasmic NPM immunostaining (14.6%).
  • All but one were female patients, and were diagnosed as de novo AML with no recurrent cytogenetic aberrations (6/23, 26.1%).
  • The NPMc+ group displayed M2 or M4 morphology, low CD34, c-kit and HLA-DR expression making a clear phenotypic distinction from the unaffected cases possible.
  • In conclusion, immunohistochemistry is well applicable for the identification of NPM mutated AML in the daily hematopathology practice.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics

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  • (PMID = 19465351.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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50. Choi Y, Elagib KE, Goldfarb AN: AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein. Crit Rev Eukaryot Gene Expr; 2005;15(3):207-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein.
  • The chromosomal translocation t(8;21), generating the AML1-ETO fusion protein, is frequently associated with French-American-British (FAB) type M2 acute myeloid leukemia (AML).
  • Several mechanistic models for the role of AML1-ETO in leukemia development have emerged over the last decade.
  • Most of these models have emphasized the capacity of the fusion protein to redirect repressive cofactors, such as histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), to RUNX target genes, thereby reversing the hematopoietic transcriptional program activated by wild-type RUNX1a phenomenon referred to collectively in this review as the "classical" corepressor model.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Animals. Cell Differentiation / genetics. Cells, Cultured. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Erythropoiesis / genetics. GATA1 Transcription Factor / physiology. Histone Deacetylases / genetics. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Signal Transduction / genetics. Translocation, Genetic

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  • (PMID = 16390317.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins, Fusion; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 58
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51. Bonadies N, Pabst T, Mueller BU: Heterozygous deletion of the PU.1 locus in human AML. Blood; 2010 Jan 14;115(2):331-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterozygous deletion of the PU.1 locus in human AML.
  • The transcription factor PU.1 is essential for myeloid development.
  • Targeted disruption of an upstream regulatory element (URE) decreases PU.1 expression by 80% and leads to acute myeloid leukemia (AML) in mice.
  • Here, we sequenced the URE sequences of PU.1 in 120 AML patients.
  • Among them, we compared samples at diagnosis and remission, and one patient with cytogenetically normal acute myeloid leukemia M2 was identified with heterozygosity in 3 of the SNPs in the URE at remission.
  • Our study suggests that heterozygous deletion of the PU.1 locus can be associated with human AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity / genetics. Polymorphism, Single Nucleotide. Promoter Regions, Genetic / genetics. Proto-Oncogene Proteins / genetics. Quantitative Trait Loci / genetics. Sequence Deletion. Trans-Activators / genetics

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  • (PMID = 19890096.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1
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52. Hauer J, Tosi S, Schuster FR, Harbott J, Kolb HJ, Borkhardt A: Graft versus leukemia effect after haploidentical HSCT in a MLL-negative infant AML with HLXB9/ETV6 rearrangement. Pediatr Blood Cancer; 2008 Apr;50(4):921-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Graft versus leukemia effect after haploidentical HSCT in a MLL-negative infant AML with HLXB9/ETV6 rearrangement.
  • Recently published data show an extremely poor survival of infants with AML and HLXB9/ETV6 rearrangement which is the fusion, resulting from the translocation t(7;12)(q36;p13).
  • Herein, we report the clinical course of an 8-month-old patient with acute myeloid leukemia, M2 subtype and with a HLXB9/TEL rearrangement.
  • This case reinforces the potential benefit of a graft-versus-leukemia effect in the haploidentical setting even in chemoresistant myeloid leukemias with poor-prognosis molecular features.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / therapy. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17960638.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Transcription Factors
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53. Corral Mdel P, Villa O, Alfaro EM, Alonso CN, Baro C, Felice MS, Rossi J, Solé F, Gallego MS: Complex chromosome 8;21 translocation with associated hyperdiploidy in acute myeloid leukemia (FAB-M2). Pediatr Blood Cancer; 2008 Mar;50(3):651-4
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  • [Title] Complex chromosome 8;21 translocation with associated hyperdiploidy in acute myeloid leukemia (FAB-M2).
  • We present a case of acute myeloblastic leukemia (AML-M2) with a complex t(8;21) translocation and additional acquired chromosomes yielding a hyperdiploid karyotype.
  • The patient was treated according to our current protocol for AML.
  • He remains in complete remission +11 months from diagnosis.
  • Further follow-up of this patient and the analysis of a larger number of children are needed to define whether the gains of the specific extra chromosomes modify the good prognosis that t(8;21) confers to this subgroup of AML.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / ultrastructure. Chromosomes, Human, Pair 8 / ultrastructure. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17405156.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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54. Liang DC, Shih LY, Huang CF, Hung IJ, Yang CP, Liu HC, Jaing TH, Wang LY, Chang WH: CEBPalpha mutations in childhood acute myeloid leukemia. Leukemia; 2005 Mar;19(3):410-4
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  • [Title] CEBPalpha mutations in childhood acute myeloid leukemia.
  • CEBPalpha: mutations have been described in adult acute myeloid leukemia (AML) and conferred a favorable prognosis.
  • We investigated 117 children with de novo AML using DNA PCR assay followed by sequencing for each PCR product.
  • CEBPalpha mutations were detected in seven patients, four had FAB M2, two M1 and one M4.
  • Our results showed that CEBPalpha mutations occurred in 6% of childhood AML and most exhibited combined mutations in both N-terminal part and bZIP domain.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 15618961.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
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55. Ko RM, Kim HG, Wolff L, Klug CA: Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1101-11
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  • [Title] Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia.
  • Inactivation of p15(Ink4b) expression by promoter hypermethylation occurs in up to 80% of acute myeloid leukemia (AML) cases and is particularly common in the FAB-M2 subtype of AML, which is characterized by the presence of the RUNX1-ETO translocation in 40% of cases.
  • To establish whether the loss of p15(Ink4b) contributes to AML progression in association with RUNX1-ETO, we have expressed the RUNX1-ETO fusion protein from a retroviral vector in hematopoietic progenitor cells isolated from wild-type, p15(Ink4b) or p16(Ink4a) knockout bone marrow.
  • Loss of p15(Ink4b) alone resulted in increased myeloid progenitor cell frequencies in bone marrow by 10-month post-transplant and a 19-fold increase in the frequency of Lin(-)c-Kit(+)Sca-1(+) (LKS) cells that was not associated with expansion of long-term reconstituting HSC.
  • These results strongly suggest that p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated AML to develop.

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  • (PMID = 18037485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096798; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01CA087549; United States / NCI NIH HHS / CA / CA096798-05; United States / NCI NIH HHS / CA / R01 CA096798-05; United States / NCI NIH HHS / CA / R01CA096798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ NIHMS49471; NLM/ PMC2430055
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56. Gu LJ, Tie LJ, Jiang LM, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP, Ye H: [Relationship between immunological characteristics and prognosis in children with acute myeloid leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):241-5
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  • [Title] [Relationship between immunological characteristics and prognosis in children with acute myeloid leukemia].
  • OBJECTIVE: The prognostic significance of immunophenotyping in acute myeloid leukemia (AML) has been controversial.
  • This study investigated the relationship of immunophenotypes with French-American-British (FAB) subtypes and chromosomal abnormalities and assessed the prognostic value of immunophenotyping in children with AML.
  • METHODS: From January 1998 to May 2003, 75 children with newly diagnosed AML were enrolled on protocol AML-XH-99.
  • According to the McAbs used, the patients were classified into five groups: panmyeloid antigens (CD13, CD33, and MPO), myeloid-lineage associated antigens (CD14, CD15), lineage-specific antigens (CD41, GlyA), progenitor-associated antigens (CD34, HLA-DR) and lymphoid-associated antigens (CD19, CD7).
  • The proportion of children with AML expressing one or more of the lymphoid-associated antigens was 24.3%.
  • Lymphoid-associated antigen CD19 was expressed by blast cells in most of FAB M2 patients.
  • The patients with acute promyelocytic leukemia were characterized by the absence of HLA-DR and lymphoid-associated antigens CD19 and CD7.
  • Multivariate analysis suggested immunophenotyping had no independent prognostic value in AML.
  • CONCLUSIONS: Immunophenotyping can not be used independently in the evaluation of risk classification in children with AML.
  • However, it is useful in the reorganization of special types of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology

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  • (PMID = 19374802.001).
  • [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] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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57. Gottardi M, Gattei V, Degan M, Bomben R, Zucchetto A, Tecchio C, Laurino L, Zanatta L, Dei Tos AP, Mordacchini M, Canal F, Gherlinzoni F: Concomitant chronic lymphocytic leukemia and acute myeloid leukemia: evidence of simultaneous expansion of two independent clones. Leuk Lymphoma; 2006 May;47(5):885-9
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  • [Title] Concomitant chronic lymphocytic leukemia and acute myeloid leukemia: evidence of simultaneous expansion of two independent clones.
  • The simultaneous appearance of chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) has been rarely reported, with AML occurring more frequently as a secondary event in patients receiving cytotoxic drugs for a primary lymphoproliferative disorder.
  • We describe a case of simultaneous CLL and AML documented by morphological and cytometric analysis in a previously untreated patient.
  • In particular, on the basis of morphological and immunological features, the patient was diagnosed as being affected by CD34 + /CD13 + /CD33 + /HLA-DR + /CD7 + FAB-M2 AML, along with a B-CLL characterized by neoplastic cells expressing a VH3-53/D3-22/JH4 Ig, bearing, on average, 3.9% IgVH mutations without evidence of antigen-driven selection.
  • These results provide evidence that the rare concomitant association of CLL and AML likely arises from simultaneous expansion of two independent clones.
  • [MeSH-major] Cell Proliferation. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myeloid / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Acute Disease. Aged. Clone Cells / pathology. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Male


58. Eshel R, Ben-Zaken O, Vainas O, Nadir Y, Minucci S, Polliack A, Naparstek E, Vlodavsky I, Katz BZ: Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells. Biochem Biophys Res Commun; 2005 Oct 7;335(4):1115-22
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  • [Title] Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells.
  • Heparanase is a heparan sulfate-degrading endoglycosidase expressed by mature monocytes and myeloid cells, but not by immature hematopoietic progenitors.
  • Heparanase gene expression is upregulated during differentiation of immature myeloid cells.
  • PML-RARalpha and PLZF-RARalpha fusion gene products associated with acute promyelocytic leukemia abrogate myeloid differentiation and heparanase expression.
  • AML-Eto, a translocation product associated with AML FAB M2, also downregulates heparanase gene expression.
  • We found that retinoic acid that dissociates PML-RARalpha from the DNA, and which is used to treat acute promyelocytic leukemia patients, restores heparanase expression to normal levels in an acute promyelocytic leukemia cell line.
  • The retinoic acid effects were also observed in primary acute promyelocytic leukemia cells and in a retinoic acid-treated acute promyelocytic leukemia patient.
  • Histone deacetylase inhibitor reverses the downregulation of heparanase expression induced by the AML-Eto fusion gene product in M2 type AML.
  • In summary, we have characterized a link between leukomogenic factors and the downregulation of heparanase in myeloid leukemic cells.
  • [MeSH-major] Glucuronidase / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes / metabolism. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism

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  • (PMID = 16112651.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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59. Udayakumar AM, Pathare AV, Al-Kindi S, Khan H, Rehmen JU, Zia F, Al-Ghazaly A, Nusrut N, Khan MI, Wali YA, Al-Lamki Z, Dennison D, Raeburn JA: Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):89-94
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  • [Title] Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia.
  • Chromosome aberrations observed at diagnosis are considered to be the most valuable prognostic factors in acute myeloid leukemia (AML).
  • There are only limited studies on the role of such variability in AML patients.
  • Here, we report the results of a cytogenetic study on 63 ethnic Omani patients with de novo AML: 18 children (<or=16 years) and 45 adults.
  • By sex, 41 were male and 22 female; median age at diagnosis was 25 years.
  • The morphological diagnosis was based on the French-American-British (FAB) WHO criteria.
  • Karyotypes with a sole abnormality accounted for 20 of 63 patients (32%).
  • Chromosome abnormalities were more common in patients with the FAB-M2 subtype (15 of 22; 68%), which was also the most frequent subtype observed (22 of 63; 35%).
  • Among the normal karyotypes (24 of 63; 38%), M2 subtype was the also most frequent (7 of 24; 29%), followed by M4 (4 of 24; 17%).
  • Our population differed morphologically, with the M2 subtype as most common, whereas M4 and M3 were more commonly in those reports.
  • [MeSH-major] Antigens, CD / metabolism. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Aberrations. Chromosomes, Human / ultrastructure. Ethnic Groups / genetics. Female. Fluorescent Antibody Technique. Humans. Immunophenotyping. Infant. Karyotyping. Male. Middle Aged. Oman / ethnology

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  • (PMID = 17854660.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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60. Roberson JR, Onciu M, Pounds S, Rubnitz JE, Pui CH, Razzouk BI: Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):542-8
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  • [Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.
  • BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.
  • PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).
  • Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.
  • RESULTS: Median MPO expression was higher in FAB M2 subtype than in other subtypes (P < 0.0001) and differed significantly across cytogenetic risk groups (P = 0.002) with highest MPO expression among those with favorable karyotypes.
  • The percentage of MPO-positive blasts was not significantly associated with the probability of complete remission (P = 0.97), event-free survival (P = 0.72), or survival (P = 0.76) in multivariate analyses that accounted for age, FAB subtype, presenting WBC count, cytogenetic and protocol treatment risk group.
  • CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.
  • [MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763467.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.11.1.7 / Peroxidase
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61. Choschzick M, Bacher U, Ayuk F, Lebeau A: Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation. J Clin Pathol; 2010 Jun;63(6):558-61
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  • [Title] Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation.
  • Myeloid sarcoma of the breast is a rare manifestation of acute myeloid leukaemia (AML).
  • This report describes a patient who was diagnosed with AML FAB M2.
  • Core needle biopsy of the lesion resulted in diagnosis of myeloid sarcoma.
  • The myeloid sarcoma showed complete transient resolution following treatment with the kinase inhibitor sorafenib.
  • However, the patient developed bone marrow relapse and died in fatal cerebral haemorrhage 1 year after initial diagnosis of AML.
  • In summary, combined molecular and immunohistochemical examination of NPM1 and FLT3 is helpful in the diagnosis of extramedullary manifestations of AML in core needle biopsies.
  • [MeSH-major] Breast Neoplasms / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Sarcoma, Myeloid / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20360144.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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62. Kawamura M, Kaku H, Taketani T, Taki T, Shimada A, Hayashi Y: Mutations of GATA1, FLT3, MLL-partial tandem duplication, NRAS, and RUNX1 genes are not found in a 7-year-old Down syndrome patient with acute myeloid leukemia (FAB-M2) having a good prognosis. Cancer Genet Cytogenet; 2008 Jan 1;180(1):74-8
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  • [Title] Mutations of GATA1, FLT3, MLL-partial tandem duplication, NRAS, and RUNX1 genes are not found in a 7-year-old Down syndrome patient with acute myeloid leukemia (FAB-M2) having a good prognosis.
  • The prognosis of leukemia developed in Down syndrome (DS) patients has improved markedly.
  • Most DS leukemia occurs before 3 years of age and is classified as acute megakaryocytic leukemia (AMKL).
  • In contrast, it has been shown that occurrence of DS acute myeloid leukemia (DS-AML) after 3 years of age may indicate a higher risk for a poor prognosis, but its frequency is very low.
  • Age is one of the significant prognostic indicators in DS-AML.
  • The prognostic factor of gene alterations has not been reported in older DS-AML patients.
  • We here describe the case of a 7-year-old DS boy with AML-M2, who had no history of transient abnormal myelopoiesis or any clinical poor prognostic factors, such as high white blood cell counts or extramedullary infiltration.
  • This suggests that a patient lacking these genes alterations might belong to a subgroup of older DS-AML patients with good prognosis.
  • Accumulation of more data on older pediatric DS-AML patients is needed.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Down Syndrome / complications. GATA1 Transcription Factor / genetics. Leukemia, Promyelocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18068539.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / MLL protein, human; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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63. Zelezníková T, Babusíková O: The value of dot plot patterns and leukemia-associated phenotypes in AML diagnosis by multiparameter flow cytometry. Neoplasma; 2005;52(6):517-22
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  • [Title] The value of dot plot patterns and leukemia-associated phenotypes in AML diagnosis by multiparameter flow cytometry.
  • The immunophenotypic features in patients with acute myeloid leukemia (AML) were investigated at diagnosis using a wide antibody panel including progenitor-associated, myeloid and lymphoid markers in quadruple combinations.
  • Analyzed were bone marrow samples from 37 adult and pediatric patients for exact identification of AML blasts according their localization on CD45/SSC dot plots and aberrant immunophenotypes in various subtype of AML.
  • We found the localization of AML blasts on CD45/SSC dot plots, which in combination with immunophenotype profile of blasts allow discrimination of several AML subtypes (M0-M2, M3, M4/M5 and other types).
  • In 27/37 AML patients (73%) at least one leukemia-associated phenotype (LAP) was found, two or more aberrancies coexisted in more than a half of them (78%).
  • Asynchronous expression was the most frequent type of LAP (77.8%, 21/27) followed by coexpression of lymphoid-associated antigens, which occurred in 18/27 (66.7%) patients.
  • Presented study showed that leukemic cells of each AML patient had a unique antigenic profile and could be discriminated from their normal counterparts based on typical light scatter profiles and aberrant antigen expression that could further be used for detection of minimal residual disease.
  • [MeSH-major] Flow Cytometry. Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD / analysis. Blast Crisis / diagnosis. Blast Crisis / immunology. Child. Child, Preschool. Female. HLA-DR Antigens / analysis. Humans. Male. Middle Aged. Neoplasm, Residual / diagnosis. Neoplasm, Residual / immunology. Phenotype

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  • (PMID = 16284699.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA-DR Antigens
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64. Kaspers GJ, Reinhardt D, Fleischhack G, Armendariz H, Stark B, Zwaan CM, Zimmermann M, Creutzig U: Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML. Pediatr Blood Cancer; 2006 Oct 15;47(5):539-42
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  • [Title] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.
  • BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.
  • PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.
  • By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.
  • CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.
  • However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use


65. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
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  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Gata-2 overexpression was associated with a low percentage of blasts in BM and males.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

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  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
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66. Manzoor NF, Azim S, Fadoo Z: Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2). J Pak Med Assoc; 2010 Nov;60(11):977-9
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  • [Title] Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2).
  • He was diagnosed with Acute Mycloid Leukemia (AML-M2).
  • This case shows the efficacy and safety of combined antifungal therapy, including voriconazole, for invasive aspergillosis complicating AML.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Leukemia, Myeloid, Acute / microbiology. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 21375212.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; JFU09I87TR / Voriconazole
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67. Franco A, Lewis KN, Blackmon JM, Manaloor EJ: Hyperostosis - an unusual radiographic presentation of Myelodysplastic Syndrome transformed to Acute Myeloid Leukemia. J Radiol Case Rep; 2010;4(11):18-25
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  • [Title] Hyperostosis - an unusual radiographic presentation of Myelodysplastic Syndrome transformed to Acute Myeloid Leukemia.
  • Acute myeloid leukemia (AML) is also referred to non-lymphocytic leukemia in the literature.
  • It comprises about 15% of the childhood leukemia.
  • There are multiple subtypes of AML from M0-M7 with approximately 45% of the cases being M0-M2 and the remaining subtypes being rare.
  • The definitive diagnosis relies on bone marrow biopsy showing bone marrow infiltration with leukemic cells.
  • We describe a rare radiographic presentation of myelodysplastic syndrome (MDS) transformed to AML in an 8 month old boy who presented with a orbital wall fracture, periosteal reaction, and mixed lytic and sclerotic lesions.

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  • (PMID = 22470698.001).
  • [ISSN] 1943-0922
  • [Journal-full-title] Journal of radiology case reports
  • [ISO-abbreviation] J Radiol Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3303354
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Hyperostosis / Myelodysplastic Syndrome
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68. Nervi B, Ramirez P, Rettig MP, Uy GL, Holt MS, Ritchey JK, Prior JL, Piwnica-Worms D, Bridger G, Ley TJ, DiPersio JF: Chemosensitization of acute myeloid leukemia (AML) following mobilization by the CXCR4 antagonist AMD3100. Blood; 2009 Jun 11;113(24):6206-14
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  • [Title] Chemosensitization of acute myeloid leukemia (AML) following mobilization by the CXCR4 antagonist AMD3100.
  • Here, we used a mouse model of acute promyelocytic leukemia (APL) and a small molecule competitive antagonist of CXCR4, AMD3100, to examine the interaction of mouse APL cells with the BM microenvironment.
  • Coculture of APL(luc) cells with M2-10B4 stromal cells protected the leukemia cells from chemotherapy-induced apoptosis in vitro.
  • These studies provide a proof-of-principle for directing therapy to the critical tethers that promote AML-niche interactions.

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  • (PMID = 19050309.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA094056; United States / NCI NIH HHS / CA / R21 CA110489; United States / NCI NIH HHS / CA / R01 CA083845; United States / NCI NIH HHS / CA / R01 CA83845; United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / P50 CA94056; United States / NCI NIH HHS / CA / P01 CA0101937
  • [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 / Anti-HIV Agents; 0 / Antimetabolites, Antineoplastic; 0 / CXCR4 protein, mouse; 0 / Heterocyclic Compounds; 0 / Receptors, CXCR4; 04079A1RDZ / Cytarabine; 155148-31-5 / JM 3100; EC 3.4.- / Cathepsins; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.20 / Cathepsin G; EC 3.4.21.20 / Ctsg protein, mouse
  • [Other-IDs] NLM/ PMC2699239
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69. Jiang SH, Shi WY, Liu H, Song GQ, Sun GX, Lu W, Liu DF: [Cytogenetic and clinical study of myeloid leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Oct;24(5):571-3
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  • [Title] [Cytogenetic and clinical study of myeloid leukemia].
  • OBJECTIVE: To explore the clinical cytogenetic features and prognosis of myeloid leukemia patients.
  • RESULTS: Among 420 patients with acute myeloid leukemia (AML), 223 cases were found to exhibit clonal chromosome abnormalities, accounted for 53.1%.
  • Out of 158 patients with chronic myeloid leukemia (CML), 96.8% (153/158) were found to exhibit clonal chromosome abnormalities.
  • T(9;22) was specifically associated with CML and some cases of M0, M1 and M2.
  • In these myeloid leukemia cases, there were 18 cases (AML 13 cases, CML 15 cases) without clonal chromosome abnormalities, accounted for 3.1% (18/578) and this phenomenon agreed with the diagnose of clinical signs, marrow morphology and immunology incompletely.
  • CONCLUSION: Karyotype analysis was not only helpful to the diagnose and differential diagnose of myeloid leukemia, but also an important standard of the remission, relapse and therapeutic effect of myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • (PMID = 17922430.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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70. Zhu ZH, Qian J, Lin J, Yao DM, Qian Z, Wang YL, Chen Q, Han LX, Xiao G: [Quantification of the PRAME transcripts in patients with acute myeloid leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Apr;27(2):149-52
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  • [Title] [Quantification of the PRAME transcripts in patients with acute myeloid leukemia].
  • OBJECTIVE: To analyze the expression level and clinical significance of the preferentially expressed antigen of melanoma (PRAME) transcripts in patients with acute myeloid leukemia (AML).
  • METHODS: Real-time quantitative polymerase chain reaction with EvaGreen dye was established to detect the expression level of PRAME transcripts in the bone marrow mononuclear cells of 56 AML cases and 20 controls.
  • RESULTS: The PRAME transcripts were 0-1.46% (median 0.18%) and 0-21 618.09% (median 9.79%) in controls and AML cases, respectively (P< 0.01).
  • Among the FAB subtypes, those with M1, M2, M3 and M4 had significantly higher level of PRAME transcripts than controls.
  • Among cases with AML-M2, those with t(8;21) had significantly higher level of PRAME transcripts (135.06% -21 618.09%, median 2201.88%) than those without t(8;21)(0.14% -1696.30%, median 17.97%)(P= 0.002).
  • CONCLUSION: The PRAME transcript was highly expressed in AML patients and was a favorable marker of prognosis.
  • Quantification of PRAME transcript can be used in monitoring disease status of AML.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20376794.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human; 0 / RNA, Messenger
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71. Faderl S, Verstovsek S, Cortes J, Ravandi F, Beran M, Garcia-Manero G, Ferrajoli A, Estrov Z, O'Brien S, Koller C, Giles FJ, Wierda W, Kwari M, Kantarjian HM: Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older. Blood; 2006 Jul 1;108(1):45-51
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  • [Title] Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older.
  • Outcome of patients with acute myeloid leukemia (AML) who are older than 60 years of age remains unsatisfactory, with low remission rates and poor overall survival.
  • We have previously established the activity of clofarabine plus cytarabine in AML relapse.
  • We have now conducted a phase 2 study of clofarabine plus cytarabine in patients aged 50 years or older with previously untreated AML.
  • Clofarabine was given at 40 mg/m2 as a 1-hour intravenous infusion for 5 days (days 2 to 6) followed 4 hours later by cytarabine at 1 g/m2/d as a 2-hour intravenous infusion for 5 days (days 1 to 5).
  • Of 60 patients, 29 (48%) had secondary AML, 30 (50%) had abnormal karyotypes (monosomy 5 and/or 7 in 15 [25%]), and 11 (21%) showed FLT3 abnormalities.
  • Clofarabine plus cytarabine has activity in adult AML, achieving a good CR rate.
  • Modifications of this combination in AML therapy of older patients warrant further evaluation.
  • [MeSH-major] Adenine Nucleotides / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Chromosome Aberrations. Drug Administration Schedule. Humans. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome


72. Syampurnawati M, Tatsumi E, Ardianto B, Takenokuchi M, Nakamachi Y, Kawano S, Kumagai S, Saigo K, Matsui T, Takahashi T, Nagai K, Gunadi, Nishio H, Yabe H, Kondo S, Hayashi Y: DR negativity is a distinctive feature of M1/M2 AML cases with NPM1 mutation. Leuk Res; 2008 Jul;32(7):1141-3
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  • [Title] DR negativity is a distinctive feature of M1/M2 AML cases with NPM1 mutation.
  • Our previous observation of a higher incidence of FLT3-ITD in DR(-) M1/M2 AML than in DR(+) M1/M2 led to an investigation of NPM1 mutation in the same samples, since DR(-) AML and AML with NPM1 mutation share such characteristics as normal karyotype, the absence of CD34, and FLT3-ITD.
  • These findings point to DR negativity as another phenotypic feature of AML with NPM1 mutation.
  • [MeSH-major] HLA-DR Antigens / analysis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18180033.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / HLA-DR Antigens
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73. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
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74. Wang L, Xu WL, Meng HT, Qian WB, Mai WY, Tong HY, Mao LP, Tong Y, Qian JJ, Lou YJ, Chen ZM, Wang YG, Jin J: FLT3 and NPM1 mutations in Chinese patients with acute myeloid leukemia and normal cytogenetics. J Zhejiang Univ Sci B; 2010 Oct;11(10):762-70
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  • [Title] FLT3 and NPM1 mutations in Chinese patients with acute myeloid leukemia and normal cytogenetics.
  • Mutations of fms-like tyrosine kinase 3 (FLT3) and nucleophosmin (NPM1) exon 12 genes are the most common abnormalities in adult acute myeloid leukemia (AML) with normal cytogenetics.
  • To assess the prognostic impact of the two gene mutations in Chinese AML patients, we used multiplex polymerase chain reaction (PCR) and capillary electrophoresis to screen 76 AML patients with normal cytogenetics for mutations in FLT3 internal tandem duplication (FLT3/ITD) and exon 12 of the NPM1 gene.
  • Significantly more FLT3/ITD aberration was detected in subjects with French-American-British (FAB) M1 (42.8%).
  • NPM1 mutation was frequently detected in subjects with M5 (47.1%) and infrequently in subjects with M2 (11.1%).
  • FLT3 and NPM1 mutations were significantly associated with a higher white blood cell count in peripheral blood and a lower CD34 antigen expression, but not age, sex, or platelet count.
  • Our results indicate that the FLT3/ITD mutation might be a prognostic factor for an unfavorable outcome in Chinese AML subjects with normal cytogenetics, while NPM1 mutation may be a favorable prognostic factor for OS and RFS in the presence of FLT3/ITD.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20872983.001).
  • [ISSN] 1862-1783
  • [Journal-full-title] Journal of Zhejiang University. Science. B
  • [ISO-abbreviation] J Zhejiang Univ Sci B
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2950237
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75. Lewis RE, Cruse JM, Webb RN, Sanders CM, Beason K: Contrasting antigenic maturation patterns in M0-M2 versus M3 acute myeloid leukemias. Exp Mol Pathol; 2007 Oct;83(2):269-73
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  • [Title] Contrasting antigenic maturation patterns in M0-M2 versus M3 acute myeloid leukemias.
  • Acute myelogenous leukemia (AML) is divided into 8 FAB subgroups based on differentiation and maturation properties of the neoplastic cells.
  • Acute promyelocytic leukemia (APL), or M3 AML, is associated with disseminated intravascular coagulation (DIC).
  • Flow cytometric immunophenotyping differentiates among the AML subtypes.
  • Key markers in this classification include the myeloid antigens CD13 and CD33 and the hematopoietic precursor markers CD34 and HLA-DR.
  • The present study analyzes and compares differences in the expression of these markers in 27 M0-M2 cases and 8 M3 cases.
  • The M0-M2 cases generally expressed all four antigens.
  • Analysis of the M3 cases revealed a different immunophenotype as CD13 and CD33 were each positive in all 8 (100%) M3 AML cases while CD34 and HLA-DR were negative in 6 (75%) and 8 (100%) of the 8 M3 cases, respectively.
  • In contrast to expression of the early markers CD34 and HLA-DR in the M0-M2 group, these were negative in the M3 cases which were characterized by heterogeneous CD13 and generally homogeneous and bright CD33 expression.
  • [MeSH-major] Antigens, Neoplasm / analysis. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 17603036.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Neoplasm; 0 / HLA-DR Antigens
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76. Ho PA, Alonzo TA, Gerbing RB, Pollard J, Stirewalt DL, Hurwitz C, Heerema NA, Hirsch B, Raimondi SC, Lange B, Franklin JL, Radich JP, Meshinchi S: Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group. Blood; 2009 Jun 25;113(26):6558-66
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  • [Title] Prevalence and prognostic implications of CEBPA mutations in pediatric acute myeloid leukemia (AML): a report from the Children's Oncology Group.
  • CEBPA mutations have been associated with improved outcome in adult acute myeloid leukemia (AML).
  • We evaluated the prevalence and prognostic significance of CEBPA mutations in 847 children with AML treated on 3 consecutive pediatric trials.
  • CEBPA mutations were significantly more common in older patients, patients with FAB M1 or M2, and patients with normal karyotype.
  • Actuarial event-free survival at 5 years was 70% versus 38% (P = .015) with a cumulative incidence of relapse from complete remission of 13% versus 44% (P = .007) for those with and without CEBPA mutations.
  • As CEBPA mutations are associated with lower relapse rate and improved survival, CEBPA mutation analysis needs to be incorporated into initial screening for risk identification and therapy allocation at diagnosis.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Clinical Trials as Topic / statistics & numerical data. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Polymorphism, Genetic. Prevalence. Prognosis. Protein Structure, Tertiary. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19304957.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002798/ NCT00070174
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009351; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2943755
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77. Chi Y, Lindgren V, Quigley S, Gaitonde S: Acute myelogenous leukemia with t(6;9)(p23;q34) and marrow basophilia: an overview. Arch Pathol Lab Med; 2008 Nov;132(11):1835-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia with t(6;9)(p23;q34) and marrow basophilia: an overview.
  • Acute myelogenous leukemia (AML) with chromosomal translocation (6;9)(p23;q34) is a rare disease with poor prognosis and distinct clinical and morphologic features. t(6;9) results in a chimeric fusion gene between DEK (6p23) and CAN/NUP214 (9q34).
  • FLT3-ITD mutation is one of the most frequent mutations in AML and correlates with poor clinical outcome.
  • Prevalence of FLT3-ITD is as high as 70% among patients with t(6;9) AML, and patients with t(6;9) AML and FLT3-ITD mutations usually have higher white blood cell counts, higher bone marrow blasts, and significantly lower rates of complete remission. t(6;9) is most commonly associated with AML-FAB-M2 and is considered by some researchers to be a separate disease entity because of its distinct clinical and morphologic features and poor prognostic implication.
  • Distinct morphologic features of this entity include marrow basophilia and myelodysplasia, and immunophenotypically, the blast cells are positive for CD9, CD13, CD33, and HLA-DR; are usually positive for CD45 and CD38; and may be positive for CD15, CD34, and terminal deoxynucleotidyl transferase.
  • [MeSH-major] Basophils / pathology. Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Translocation, Genetic

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  • (PMID = 18976025.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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78. Morerio C, Acquila M, Rosanda C, Rapella A, Tassano E, Micalizzi C, Panarello C: t(9;11)(p22;p15) with NUP98-LEDGF fusion gene in pediatric acute myeloid leukemia. Leuk Res; 2005 Apr;29(4):467-70
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  • [Title] t(9;11)(p22;p15) with NUP98-LEDGF fusion gene in pediatric acute myeloid leukemia.
  • The rare t(9;11)(p22;p15) translocation is associated with adult acute myeloid leukemia (AML) with immature forms.
  • We report a novel fusion of the NUP98 and LEDGF genes in a pediatric AML with intermediate characteristics between M2-M3 French-American-British (FAB) subtypes exhibiting the same chromosomal rearrangement.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 22. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Translocation, Genetic

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  • (PMID = 15725483.001).
  • [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
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / lens epithelium-derived growth factor
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79. Syampurnawati M, Tatsumi E, Furuta K, Takenokuchi M, Nakamachi Y, Kawano S, Kumagai S, Saigo K, Matsui T, Takahashi T, Nagai K, Yabe H, Kondo S, Hayashi Y: HLA-DR-negative AML (M1 and M2): FLT3 mutations (ITD and D835) and cell-surface antigen expression. Leuk Res; 2007 Jul;31(7):921-9
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  • [Title] HLA-DR-negative AML (M1 and M2): FLT3 mutations (ITD and D835) and cell-surface antigen expression.
  • FLT3 mutations and cell-surface antigen were investigated in 29 DR-negative (DR(-)) M1/M2 AML samples in comparison with 30 DR-positive (DR(+)) M1/M2 AML samples.
  • Our results indicated that FLT3 mutation is the most common gene alteration found in the DR(-) M1/M2 AML.
  • These results are important for further characterizing this phenotypic AML entity.
  • [MeSH-major] Antigens, Surface / metabolism. HLA-DR Antigens / metabolism. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17056111.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Surface; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / Antigens, CD45
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80. Bhatla D, Gerbing RB, Alonzo TA, Conner H, Ross JA, Meshinchi S, Zhai X, Zamzow T, Mehta PA, Geiger H, Perentesis J, Davies SM: Cytidine deaminase genotype and toxicity of cytosine arabinoside therapy in children with acute myeloid leukemia. Br J Haematol; 2009 Feb;144(3):388-94
Hazardous Substances Data Bank. CYTARABINE .

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  • [Title] Cytidine deaminase genotype and toxicity of cytosine arabinoside therapy in children with acute myeloid leukemia.
  • CDA A79C genotypes were determined in 457 children with acute myeloid leukaemia (AML) treated on the Children's Cancer Group (CCG) 2941 and 2961 protocols and analyzed the impact of CDA genotype on therapy outcomes.
  • Postinduction treatment-related mortality (TRM) was significantly elevated in children with the CC genotype (5-year TRM 17 +/- 13% CC vs. 7 +/- 4% AA, 5 +/- 4% AC, P = 0.05).
  • This was more notable in children who received idarubicin, fludarabine, ara-C, and granulocyte colony-stimulating factor (IDA-FLAG; ara-C = 7590 mg/m2) (5-year TRM 24 +/- 21% CC vs. 6 +/- 6% AA, 6 +/- 7% AC, P = 0.07) as consolidation therapy compared to idarubicin, dexamethasone, cytarabine, thioguanine, etoposide and daunomycin (IDA-DCTER; ara-C = 800 mg/m2) (5-year TRM 15 +/- 20% CC vs. 8 +/- 6% AA, 4 +/- 6% AC; P = 0.29).
  • Relapse-free survival was non-significantly increased in children with the CC genotype treated with IDA-FLAG (76 +/- 20% CC vs. 59 +/- 12% AA and 55 +/- 14% AC; P = 0.40).
  • These data indicate that children with a low activity CDA genotype are at increased risk of TRM with ara-C based therapy for AML.

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  • (PMID = 19036079.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA098543-01; United States / NCI NIH HHS / CA / CA093552-01; United States / NCI NIH HHS / CA / CA114563-01
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 3.5.4.1 / Cytosine Deaminase
  • [Other-IDs] NLM/ NIHMS107031; NLM/ PMC3083240
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81. El-Sissy AH, El-Mashari MA, Bassuni WY, El-Swaayed AF: Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia. J Egypt Natl Canc Inst; 2006 Sep;18(3):244-9
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  • [Title] Aberrant lymphoid antigen expression in acute myeloid leukemia in Saudi Arabia.
  • BACKGROUND: Immunophenotyping improves both accuracy and reproducibility of acute leukemia classification and is considered particularly useful for identifying aberrant lineage association of acute leukemia, biphenotypic and bilineal acute leukemia, as well as monitoring minimal residual disease.
  • THE AIM OF OUR STUDY: Is to determine aberrant lymphoid antigen expression in Saudi acute myeloid leukemia (AML), correlate them with FAB subtypes, evaluate early surface markers CD7 and CD56, and to investigate the role of cytoplasmic CD79a (a B cell marker that is assigned a high score of 2.0 in the WHO classification).
  • PATIENTS AND METHODS: Thirty four newly diagnosed AML cases were included in this study, 47% showed aberrant lymphoid antigen expression.
  • CD9 was expressed in 3/6 (50%) of M3 cases, CD7 was expressed in 11.8% and was mostly confined to FAB M1 and M2 and associated with immature antigens CD34, HLA-DR and TdT.
  • CD56 was expressed in 2/7 (28.6%) M2 cases, and was associated with t (8;21) (q22;q22) together with CD19.
  • CD79a was expressed in one case together with CD19, diagnosed as acute biphenotypic leukemia, and was associated with t(8;21) (q22;q22).
  • CONCLUSION: Minimal residual disease in AML is very difficult to trace, detection of aberrant expression of lymphoid antigens will make it easier.
  • [MeSH-major] Antigens, CD56 / analysis. Antigens, CD7 / analysis. Antigens, CD79 / analysis. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / diagnosis

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  • (PMID = 17671534.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
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82. Monma F, Nishii K, Shiga J, Sugahara H, Lorenzo F 5th, Watanabe Y, Kawakami K, Hosokai N, Yamamori S, Katayama N, Shiku H: Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients. Leuk Res; 2007 Apr;31(4):471-6
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  • [Title] Detection of the CBFB/MYH11 fusion gene in de novo acute myeloid leukemia (AML): a single-institution study of 224 Japanese AML patients.
  • The cytogenetic findings in acute myeloid leukemia (AML) are a powerful prognostic indicator.
  • Among these abnormalities, the World Health Organization has classified inv(16)(p13q22), which is closely associated with the M4E classification in the French-American-British system, as indicating a good-risk AML.
  • However, this chromosomal abnormality can often be difficult to detect.
  • In this study, we used RT-PCR and FISH analysis to examine 224 Japanese adult de novo AML patients for the presence of the CBFB/MYH11 fusion transcript at the time of diagnosis.
  • AML with the CBFB/MYH11 fusion gene but without inv(16) was found in M2, M4, and M5, but not in M4E patients.
  • These results indicate that even if eosinophilia is not found, molecular screening for CBFB/MYH11 fusion gene should be performed in all AML patients at the time of diagnosis to help guide disease management.
  • [MeSH-major] Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Adult. Chromosome Inversion / genetics. Chromosomes, Human, Pair 16. Humans. In Situ Hybridization, Fluorescence. Incidence. Japan. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17052753.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm
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83. Slavcheva V, Lukanov T, Tzvetkov N: Two cases of extramedullary myeloid tumor in patients with continuous remission of acute myeloblastic leukemia. J BUON; 2008 Oct-Dec;13(4):589-92
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  • [Title] Two cases of extramedullary myeloid tumor in patients with continuous remission of acute myeloblastic leukemia.
  • Myeloid sarcoma is described as tumor mass consisting of myeloblasts or immature myeloid cells, involving extramedullary tissues.
  • It can be initial manifestation of myeloproliferative disorders or relapse of previously treated acute myeloblastic leukemia (AML).
  • We present two patients, one with AML-M2 and the other with acute promyelocytic leukemia (APL)-M3.
  • After remission induced by conventional chemotherapy, which continued for 3 and 10 years respectively, a myeloid sarcoma was diagnosed.
  • Two years after the diagnosis of myeloid sarcoma the patient died of haemorrhagic stroke.
  • The patient with AML-M2 continued treatment with polychemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Promyelocytic, Acute / pathology. Sarcoma, Myeloid / pathology

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  • (PMID = 19145688.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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84. Cashen AF, Shah AK, Todt L, Fisher N, DiPersio J: Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Cancer Chemother Pharmacol; 2008 Apr;61(5):759-66
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  • [Title] Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • PURPOSE: In this study, pharmacokinetics (PK) of decitabine administered as a 3-h intravenous infusion of 15 mg/m2 every 8 h for 3 days (cycles repeated every 6 weeks) was evaluated in patients with MDS or AML.
  • METHODS: The PK of this dosing regimen was evaluated in sixteen patients with MDS or AML.
  • The mean values for terminal phase elimination half-life (0.62-0.78 h), total body clearance (125-132 l/h per m2), and volume of distribution at steady state (62.7-89.2 l/m2), remained unchanged during the every 8 h dosing (P>0.05).
  • CONCLUSIONS: Decitabine dosed at 15 mg/m2 iv every 8 h for 3 days resulted in a predictable and manageable toxicity profile in patients with MDS/AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


85. Mahadevan D, DiMento J, Croce KD, Riley C, George B, Fuchs D, Mathews T, Wilson C, Lobell M: Transcriptosome and serum cytokine profiling of an atypical case of myelodysplastic syndrome with progression to acute myelogenous leukemia. Am J Hematol; 2006 Oct;81(10):779-86
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  • [Title] Transcriptosome and serum cytokine profiling of an atypical case of myelodysplastic syndrome with progression to acute myelogenous leukemia.
  • The patient ultimately progressed to acute myelogenous leukemia (AML, FAB M2) and had a normal karyotype throughout her course.
  • Transformation to AML was characterized by a BM blast percentage of 49%.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Cytokines / blood. Gene Expression Profiling. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


86. Mori M, Ohta M, Miyata A, Higashihara M, Oshimi K, Kimura H, Yagasaki F, Sunami K: Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG). Leuk Lymphoma; 2006 Oct;47(10):2062-9
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  • [Title] Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG).
  • The feasibility and effects of combination chemotherapy for very elderly patients with acute myeloid leukemia was examined in 65 patients (including previous myelodysplastic syndrome) aged 76 years or morewith a performance status of 0 - 3.
  • Induction chemotherapy was performed with 30 mg/m2 daunorubicin on days 1 - 3, 150 mg/m2 behenoyl cytosine arabinoside on days 1 - 7, and 70 mg/m2 6-mercaptopurine with 300 mg allopurinol taken orally on days 1 - 7 (BHAC-DM).
  • BHAC-DM is feasible and effective for selected very elderly acute myeloid leukemia patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17071477.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 9YVR68W306 / enocitabine
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87. Christakis G, Perlorentzou S, Aslanidou M, Megalakaki A, Velegraki A: Fatal Blastoschizomyces capitatus sepsis in a neutropenic patient with acute myeloid leukemia: first documented case from Greece. Mycoses; 2005 May;48(3):216-20
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  • [Title] Fatal Blastoschizomyces capitatus sepsis in a neutropenic patient with acute myeloid leukemia: first documented case from Greece.
  • Blastoschizomyces capitatus was isolated from peripheral blood cultures of a profoundly neutropenic patient with acute myeloid leukemia (M2 FAB).
  • [MeSH-major] Geotrichosis / microbiology. Geotrichum / isolation & purification. Leukemia, Myeloid, Acute / complications. Neutropenia / complications. Sepsis / microbiology

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  • (PMID = 15842341.001).
  • [ISSN] 0933-7407
  • [Journal-full-title] Mycoses
  • [ISO-abbreviation] Mycoses
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
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88. Ma Y, Tong HX, Deng X, Zhao Y, Liu ZG, Zhang JH: [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Feb;17(1):12-6
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  • [Title] [MICM characteristics and typing diagnosis in acute myelogenous leukemia patients (AML-M2) with complex karyotype t (2;21;8)(p12;q22;q22)].
  • This study was purposed to investigate the acute myeloid leukemia with complex karyotype t(2;21;8)(p12;q22;q22) (AML-M(2)) by using morphologic, immunologic, cytogenetic and molecular biologic classification technique (MICM) and to analyze the MICM characteristics of AML-M(2) and their diagnostic significance.
  • The FAB typing of bone marrow cells (BMCs) was performed by Wright-Giemsa staining and histochemical staining of BM smears; the immunophenotype of leukemic cells was detected by flow cytometry; the karyotypes of chromosome samples prepared by short-term (48 hours) conventional culture of fresh BMCs were analyzed by RHG banding technique; the FISH signaling in mitotic metaphase was determined by dual color and dual fusion AML/ETO probe and chromosome painting probe, and was compared with results of conventional cytogenetic assay; the AML/ETO fusion transcripts were detected by nested RT-PCR.
  • Case 2 accorded with AML-M(2b) in which abnormal increase of myelocytes mainly appeared.
  • It is concluded that application of MICM has an important significance for correct diagnostic typing of AML-M2 with complex karyotype variant of t(8; 21)(p12;q22;q22).

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  • (PMID = 19236738.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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89. van Binsbergen E, de Weerdt O, Buijs A: A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review. Cancer Genet Cytogenet; 2007 Jul 1;176(1):72-5
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  • [Title] A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review.
  • The t(2;11)(q37;q23) is a rare recurrent cytogenetic abnormality associated with de novo and therapy-related acute myeloid leukemia, resulting in a MLL-SEPT2 fusion gene.
  • We report on a case of therapy-related acute myeloid leukemia M2 showing a t(2;11)(q37;q23) and resulting in a new subtype of a MLL-SEPT2 chimeric transcript.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

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  • (PMID = 17574968.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Number-of-references] 9
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90. Kebriaei P, Kline J, Stock W, Kasza K, Le Beau MM, Larson RA, van Besien K: Impact of disease burden at time of allogeneic stem cell transplantation in adults with acute myeloid leukemia and myelodysplastic syndromes. Bone Marrow Transplant; 2005 May;35(10):965-70
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  • [Title] Impact of disease burden at time of allogeneic stem cell transplantation in adults with acute myeloid leukemia and myelodysplastic syndromes.
  • The impact of disease burden on the outcome of patients with acute myeloid leukemia (AML) undergoing allogeneic stem cell transplantation (SCT) has not been well defined.
  • Data from several retrospective series suggest that overt leukemia at the time of transplant increases the risk of relapse.
  • We reviewed the outcomes of 68 consecutive adults with AML (n=60) or myelodysplastic syndromes (MDS) (n=8) who received an allogeneic SCT at the University of Chicago between May 1986 and October 2002 to confirm the importance of currently recognized risk factors for overall survival (OS) and progression-free survival (PFS).
  • AML subtypes based on the FAB classification were as follows: M0=9, M1=9, M2=16, M3=2, M4=16, M5=3, M6=5.
  • Using standard morphologic criteria, 34 patients were in complete remission (CR) and 34 had visible leukemia present.
  • (1) increased percentage of blasts in the bone marrow at the time of SCT, (2) presence of acute graft-versus-host disease, (3) mismatched donor, (4) Zubrod performance score of >/=2, and (5) age >/=45 years.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


91. Peterson LF, Yan M, Zhang DE: The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO. Blood; 2007 May 15;109(10):4392-8
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  • The 8;21 translocation is a major contributor to acute myeloid leukemia (AML) of the M2 classification occurring in approximately 40% of these cases.
  • Thus, loss of p21(WAF1) facilitates AML1-ETO-induced leukemogenesis, suggesting that mutagenic events in the p21(WAF1) pathway to bypass the growth inhibitory effect from AML1-ETO-induced p21(WAF1) expression can be a significant factor in AML1-ETO-associated acute myeloid leukemia.

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  • (PMID = 17284535.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096735; United States / NCI NIH HHS / CA / CA96735
  • [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 / AML1-ETO fusion protein, human; 0 / CDKN1A protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1885483
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92. 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] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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93. Kim H, Park JH, Lee JH, Lee JH, Joo YD, Lee WS, Bae SH, Mo Ryoo H, Lee KH, Cooperative Study Group A for Hematology: Continuous infusion of intermediate-dose cytarabine and fludarabine with idarubicin for patients younger than 60 years with resistant acute myeloid leukemia: a prospective, multicenter phase II study. Am J Hematol; 2009 Mar;84(3):161-6
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  • [Title] Continuous infusion of intermediate-dose cytarabine and fludarabine with idarubicin for patients younger than 60 years with resistant acute myeloid leukemia: a prospective, multicenter phase II study.
  • We assessed continuous infusion (CI) of fludarabine and cytarabine (FLAG) plus idarubicin for patients under 60-years old with resistant acute myeloid leukemia (AML).
  • Induction chemotherapy consisted of idarubicin (12 mg/m(2) iv infusion over 30 min on Days 1-3), plus fludarabine (30 mg/m2/day) and cytarabine (1,000 mg/m(2)/day) on Days 1-5 as a 24-hr CI.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19195034.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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94. Lemez P, Urbánek V: Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients. Neoplasma; 2005;52(5):398-401
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  • [Title] Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients.
  • The aim was to follow-up gonadal functions in long-term survivors of acute myeloid leukemias (AML) after intensive chemotherapy based on high-doses of cytosine arabinoside (Ara-C) and anthracyclines in the study UHKT-911.
  • Adult patients were treated with at least 3 cycles of chemotherapy including 1-3 courses of Ara-C 10 x 2000 mg/m2/12 h and daunorubicin (DNR) 2 x 45 mg/m2/d.
  • The patient received 4 cycles of Ara-C and DNR plus one cycle with etoposide 350 mg/m2 and mitoxantrone 30 mg/m2.
  • They received the same chemotherapy including cumulative doses of etoposide 500 mg/m2 and mitoxantrone 36 mg/m2.
  • Intensive chemotherapy with high-doses of Ara-C and DNR plus one cycle of etoposide and mitoxantrone may cause permanent gonadal dysfunction in middle-aged patients with AML.
  • [MeSH-major] Amenorrhea / chemically induced. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / drug therapy. Spermatozoa / drug effects
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Transplantation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Oligospermia / chemically induced. Sperm Motility / drug effects

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  • (PMID = 16151584.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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95. Sorour A, Nafea D: Dual color FISH on CBF primary acute myeloid leukemia. Egypt J Immunol; 2008;15(2):25-31
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  • [Title] Dual color FISH on CBF primary acute myeloid leukemia.
  • In acute myeloid leukemia (AML), clonal chromosomal aberrations constitute markers of diagnostic value and the molecular characterization of numerous abnormalities has greatly improved the understanding of the biology of distinct subtypes of the disease.
  • Two of the most common recurring chromosomal abnormalities in AML are t(8;21) and inversion of chromosome 16 or its variant which belong to core binding factor (CBF) AML group.
  • We aimed to compare between cytogenetics and dual color Fluorescence In Situ Hybridization (FISH) regarding their sensitivity for detection of CBF AML associated translocations including t(8;21) and inv(16)/t(16;16).
  • Fifty five consecutive patients diagnosed as de novo AML were studied by chromosome banding analysis.
  • Four cases of AML (M2) subtype were positive for t(8;21) and 1 (M4) subtype was positive for inv(16) by karyotyping analysis.
  • When FISH was applied 6 cases all of AML (M2) subtype were positive for t(8;21), 2 of them were of normal karyotype, and 5 cases all of M4EO subtype were found to be positive for inv(16)/ t(16;16) and 4 of them showed normal karyotypes.
  • In conclusion, FISH can be used as a complementary technique to identify t(8;21) and inv16/t(16;16) in de novo AML as these abnormalities are difficult to diagnose in most cases by conventional cytogenetics alone.

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  • (PMID = 20306685.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factors; 0 / Oncogene Proteins, Fusion
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96. Zaker F, Mohammadzadeh M, Mohammadi M: Detection of KIT and FLT3 mutations in acute myeloid leukemia with different subtypes. Arch Iran Med; 2010 Jan;13(1):21-5
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  • [Title] Detection of KIT and FLT3 mutations in acute myeloid leukemia with different subtypes.
  • BACKGROUND: Mutations in KIT and fms-like tyrosine kinase 3 genes lead to uncontrolled proliferation of leukemic cells with a poor prognosis.
  • Since, data concerning the incidence and associations with patients characteristics vary amongst different studies, the aim of the present study is to identify and quantify the frequency of mutations in Iranian patients suffering from acute myeloid leukemia.
  • METHODS: Internal tandem duplication and D835 mutations in the fms-like tyrosine kinase 3 gene of acute myeloid leukemia patients were studied through polymerase chain reaction and polymerase chain reaction-RFLP analysis.
  • RESULTS: Internal tandem duplication and D835 mutations in the fms-like tyrosine kinase 3 gene occurred in 18% and 6% of AML patients, respectively.
  • Frequencies of mutation were 1.4% and 4.7% in exon 8 and D816 of the KIT gene in acute myeloid leukemia patients.
  • CONCLUSION: This study revealed that approximately 30% of acute myeloid leukemia patients have either KIT or fms-like tyrosine kinase 3 genetic mutations.
  • The presence of fms-like tyrosine kinase 3 was significantly associated with M3 morphology and mutations of KIT were significantly associated with M2 and M4 subtypes.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Mutation / genetics. Proto-Oncogene Proteins c-kit / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 20039765.001).
  • [ISSN] 1735-3947
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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97. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
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  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • The commonly used method for diagnosis and classification is based on FAB criteria using morphology and cytochemical stains.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • The patients were diagnosed on the basis of bone marrow morphology using FAB classification.
  • The age ranged between 6 months to 85 years with a mean age of 32 years.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

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  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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98. 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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99. Kokate P, Ahmad F, Dalvi R, Das BR, Mandava S: Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype. Cancer Genet Cytogenet; 2008 Jul;184(1):52-6
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  • [Title] Molecular cytogenetic investigations in a novel complex variant of t(8;21)(q22;q22) with ins(15;21)(q15;q22.2q22.3) in a patient with AML-M2 subtype.
  • Acute myeloid leukemia (AML) is a clinically and molecularly heterogeneous disease characterized by the aberrant proliferation of myeloid stem cells, reduced apoptosis and blockage in cellular differentiation.
  • The present report describes the results of hematological, cytogenetic, and fluorescence in situ hybridization (FISH) analysis in a 25-year-old man diagnosed with AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18558290.001).
  • [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
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100. Ahmad F, Kokate P, Chheda P, Dalvi R, Das BR, Mandava S: Molecular cytogenetic findings in a three-way novel variant of t(1;8;21)(p35;q22;q22): a unique relocation of the AML1/ETO fusion gene 1p35 in AML-M2. Cancer Genet Cytogenet; 2008 Jan 15;180(2):153-7
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  • [Title] Molecular cytogenetic findings in a three-way novel variant of t(1;8;21)(p35;q22;q22): a unique relocation of the AML1/ETO fusion gene 1p35 in AML-M2.
  • Acute myeloid leukemia (AML) is a malignant neoplasm of hematopoietic stem cells characterized by an abnormal proliferation of myeloid precursors, a reduced rate of apoptosis, and an arrest in cellular differentiation.
  • The present report deals with the results of hematologic, immunophenotypic, cytogenetic, fluorescence in situ hybridization (FISH), and molecular analyses of a 53-year-old female patient diagnosed with AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18206543.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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