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33. Bernardini P, Giannandrea F, Voso MT, Sica S: [Myeloproliferative disorders due to the use of gasoline as a solvent: report of three cases]. Med Lav; 2005 Mar-Apr;96(2):119-25
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  • METHODS: Clinical diagnosis was performed using standard immuno-phenotypic and morphological criteria; the hypothesis of an occupational origin was derived from analysis of the occupational histories.
  • RESULTS: The first case was a 59 year-old blacksmith suffering from acute myeloid leukaemia (AML) FAB M2, who had used petrol for 36 years to degrease the forged metal parts before painting them.
  • The second was a 53 year-old mechanic with AML FAB M3 who had used petrol for 15 years to degrease mechanical parts of tanker motors.
  • If it cannot, how many cases of benzene-related diseases escape aetiological diagnosis?
  • [MeSH-major] Gasoline / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Promyelocytic, Acute / chemically induced. Metallurgy. Motor Vehicles. Occupational Diseases / chemically induced. Primary Myelofibrosis / chemically induced. Solvents / adverse effects

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  • [CommentIn] Med Lav. 2005 Sep-Oct;96(5):447-51 [16711648.001]
  • [ErratumIn] Med Lav. 2005 Sep-Oct;96(5):418
  • (PMID = 16001511.001).
  • [ISSN] 0025-7818
  • [Journal-full-title] La Medicina del lavoro
  • [ISO-abbreviation] Med Lav
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Gasoline; 0 / Solvents; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.5.1.18 / glutathione transferase T1-1, human
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4. Manola KN, Georgakakos VN, Margaritis D, Stavropoulou C, Panos C, Kotsianidis I, Pantelias GE, Sambani C: Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer. Cancer Genet Cytogenet; 2008 Jan 1;180(1):37-42
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  • [Title] Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer.
  • We describe a case of treatment-induced acute myeloid leukemia M2 after breast cancer with a rare reciprocal t(12;12)(p13;q13) as a secondary cytogenetic abnormality in addition to the t(11;19)(q23;p13.1).
  • To the best of our knowledge, our patient represents the first report of the rare t(12;12)(p13;q13) described in treatment-induced leukemia and the possible formation of a new fusion gene.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / drug therapy. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic


35. 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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36. 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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37. 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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38. 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


39. 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.
  • 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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40. 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] Japan
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41. 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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  • [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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42. Chen JP, Chen L, Leek J, Lin C: Antisense c-myc fragments induce normal differentiation cycles in HL-60 cells. Eur J Clin Invest; 2006 Jan;36(1):49-57
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  • BACKGROUND: We have investigated the potential for using antisense technology as a means of delivering treatment for acute myeloblastic leukaemia (FAB-M2) by gene therapy.
  • Thus, we believe that further study of this construct is warranted as a potential gene therapy reagent for treatment of acute myeloblastic leukaemia.
  • [MeSH-major] Antisense Elements (Genetics). Leukemia, Myeloid, Acute / pathology. Proto-Oncogene Proteins c-myc / metabolism

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  • (PMID = 16403010.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antisense Elements (Genetics); 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-myc
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43. 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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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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45. 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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46. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • The deletion was identified at initial diagnosis in one patient and at relapse in the other two.
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • 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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47. Romani C, Pettinau M, Dessalvi P, Murru R, Angelucci E: Unexpected CNS localization in M2 acute myeloid leukemia: a link with past heroin addiction? Am J Hematol; 2008 Aug;83(8):682-3
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  • [Title] Unexpected CNS localization in M2 acute myeloid leukemia: a link with past heroin addiction?
  • [MeSH-major] Central Nervous System Neoplasms / etiology. Heroin Dependence / complications. Leukemia, Myeloid, Acute / pathology


48. Tachikawa Y, Abe Y, Choi I, Ohtsuka R, Nagasawa E, Shibata K, Nishimura J, Nawata H, Muta K: [Second nonmyeloablative allogeneic peripheral blood stem cell transplantation with more immunosuppressive conditioning regimen for the late graft failure of the patient with acute myeloid leukemia]. Fukuoka Igaku Zasshi; 2005 Nov;96(11):378-82
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  • [Title] [Second nonmyeloablative allogeneic peripheral blood stem cell transplantation with more immunosuppressive conditioning regimen for the late graft failure of the patient with acute myeloid leukemia].
  • A 53-year-old woman with acute myeloid leukemia (M2; normal karyotype) in first remission underwent the nonmyeloablative allogeneic peripheral blood stem cell transplantation from her HLA-identical brother, with conditioning consisting of fludarabine and low dose total body irradiation (2Gy).
  • [MeSH-major] Immunosuppression / methods. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning / methods

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  • (PMID = 16502857.001).
  • [ISSN] 0016-254X
  • [Journal-full-title] Fukuoka igaku zasshi = Hukuoka acta medica
  • [ISO-abbreviation] Fukuoka Igaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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49. 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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50. 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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51. 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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52. 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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53. 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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  • [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).
  • 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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54. 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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55. Gozzetti A, Crupi R, Rondoni M, Daviddi B, Defina M, Bocchia M, Pietrini A, Raspadori D, Lauria F: Translocation(X;2)(q26;q11.2) in a patient with acute myeloid leukemia M2 evolved from essential thrombocytemia. Cancer Genet Cytogenet; 2010 Feb;197(1):84-5
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  • [Title] Translocation(X;2)(q26;q11.2) in a patient with acute myeloid leukemia M2 evolved from essential thrombocytemia.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, X. Leukemia, Myeloid, Acute / genetics. Thrombocythemia, Essential / complications. Translocation, Genetic

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  • (PMID = 20113843.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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56. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


57. 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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  • [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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58. Roosild TP, Castronovo S, Choe S: Structure of anti-FLAG M2 Fab domain and its use in the stabilization of engineered membrane proteins. Acta Crystallogr Sect F Struct Biol Cryst Commun; 2006 Sep 1;62(Pt 9):835-9
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  • [Title] Structure of anti-FLAG M2 Fab domain and its use in the stabilization of engineered membrane proteins.
  • Here, the stabilization of a detergent-solubilized K(+) channel protein, KvPae, by engineering a FLAG-binding epitope into a known loop region of the protein and creating a complex with Fab fragments from commercially available anti-FLAG M2 monoclonal antibodies is reported.
  • Although well diffracting crystals of the complex have not yet been obtained, during the course of crystallization trials the structure of the anti-FLAG M2 Fab domain was solved to 1.86 A resolution.
  • Thus, the use of antibody fragments for improving the stability of target proteins can be rapidly applied to the study of membrane-protein structure by placing the short DKYD motif within a predicted peripheral loop of that protein and utilizing commercially available anti-FLAG M2 antibody fragments.

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  • (PMID = 16946459.001).
  • [ISSN] 1744-3091
  • [Journal-full-title] Acta crystallographica. Section F, Structural biology and crystallization communications
  • [ISO-abbreviation] Acta Crystallogr. Sect. F Struct. Biol. Cryst. Commun.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 2G60
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM074821; United States / NIGMS NIH HHS / GM / GM6653; United States / NIGMS NIH HHS / GM / GM74821
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Immunoglobulin Fab Fragments; 0 / Oligopeptides; 0 / Peptides; 98849-88-8 / FLAG peptide
  • [Other-IDs] NLM/ PMC2242885
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59. 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


60. 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


61. 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
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  • [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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62. 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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63. 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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64. 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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  • [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.
  • 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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65. 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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  • [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


66. Yılmaz M, Vural F, Töbü M, Ertan Y, Büyük F: Hemophagocytic syndrome with erythrocyte phagocytosis by the myeloid precursors in a patient with AML -M2. Turk J Haematol; 2008 Mar 5;25(1):42-4
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  • [Title] Hemophagocytic syndrome with erythrocyte phagocytosis by the myeloid precursors in a patient with AML -M2.
  • [Transliterated title] Myeloid öncül hücreleri ve myeloblastlar tarafından eritroid fagositozu ile seyreden hemopagositik sendromlu AML-M2 olgusu.
  • We present a 73-year-old man with acute myeloblastic leukemia FAB M2 type (AML M2) whose bone marrow histology showed unusual hemophagocytosis by myeloid cells and myeloblasts.

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  • (PMID = 27264149.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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67. 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


68. 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


69. Jang JH, Yoo EH, Kim HJ, Kim DH, Jung CW, Kim SH: Acute myeloid leukemia with del(X)(p21) and cryptic RUNX1/RUNX1T1 from ins(8;21)(q22;q22q22) revealed by atypical FISH signals. Ann Clin Lab Sci; 2010;40(1):80-4
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  • [Title] Acute myeloid leukemia with del(X)(p21) and cryptic RUNX1/RUNX1T1 from ins(8;21)(q22;q22q22) revealed by atypical FISH signals.
  • A 57-yr-old woman was diagnosed with acute myeloid leukemia (AML) with maturation, based on morphological and cytochemical/immunophenotypic findings on bone marrow studies.
  • In addition to the cryptic RUNX1/RUNX1T1 rearrangement, this is the first report of partial deletion of an X chromosome as an additional cytogenetic aberration in AML with RUNX1/RUNX1T1.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, X / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20124335.001).
  • [ISSN] 1550-8080
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [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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70. Iguchi T, Yamada Y, Awaya N, Ikeda Y, Okamoto S, Kizaki M: Multilineage involvement of light microscopic myeloperoxidase-negative acute leukemia. Int J Hematol; 2005 Nov;82(4):315-8
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  • [Title] Multilineage involvement of light microscopic myeloperoxidase-negative acute leukemia.
  • The classification of acute leukemia has traditionally been based on a combination of morphology and cytochemical staining data, including myeloperoxidase (MPO) reaction; however, a recent World Health Organization (WHO) classification entails use of cytogenetic and molecular findings in addition to the classic morphological and immunophenotypic analyses.
  • These cases may be classified as acute leukemia of ambiguous lineage in the recent WHO classification.
  • We report the case of a 49-year-old man with acute leukemia with multilineage phenotypes.
  • Morphological findings led to a diagnosis of acute myeloid leukemia M2 by the French-American-British classification, but at light microscopy the results of MPO staining were negative for blast cells.
  • We concluded that the multiparameter analyses conducted in this case, including immunological and ultrastructural assays, were important in arriving at the appropriate diagnosis of acute leukemia of ambiguous lineage in the new WHO classification.
  • [MeSH-major] Bone Marrow Cells / pathology. Leukemia / pathology. Peroxidase / genetics
  • [MeSH-minor] Acute Disease. Antigens, CD / analysis. Antigens, CD / genetics. Gene Rearrangement. HLA-DR Antigens / analysis. HLA-DR Antigens / genetics. Humans. Immunophenotyping. Male. Middle Aged

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  • (PMID = 16298822.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA-DR Antigens; EC 1.11.1.7 / Peroxidase
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71. 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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  • [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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72. Owaidah TM, Al Beihany A, Iqbal MA, Elkum N, Roberts GT: Cytogenetics, molecular and ultrastructural characteristics of biphenotypic acute leukemia identified by the EGIL scoring system. Leukemia; 2006 Apr;20(4):620-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetics, molecular and ultrastructural characteristics of biphenotypic acute leukemia identified by the EGIL scoring system.
  • Biphenotypic acute leukemia (BAL) is a rare, difficult to diagnose entity.
  • Its identification is important for risk stratification in acute leukemia (AL).
  • The scoring proposal of the European Group for the Classification of Acute Leukemia (EGIL) is useful for this purpose, but its performance against objective benchmarks is unclear.
  • Mixed, small and large blast cells predominated, with FAB M2 and L1 constituting the majority.
  • All patients were positive for myeloid (M) markers and either B cell (B) (17 or 74%) or T cell (T) (8 or 34%) markers with two exceptional patients demonstrating trilineage phenotype.
  • In six (26%) patients myeloid lineage commitment was also demonstrable by electron cytochemistry.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Cytogenetic Analysis / methods. Leukemia / diagnosis. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Lineage. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Female. Gene Rearrangement. Guidelines as Topic. Humans. In Situ Hybridization, Fluorescence / methods. In Vitro Techniques. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Phenotype. Risk Factors. Sensitivity and Specificity

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  • (PMID = 16437134.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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73. 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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74. 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
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  • [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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  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
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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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75. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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76. Tirado CA, Chen W, Valdez FJ, Henderson S, Doolittle J, Garcia R, Patel S, Holdridge S, Chastain C, Collins RH: Acute myeloid leukemia (M2) with a cryptic RUNX1/RUNX1T1 t(1;21;8)(p36;q22;q22) variant. Cancer Genet Cytogenet; 2009 Aug;193(1):67-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (M2) with a cryptic RUNX1/RUNX1T1 t(1;21;8)(p36;q22;q22) variant.
  • [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

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  • (PMID = 19602466.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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77. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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78. Jung SH, Kim HC, Yu CS, Kim JC: Solitary preleukemic granulocytic sarcoma as a cause of small bowel obstruction. Gut Liver; 2007 Jun;1(1):82-6
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  • [Title] Solitary preleukemic granulocytic sarcoma as a cause of small bowel obstruction.
  • Granulocytic sarcoma is an extramedullary tumor composed of immature granulocytic cells.
  • These tumors usually occur simultaneously with or follow after the onset of acute myeloid leukemia (AML) or other myeloproliferative disorders.
  • Rarely, it is the first manifestation of AML which appears several months before the onset of leukemia.
  • Immunohistochemical studies showed that the neoplastic cells were of myeloid lineage positive for myeloperoxidase and leukocyte common antigen, but negative for CD3, 20, 56, 79a, and cytokeratin.
  • Initially, there was no evidence of blood or bone marrow involvement suggesting acute leukemia or other myeloproliferative disorders.
  • The findings were consistent with the diagnostic findings of solitary granulocytic sarcoma (preleukemic).
  • Sequentially, the patient developed FAB M2 acute myeloid leukemia.

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  • (PMID = 20485664.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2871656
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Granulocytic sarcoma / Small bowel obstruction
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79. Yan M, Kanbe E, Peterson LF, Boyapati A, Miao Y, Wang Y, Chen IM, Chen Z, Rowley JD, Willman CL, Zhang DE: A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis. Nat Med; 2006 Aug;12(8):945-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(8;21)(q22;q22) translocation is one of the most common genetic abnormalities in acute myeloid leukemia (AML), identified in 15% of all cases of AML, including 40-50% of FAB M2 subtype and rare cases of M0, M1 and M4 subtypes.
  • Although alterations of gene expression and hematopoietic cell proliferation have been reported in the presence of AML1-ETO, its expression does not lead to the development of leukemia.
  • Expression of AML1-ETO9a leads to rapid development of leukemia in a mouse retroviral transduction-transplantation model.
  • More importantly, coexpression of AML1-ETO and AML1-ETO9a results in the substantially earlier onset of AML and blocks myeloid cell differentiation at a more immature stage.
  • [MeSH-major] Alternative Splicing. 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 = 16892037.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA096735; United States / NCI NIH HHS / CA / CA104509; United States / NHLBI NIH HHS / HL / F32HL079900
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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