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1. 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


2. 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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3. 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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4. 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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  • [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.
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):852-63 [18452067.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] Leuk Lymphoma. 2002 Aug;43(8):1541-7 [12400596.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Leukemia. 2003 Apr;17(4):707-15 [12682628.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):650-65 [12951584.001]
  • [Cites] Am J Clin Pathol. 2004 Sep;122(3):348-58 [15362364.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1591-8 [15343344.001]
  • [Cites] Blood. 1994 Jul 1;84(1):244-55 [7517211.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Int J Hematol. 2005 Aug;82(2):85-92 [16146837.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1783-4 [16926303.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2052-4; author reply 2054; discussion 2055-6 [17637816.001]
  • [Cites] Haematologica. 2008 Feb;93(2):283-6 [18223289.001]
  • [Cites] Haematologica. 2008 Mar;93(3):439-42 [18268276.001]
  • [Cites] Blood. 2002 Jul 1;100(1):59-66 [12070009.001]
  • (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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5. 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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6. 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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  • [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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  • [Cites] Cancer. 2000 Jan 15;88(2):480-90 [10640983.001]
  • [Cites] J Assoc Physicians India. 2002 Nov;50:1435-7 [12583479.001]
  • [Cites] Ann Hematol. 2003 Apr;82(4):231-5 [12707726.001]
  • [Cites] Am J Hematol. 2007 May;82(5):405-8 [17133422.001]
  • [Cites] Bildgebung. 1994 Mar;61(1):37-9 [8193516.001]
  • [Cites] Ann Hematol. 1996 Dec;73(6):297-302 [9003161.001]
  • [Cites] Haematologica. 1998 Aug;83(8):760-1 [9793269.001]
  • [Cites] Jpn J Med. 1987 May;26(2):234-6 [3476781.001]
  • (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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7. 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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8. 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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9. 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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10. 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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11. 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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12. 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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13. 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
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  • [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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14. 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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  • [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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15. 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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16. Villa O, Salido M, Pérez-Vila ME, Ferrer A, Arenillas L, Pedro C, Espinet B, Corzo C, Serrano S, Woessner S, Florensa L, Solé F: Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):32-6
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  • [Title] Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia.
  • We report three cases of acute myeloid leukemia without maturation [AML-M1 subtype according to the French-American-British classification (FAB)] with the presence of MYC oncogene amplification in form of double minutes (dmin) or homogeneously staining region (hsr).
  • [MeSH-major] Cell Nucleus / pathology. Genes, myc. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 18656691.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
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17. 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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18. 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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19. 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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  • [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


20. 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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  • [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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21. 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


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

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  • (PMID = 19893346.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human
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23. 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


24. 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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25. 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


26. 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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27. 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
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  • [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]
  • [Cites] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Aug;24(4):369-72 [17680522.001]
  • [Cites] Leukemia. 2003 Apr;17(4):731-7 [12682630.001]
  • [Cites] Leuk Res. 1998 Oct;22(10):899-903 [9766750.001]
  • (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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28. 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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29. 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


30. Garattini E, Terao M: Granulocytic maturation in cultures of acute myeloid leukemia is not always accompanied by increased apoptosis. Leuk Res; 2006 May;30(5):519-20
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  • [Title] Granulocytic maturation in cultures of acute myeloid leukemia is not always accompanied by increased apoptosis.
  • In this issue of the Journal, Soucek et al. challenge the assumption that increased functional granulocytic maturation of HL-60, an ATRA-responsive acute myeloid leukemia cell line devoid of the APL-specific PML-RARalpha fusion protein, results in more rapid or more sustained cell death.
  • [MeSH-major] Apoptosis. Cell Differentiation. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins / metabolism. Apoptosis Regulatory Proteins / pharmacology. CASP8 and FADD-Like Apoptosis Regulating Protein. Caspase 8. Caspases / drug effects. Caspases / metabolism. Cell Proliferation / drug effects. Granulocytes / cytology. HL-60 Cells. Humans. Intracellular Signaling Peptides and Proteins / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Membrane Glycoproteins / metabolism. Membrane Glycoproteins / pharmacology. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / drug effects. Neoplasm Proteins / metabolism. Peptide Fragments / pharmacology. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. TNF-Related Apoptosis-Inducing Ligand. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta1. Tretinoin / antagonists & inhibitors. Tretinoin / pharmacology. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • [CommentOn] Leuk Res. 2006 May;30(5):607-23 [16242776.001]
  • (PMID = 16246418.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 0 / transforming growth factor beta1 (41-65); 5688UTC01R / Tretinoin; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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31. 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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32. 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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33. 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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34. 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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35. Gozzini A, Santini V: Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts. Ann Hematol; 2005 Dec;84 Suppl 1:54-60
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  • [Title] Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts.
  • In leukemic cells, hypermethylation of CpG islands in the promoter region of genes critical for cell cycle and maturation is frequent, and DNMTs were found to be overexpressed, findings paralleled by evidence of transcriptional repression of downstream genes.
  • Therefore, the combination of HDAC and DNMT inhibitors has been considered to be a possible therapeutic approach to restore normal gene expression in acute myeloid leukemia (AML) and other diseases.
  • Thus, treatment of AML with HDAC inhibitors such as D1 and DNMT inhibitors such as decitabine might have clinical benefit for patients, especially these presenting subtypes of AML, like AML1/ETO, in which the leukemogenic mechanism involves corepressor protein complexes containing HDAC and DNMT.
  • [MeSH-major] Azacitidine / analogs & derivatives. Butyrates / pharmacology. DNA Modification Methylases / antagonists & inhibitors. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / genetics. Mannose / analogs & derivatives

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  • (PMID = 16228241.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histone Deacetylase Inhibitors; 0 / O-n-butanoyl-2,3-O-isopropylidenemannofuranoside; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine; PHA4727WTP / Mannose
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36. 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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37. 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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38. 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]
  • [Cites] Blood. 1992 Jan 15;79(2):295-8 [1346094.001]
  • [Cites] Blood. 1992 Jan 15;79(2):473-6 [1370388.001]
  • [Cites] Br J Haematol. 1991 Jan;77(1):50-3 [1671821.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1237-47 [8644864.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1202-10 [12663440.001]
  • [Cites] Oncol Rep. 2004 Dec;12(6):1201-7 [15547738.001]
  • [Cites] J Pathol. 1989 Jul;158(3):185-8 [2475599.001]
  • [Cites] Br J Haematol. 1981 Apr;47(4):553-61 [6938236.001]
  • [Cites] Blood. 1993 May 1;81(9):2394-8 [8097634.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3480-1 [8507883.001]
  • [Cites] Leuk Lymphoma. 1995 Sep;19(1-2):135-40 [8574159.001]
  • [Cites] Cancer Lett. 1996 Nov 12;108(1):87-91 [8950214.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1673-80 [9324288.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1512-8 [9552060.001]
  • [Cites] Am J Hematol. 1999 Jun;61(2):149-52 [10367797.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):309-14 [11999562.001]
  • [Cites] Mol Cancer Res. 2004 Jun;2(6):339-47 [15235109.001]
  • [Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):641-51 [15494300.001]
  • (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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39. 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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  • [Cites] Cancer Res. 2004 Jan 1;64(1):370-7 [14729647.001]
  • [Cites] J Cell Physiol. 2004 Mar;198(3):333-42 [14755538.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):233-8 [15225777.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):365-70 [15225802.001]
  • [Cites] Exp Cell Res. 2004 Aug 15;298(2):339-58 [15265684.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5425-33 [15289351.001]
  • [Cites] Steroids. 2004 Sep;69(10):629-35 [15465107.001]
  • [Cites] Blood. 1979 Sep;54(3):713-33 [288488.001]
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17276-80 [10764733.001]
  • [Cites] Exp Cell Res. 2000 Aug 1;258(2):425-37 [10896794.001]
  • [Cites] J Cell Biochem. 2001;80(4):471-82 [11169731.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):963-9 [11221891.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] J Cell Sci. 2001 May;114(Pt 9):1609-12 [11309192.001]
  • [Cites] J Cell Biochem. 2001 Apr 2-27;82(1):68-77 [11400164.001]
  • [Cites] Exp Cell Res. 2001 Aug 15;268(2):294-300 [11478855.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 15;93(16):1224-33 [11504768.001]
  • [Cites] Biol Signals Recept. 2001 Nov-Dec;10(6):341-9 [11721090.001]
  • [Cites] Steroids. 2002 Aug;67(9):789-98 [12123791.001]
  • [Cites] Acta Biochim Pol. 2002;49(2):393-406 [12362981.001]
  • [Cites] Cell Cycle. 2002 Mar-Apr;1(2):103-10 [12429916.001]
  • [Cites] Cell Cycle. 2002 Nov-Dec;1(6):410-5 [12548017.001]
  • [Cites] J Cell Biochem. 2003 Mar 1;88(4):695-705 [12577303.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9402-6 [12522135.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1325-32 [12649194.001]
  • [Cites] J Cell Biochem. 2003 Aug 15;89(6):1087-101 [12898508.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52651-9 [14517214.001]
  • [Cites] Biochemistry. 1990 Jan 9;29(1):190-6 [2322540.001]
  • [Cites] J Biol Chem. 1990 Sep 15;265(26):15823-31 [2394750.001]
  • [Cites] J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):231-40 [1314073.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27489-94 [7499206.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] J Natl Cancer Inst. 1997 Aug 20;89(16):1199-206 [9274914.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):12792-6 [9371754.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23242-8 [10438498.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):472-87 [15601867.001]
  • (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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40. 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


41. Chen WL, Hsu YJ, Tsai WC, Tsao YT: An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen. J Natl Med Assoc; 2008 Aug;100(8):957-9
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  • [Title] An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen.
  • Differential diagnosis of a focal splenic lesion in the context of acute leukemia is quite challenging.
  • The results of hematological work-up were consistent with acute myeloblastic leukemia (M2, French-American-British classification).
  • Being susceptible to infection in this leukemic patient with severe neutropenia, a diagnosis of splenic abscess was straightforward, plausibly supported by the radiographic findings.
  • Histological sections from ultrasound-guided percutaneous core-needle biopsy of the spleen confirmed the diagnosis of myeloid sarcoma.
  • However, delayed leukemia-targeted therapy, unfortunately, resulted in catastrophic mortality.
  • It should be addressed that, even with the advent of modern imaging modalities, there can be a diagnostic pitfall when managing solitary splenic lesion in acute leukemic patients without histological examination.
  • [MeSH-major] Fever / etiology. Leukemia, Myeloid, Acute / diagnosis. Neutropenia / etiology. Sarcoma, Myeloid / diagnosis. Splenic Neoplasms / diagnosis
  • [MeSH-minor] Biopsy, Needle. Diagnosis, Differential. Diagnostic Errors. Fatal Outcome. Female. Humans. Middle Aged. Spleen / pathology. Tomography, X-Ray Computed


42. 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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43. 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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44. 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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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. Ghanem L, Steinman RA: p21Waf1 inhibits granulocytic differentiation of 32Dcl3 cells. Leuk Res; 2006 Oct;30(10):1285-92
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  • [Title] p21Waf1 inhibits granulocytic differentiation of 32Dcl3 cells.
  • Defining the molecular mechanisms that prevent myeloid progenitor cells from maturing is important because defects in maturation contribute to the development of myeloproliferative and myelodysplastic diseases.
  • IL-3 is an important developmental factor for myeloid progenitor cells in vivo and is required to maintain the undifferentiated state in the 32Dcl3 cell line.
  • 32Dcl3 cells are myeloid progenitor cells of murine origin with high basal levels of p21waf1/cip1 (p21) expression.
  • Our laboratory has previously reported that p21 levels decreased as CD34+-derived myeloid progenitor cells underwent terminal granulopoiesis in vitro.
  • The effect of p21 upon the expression of genes associated with granulocytic differentiation has been unexplored, however.
  • Since IL-3 maintains high levels of p21 in 32Dcl3 cells, we tested the hypothesis that p21 is an inhibitor of myeloid differentiation.
  • Rescue with human p21 in these cells suppressed premature granule protein expression. p21 knockdown was also found to accelerate morphologic granulocytic differentiation in 32Dcl3 cells stimulated with G-CSF.
  • Since high expression levels of p21 and overexpression of the IL-3 receptor have been correlated with poor outcomes in acute myeloid leukemias (AML), differentiation blockade by p21 may be one mechanism that contributes to AML pathogenesis.
  • [MeSH-minor] Animals. Base Sequence. Blotting, Northern. Cell Division / drug effects. Cell Line. Cell Survival / drug effects. DNA Primers. Gene Expression Regulation. Interleukin-3 / pharmacology. Leukemia, Myeloid, Acute / pathology. Mice. Molecular Sequence Data. Plasmids. Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 16499966.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA Primers; 0 / Interleukin-3; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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47. Veyret C, Levy C, Chollet P, Merrouche Y, Roche H, Kerbrat P, Fumoleau P, Fargeot P, Clavere P, Chevallier B: Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial. Cancer; 2006 Dec 1;107(11):2535-44
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  • [Title] Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial.
  • In the lenograstim group, 1 patient developed acute myeloblastic leukemia M2, and 1 patient developed myelodysplastic syndrome.
  • CONCLUSIONS: FEC-HD induction chemotherapy followed by FEC 75 maintenance regimen had moderate and acute long-term toxicities and lead to high DFS and OS rates in patients with IBC.

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17054108.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Placebos; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 6WS4C399GB / lenograstim; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
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48. Gutiérrez NC, López-Pérez R, Hernández JM, Isidro I, González B, Delgado M, Fermiñán E, García JL, Vázquez L, González M, San Miguel JF: Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia. Leukemia; 2005 Mar;19(3):402-9
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  • [Title] Gene expression profile reveals deregulation of genes with relevant functions in the different subclasses of acute myeloid leukemia.
  • Bone marrow samples from 43 adult patients with de novo diagnosed acute myeloid leukemia (AML)--10 acute promyelocytic leukemias (APL) with t(15;17), four AML with inv(16), seven monocytic leukemias and 22 nonmonocytic leukemias--were analyzed using high-density oligonucleotide microarrays.
  • Hierarchical clustering analysis segregated APL, AML with inv(16), monocytic leukemias and the remaining AML into separate groups.
  • A set of only 21 genes was able to assign AML to one of these three classes: APL, inv(16) and other AML subtype without a specific translocation.
  • AML with inv(16) showed an upregulation of MYH11 and a downregulation of a gene encoding a core-binding factor protein, RUNX3.
  • Two major groups emerged from the remaining 22 AML: cluster A with 10 samples and cluster B with 12.
  • In the latter cluster, CD34 upregulation and serine proteases downregulation is consistent with a maturation arrest and lack of granulocytic differentiation.
  • [MeSH-major] Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cluster Analysis. Female. Humans. Leukemia, Monocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Phylogeny. Retrospective Studies


49. Lulli V, Romania P, Riccioni R, Boe A, Lo-Coco F, Testa U, Marziali G: Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation. Haematologica; 2010 Oct;95(10):1633-41
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  • [Title] Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation.
  • This study focuses on the role of Ets-1 during granulocytic differentiation of NB4 promyelocytic and HL60 myeloblastic leukemia cell lines induced by all-trans retinoic acid.
  • Expression of Ets-1 was also reduced during dimethylsulfoxide-induced differentiation and during granulocytic differentiation of human CD34(+) hematopoietic progenitor cells but not in NB4.R2 and HL60R cells resistant to all-trans retinoic acid.
  • In line with these observations, transduction of a transdominant negative molecule of Ets-1, which inhibited DNA binding and transcriptional activity of the wild-type Ets-1, significantly increased chemical-induced differentiation.
  • Interestingly, p51 Ets-1 over-expression was frequently observed in CD34(+) hematopoietic progenitor cells derived from patients with acute myeloid leukemia, as compared to its expression in normal CD34(+) cells.
  • CONCLUSIONS: Our results indicated that a decreased expression of Ets-1 protein generalizes to granulocytic differentiation and may represent a crucial event for granulocytic maturation.
  • [MeSH-minor] Cell Line, Tumor. HL-60 Cells. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Leukemia / pathology. Leukemia, Promyelocytic, Acute. RNA, Small Interfering / pharmacology


50. Naeem M, Harrison K, Barton K, Nand S, Alkan S: A unique case of acute promyelocytic leukemia showing monocytic differentiation after ATRA (all-trans retinoic acid) therapy. Eur J Haematol; 2006 Feb;76(2):164-6
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  • [Title] A unique case of acute promyelocytic leukemia showing monocytic differentiation after ATRA (all-trans retinoic acid) therapy.
  • Acute promyelocytic leukemia (PML) is characterized by a reciprocal translocation between chromosomes 15 and 17 resulting in a chimeric PML and retinoic acid receptor alpha (RARA) oncogene.
  • In vitro and in vivo studies have shown that the large majority of APL cells undergo granulocytic maturation after ATRA therapy.
  • We discuss potential dual capability for granulocytic/monocytic differentiation of PML/RARA positive APL cells and implications of monocytic differentiation in the management of APL patients treated with ATRA.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Differentiation. Leukemia, Promyelocytic, Acute / drug therapy. Monocytes / cytology. Tretinoin / therapeutic use

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  • (PMID = 16405439.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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51. 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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  • [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


52. 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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53. Nitta M, Hoshi A, Shinozaki T, Soeda S, Kawakami M, Kin H, Nakajima N, Hanai K, Kato S, Nomoto T, Usui Y, Terachi T: [Granulocytic sarcoma of the prostate]. Hinyokika Kiyo; 2010 Sep;56(9):521-5
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  • [Title] [Granulocytic sarcoma of the prostate].
  • Histological examination revealed leukemia-like cells, and bone-marrow examination (aspiration) was performed to determine the location of the original lesion.
  • However, no leukemia-like cells or any other form of malignant cells were identified.
  • Clinical imaging confirmed the absence of any other lesions, and granulocytic sarcoma of the prostate was subsequently diagnosed.
  • Four months after initial presentation, the patient developed acute myeloid leukemia [M2 by French-American-British classification].
  • [MeSH-major] Prostatic Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Aged. Humans. Leukemia, Myeloid, Acute / etiology. Male

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  • (PMID = 20940529.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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54. Schanz J, Weiss B, Henrich D, Bohrer MH, Uppenkamp M: [30 year-old patient with multiple pelvic lesions and fecal incontinence]. Internist (Berl); 2009 Sep;50(9):1155, 1157-60
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  • The results of a bone marrow aspiration showed acute myeloid leukemia M2 with translocation t(8,21) associated with granulocytic sarcoma.
  • [MeSH-major] Fecal Incontinence / prevention & control. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Pelvic Neoplasms / diagnosis. Pelvic Neoplasms / surgery. Stem Cell Transplantation

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  • (PMID = 19585093.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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55. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
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  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • RESULTS: In non-APL AML we observed frequent expression of TRAIL decoy receptors (TRAIL-R3 and TRAIL-R4), while TRAIL-R1 and TRAIL-R2 expression was restricted to AML exhibiting monocytic features.
  • Total leukemic blasts, as well as AML colony-forming units (AML-CFU), were invariably resistant to TRAIL-mediated apoptosis.
  • APL express membrane-bound TRAIL on their surface and exhibit a pattern of TRAIL-R expression similar to that observed in the other types of AML.
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • We suggest that AML blasts, including APL blasts, are resistant to TRAIL-mediated apoptosis, a phenomenon seemingly related to the expression of TRAIL decoy receptors on these cells.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

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  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
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56. 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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57. Idres N, Marill J, Chabot GG: Regulation of CYP26A1 expression by selective RAR and RXR agonists in human NB4 promyelocytic leukemia cells. Biochem Pharmacol; 2005 Jun 1;69(11):1595-601
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  • [Title] Regulation of CYP26A1 expression by selective RAR and RXR agonists in human NB4 promyelocytic leukemia cells.
  • All-trans retinoic acid (ATRA) can induce complete remission in acute promyelocytic leukemia (APL), but resistance to this treatment develops rapidly partly due to increased ATRA metabolism.
  • Among the cytochrome P450s (CYPs) involved in ATRA metabolism, the ATRA-inducible cytochrome P450 26A1 (CYP26A1) is particularly active although the molecular mechanisms involved in its regulation are not well defined in the target leukemia cells.
  • To study CYP26A1 expression and regulation in APL cells, we used the NB4 promyelocytic leukemia cell line.
  • To further define CYP26A1 induction mechanisms in the NB4 leukemia cells, we used RARs and RXR selective agonists.
  • The RARalpha agonist BMS753 could elicit maturation, as expected, but not CYP26A1 expression.
  • Treatment with the RARbeta agonist BMS641, or the RARbeta/gamma agonist BMS961, could not elicit maturation, as expected, nor induce CYP26A1 expression.
  • In conclusion, we have shown that CYP26A1 induction is not essential for the granulocytic maturation of NB4 leukemia cells, and that CYP26A1 induction requires the activation of both RARalpha and RXR in these cells.
  • [MeSH-major] Cytochrome P-450 Enzyme System / biosynthesis. Leukemia, Promyelocytic, Acute / enzymology. Receptors, Retinoic Acid / agonists. Retinoid X Receptors / agonists

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  • (PMID = 15896339.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / retinoic acid receptor alpha; 0 / retinoic acid receptor beta; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / retinoic acid 4-hydroxylase
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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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  • [Cites] J Immunol Methods. 1994 Jan 3;167(1-2):279-87 [7508479.001]
  • [Cites] Science. 1993 Oct 29;262(5134):734-8 [8235592.001]
  • [Cites] Nat Struct Biol. 1995 Oct;2(10):842-6 [7552705.001]
  • [Cites] J Bioenerg Biomembr. 1996 Feb;28(1):13-27 [8786233.001]
  • [Cites] J Mol Graph. 1996 Feb;14(1):51-5, 29-32 [8744573.001]
  • [Cites] Structure. 1995 Dec 15;3(12):1291-3 [8747455.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14532-5 [8962086.001]
  • [Cites] Curr Opin Struct Biol. 1997 Oct;7(5):697-701 [9345629.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):28576-82 [9786848.001]
  • [Cites] Protein Sci. 2005 Mar;14(3):836-40 [15689517.001]
  • [Cites] Science. 2005 Feb 25;307(5713):1317-21 [15731457.001]
  • [Cites] Protein Eng Des Sel. 2005 Feb;18(2):79-84 [15788421.001]
  • [Cites] J Struct Funct Genomics. 2005;6(2-3):171-5 [16211515.001]
  • [Cites] Structure. 2000 Jun 15;8(6):669-84 [10873857.001]
  • [Cites] Biochemistry. 2001 Jun 5;40(22):6636-45 [11380258.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):43-8 [11689936.001]
  • [Cites] J Mol Biol. 2002 Feb 8;316(1):1-6 [11829498.001]
  • [Cites] J Mol Biol. 2002 Apr 19;318(1):135-47 [12054774.001]
  • [Cites] Curr Opin Struct Biol. 2002 Aug;12(4):503-8 [12163074.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 2002 Oct;58(Pt 10 Pt 1):1715-21 [12351893.001]
  • [Cites] Protein Sci. 2003 Feb;12(2):337-48 [12538897.001]
  • [Cites] Nat Biotechnol. 2003 Feb;21(2):171-6 [12524549.001]
  • [Cites] Science. 2003 Apr 4;300(5616):108-12 [12649487.001]
  • [Cites] Nature. 2003 May 1;423(6935):33-41 [12721618.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1828-33 [14766985.001]
  • [Cites] FEBS Lett. 2004 Apr 30;564(3):340-8 [15111119.001]
  • [Cites] J Mol Biol. 2004 Oct 22;343(3):747-58 [15465059.001]
  • [Cites] Biotechniques. 1994 Oct;17(4):754-61 [7530459.001]
  • (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. Mathieu J, Giraudier S, Lanotte M, Besançon F: Retinoid-induced activation of NF-kappaB in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells. Oncogene; 2005 Nov 3;24(48):7145-55
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  • [Title] Retinoid-induced activation of NF-kappaB in APL cells is not essential for granulocytic differentiation, but prolongs the life span of mature cells.
  • All-trans retinoic acid (ATRA) significantly improves the survival of patients with acute promyelocytic leukemia (APL) by inducing granulocytic differentiation of leukemia cells.
  • Since an activation of the transcription factor NF-kappaB occurs during ATRA-induced maturation of APL cells, a mechanistic link between these two processes was investigated.
  • Using an in vitro model for APL, we report that ectopic overexpression of a repressor of NF-kappaB activation did not affect granulocytic differentiation.
  • [MeSH-major] Cell Aging / drug effects. Cell Differentiation / drug effects. Granulocytes / physiology. Leukemia, Promyelocytic, Acute / pathology. NF-kappa B / metabolism. Tretinoin / pharmacology

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  • [Copyright] Oncogene (2005) 24, 7145-7155. doi:10.1038/sj.onc.1208889; published online 25 July 2005.
  • (PMID = 16044154.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11c; 0 / Antioxidants; 0 / NF-kappa B; 0 / Reactive Oxygen Species; 25013-16-5 / Butylated Hydroxyanisole; 5688UTC01R / Tretinoin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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60. 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


61. Rizzi M, Tschan MP, Britschgi C, Britschgi A, Hügli B, Grob TJ, Leupin N, Mueller BU, Simon HU, Ziemiecki A, Torbett BE, Fey MF, Tobler A: The death-associated protein kinase 2 is up-regulated during normal myeloid differentiation and enhances neutrophil maturation in myeloid leukemic cells. J Leukoc Biol; 2007 Jun;81(6):1599-608
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  • [Title] The death-associated protein kinase 2 is up-regulated during normal myeloid differentiation and enhances neutrophil maturation in myeloid leukemic cells.
  • In primary leukemia, low expression of DAPK2 was seen in acute myeloid leukemia samples, whereas chronic myeloid leukemia samples in chronic phase showed intermediate expression levels.
  • Lentiviral vector-mediated expression of DAPK2 in NB4 cells enhanced, whereas small interfering RNA-mediated DAPK2 knockdown reduced ATRA-induced granulocytic differentiation, as evidenced by morphology and neutrophil stage-specific maturation genes, such as CD11b, G-CSF receptor, C/EBPepsilon, and lactoferrin.
  • In summary, our findings implicate a role for DAPK2 in granulocyte maturation.
  • [MeSH-major] Calcium-Calmodulin-Dependent Protein Kinases / biosynthesis. Leukemia, Myeloid / pathology. Myeloid Cells / cytology. Myelopoiesis / physiology. Neutrophils / cytology
  • [MeSH-minor] Acute Disease. Antigens, CD34 / metabolism. Antigens, Differentiation / metabolism. Apoptosis Regulatory Proteins. Cell Differentiation. Cell Line, Tumor. Chronic Disease. Death-Associated Protein Kinases. Gene Expression Profiling. Granulocytes / cytology. Granulocytes / physiology. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. RNA, Small Interfering / biosynthesis. Tretinoin / pharmacology. Up-Regulation

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  • (PMID = 17347302.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI49165; United States / NIDDK NIH HHS / DK / DK54938
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, Differentiation; 0 / Apoptosis Regulatory Proteins; 0 / RNA, Small Interfering; 5688UTC01R / Tretinoin; EC 2.7.11.1 / DAPK2 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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62. 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


63. 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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64. 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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  • [Cites] Science. 1997 Sep 26;277(5334):1996-2000 [9302295.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1696-9 [9324291.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3707-13 [9345056.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1812-7 [9465099.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4028-37 [9596646.001]
  • [Cites] Leukemia. 1998 Jun;12(6):893-8 [9639417.001]
  • [Cites] Gene. 1998 May 28;212(1):103-9 [9661669.001]
  • [Cites] EMBO J. 1999 Mar 1;18(5):1223-34 [10064589.001]
  • [Cites] Blood. 1999 Mar 15;93(6):2067-74 [10068680.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1259-67 [10096557.001]
  • [Cites] Genes Dev. 1999 Jun 15;13(12):1501-12 [10385618.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4055-62 [10435586.001]
  • [Cites] Oncogene. 1999 Sep 23;18(39):5381-92 [10498892.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2890-904 [15024077.001]
  • [Cites] Mol Cell Biol. 1996 Jun;16(6):2987-97 [8649410.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2419-30 [15743834.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4523-6 [15705784.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1357-60 [15936816.001]
  • [Cites] Gene Ther. 2005 Oct;12(19):1444-52 [15877047.001]
  • [Cites] Cell Cycle. 2005 Aug;4(8):1113-9 [16082198.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10205-19 [16287839.001]
  • [Cites] Am J Hematol. 2005 Dec;80(4):282-7 [16315255.001]
  • [Cites] Leukemia. 2006 Feb;20(2):224-9 [16357831.001]
  • [Cites] J Cell Physiol. 2006 Jun;207(3):582-93 [16250015.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3303-12 [16380455.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):249-60 [16616331.001]
  • [Cites] J Cell Physiol. 2006 Sep;208(3):594-601 [16741927.001]
  • [Cites] J Biol Chem. 1996 Jun 28;271(26):15782-6 [8663132.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4255-62 [15156181.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4547-54 [15231665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Blood. 1984 Jul;64(1):318-20 [6329379.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):4004-8 [8171026.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):574-8 [7911228.001]
  • [Cites] Nature. 1994 Oct 6;371(6497):534-7 [7935768.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5545-9 [7777546.001]
  • [Cites] Cell. 1995 Aug 25;82(4):675-84 [7664346.001]
  • [Cites] Oncogene. 1995 Nov 2;11(9):1761-9 [7478604.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Assoc Am Physicians. 1995 Jul;107(2):175-80 [8624850.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2676-86 [10733570.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2511-22 [10851050.001]
  • [Cites] J Biol Chem. 2000 Jun 23;275(25):18794-800 [10764767.001]
  • [Cites] Blood. 2000 Jul 15;96(2):655-63 [10887131.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5660-79 [11607817.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] Leukemia. 2002 May;16(5):874-85 [11986950.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47338-47 [12354776.001]
  • [Cites] Cell Cycle. 2002 Sep-Oct;1(5):343-50 [12461297.001]
  • [Cites] Gene. 2003 Jan 16;303:1-10 [12559562.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3157-63 [12480707.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1665-6 [12886257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9506-11 [12881486.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5646-57 [12944913.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1751-61 [14660751.001]
  • [Cites] Blood. 2004 Jan 15;103(2):743-6 [14702288.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):825-30 [14561740.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):571-81 [14978235.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Mar 26;316(1):85-92 [15003515.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14059-64 [8943060.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2251-8 [9036972.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Leuk Lymphoma. 1997 Jun;26(1-2):35-41 [9250785.001]
  • (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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65. Wagner K, Zhang P, Rosenbauer F, Drescher B, Kobayashi S, Radomska HS, Kutok JL, Gilliland DG, Krauter J, Tenen DG: Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy. Proc Natl Acad Sci U S A; 2006 Apr 18;103(16):6338-43
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  • [Title] Absence of the transcription factor CCAAT enhancer binding protein alpha results in loss of myeloid identity in bcr/abl-induced malignancy.
  • The lineage-determining transcription factor CCAAT enhancer binding protein alpha (C/EBPalpha) is required for myeloid differentiation.
  • Decreased function or expression of C/EBPalpha is often found in human acute myeloid leukemia.
  • However, the precise impact of C/EBPalpha deficiency on the maturation arrest in leukemogenesis is not well understood.
  • The expression of bcr/abl in C/EBPalphapos fetal liver cells led to a chronic myeloid leukemia-like disease.
  • Surprisingly, bcr/abl-expressing C/EBPalpha-/- fetal liver cells failed to induce a myeloid disease in transplanted mice, but caused a fatal, transplantable erythroleukemia instead.
  • The mechanism for the lineage shift from myeloid to erythroid leukemia was studied in a bcr/abl-positive cell line.
  • Down-regulation of Id1 by RNA interference impaired C/EBPalpha-induced granulocytic differentiation.
  • Taken together, our study provides evidence that myeloid lineage identity of malignant hematopoietic progenitor cells requires the residual expression of C/EBPalpha.

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  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8393-9 [10567564.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4272-81 [15701714.001]
  • [Cites] Gene Ther. 2000 Jun;7(12):1063-6 [10871756.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Cell. 2001 Jan 12;104(1):21-32 [11163237.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3261-73 [11719363.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7622-7 [12032333.001]
  • [Cites] Blood. 2002 Jul 1;100(1):238-45 [12070033.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):33968-77 [12121983.001]
  • [Cites] Nat Rev Cancer. 2003 Feb;3(2):89-101 [12563308.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):992-7 [12552125.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2206-14 [12406909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):10002-7 [12890867.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3163-71 [12869508.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3575-83 [12893747.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52651-9 [14517214.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Nat Immunol. 2004 Jul;5(7):738-43 [15170211.001]
  • [Cites] Blood. 1983 Sep;62(3):591-6 [6576813.001]
  • [Cites] Nucleic Acids Res. 1991 May 11;19(9):2499 [2041787.001]
  • [Cites] Mol Cell Biol. 1995 Mar;15(3):1513-21 [7862144.001]
  • [Cites] J Biol Chem. 1995 Jul 28;270(30):17939-46 [7629100.001]
  • [Cites] Science. 1995 Aug 25;269(5227):1108-12 [7652557.001]
  • [Cites] Mol Cell Biol. 1997 Feb;17(2):844-50 [9001238.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Immunity. 2004 Dec;21(6):853-63 [15589173.001]
  • [Cites] Gene Ther. 2005 Jan;12(1):12-21 [15602589.001]
  • [Cites] J Exp Med. 2005 Jul 4;202(1):85-96 [15983063.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1590-600 [15914556.001]
  • [Cites] Nature. 2000 Mar 9;404(6774):193-7 [10724173.001]
  • (PMID = 16606850.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA66996; United States / NIDDK NIH HHS / DK / K01 DK062064; United States / NCI NIH HHS / CA / P30CA6516; United States / NCI NIH HHS / CA / P01 CA066996; United States / NIDDK NIH HHS / DK / DK62064; United States / NCI NIH HHS / CA / CA88046; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / R01 CA088046
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Inhibitor of Differentiation Protein 1; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC1458879
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66. 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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67. 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


68. Yoshida H, Ichikawa H, Tagata Y, Katsumoto T, Ohnishi K, Akao Y, Naoe T, Pandolfi PP, Kitabayashi I: PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation. Mol Cell Biol; 2007 Aug;27(16):5819-34
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  • [Title] PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation.
  • PML and PU.1 play important roles in myeloid differentiation.
  • PML-deficient mice have an impaired capacity for terminal maturation of their myeloid precursor cells.
  • We showed that PU.1 directly activates the transcription of the C/EBPepsilon gene that is essential for granulocytic differentiation.
  • The type IV isoform of PML interacted with PU.1, promoted its association with p300, and then enhanced PU.1-induced transcription and granulocytic differentiation.
  • In contrast to PML IV, the leukemia-associated PML-retinoic acid receptor alpha fusion protein dissociated the PU.1/PML IV/p300 complex and inhibited PU.1-induced transcription.
  • These results suggest a novel pathogenic mechanism of the PML-retinoic acid receptor alpha fusion protein in acute promyelocytic leukemia.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / metabolism. Cell Differentiation. Myeloid Cells / cytology. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism

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  • [Cites] Nat Genet. 1999 Nov;23(3):287-95 [10610177.001]
  • [Cites] Mol Cell Biol. 1997 Mar;17(3):1375-86 [9032264.001]
  • [Cites] Nat Cell Biol. 2000 May;2(5):E85-90 [10806494.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3349-56 [10828015.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1297-308 [10942371.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1314-20 [11222375.001]
  • [Cites] Stem Cells. 2001;19(2):125-33 [11239167.001]
  • [Cites] Leuk Res. 2001 Nov;25(11):981-95 [11597733.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7178-85 [11704846.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7186-203 [11704847.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7216-22 [11704849.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6462-7 [9177240.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13187-92 [9371821.001]
  • [Cites] Stem Cells. 1998;16(1):25-37 [9474745.001]
  • [Cites] Science. 1998 Mar 6;279(5356):1547-51 [9488655.001]
  • [Cites] Oncogene. 1999 Feb 18;18(7):1495-501 [10050886.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] J Clin Invest. 1999 May 15;103(10):1399-408 [10330422.001]
  • [Cites] Blood. 1999 Jul 15;94(2):560-71 [10397723.001]
  • [Cites] Blood. 2005 Jan 1;105(1):292-300 [15331439.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12513-8 [16113082.001]
  • [Cites] Cancer Cell. 2006 Feb;9(2):81-94 [16473276.001]
  • [Cites] J Exp Med. 2006 Apr 17;203(4):821-8 [16549595.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7223-33 [11704850.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3377-90 [12032776.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4406-12 [12036869.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1141-8 [12393450.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3265-73 [12515729.001]
  • [Cites] EMBO J. 2003 Nov 3;22(21):5806-16 [14592978.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3727-36 [12893766.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Cell. 1990 Apr 6;61(1):113-24 [2180582.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1257-66 [1708811.001]
  • [Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]
  • [Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]
  • [Cites] Science. 1994 Sep 9;265(5178):1573-7 [8079170.001]
  • [Cites] Oncogene. 1995 Oct 19;11(8):1549-60 [7478579.001]
  • [Cites] Immunity. 1995 Dec;3(6):703-14 [8777716.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2945-8 [8674046.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5647-58 [8896458.001]
  • [Cites] Blood. 2000 May 1;95(9):2748-52 [10779416.001]
  • (PMID = 17562868.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Cebpe protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1; 142805-41-2 / CEBPE protein, human; 143220-95-5 / PML protein, human; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 2.3.1.48 / EP300 protein, human
  • [Other-IDs] NLM/ PMC1952121
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69. 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


70. 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


71. 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


72. 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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73. Kotru M, Batra M, Gomber S, Rusia U: Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia. Indian J Pathol Microbiol; 2009 Jan-Mar;52(1):113-4
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  • [Title] Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia.
  • It is rarely seen in acute leukemia.
  • A 12-year-old girl with acute myeloblastic leukemia (FAB M2) in remission presented with pyoderma.
  • This case has been presented because thrombocytosis is rare in AML and its appearance calls for a close follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / pathology. Thrombocytosis / pathology

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  • (PMID = 19136802.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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74. 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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75. 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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  • [Cites] Cancer. 2000 Dec 25;90(6):364-72 [11156520.001]
  • [Cites] Hong Kong Med J. 2005 Jun;11(3):204-6 [15951586.001]
  • [Cites] Acta Chir Belg. 1999 Apr;99(2):78-81 [10352737.001]
  • [Cites] Histopathology. 1999 May;34(5):391-8 [10231412.001]
  • [Cites] Am J Gastroenterol. 1998 Dec;93(12):2586-8 [9860434.001]
  • [Cites] Cancer. 2002 Mar 15;94(6):1739-46 [11920536.001]
  • [Cites] Cancer. 1981 Sep 15;48(6):1426-37 [7023656.001]
  • [Cites] Cancer. 1973 Jun;31(6):1315-27 [4513690.001]
  • [Cites] Cancer. 1975 May;35(5):1333-40 [1054617.001]
  • [Cites] Acta Cytol. 2004 Sep-Oct;48(5):641-4 [15471256.001]
  • [Cites] Leukemia. 2003 Jun;17(6):1100-3 [12764375.001]
  • [Cites] Cancer. 1986 Dec 15;58(12):2697-709 [3465429.001]
  • (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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76. 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] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA-DR Antigens; EC 1.11.1.7 / Peroxidase
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77. 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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78. 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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79. 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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80. 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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81. McNamara S, Nichol JN, Wang H, Miller WH Jr: Targeting PKC delta-mediated topoisomerase II beta overexpression subverts the differentiation block in a retinoic acid-resistant APL cell line. Leukemia; 2010 Apr;24(4):729-39
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  • Retinoic acid (RA) relieves the maturation block in t(15:17) acute promyelocytic leukemia (APL), leading to granulocytic differentiation.
  • Furthermore, the co-treatment overcame the differentiation block in RA-resistant cells, as assessed by morphological analysis, restoration of promyelocytic leukemia nuclear bodies, induction of CD11c cell surface expression and an increase in nitro-blue-tetrazolium reduction.
  • Cumulatively, our data suggest a model whereby inhibition of PRKCD decreases TOP2B protein levels, leading to a loss of TOP2B-mediated repressive effects on RA-induced transcription and granulocytic differentiation.
  • [MeSH-major] Cell Differentiation / drug effects. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Protein Kinase C-delta / antagonists & inhibitors. Tretinoin / pharmacology

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  • (PMID = 20200558.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 5688UTC01R / Tretinoin; EC 2.7.11.13 / Protein Kinase C-delta; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II beta
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82. 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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83. 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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84. Bertagnolo V, Brugnoli F, Mischiati C, Sereni A, Bavelloni A, Carini C, Capitani S: Vav promotes differentiation of human tumoral myeloid precursors. Exp Cell Res; 2005 May 15;306(1):56-63
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  • [Title] Vav promotes differentiation of human tumoral myeloid precursors.
  • In T and B cells, it appears crucial for both development and functions, while, in non-lymphoid hematopoietic cells, Vav seems not involved in cell maturation, but rather in the response of mature cells to agonist-dependent proliferation and phagocytosis.
  • We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine-phosphorylated Vav does not display any ATRA-induced GEF activity but contributes to the regulation of PI 3-K activity.
  • In this study, we report that Vav accumulates in nuclei of ATRA-treated APL-derived cells and that the down-modulation of Vav prevents differentiation of tumoral promyelocytes, indicating that it is a key molecule in ATRA-dependent myeloid maturation.
  • On the other hand, the overexpression of Vav induces an increased expression of surface markers of granulocytic differentiation without affecting the maturation-related changes of the nuclear morphology.
  • Our data support the unprecedented notion that Vav plays crucial functions in the maturation process of myeloid cells, and suggest that Vav can be regarded as a potential target for the therapeutic treatment of myeloproliferative disorders.
  • [MeSH-major] Cell Cycle Proteins / physiology. Cell Differentiation / physiology. Myeloid Progenitor Cells / metabolism. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Gene Expression / genetics. Gene Expression / physiology. Gene Expression Regulation, Leukemic / drug effects. Granulocytes / physiology. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Phosphorylation. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-vav. RNA, Small Interfering / genetics. Stilbenes / pharmacology. Transfection. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15878332.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Stilbenes; 0 / VAV1 protein, human; 4339-71-3 / 3,3',4,5'-tetrahydroxystilbene; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Protein-Tyrosine Kinases
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85. Campioni D, Secchiero P, Corallini F, Melloni E, Capitani S, Lanza F, Zauli G: Evidence for a role of TNF-related apoptosis-inducing ligand (TRAIL) in the anemia of myelodysplastic syndromes. Am J Pathol; 2005 Feb;166(2):557-63
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  • We focused our study on the cytokine TRAIL (TNF-related apoptosis-inducing ligand), which has been shown to exhibit an anti-differentiation activity on erythroid maturation.
  • Immunocytochemical analysis of bone marrow mononuclear cells (BMMC) showed an increased expression of TRAIL in MDS patients with respect to acute myeloid leukemia (AML) patients and normal BM donors.
  • TRAIL expression was increased predominantly in myeloid precursors of granulocytic lineage and in a subset of monocytes and pro-erythroblasts.
  • On the other hand, TRAIL was detected less frequently in the culture supernatants of AML (4 of 33) and normal BMMC (0 of 22).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Apoptosis. Apoptosis Regulatory Proteins. Bone Marrow Cells / metabolism. Culture Media, Conditioned / pharmacology. Culture Media, Serum-Free / metabolism. Enzyme-Linked Immunosorbent Assay. Erythrocytes / metabolism. Female. Fetal Blood / metabolism. Flow Cytometry. Glycophorin / metabolism. Humans. Immunohistochemistry. Leukemia, Myeloid, Acute / blood. Leukocytes, Mononuclear / metabolism. Ligands. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand. Time Factors


86. 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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87. 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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88. 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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  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6 [10861016.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):296-308 [10460585.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):5869-79 [15988004.001]
  • [Cites] J Exp Med. 2005 Dec 5;202(11):1599-611 [16330818.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):249-60 [16616331.001]
  • [Cites] J Cell Physiol. 2006 Sep;208(3):594-601 [16741927.001]
  • [Cites] Exp Hematol. 2007 Mar;35(3):394-406 [17309820.001]
  • [Cites] Blood. 2007 May 15;109(10):4392-8 [17284535.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3438-45 [10652337.001]
  • [Cites] Blood. 2000 Mar 15;95(6):1942-9 [10706859.001]
  • [Cites] Oncogene. 2000 May 18;19(22):2695-703 [10851069.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] Mol Cell Biol. 2002 Dec;22(23):8278-91 [12417730.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4342-6 [12560221.001]
  • [Cites] Ann Hematol. 2003 Dec;82(12):738-42 [14513284.001]
  • [Cites] Oncogene. 2003 Dec 18;22(58):9265-74 [14681685.001]
  • [Cites] J Biol Chem. 2004 Apr 9;279(15):15678-87 [14747476.001]
  • [Cites] Ann Genet. 1973 Jun;16(2):109-12 [4125056.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1825-31 [1391946.001]
  • [Cites] Blood. 1993 Jun 1;81(11):2860-5 [8499624.001]
  • [Cites] EMBO J. 1993 Jul;12(7):2715-21 [8334990.001]
  • [Cites] Blood. 1993 Aug 1;82(3):712-5 [8338940.001]
  • [Cites] Blood. 1995 Jul 1;86(1):1-14 [7795214.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1548-56 [7632963.001]
  • [Cites] Cancer Res. 1996 Feb 15;56(4):722-7 [8631003.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8508-11 [8710900.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):837-41 [9041182.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):322-33 [9418879.001]
  • [Cites] Leukemia. 1998 Jun;12(6):845-59 [9639410.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7176-84 [9819404.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7185-91 [9819405.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3496-506 [10880462.001]
  • (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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89. Zhu YL, Zhang Y, Zhu P, Yang Y, Du JW, Liu J: [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):236-9
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  • [Title] [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia].
  • OBJECTIVE: To assess the value of common fusion genes analysis in the diagnosis and classification of leukemia by multiplex RT-PCR.
  • METHODS: The multiplex RT-PCR, including 8 parallel PCR reactions, could screen 86 mRNA breakpoints or splice variants at the same time, which was important for the diagnosis and prognosis of leukemia.
  • Bone marrow samples from 161 cases of leukemia and 8 cases of myelodysplastic syndrome (MDS) were involved in the study.
  • The distribution of common fusion genes in leukemia was analyzed by the method mentioned above in combination with clinical and morphological features.
  • RESULTS: Ten fusion genes were detected in 115 cases of leukemia, including AML1/ETO, PML/RAR alpha, PLZF/RAR alpha, dupMLL, MLL/AF6, MLL/AF10, CBFbeta/MYH11, BCR/ABL, Hox11, and EVI1 BCR/ABL was positive in all the 52 cases of chronic myeloid leukemia; PML/RAR alpha was found in 21 of 25 acute promyelocytic leukemia (APL), and PLZF/RAR alpha was detected in one case of APL.
  • Sixteen cases of 17 AML1/ETO-positive acute leukemia (AL) belonged to FAB-M2 subtype, and one case was mixed leukemia.
  • Furthermore, BCR/ABL was detected in 5 acute lymphoblastic leukemia (ALL) cases.
  • Fusion genes were also found in 2 MDS cases, of which AML1/ETO positive-MDS-RAEB progressed to AML rapidly.
  • CONCLUSION: Screening of common fusion genes by multiplex RT-PCR is an important tool which could provide useful and reliable molecular genetic information for the diagnosis and treatment of leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 15968309.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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90. 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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91. Brugnoli F, Bovolenta M, Benedusi M, Miscia S, Capitani S, Bertagnolo V: PLC-beta2 monitors the drug-induced release of differentiation blockade in tumoral myeloid precursors. J Cell Biochem; 2006 May 1;98(1):160-73
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  • [Title] PLC-beta2 monitors the drug-induced release of differentiation blockade in tumoral myeloid precursors.
  • The differentiation therapy in treatment of acute promyelocytic leukemia (APL), based on the administration of all-trans retinoic acid (ATRA), is currently flanked with the use of As2O3, a safe and effective agent for patients showing a resistance to ATRA treatment.
  • A synergy between ATRA and As3O3 was also reported in inducing granulocytic differentiation of APL-derived cells.
  • Here we report that, in APL-derived cells, low doses of As3O3 induce a slight increase of PLC-beta2 together with a moderate maturation, and cooperate with ATRA to provoke a significant increase of PLC-beta2 expression.
  • PLC-beta2 is not necessary for the progression of tumoral promyelocytes along the granulocytic lineage and is unable to overcome the differentiation block or to potentiate the agonist-induced maturation.
  • On the other hand, since its expression closely correlates with the differentiation level reached by APL-derived cells induced to maturate by drugs presently employed in APL therapies, PLC-beta2 represents indeed a specific marker to test the ability of differentiation agents to induce the release of the maturation blockade of tumoral myeloid precursors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Cell Differentiation / drug effects. Growth Inhibitors / pharmacology. Myeloid Progenitor Cells / enzymology. Myeloid Progenitor Cells / pathology. Oxides / pharmacology. Phospholipase C beta / physiology. Tretinoin / physiology

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  • (PMID = 16408290.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Growth Inhibitors; 0 / Oxides; 5688UTC01R / Tretinoin; EC 3.1.4.11 / PLCB2 protein, human; EC 3.1.4.11 / Phospholipase C beta; S7V92P67HO / arsenic trioxide
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92. Boyapati A, Yan M, Peterson LF, Biggs JR, Le Beau MM, Zhang DE: A leukemia fusion protein attenuates the spindle checkpoint and promotes aneuploidy. Blood; 2007 May 1;109(9):3963-71
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  • [Title] A leukemia fusion protein attenuates the spindle checkpoint and promotes aneuploidy.
  • The 8;21 chromosomal translocation occurs in 15% to 40% of patients with the FAB M2 subtype of acute myeloid leukemia (AML).
  • This chromosomal abnormality fuses part of the AML1/RUNX1 gene to the ETO/MTG8 gene and generates the AML1-ETO protein.
  • We previously identified a C-terminal truncated AML1-ETO protein (AEtr) in a mouse leukemia model.
  • AEtr is almost identical to the AML1-ETO exon 9a isoform expressed in leukemia patients.
  • Additionally, primary leukemia cells and cell lines expressing AEtr were aneuploid.
  • These results suggest that inactivation of the spindle checkpoint may contribute to the development of aneuploidy described in t(8;21) leukemia patients.

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  • [Cites] Dev Cell. 2004 Nov;7(5):637-51 [15525526.001]
  • [Cites] Nat Med. 2006 Aug;12(8):945-9 [16892037.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Cell. 2000 Oct 27;103(3):375-86 [11081625.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):156-63 [11113190.001]
  • [Cites] Nature. 2001 Jan 18;409(6818):355-9 [11201745.001]
  • [Cites] Leuk Res. 2001 Apr;25(4):313-22 [11248328.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9889-95 [11150306.001]
  • [Cites] Cell. 2001 May 18;105(4):445-57 [11371342.001]
  • [Cites] Leuk Lymphoma. 2000 Dec;40(1-2):67-77 [11426630.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6470-83 [11533236.001]
  • [Cites] Mol Endocrinol. 2001 Nov;15(11):1870-9 [11682618.001]
  • [Cites] Dev Cell. 2001 Aug;1(2):227-37 [11702782.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5187-93 [11729202.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Curr Biol. 2002 Aug 20;12(16):1368-78 [12194817.001]
  • [Cites] FEBS Lett. 2002 Sep 25;528(1-3):246-50 [12297314.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] Blood. 2003 Jan 1;101(1):289-91 [12393441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4574-9 [12672959.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):440-5 [14744753.001]
  • [Cites] Oncogene. 2004 Mar 15;23(11):2016-27 [15021889.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4459-64 [15070740.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2825-37 [15077146.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 8;101(23):8699-704 [15159543.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Cancer Genet Cytogenet. 1986 Aug;22(4):331-8 [3460687.001]
  • [Cites] Eur J Immunol. 1988 Jan;18(1):97-104 [2831066.001]
  • [Cites] Cancer Genet Cytogenet. 1990 Feb;44(2):169-79 [2297675.001]
  • [Cites] Blood. 1991 May 1;77(9):2031-6 [2018839.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Cancer Genet Cytogenet. 1993 Oct 1;70(1):6-11 [8221614.001]
  • [Cites] Leukemia. 1994 Mar;8(3):465-75 [7907395.001]
  • [Cites] J Tongji Med Univ. 1994;14(1):35-7 [7877191.001]
  • [Cites] Leuk Lymphoma. 1994 Dec;16(1-2):51-6 [7696931.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):805-11 [7772516.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Genes Dev. 1996 Dec 15;10(24):3081-93 [8985178.001]
  • [Cites] Leuk Lymphoma. 1996 Oct;23(3-4):227-34 [9031103.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3604-11 [9584201.001]
  • [Cites] Cell. 1998 Jun 12;93(6):1067-76 [9635435.001]
  • [Cites] Clin Lab Haematol. 1999 Feb;21(1):17-20 [10197258.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1456-66 [15522959.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2452-61 [15972450.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):773-85 [16195750.001]
  • [Cites] Nature. 2005 Oct 13;437(7061):1043-7 [16222300.001]
  • [Cites] Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2005 Oct;13(5):733-40 [16277833.001]
  • [Cites] PLoS Biol. 2005 Dec;3(12):e416 [16292982.001]
  • [Cites] Cancer Treat Rev. 2006 May;32(3):166-79 [16527420.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • (PMID = 17197431.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / U01 CA 84221; United States / NHLBI NIH HHS / HL / F32 HL079900; United States / NHLBI NIH HHS / HL / 5F32 HL 079900; United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA 104509; United States / NCI NIH HHS / CA / CA 096735; United States / NCI NIH HHS / CA / R01 CA096735
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Bub1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / SPAG5 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / BUB1 protein, human; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; SH1WY3R615 / Nocodazole
  • [Other-IDs] NLM/ PMC1874577
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93. 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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94. 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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  • [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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95. Valente C, André S, Catarino A, Fradinho F, Gamboa F, Loureiro M, Fontes Baganha M: [Lymphangioleiomyomatosis - report of three cases]. Rev Port Pneumol; 2010 Jan-Feb;16(1):187-95
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  • [Transliterated title] Linfangioleiomiomatose - A propósito de três casos clínicos.
  • Pulmonary lymphangioleiomyomatosis (LAM) is a rare disease of unknown aetiology.
  • LAM may occur sporadically, in association with tuberous sclerosis complex (TSC) or inheritable multiorgan hamartomatosis.
  • In either situation, LAM occurs almost exclusively in women of reproductive age, and approximately one third of the patients with TSC have LAM2.
  • The authors review the cases of three female patients diagnosed with LAM based on clinical and radiological findings.

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  • (PMID = 20054519.001).
  • [ISSN] 2172-6825
  • [Journal-full-title] Revista portuguesa de pneumologia
  • [ISO-abbreviation] Rev Port Pneumol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Portugal
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96. 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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  • 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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97. 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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98. Song LP, Zhang J, Wu SF, Huang Y, Zhao Q, Cao JP, Wu YL, Wang LS, Chen GQ: Hypoxia-inducible factor-1alpha-induced differentiation of myeloid leukemic cells is its transcriptional activity independent. Oncogene; 2008 Jan 17;27(4):519-27
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  • [Title] Hypoxia-inducible factor-1alpha-induced differentiation of myeloid leukemic cells is its transcriptional activity independent.
  • Hypoxia or hypoxia mimetic has been shown to induce differentiation together with the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) protein of myeloid leukemic cells and normal hematopoietic progenitors.
  • To provide direct evidence for the role of HIF-1alpha in acute myeloid leukemia (AML) cell differentiation and its mechanisms, we generated myeloid leukemic U937T transformants, in which HIF-1alpha was tightly induced by tetracycline withdrawal.
  • The results showed that the conditional HIF-1alpha induction triggered granulocytic differentiation of these transformants, while the suppression of HIF-1alpha expression by specific short hairpin RNAs (shRNAs) effectively inhibited hypoxia-induced differentiation of U937 cells, as evidenced by morphology, maturation-related antigens as well as expressions of myeloid differentiation signatures and hematopoietic cells-specific cytokine receptors.
  • The specific shRNAs-inhibited expression of HIF-1beta, an essential partner for transcription activity of HIF-1, failed, while the inhibition of hematopoietic differentiation-critical CCAAT/enhancer-binding protein-alpha (C/EBPalpha) significantly eliminated HIF-1alpha-mediated myeloid leukemic cell differentiation.
  • Collectively, this work provided several lines of direct evidence for the role of HIF-1alpha protein through its nontranscriptional activity in myeloid cell differentiation, in which C/EBPalpha elicits a role as an effector downstream to HIF-1alpha.
  • These discoveries would shed new insights for understanding mechanisms underlying leukemogenesis and designing the new therapeutic strategy for differentiation induction of AML.
  • [MeSH-major] Cell Differentiation / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Leukemia, Myeloid / pathology. Transcriptional Activation / physiology

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  • (PMID = 17637739.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Colony-Stimulating Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering
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99. 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


100. 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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