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1. Ozyurek E, Alioglu B, Coskun M, Ozbek N: Successful use of short-course high-dose methylprednisolone in a child with acute myeloblastic leukemia (FAB M2) and myeloid tumor. Leuk Lymphoma; 2006 May;47(5):923-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful use of short-course high-dose methylprednisolone in a child with acute myeloblastic leukemia (FAB M2) and myeloid tumor.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methylprednisolone / therapeutic use. Sarcoma, Myeloid / drug therapy

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  • (PMID = 16753881.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] X4W7ZR7023 / Methylprednisolone
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2. 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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3. Cui JW, Wang J, He K, Jin BF, Wang HX, Li W, Kang LH, Hu MR, Li HY, Yu M, Shen BF, Wang GJ, Zhang XM: Two-dimensional electrophoresis protein profiling as an analytical tool for human acute leukemia classification. Electrophoresis; 2005 Jan;26(1):268-79
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  • [Title] Two-dimensional electrophoresis protein profiling as an analytical tool for human acute leukemia classification.
  • Two-dimensional electrophoresis (2-DE) was used to profile the proteins of leukemic cells from 61 cases of akute leukemia (AL) characterized by the French-American-British (FAB) classification.
  • The distinct protein profiles (DPPs) of AL FAB subtypes were explored successfully, including acute myeloid leukemia (AML), its subtypes (M2, M3, and M5), and acute lymphoid leukemia (ALL), which were homogeneous within different samples of the same subgroup but clearly differed from all other subgroups.
  • Among the DPPs of AL subtypes, some proteins have been reported, but most of them were first reported here to mark AML differentiation and to discriminate AML from ALL.
  • These data show that 2-DE protein profiling could be used as an analytical tool for facilitating molecular definition of human AL classification and understanding the mechanism of leukemogensis, and the extension of the present analysis to the currently less well-defined AL will identify additional subgroups and may promote the identification of new targets for specific treatment approaches.
  • [MeSH-major] Electrophoresis, Gel, Two-Dimensional. Leukemia / classification. Neoplasm Proteins / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers, Tumor / analysis. Female. Humans. Male. Peptide Mapping

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  • (PMID = 15624164.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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4. Lee C, Lin Y, Huang M, Lin C, Liu C, Chow J, Liu HE: Increased cellular glutathione and protection by bone marrow stromal cells account for the resistance of non-acute promylocytic leukemia acute myeloid leukemia cells to arsenic trioxide in vivo. Leuk Lymphoma; 2006 Mar;47(3):521-9
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  • [Title] Increased cellular glutathione and protection by bone marrow stromal cells account for the resistance of non-acute promylocytic leukemia acute myeloid leukemia cells to arsenic trioxide in vivo.
  • Arsenic trioxide (ATO) is a novel agent for acute promylocytic leukemia (APL).
  • Studies performed in vitro have demonstrated that ATO also induces cell-cycle arrest and apoptosis in multiple cancers, including non-APL acute myeloid leukemia (AML).
  • To explore the potential use of ATO on non-APL AML, we treated the leukemic cells in vivo using a NOD/SCID animal model.
  • Mice harboring HL-60 or NB-4 leukemia or primary AML-M2 cells were treated daily with 5 mug/g ATO intraperitoneally for a maximum of 6 weeks.
  • ATO also failed to eradicate the primary AML cells in vivo.
  • [MeSH-major] Arsenicals / administration & dosage. Bone Marrow Cells / drug effects. Drug Resistance, Neoplasm. Glutathione / metabolism. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Oxides / administration & dosage. Stromal Cells / drug effects
  • [MeSH-minor] Acute Disease. Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Buthionine Sulfoximine / pharmacology. Cell Count. Cell Line, Tumor. Coculture Techniques. Disease Models, Animal. Humans. Injections, Intraperitoneal. Mice. Mice, Inbred NOD. Mice, SCID. Treatment Failure


5. Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS: Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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  • [Title] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
  • PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.
  • Reduced-intensity allogeneic SCT may offer a less toxic approach to patients with AML.
  • Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.
  • Therefore, we explored the feasibility and toxicity of targeted immunotherapy following reduced-intensity allogeneic SCT in children with CD33+ AML.
  • EXPERIMENTAL DESIGN: Eight patients with CD33+ AML received a reduced-intensity allogeneic SCT following fludarabine 30 mg/m2 for 6 days and busulfan 3.2 mg/kg (<4 years, 4 mg/kg/d) for 2 days.
  • CONCLUSIONS: The administration of gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with average risk AML is feasible and well tolerated with minimal toxicity.
  • The maximal tolerated dose has yet to be determined for gemtuzumab ozogamicin post reduced-intensity allogeneic SCT in children with CD33+ AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods

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  • (PMID = 16203817.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL07968
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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6. Watanabe-Okochi N, Oki T, Komeno Y, Kato N, Yuji K, Ono R, Harada Y, Harada H, Hayashi Y, Nakajima H, Nosaka T, Kitaura J, Kitamura T: Possible involvement of RasGRP4 in leukemogenesis. Int J Hematol; 2009 May;89(4):470-81
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  • To understand the molecular mechanism of leukemogenesis, particularly progression of myelodysplastic syndrome (MDS) to acute leukemia, we made cDNA libraries from the samples of patients and screened them by expression-cloning to detect class I mutations that render HF6 cells factor-independent.
  • We identified RasGRP4, an activator of Ras, as a candidate for class I mutation from three of six patients (MDS/MPD = 1, MDS-RA = 1, MDS/AML = 2, CMMoL/AML = 1 and AML-M2 = 1).
  • C57BL/6J mice transplanted with RasGRP4-transduced primary bone marrow cells died of T cell leukemia, myeloid leukemia, or myeloid leukemia with T cell leukemia.
  • The double transduction led to early onset of T cell leukemia but not of AML in the transplanted mice when compared to transduction of RasGRP4 alone.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. ras Guanine Nucleotide Exchange Factors / metabolism

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  • (PMID = 19350351.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RASGRP4 protein, human; 0 / Rasgrp4 protein, mouse; 0 / ras Guanine Nucleotide Exchange Factors
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7. 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.
  • AEtr cells had a reduced mitotic index following nocodazole treatment, suggesting a failure in a subset of cells to arrest in mitosis with a functional spindle checkpoint.
  • 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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  • (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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8. Slavcheva V, Lukanov T, Tzvetkov N: Two cases of extramedullary myeloid tumor in patients with continuous remission of acute myeloblastic leukemia. J BUON; 2008 Oct-Dec;13(4):589-92
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  • [Title] Two cases of extramedullary myeloid tumor in patients with continuous remission of acute myeloblastic leukemia.
  • Myeloid sarcoma is described as tumor mass consisting of myeloblasts or immature myeloid cells, involving extramedullary tissues.
  • It can be initial manifestation of myeloproliferative disorders or relapse of previously treated acute myeloblastic leukemia (AML).
  • We present two patients, one with AML-M2 and the other with acute promyelocytic leukemia (APL)-M3.
  • After remission induced by conventional chemotherapy, which continued for 3 and 10 years respectively, a myeloid sarcoma was diagnosed.
  • Two years after the diagnosis of myeloid sarcoma the patient died of haemorrhagic stroke.
  • The patient with AML-M2 continued treatment with polychemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Promyelocytic, Acute / pathology. Sarcoma, Myeloid / pathology

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  • (PMID = 19145688.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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9. Al-Sobhi EM, Jeha TM, Al-Taher MI: Granulocytic sarcoma causing cord compression in a pregnant woman with acute myeloid leukemia and t(8;21). Saudi Med J; 2008 Nov;29(11):1658-61
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  • [Title] Granulocytic sarcoma causing cord compression in a pregnant woman with acute myeloid leukemia and t(8;21).
  • Chloroma or granulocytic sarcomas (GSs) are solid tumors originating from myeloid precursors.
  • Most frequently they occur in acute myeloid leukemia (AML), myeloproliferative disorder, and myelodysplasia.
  • Granulocytic sarcoma resulting in spinal cord compression is rare.
  • In spite of the fact that t(8;21) is considered to be associated with good prognosis, patients with GS and spinal cord compression had less favorable prognosis than other AML patients with t(8;21).
  • Pregnancy associated with AML is rare.
  • In our research, only one case of pregnancy with GS and AML has been previously reported.
  • We are reporting a pregnant female diagnosed with AML/M2 with t(8;21) at the first trimester, who relapsed with GS, and cord compression at full term.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / complications. Pregnancy Complications, Neoplastic / pathology. Sarcoma, Myeloid / pathology. Translocation, Genetic. Umbilical Cord / pathology


10. Hiçsönmez G: A novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells. Turk J Haematol; 2010 Mar 5;27(1):1-7
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  • [Title] A novel approach to treatment in childhood acute myeloblastic leukemia and myelodysplastic syndrome with high-dose methylprednisolone as a differentiation- and apoptosis-inducing agent of myeloid leukemic cells.
  • [Transliterated title] Çocukluk yaşı akut myeloblastik lösemi ve myelodisplastik sendromunda myeloid lösemik hücrelerde farklılaşma ve apoptosisi sağlayan yüksek doz metilprednizolon ile yeni bir tedavi yaklaşımı.
  • Differentiation-inducing therapy with all-trans retinoic acid significantly improved the outcome in children with acute promyelocytic leukemia (APL).
  • Based on the experimental studies in mice, we have shown that short-course high-dose methylprednisolone (HDMP) treatment can induce terminal differentiation of leukemic cells in children with various subtypes of acute myeloblastic leukemia (AML-M1,-M2,-M3,-M4,-M7).
  • It has also been shown to induce apoptosis of myeloid leukemic cells with or without differentiation.
  • Administration of HDMP as a single agent resulted in a rapid clinical improvement, a marked decrease in blast cells in both peripheral blood and bone marrow and dramatic decreases in the size of extramedullary leukemic mass in children with AML and myelodysplastic syndrome (MDS).

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  • (PMID = 27265790.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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11. Dobashi N, Asai O, Yano S, Osawa H, Takei Y, Yamaguchi Y, Saito T, Yamazaki H, Kobayashi T, Usui N: Aclarubicin plus behenoyl cytarabine and prednisolone for previously treated acute myeloid leukemia patients. Leuk Lymphoma; 2006 Oct;47(10):2203-7
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  • [Title] Aclarubicin plus behenoyl cytarabine and prednisolone for previously treated acute myeloid leukemia patients.
  • This study analysed the clinical outcome of salvage therapy consisting of aclarubicin (ACR) plus behenoyl cytarabine (BHAC) and prednisolone (PSL) for patients with acute myeloid leukemia (AML).
  • ACR was administered at a dose of 13 mg/m2 per day for 14 days; BHAC, at 130 mg/m2 per day for 14 days; and PSL was administered orally at a dose of 60 mg/m2 per day for 5 days.
  • ACR in combination with BHAC showed a substantial anti-leukemic efficacy in previously treated AML patients and the role of ACR and BHAC may be considered while devising strategies for AML treatments.
  • [MeSH-major] Aclarubicin / administration & dosage. Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology. Prednisolone / administration & dosage

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  • (PMID = 17071496.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibiotics, Antineoplastic; 04079A1RDZ / Cytarabine; 74KXF8I502 / Aclarubicin; 9PHQ9Y1OLM / Prednisolone; 9YVR68W306 / enocitabine
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12. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
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  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Gata-2 overexpression was associated with a low percentage of blasts in BM and males.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

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  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
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13. Petropoulos D, Worth LL, Mullen CA, Madden R, Mahajan A, Choroszy M, Ha CS, Champlin RC, Chan KW: Total body irradiation, fludarabine, melphalan, and allogeneic hematopoietic stem cell transplantation for advanced pediatric hematologic malignancies. Bone Marrow Transplant; 2006 Mar;37(5):463-7
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  • We evaluated the efficacy and toxicity of adding 9 Gy of total body irradiation (TBI), in three single daily fractions of 3 Gy, to the reduced intensity regimen of fludarabine 30 mg/m2 i.v. x 4 days and melphalan 140 mg/m2 i.v. x 1 day in advanced pediatric hematologic malignancies.
  • Twenty-two acute lymphoblastic leukemia (ALL), six acute myeloid leukemia (AML), and one non-Hodgkin lymphoma patients were transplanted.
  • With a median follow-up of 52 months, seven of 22 ALL, five of six AML, and one of one lymphoma patients are alive and in remission.

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  • (PMID = 16435013.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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14. Chou WC, Chen CY, Hou HA, Lin LI, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Tseng MH, Huang CF, Tien HF: Acute myeloid leukemia bearing t(7;11)(p15;p15) is a distinct cytogenetic entity with poor outcome and a distinct mutation profile: comparative analysis of 493 adult patients. Leukemia; 2009 Jul;23(7):1303-10
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  • [Title] Acute myeloid leukemia bearing t(7;11)(p15;p15) is a distinct cytogenetic entity with poor outcome and a distinct mutation profile: comparative analysis of 493 adult patients.
  • Acute myeloid leukemia (AML) with t(7;11)(p15;p15), which results in a NUP98-HOXA9 fusion, is a distinct entity, but this subtype has not been characterized in detail.
  • In a comprehensive study comparing 11 such patients with another 482 adult patients, we found that those with t(7;11) were younger (P=0.0076) and female (P=0.0111), with almost all having the M2-subtype of AML (P<0.0001).
  • Even when those with low-risk karyotypes were excluded, patients with t(7;11) had poorer overall survival than the other AML group (median 13.5 and 20 months, respectively, P=0.045) and poorer relapse-free survival (median 6 and 12 months, respectively, P=0.003).
  • AML with NUP98-HOXA9 fusion therefore appears to have a distinct clinical and biological profile, and should be regarded as a poor prognostic group.
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 7. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic


15. Manola KN, Sambani C, Karakasis D, Kalliakosta G, Harhalakis N, Papaioannou M: Leukemias associated with Turner syndrome: report of three cases and review of the literature. Leuk Res; 2008 Mar;32(3):481-6
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  • Cases of leukemia associated with Turner syndrome (TS) are rare.
  • Here we report three TS patients with leukemia including one case of T-large granular lymphocyte leukemia (T-LGL), one rare case of coexistence of chronic lymphocytic leukemia (CLL) and idiopathic myelofibrosis (IMF) and one case of a patient with AML-M2 who received autologous stem cell transplantation (SCT).
  • T-LGL and coexistence of CLL and IMF associated with TS are reported for the first time while the last case represents the first report of SCT in a leukemia patient with TS.
  • Our cases and the limited data of previously reported leukemia patients with TS suggest that TS is not associated with a specific type of leukemia and that presentation, clinical course and response to treatment are similar to that of the non-TS leukemia patients.
  • Even in cases with no additional chromosome abnormalities, the ratio of X/XX cells in bone marrow cells was significantly increased compared to that in constitutional karyotype, indicating that monosomic cells possibly provide a survival advantage for leukemia cells or that reduced programmed cell death may be responsible for the expansion of the monosomic cells.
  • [MeSH-major] Leukemia / complications. Turner Syndrome / complications
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Large Granular Lymphocytic / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Myeloid, Acute / complications. Middle Aged. Monosomy. Treatment Outcome

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  • (PMID = 17669490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
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16. Øyan AM, Bø TH, Jonassen I, Gjertsen BT, Bruserud Ø, Kalland KH: cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation. Int J Oncol; 2006 May;28(5):1065-80
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  • [Title] cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to biology and clinical course.
  • In an attempt to address this question, we performed cDNA microarray analysis on peripheral blood samples of 25 patients with newly diagnosed AML with high blast counts.
  • Leave-one-out crossvalidation (LOOCV) showed with high accuracy that gene expression classifiers could predict if leukaemia samples belonged to the FAB AML-M1 or to the FAB AML-M2 groups.
  • Except for an accumulation of samples classified as FAB M1 and M2 in cluster 3, there was no evident relationship between the clusters and the FAB classification.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


17. Chen SW, Li CF, Chuang SS, Tzeng CC, Hsieh YC, Lee PS, Chen CH, Huang WT, Hwang WS, Tsao CJ: Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan. Int J Lab Hematol; 2008 Apr;30(2):133-8
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  • [Title] Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan.
  • Aberrant antigen expression in acute myeloid leukemia (AML) has been extensively studied in the West with limited reports from Taiwan.
  • We carried out this retrospective study to characterize the frequency and significance of aberrant antigen expression of AML in Taiwan.
  • Aberrant CD7 expression was observed in all non-AML-M3 subtypes, most frequently in AML-M7 (4/6, 67%); while CD19 expression was only observed in AML-M2 (5/36, 14%).
  • CD56 expression was most common in AML-M5 (4/8, 50%).
  • The relative frequency of CD19 and CD56 expression in AML with t(8;21) was higher than those with other chromosomal abnormalities or normal karyotype (P = 0.011 and 0.005, respectively).
  • In non-M3 AML, aberrant antigen expression was identified in 56/96 (58%) cases, in contrast to 2/15 (13%) AML-M3 cases (P = 0.001).
  • The relative frequency of CD19 and/or CD56 expression in AML with t(8;21) was significantly higher than those without this translocation and co-expression of these two antigens may serve as the surrogate markers for AML with t(8;21).
  • [MeSH-major] Antigens, CD / metabolism. Antigens, CD19 / metabolism. Antigens, CD56 / metabolism. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18333845.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD56
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18. Wang J, Lü S, Yang J, Song X, Chen L, Huang C, Hou J, Zhang W: A homoharringtonine-based induction regimen for the treatment of elderly patients with acute myeloid leukemia: a single center experience from China. J Hematol Oncol; 2009;2:32
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  • [Title] A homoharringtonine-based induction regimen for the treatment of elderly patients with acute myeloid leukemia: a single center experience from China.
  • BACKGROUND AND PURPOSE: The response to remission induction in elderly patients with acute myeloid leukemia (AML) remains poor.
  • The purpose of this paper is to evaluate the efficacy and toxicity of a plant alkaloid, homoharringtonine, in combination with cytarabine as an induction therapy for AML in elderly patients (> or =60 years).
  • RESULTS: Twenty-three patients were treated with the HA regimen consisting of homoharringtonine (2 mg/m2/day for 7 days) and cytarabine (Ara-C, 100 mg/m2/day for 7 days).
  • CONCLUSION: HA is a suitable induction regimen for elderly patients with AML, with relatively low toxicity and reasonable response rate.
  • [MeSH-major] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Harringtonines / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19642997.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 6FG8041S5B / homoharringtonine
  • [Other-IDs] NLM/ PMC2731035
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19. Manzoor NF, Azim S, Fadoo Z: Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2). J Pak Med Assoc; 2010 Nov;60(11):977-9
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  • [Title] Successful management of invasive aspergillosis with voriconazole and amphoteracin B therapy in a patient with acute mycloid leukemia (AML-M2).
  • He was diagnosed with Acute Mycloid Leukemia (AML-M2).
  • This case shows the efficacy and safety of combined antifungal therapy, including voriconazole, for invasive aspergillosis complicating AML.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Leukemia, Myeloid, Acute / microbiology. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 21375212.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; JFU09I87TR / Voriconazole
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20. Frater JL, Hoover RG, Bernreuter K, Batanian JR: Deletion of MYC and presence of double minutes with MYC amplification in a morphologic acute promyelocytic leukemia-like case lacking RARA rearrangement: could early exclusion of double-minute chromosomes be a prognostic factor? Cancer Genet Cytogenet; 2006 Apr 15;166(2):139-45
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  • [Title] Deletion of MYC and presence of double minutes with MYC amplification in a morphologic acute promyelocytic leukemia-like case lacking RARA rearrangement: could early exclusion of double-minute chromosomes be a prognostic factor?
  • Gene amplification on double minutes is rarely found in acute myeloid leukemia (AML) and is often linked to poor prognosis.
  • It is often associated with acute myeloid leukemia with differentiation (AML-M2) and is rarely reported in acute promyelocytic leukemia (APL), which is characterized in the vast majority of cases by the reciprocal t(15;17)(q22;q21) with resultant translation of an abnormal PML-RARA fusion protein.
  • We report on a morphologic APL-like case lacking t(15;17) and the RARA breakpoint and also has the deletion MYC of 8q24 associated with the occurrence of MYC amplification on double-minute chromosomes (dmin).
  • Excessive exclusion of dmin was observed at the initial diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Gene Amplification / genetics. Gene Deletion. Genes, myc / genetics. Leukemia, Promyelocytic, Acute / genetics. Receptors, Retinoic Acid / genetics

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  • (PMID = 16631470.001).
  • [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 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha
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21. Kajiwara R, Goto H, Yokosuka T, Yanagimachi M, Kuroki F, Fujii H, Takahashi H, Yokota S: [Acute appendicitis during bone marrow suppression following chemotherapy for acute leukemia; report of three cases]. Rinsho Ketsueki; 2007 Mar;48(3):223-8
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  • [Title] [Acute appendicitis during bone marrow suppression following chemotherapy for acute leukemia; report of three cases].
  • We report here on the clinical courses of three cases of acute appendicitis during a period of myelosuppression after chemotherapy for acute leukemia.
  • The patients were two boys and one girl with a mean age 11 years (range, 10-12).
  • Two of the patients had acute myeloid leukemia (AML) in subtypes M1 and M2, while the third had acute lymphoblostic leukemia of subtype L1 (FAB classification).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Appendicitis / diagnosis. Appendicitis / etiology. Appendicitis / surgery. Bone Marrow Cells / immunology. Immunosuppression. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Perioperative Care. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Appendectomy. Child. Diagnosis, Differential. Female. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 17441480.001).
  • [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
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22. Saito M, Mori A, Irie T, Tanaka M, Morioka M: [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer]. Rinsho Ketsueki; 2009 Mar;50(3):192-6
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  • [Title] [Therapy-related acute myeloid leukemia with 11q23 abnormality due to paclitaxel coexisting with bone marrow metastasis of breast cancer].
  • Among cases of therapy-related acute myeloid leukemia (t-AML) due to DNA topoisomerase II inhibitors, 11q23 abnormality is often detected.
  • Few studies have reported t-AML due to paclitaxel.
  • In this study, we report a patient who developed t-AML with 11q23 abnormality and bone marrow metastasis after breast cancer treatment with paclitaxel.
  • Weekly therapy with paclitaxel at 80 mg/m2 was administered for 10 weeks (total dose: 1,200 mg), and radiotherapy was performed; thereafter, the extent of bone metastasis increased.
  • Bone marrow aspiration suggested AML (M4) with (11;19)(q23;p13) chromosome abnormalities.
  • Based on the clinical course, t-AML may have developed after paclitaxel therapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Bone Marrow Neoplasms / secondary. Breast Neoplasms / pathology. Chromosome Aberrations / drug effects. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / etiology. Neoplasms, Second Primary. Paclitaxel / adverse effects


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

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  • (PMID = 15674366.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 39
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24. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Liu YR, Shi Y, Dang H, He Q, Lu DP: [Analysis of characteristics of 72 cases of t(8;21) acute myeloid leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):245-8
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  • [Title] [Analysis of characteristics of 72 cases of t(8;21) acute myeloid leukemia].
  • OBJECTIVE: To investigate the laboratorial and clinical characteristics of t(8;21) AML, and to compare the differences between patients with additional chromosomal abnormalities and those without additional aberrations.
  • METHODS: Seventy-two cases of t(8;21) AML were analyzed retrospectively, including features of morphology, initial blood cells, cytogenetic G-banding karyotype, immunophenotype, AML1/ETO fusion gene and clinical outcome.
  • RESULTS: According to FAB classification, there were 65 cases of M2, 5 cases of M4 and 2 of M5.
  • There were no obvious differences between these two groups in their features of age distribution, bone marrow blast cells, Auer rods, eosinophilia, immunophenotype, as well as central nervous system leukemia occurrence and complete remission rate of induction, but a male prevalence and a lower initial WBC were observed in Group B.
  • With a follow up of 1-96 months, the median survival time was much longer in group A (65 months) compared with group B (12 months), but there was no difference between the four main subgroups of group B.
  • CONCLUSION: Additional chromosomal abnormality is an adverse factor for prognosis of t(8;21) AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 15968311.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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25. Hidaka H, Yagasaki H, Takahashi Y, Hama A, Nishio N, Tanaka M, Yoshida N, Villalobos IB, Wang Y, Xu Y, Horibe K, Chen S, Kadomatsu K, Kojima S: Increased midkine gene expression in childhood B-precursor acute lymphoblastic leukemia. Leuk Res; 2007 Aug;31(8):1045-51
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  • [Title] Increased midkine gene expression in childhood B-precursor acute lymphoblastic leukemia.
  • However, expression in acute leukemia has not been clarified.
  • We examined MK gene expression using real-time PCR in 94 children with acute leukemia.
  • MK gene was also overexpressed in more than half of patients with FAB M1 and M2 types of AML.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, B-Cell / genetics. Leukemia, Myeloid / genetics. Neoplasm Proteins / genetics. Nerve Growth Factors / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


26. Lin HR, Wang YZ, Wang DX, Chang Y, Hao L, Qin YZ, Li JL, Li LD, Huang XJ, Liu YR: [Quantitative analysis of dendritic cell subsets in bone marrow of patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Oct;17(5):1249-54
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  • [Title] [Quantitative analysis of dendritic cell subsets in bone marrow of patients with acute myeloid leukemia].
  • In order to study the quantity of dendritic cell (DC) subsets of bone marrow in patients with acute myeloid leukemia (AML), the bone marrow aspirate were collected from 77 newly diagnosed AML patients and from 30 healthy persons.
  • The quantity of DC subsets (myeloid dendritic cells, mDC and plasmacytoid dendritic cells, pDC) were detected by flow cytometry and analysed by 3-color and 4-color cytometric gate.
  • In subtypes of AML-M2, AML-M3 or AML-M4/5, 81.4%, 100% and 42.1% patients showed mDC decrease and 88.4%, 100% and 89.5% patients showed pDC decrease respectively by 4-color cytometric analysis.
  • It is concluded that the 4-color cytometric gate is better method for detection of mDC and pDC from bone marrow of newly diagnosed AML patients as compared with 3-color cytometric gate, the majority of AML patients showed reduction of mDC and pDC.
  • The percentages of patients with mDC normal or mDC increase in AML-M4/5 subtypes are more than that in AML-M2/3 subtypes, while the pDC does not show difference between AML subtypes.

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  • (PMID = 19840461.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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27. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


28. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • The deletion was identified at initial diagnosis in one patient and at relapse in the other two.
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

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  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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29. 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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30. Song KW, Mollee PN, Hogge DE, Gupta V, Barnett MJ, Forrest DL, Lavoie JC, Nevill TJ, Nantel SH, Shepherd JD, Smith CA, Sutherland HJ, Toze CL, Crump M, Keating A: Predictive value of karyotype on outcome of autotransplants for acute myeloid leukemia in second remission. Leuk Lymphoma; 2005 Apr;46(4):525-31
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  • [Title] Predictive value of karyotype on outcome of autotransplants for acute myeloid leukemia in second remission.
  • The impact of karyotype on the outcome of patients who undergo autotransplant for acute myeloid leukemia (AML) in second remission (CR2) has not been explored.
  • We evaluated the outcomes of 40 patients who proceeded to autotransplant for AML in CR2 at 2 centers.
  • High-dose therapy was melphalan 140-160 mg/m2 plus etoposide 60 mg/kg with or without total body irradiation (22), a busulfan-based regimen (17), and cyclophosphamide alone (1).
  • Graft purging did not significantly influence survival outcome (P=0.94), although platelet engraftment was significantly delayed (P=0.02).
  • We conclude that patients with AML in CR2 who undergo autotransplant can have durable remissions and those with a good risk karyotype are the most likely to obtain long-term disease-free survival.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Disease-Free Survival. Female. Humans. Karyotyping. Male. Middle Aged. Predictive Value of Tests. Remission Induction. Retrospective Studies. Risk Factors. Transplantation, Autologous. Treatment Failure. Treatment Outcome. Whole-Body Irradiation

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  • (PMID = 16019480.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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31. de Lima M, Giralt S, Thall PF, de Padua Silva L, Jones RB, Komanduri K, Braun TM, Nguyen HQ, Champlin R, Garcia-Manero G: Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study. Cancer; 2010 Dec 01;116(23):5420-31
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  • [Title] Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study.
  • BACKGROUND: Recurrence is a major cause of treatment failure after allogeneic transplantation for acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), and treatment options are very limited.
  • Azacitidine is a DNA methyltransferase inhibitor with activity in myeloid disease.
  • By using a Bayesian adaptive method to determine the best dose/schedule combination based on time to toxicity, the authors investigated combinations of 5 daily azacitidine doses, 8, 16, 24, 32, and 40 mg/m2, and 4 schedules: 1, 2, 3, or 4 cycles, each with 5 days of drug and 25 days of rest.
  • The optimal combination was 32 mg/m2 given for 4 cycles.
  • CONCLUSIONS: Azacitidine at 32 mg/m2 given for 5 days is safe and can be administered after allogeneic transplant for at least 4 cycles to heavily pretreated AML/MDS patients.
  • [MeSH-major] Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery


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

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  • (PMID = 18206543.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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33. Al-Tonbary Y, Mansour AK, Ghazy H, Elghannam DM, Abd-Elghaffar HA: Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia. Int J Lab Hematol; 2009 Jun;31(3):320-6
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  • [Title] Prognostic significance of foetal-like tyrosine kinase 3 mutation in Egyptian children with acute leukaemia.
  • In children with acute myelogenous leukaemia (AML), internal tandem duplication of the Flt3 gene (Flt3/ITD) was previously reported and correlated to poor prognosis.
  • Limited data are available about childhood acute lymphoblastic leukaemia (ALL).
  • We analysed bone marrow specimens from 55 newly diagnosed acute leukaemia cases including 30 AML and 25 ALL by genomic PCR for the presence of Flt3/ITD and correlated its presence with clinical outcome.
  • Tandem duplication was found in 6/30(20%) AML cases: 2/8 M1, 1/8 M2, 2/6 M3, 1/6 M4 with loss of heterozygosity (LOH) in two cases.
  • Patients with Flt3/ITD appear to be refractory to primary induction therapy, and for those who achieve remission, there is a high rate of relapse and death so there may be an association between this type of mutation and patient outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18336585.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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34. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92
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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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35. Potenza L, Luppi M, Riva G, Morselli M, Ferrari A, Imovilli A, Giacobbi F, Temperani P, Donelli A, Narni F, Torelli G: Isolated extramedullary relapse after autologous bone marrow transplantation for acute myeloid leukemia: case report and review of the literature. Am J Hematol; 2006 Jan;81(1):45-50
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  • [Title] Isolated extramedullary relapse after autologous bone marrow transplantation for acute myeloid leukemia: case report and review of the literature.
  • Isolated extramedullary relapse (IEMR) is a pattern of acute myeloid leukemia (AML) relapse post-allogeneic bone marrow transplantation (alloBMT).
  • We report a case of a woman with M4 AML who experienced IEMR post-autoBMT and review the related literature.
  • The review suggests that an M2 or M4 French-American-British (FAB) phenotype, intermediate cytogenetic risk group, and chromosome 8 abnormalities are more frequently associated with the occurrence of IEMR.
  • When we searched the European Bone Marrow Transplant Registry (EBMTR) database, we found the incidence of IEMR to be statistically greater in alloBMT than in autoBMT (11% vs. 6%; P = 0.02), but no correlations have been found with the conditioning transplant regimen used.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / therapy


36. Gleissner B, Schlenk R, Bornhäuser M, Berdel WE: Gemtuzumab ozogamicin (mylotarg) for the treatment of acute myeloid leukemia--ongoing trials. Onkologie; 2007 Dec;30(12):657-62
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  • [Title] Gemtuzumab ozogamicin (mylotarg) for the treatment of acute myeloid leukemia--ongoing trials.
  • The value of the combination of gemtuzumab ozogamicin (GO) and chemotherapy for the treatment of acute myeloid leukemia (AML) is currently analyzed within clinical trials.
  • GO (6 mg/m2) and standard-dose cytarabine (100 mg/m2) is evaluated for the treatment of newly diagnosed AML in elderly patients in the SAL phase II trial.
  • Preliminary results of the MRC AML15 trial support the application of GO 3 mg/m2 with standard- and high-dose cytarabine and anthracyclines for the treatment of de novo AML.
  • The combination of GO (3 mg/m2) and high-dose cytarabine (3 g/m2) is safe and more effective for the treatment of refractory AML than previous combinations from the AMLSG study group.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Clinical Trials as Topic / trends. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18063879.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 93NS566KF7 / gemtuzumab
  • [Number-of-references] 35
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37. 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


38. 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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39. Zhang XH, Zhang R, Li Y: Granulocytic sarcoma of abdomen in acute myeloid leukemia patient with inv(16) and t(6;17) abnormal chromosome: case report and review of literature. Leuk Res; 2010 Jul;34(7):958-61
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  • [Title] Granulocytic sarcoma of abdomen in acute myeloid leukemia patient with inv(16) and t(6;17) abnormal chromosome: case report and review of literature.
  • Granulocytic sarcoma (GS) is composed of immature granulocytic precursors and is usually found in acute myeloid leukemia (AML) patients with t(8;21).
  • Inv(16) is rarely associated with GS comparing with t(8;21) leukemia.
  • Here we describe an abdominal GS patient in AML-M2 with acquired translocation between chromosomes 6 and 17 and inv (16).
  • Intestine maybe a tissue specific target for the expression of inv(16) leukemia.
  • Complete physical examination and molecular diagnosis are necessary for AML patients to benefit from the diagnosis and therapeutic strategy.
  • [MeSH-major] Abdominal Neoplasms / genetics. Chromosome Inversion. Chromosomes, Human, Pair 16 / ultrastructure. Chromosomes, Human, Pair 17 / ultrastructure. Chromosomes, Human, Pair 6 / ultrastructure. Leukemia, Myeloid, Acute / genetics. Sarcoma, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Humans. Idarubicin / administration & dosage. Male. Remission Induction


40. Ohtake S, Miyawaki S, Kiyoi H, Miyazaki Y, Okumura H, Matsuda S, Nagai T, Kishimoto Y, Okada M, Takahashi M, Handa H, Takeuchi J, Kageyama S, Asou N, Yagasaki F, Maeda Y, Ohnishi K, Naoe T, Ohno R: Randomized trial of response-oriented individualized versus fixed-schedule induction chemotherapy with idarubicin and cytarabine in adult acute myeloid leukemia: the JALSG AML95 study. Int J Hematol; 2010 Mar;91(2):276-83
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  • [Title] Randomized trial of response-oriented individualized versus fixed-schedule induction chemotherapy with idarubicin and cytarabine in adult acute myeloid leukemia: the JALSG AML95 study.
  • A multicenter, prospective, randomized study was conducted to compare a response-oriented individualized remission induction therapy with a standard fixed-schedule induction therapy, using idarubicin (IDR) and cytarabine (Ara-C), in adult patients with acute myeloid leukemia (AML).
  • Newly diagnosed patients with AML of age less than 65 were randomly assigned to receive either of the two schedules.
  • Both groups received IDR (12 mg/m2) for 3 days and Ara-C (100 mg/m2) for 7 days.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Cytarabine / administration & dosage. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy

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  • [Cites] J Clin Oncol. 1986 Dec;4(12):1740-7 [3465875.001]
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  • (PMID = 20054669.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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41. Bhatia S, Krailo MD, Chen Z, Burden L, Askin FB, Dickman PS, Grier HE, Link MP, Meyers PA, Perlman EJ, Rausen AR, Robison LL, Vietti TJ, Miser JS: Therapy-related myelodysplasia and acute myeloid leukemia after Ewing sarcoma and primitive neuroectodermal tumor of bone: A report from the Children's Oncology Group. Blood; 2007 Jan 1;109(1):46-51
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  • [Title] Therapy-related myelodysplasia and acute myeloid leukemia after Ewing sarcoma and primitive neuroectodermal tumor of bone: A report from the Children's Oncology Group.
  • This study describes the magnitude of risk of therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) in 578 individuals diagnosed with Ewing sarcoma and enrolled on Children's Oncology Group therapeutic protocol, INT-0091.
  • Median age at diagnosis of Ewing sarcoma was 12 years, and median length of follow-up, 8 years.
  • Eleven patients developed t-MDS/AML, resulting in a cumulative incidence of 2% at 5 years.
  • While patients treated on regimens A and B were at a low risk for development of t-MDS/AML (cumulative incidence: 0.4% and 0.9% at 5 years, respectively), patients treated on regimen C were at a 16-fold increased risk of developing t-MDS/AML (cumulative incidence: 11% at 5 years), when compared with those treated on regimen A.
  • Increasing exposure to ifosfamide from 90 to 140 g/m2, cyclophosphamide from 9.6 to 17.6 g/m2, and doxorubicin from 375 to 450 mg/m2 increased the risk of t-MDS/AML significantly.


42. Wang Y, Xue Y, Chen S, Wu Y, Pan J, Zhang J, Shen J: [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Feb;27(1):34-7
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  • [Title] [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)].
  • OBJECTIVE: To explore the clinical and laboratory features of 6 cases of acute myeloid leukemia (AML) with t(6;9)(p23;q34).
  • RESULTS: The t(6;9)(p23;q34) was found in all the 6 cases including 4 cases of M2 and 2 cases of M4.
  • Follow-up showed that 3 patients died with a survival time of 3 months, 5 months and 6 months, respectively.
  • AML with t(6;9)(p23;q34) has unique clinical and laboratory features and its prognosis is poor in most cases.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 20140864.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
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43. Cen D, Lü JX, Pei RZ, Tu ZG, Yu XL, Wen YA: [The clinical significance of real-time fluorescence PCR quantification of hepatocyte growth factor mRNA expression in acute leukemia]. Zhonghua Nei Ke Za Zhi; 2008 May;47(5):401-4
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  • [Title] [The clinical significance of real-time fluorescence PCR quantification of hepatocyte growth factor mRNA expression in acute leukemia].
  • OBJECTIVE: To detect quantitatively hepatocyte growth factor (HGF) mRNA expressions of bone marrow mononuclear cells (MNCs) in acute leukemia (AL) and investigate its clinical significance.
  • METHODS: Total mRNA of quantitated bone marrow MNCs isolated from 67 de novo AL cases was extracted and then cDNA was synthesized.
  • RESULTS: Expressions of HGF mRNA in a group of AL were higher significantly than these in a control group (6.936 +/- 1.613, 0.407 +/- 0.170, P < 0.001), but there was similarity between a group of acute myeloid leukemia (AML) and group of acute lymphoblastic leukemia (ALL) (7.127 +/- 1.911, 6.635 +/- 0.934, P > 0.05).
  • In AL subtypes, the expression of M5 (9.998 +/- 1.454) was higher than that of M2, M3, M4, L1, L2 and L3 (P < 0.001), but there were no differences among the latters (P > 0.05).
  • As to AL subtypes, there are no statistically significant differences between AML and ALL as well as between different age and sex.
  • It is suggested that HGF mRNA is a suitable index for AL diagnosis and treatment.
  • [MeSH-major] Hepatocyte Growth Factor / genetics. Leukemia / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Child, Preschool. Female. Fluorescence. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Young Adult

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  • (PMID = 18953951.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 67256-21-7 / Hepatocyte Growth Factor
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44. 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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45. 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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46. Amadori S, Suciu S, Stasi R, Willemze R, Mandelli F, Selleslag D, Denzlinger C, Muus P, Stauder R, Berneman Z, Pruijt J, Nobile F, Cassibba V, Marie JP, Beeldens F, Baila L, Vignetti M, de Witte T: Gemtuzumab ozogamicin (Mylotarg) as single-agent treatment for frail patients 61 years of age and older with acute myeloid leukemia: final results of AML-15B, a phase 2 study of the European Organisation for Research and Treatment of Cancer and Gruppo Italiano Malattie Ematologiche dell'Adulto Leukemia Groups. Leukemia; 2005 Oct;19(10):1768-73
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  • [Title] Gemtuzumab ozogamicin (Mylotarg) as single-agent treatment for frail patients 61 years of age and older with acute myeloid leukemia: final results of AML-15B, a phase 2 study of the European Organisation for Research and Treatment of Cancer and Gruppo Italiano Malattie Ematologiche dell'Adulto Leukemia Groups.
  • The therapeutic activity and toxicity profile of gemtuzumab ozogamicin were assessed in 40 patients >60 years of age with acute myeloid leukemia (AML) who were not considered eligible for conventional chemotherapy because of advanced age or poor performance status.
  • The drug was administered at the dose of 9 mg/m2 as a single 2-h i.v. infusion on days 1 and 15.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Frail Elderly. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Female. Humans. Male. Middle Aged. Remission Induction. Survival Rate

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  • (PMID = 16079891.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5U10-CA11488-29; United States / NCI NIH HHS / CA / 5U10-CA11488-35
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Immunotoxins; 0 / gemtuzumab
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47. Qiu HY, Xue YQ, Zhang J, Dai HP, Pan JL, Wu YF, Chen SN, Wang Y, Shen J, Sun AN, Wu DP: [Establishment and characterization of a new human myeloid leukemia cell line SH-2]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jul;30(7):458-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Establishment and characterization of a new human myeloid leukemia cell line SH-2].
  • OBJECTIVE: To establish and characterize a novel human myeloid leukemia cell line SH-2.
  • METHODS: Bone marrow mononuclear cells (BMMNC) isolated from a AML-M2 patient, who failed to obtain complete remission after chemotherapy and allogenic bone marrow transplantation were passed in a long term IMDM culture medium supplemented with 20% fetal calf serum.
  • A new human myeloid leukemia cell line SH-2 was successfully established with a cytogenetic characteristics of a loss of Y chromosome (-Y), a derivative chromosome 16 resulting from unbalanced translocation between chromosome 16 and 17, monosome 17, trisomy 19 and p53 alteration.
  • SH-2 cells had the basically same morphological, immunophenotypic and cytogenetic features as the patient's leukemia cells did, such as myeloid morphology, an immunophenotype of CD13+, CD33+, CD56+, CD16/56+ and a hypodiploid karyotype of 45, X, -Y, der(16)t(16;17)(q24;ql2), -17, +19, which were gradually decreased and replaced by the near-tetraploid cells with a karyotype of 73-102(80), XX, -Y, -Y, del (q131)x2, der(16)t(16;17)(q24;q12)x2, -17, -17, +19, +19.
  • Short tandem repeat PCR provided powerful evidence for the derivation of SH-2 cell line from the patient's leukemia cells.
  • CONCLUSION: SH-2 is a new myeloid leukemia cell line with a unique biology background, and will provide a useful tool for leukemia research.
  • [MeSH-major] Cell Line, Tumor. Leukemia, Myeloid, Acute / pathology


48. Gozzetti A, Crupi R, Rondoni M, Defina M, Bocchia M, Pietrini A, Raspadori D, Lauria F: A der(1)t(1;21)(p36.3;q22) in a patient with acute myelogenous leukemia M2. Acta Haematol; 2010;124(1):44-5
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  • [Title] A der(1)t(1;21)(p36.3;q22) in a patient with acute myelogenous leukemia M2.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20606416.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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49. Yılmaz M, Vural F, Töbü M, Ertan Y, Büyük F: Hemophagocytic syndrome with erythrocyte phagocytosis by the myeloid precursors in a patient with AML -M2. Turk J Haematol; 2008 Mar 5;25(1):42-4
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  • [Title] Hemophagocytic syndrome with erythrocyte phagocytosis by the myeloid precursors in a patient with AML -M2.
  • [Transliterated title] Myeloid öncül hücreleri ve myeloblastlar tarafından eritroid fagositozu ile seyreden hemopagositik sendromlu AML-M2 olgusu.
  • We present a 73-year-old man with acute myeloblastic leukemia FAB M2 type (AML M2) whose bone marrow histology showed unusual hemophagocytosis by myeloid cells and myeloblasts.

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  • (PMID = 27264149.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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50. Choi Y, Elagib KE, Goldfarb AN: AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein. Crit Rev Eukaryot Gene Expr; 2005;15(3):207-16
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  • [Title] AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein.
  • The chromosomal translocation t(8;21), generating the AML1-ETO fusion protein, is frequently associated with French-American-British (FAB) type M2 acute myeloid leukemia (AML).
  • Several mechanistic models for the role of AML1-ETO in leukemia development have emerged over the last decade.
  • Most of these models have emphasized the capacity of the fusion protein to redirect repressive cofactors, such as histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), to RUNX target genes, thereby reversing the hematopoietic transcriptional program activated by wild-type RUNX1a phenomenon referred to collectively in this review as the "classical" corepressor model.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Animals. Cell Differentiation / genetics. Cells, Cultured. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Erythropoiesis / genetics. GATA1 Transcription Factor / physiology. Histone Deacetylases / genetics. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Signal Transduction / genetics. Translocation, Genetic

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  • (PMID = 16390317.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins, Fusion; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 58
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51. Wang J, Wang T, Li S, Lin L, Gang Y: [Flt-3/ITD mutation in pediatric leukemia and its clinical significance]. Ai Zheng; 2007 Jan;26(1):58-63
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  • [Title] [Flt-3/ITD mutation in pediatric leukemia and its clinical significance].
  • BACKGROUND & OBJECTIVE: Flt-3 internal tandem duplication (Flt-3/ITD) in transmembrane region is the most frequently identified mutation in Flt-3 gene, which is the most frequently happened in acute myeloid leukemia (AML) and correlated to prognosis.
  • This study was to explore the correlation of Flt-3/ITD mutation to the occurrence of pediatric leukemia, and analyze its clinical significance.
  • METHODS: Flt-3/ITD mutation status in bone marrow samples from 302 children with leukemia, including 122 cases of AML, 124 cases of acute lymphoblastic leukemia (ALL), 17 cases of juvenile chronic myelogenous leukemia (JCML), and 39 cases of myelodysplastic syndromes (MDS), were examined by polymerase chain reaction (PCR) and sequencing.
  • RESULTS: Of the 122 AML patients, 98 (80.32%) had Flt-3 gene products in bone marrow.
  • Flt-3/ITD mutation was detected in 21 (17.21%) of the 122 patients; the mutation rates were 42.86% (3/7) in M0, 22.22% (2/9) in M1, 12.90% (4/31) in M2, 44.44% (8/18) in M4, and 15.38% (4/26) in M5.
  • Of the 19 AML patients with Flt3/ITD mutation, the median survival time was 13.5 months (0-47 months), which was significantly shorter than that of the patients without Flt-3/ITD mutation (P<0.05).
  • Chromosome karyotype analysis showed chromosome abnormity, including t(11; 12)(p15; q13), inv16(q21; q23), and t(6; 9)(p23; q23), in 3 AML patients with Flt-3/ITD.
  • CONCLUSIONS: Flt-3/ITD mutations are usually detected in AML, seldom in ALL, not in MDS and JCML.
  • Flt-3/ITD mutation is correlated to AML onset and progress.
  • Flt-3/ITD is a significant marker to analyze AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Base Sequence. Child. Child, Preschool. Chromosome Aberrations. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Infant. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / metabolism. Male. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Prognosis

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  • (PMID = 17222369.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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52. 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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53. 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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54. Wang Q, Harrison JS, Uskokovic M, Kutner A, Studzinski GP: Translational study of vitamin D differentiation therapy of myeloid leukemia: effects of the combination with a p38 MAPK inhibitor and an antioxidant. Leukemia; 2005 Oct;19(10):1812-7
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  • [Title] Translational study of vitamin D differentiation therapy of myeloid leukemia: effects of the combination with a p38 MAPK inhibitor and an antioxidant.
  • Human myeloid leukemia cell lines are induced to terminal differentiation into monocyte lineage by 1,25-dihydroxyvitamin D3 (1,25D3) or its analogs (deltanoids).
  • Our studies suggest that patients with CML or AML subtypes M2 and M4, but not M1, M3 or M4eo, are particularly suitable for this combination therapy.
  • We conclude that the established cell line HL60 presents a good model for some, but not all, subtypes of myeloid leukemia, and that the JNK pathway plays an important role in monocytic differentiation of human leukemic cells ex vivo, as well as in vitro.
  • [MeSH-major] Antioxidants / therapeutic use. Cell Differentiation / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid / drug therapy. Vitamin D / analogs & derivatives. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Calcium / metabolism. Cell Lineage. Drug Therapy, Combination. Female. Humans. Male. Middle Aged. Monocytes / metabolism

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  • (PMID = 16107889.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Enzyme Inhibitors; 1406-16-2 / Vitamin D; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; SY7Q814VUP / Calcium
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55. 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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56. Jiang SH, Shi WY, Liu H, Song GQ, Sun GX, Lu W, Liu DF: [Cytogenetic and clinical study of myeloid leukemia]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2007 Oct;24(5):571-3
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  • [Title] [Cytogenetic and clinical study of myeloid leukemia].
  • OBJECTIVE: To explore the clinical cytogenetic features and prognosis of myeloid leukemia patients.
  • RESULTS: Among 420 patients with acute myeloid leukemia (AML), 223 cases were found to exhibit clonal chromosome abnormalities, accounted for 53.1%.
  • Out of 158 patients with chronic myeloid leukemia (CML), 96.8% (153/158) were found to exhibit clonal chromosome abnormalities.
  • T(9;22) was specifically associated with CML and some cases of M0, M1 and M2.
  • In these myeloid leukemia cases, there were 18 cases (AML 13 cases, CML 15 cases) without clonal chromosome abnormalities, accounted for 3.1% (18/578) and this phenomenon agreed with the diagnose of clinical signs, marrow morphology and immunology incompletely.
  • CONCLUSION: Karyotype analysis was not only helpful to the diagnose and differential diagnose of myeloid leukemia, but also an important standard of the remission, relapse and therapeutic effect of myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology

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  • (PMID = 17922430.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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57. 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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58. Cripe LD, Rader K, Tallman MS, Gordon MS, Paietta E, Bennett J, Neuberg D, Litzow MR, O'brien TE, Rowe JM: Phase II trial of subcutaneous recombinant human interleukin 11 with subcutaneous recombinant human granulocyte-macrophage colony stimulating factor in patients with acute myeloid leukemia (AML) receiving high-dose cytarabine during induction: ECOG 3997. Leuk Res; 2006 Jul;30(7):823-7
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  • [Title] Phase II trial of subcutaneous recombinant human interleukin 11 with subcutaneous recombinant human granulocyte-macrophage colony stimulating factor in patients with acute myeloid leukemia (AML) receiving high-dose cytarabine during induction: ECOG 3997.
  • Randomized trials of substituting high-dose cytarabine (HiDAC) for standard dose cytarabine (SDAC) during induction therapy for newly diagnosed AML have not demonstrated an improvement in the complete remission (CR) rate.
  • Therefore, 34 patients were treated, with newly diagnosed AML less than 56 years of age, with daunorubicin 45 mg/m2 on days 1-3, cytarabine 100mg/m2 days 1-7 and cytarabine 2g/m2 for 12 h on days 8-10 (7+3+3).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Interleukin-11 / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Injections, Subcutaneous. Male. Middle Aged. Recombinant Proteins / administration & dosage. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 16413056.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA11083; United States / NCI NIH HHS / CA / CA13650; United States / NCI NIH HHS / CA / CA14548; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA49883; United States / NCI NIH HHS / CA / CA66636
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL11 protein, human; 0 / Interleukin-11; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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59. Silverman LR, McKenzie DR, Peterson BL, Holland JF, Backstrom JT, Beach CL, Larson RA, Cancer and Leukemia Group B: Further analysis of trials with azacitidine in patients with myelodysplastic syndrome: studies 8421, 8921, and 9221 by the Cancer and Leukemia Group B. J Clin Oncol; 2006 Aug 20;24(24):3895-903
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  • [Title] Further analysis of trials with azacitidine in patients with myelodysplastic syndrome: studies 8421, 8921, and 9221 by the Cancer and Leukemia Group B.
  • We report the combined results of three previously reported clinical trials (n = 309) with azacitidine using the WHO classification system for MDS and acute myeloid leukemia (AML) and IWG criteria for response.
  • PATIENTS AND METHODS: Data from three sequential Cancer and Leukemia Group B trials with azacitidine were recollected and reanalyzed as part of the New Drug Application process.
  • The trials were conducted with either intravenous or subcutaneous azacitidine (75 mg/m2/d for 7 days every 28 days).
  • Using current WHO criteria, 103 patients had AML at baseline; 35% to 48% had HI or better responses.
  • The median survival time for the 27 AML patients randomly assigned to azacitidine was 19.3 months compared with 12.9 months for the 25 patients assigned to observation.

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  • (PMID = 16921040.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA02599; United States / NCI NIH HHS / CA / CA03927; United States / NCI NIH HHS / CA / CA04326; United States / NCI NIH HHS / CA / CA04457; United States / NCI NIH HHS / CA / CA07968; United States / NCI NIH HHS / CA / CA08025; United States / NCI NIH HHS / CA / CA11789; United States / NCI NIH HHS / CA / CA12046; United States / NCI NIH HHS / CA / CA12449; United States / NCI NIH HHS / CA / CA16450; United States / NCI NIH HHS / CA / CA21060; United States / NCI NIH HHS / CA / CA26806; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA31983; United States / NCI NIH HHS / CA / CA32291; United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / CA35279; United States / NCI NIH HHS / CA / CA37135; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / CA47545; United States / NCI NIH HHS / CA / CA47555; United States / NCI NIH HHS / CA / CA47559; United States / NCI NIH HHS / CA / CA47577; United States / NCI NIH HHS / CA / CA47642; United States / NCI NIH HHS / CA / CA52784; United States / NCI NIH HHS / CA / CA60138; United States / NCI NIH HHS / CA / CA77406; United States / NCI NIH HHS / CA / CA77440
  • [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 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
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60. Manvelyan M, Kempf P, Weise A, Mrasek K, Heller A, Lier A, Höffken K, Fricke HJ, Sayer HG, Liehr T, Mkrtchyan H: Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics. Int J Mol Med; 2009 Sep;24(3):335-41
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  • [Title] Preferred co-localization of chromosome 8 and 21 in myeloid bone marrow cells detected by three dimensional molecular cytogenetics.
  • In this study, BM of three secondary acute myelogenous leukemia (AML) cases with trisomy 8 and otherwise normal karyotype were evaluated.
  • Bone marrow cells of one AML and one ALL (acute lymphoblastic leukemia) case, peripheral blood lymphocytes and human sperm, all of them with normal karyotype, served as controls.
  • Interestingly, in myeloid bone marrow cells chromosomes 8 (di- and trisomic) and 21 tended to co-localize with their homologue chromosome(s), rather than to be separated.
  • Thus, the co-localization of chromosomes 8 and 21 might promote a translocation providing a selective advantage of t(8;21) cells in AML-M2.
  • [MeSH-major] Bone Marrow Cells / metabolism. Chromosomes, Human, Pair 21 / metabolism. Chromosomes, Human, Pair 8 / metabolism. Cytogenetic Analysis / methods. Myeloid Cells / metabolism

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  • (PMID = 19639225.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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61. Hashmi KU, Khan B, Ahmed P, Raza S, Hussain I, Mahmood A, Iqbal H, Malik HS, Anwar M: FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study. J Pak Med Assoc; 2005 Jun;55(6):234-8
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  • [Title] FLAG-IDA in the treatment of refractory/relapsed acute leukaemias: single centre study.
  • OBJECTIVE: To evaluate the efficacy and toxicity profile of the combination of fludarabine, high dose cytarabine, idarubicin, and granulocyte colony stimulating factor in refractory relapsed cases of acute leukaemia, a study is being conducted at Armed Forces Bone Marrow Transplant Centre (AFBMTC) Rawalpindi since January 2003.
  • METHODS: Twelve Patients with refractory/relapsed (Ref/Rel) acute leukaemia (AL) were treated with fludarabine 30 mg/m2 and cytosine arabinoside (AraC) Arac 2 g/m2 for 5 days, idarubicin 10 mg/m2 for 3 days, and granulocyte colony stimulating factor G-CSF 5 micro g/kg from day 0 till neutrophil recovery (ANC > 1.0 x 10(9)/1).
  • RESULTS: Patients included were refractory acute lymphoblastic leukaemia (ALL) (n=2), relapsed ALL (n = 3), refractory acute myeloid leukaemia (AML) (n = 3), secondary AML (n=2) relapsed AML (n = 1) and acute undifferentiated leukaemia (AUL) (n = 1).
  • CONCLUSION: In our experience, FLAG-IDA is well tolerated and effective regimen in relapsed/refractory acute leukaemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Child. Cytarabine / therapeutic use. Female. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Idarubicin / therapeutic use. Male. Middle Aged. Recurrence

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  • (PMID = 16045091.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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62. Kornblau SM, Banker DE, Stirewalt D, Shen D, Lemker E, Verstovsek S, Estrov Z, Faderl S, Cortes J, Beran M, Jackson CE, Chen W, Estey E, Appelbaum FR: Blockade of adaptive defensive changes in cholesterol uptake and synthesis in AML by the addition of pravastatin to idarubicin + high-dose Ara-C: a phase 1 study. Blood; 2007 Apr 1;109(7):2999-3006
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  • [Title] Blockade of adaptive defensive changes in cholesterol uptake and synthesis in AML by the addition of pravastatin to idarubicin + high-dose Ara-C: a phase 1 study.
  • Following exposure to cytotoxic agents, acute myeloid leukemia (AML) blasts elevate cellular cholesterol in a defensive adaptation that increases chemoresistance, but blockade of HMG-CoA reductase with statins restores chemosensitivity in vitro.
  • This phase 1 study evaluated adding pravastatin (PV) (40-1680 mg/day, days 1-8) to idarubicin (Ida) ([12 mg/ (M2 x day), days 4-6]) + high-dose cytarabine (Ara-C;.
  • HDAC) [1.5 g/(M2 x day) by CI, days 4-7] in 15 newly diagnosed and 22 salvage patients with unfavorable (n = 26) or intermediate (n = 10) prognosis cytogenetics.
  • Addition of PV to Ida-HDAC was safe, and the encouraging response rates support conducting further trials evaluating the effect of cholesterol modulation on response in AML.

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  • (PMID = 17158228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA115044; United States / NCI NIH HHS / CA / R21 CA-115044
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 04079A1RDZ / Cytarabine; 97C5T2UQ7J / Cholesterol; KXO2KT9N0G / Pravastatin; ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ PMC1852228
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63. 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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  • (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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64. Shman TV, Belevtsev MV, Buglova SE: [Drug sensitivity of tumor cells in varieties of acute childhood leukemia]. Vopr Onkol; 2005;51(5):558-62
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  • [Title] [Drug sensitivity of tumor cells in varieties of acute childhood leukemia].
  • Drug sensitivity of tumor cells was studied in 154 children diagnosed with acute leukemia.
  • Cellular sensitivity in acute lymphoblastic leukemia (ALL) was higher than in acute myeloid one (AML), while T-line ALL cells were more sensitive to dexamethasone than those of B-line.
  • Among AML cells, M3 variant was less sensitive to cytozar while M4 - to vepeside.
  • Reduced sensitivity to vincristine was found in series M3 > M1 - M2 > M4 while that to L-asparaginase was in M1- M2 > M4 > M3.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16756010.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7006-34-0 / Asparagine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone
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65. 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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66. Kaspers GJ, Reinhardt D, Fleischhack G, Armendariz H, Stark B, Zwaan CM, Zimmermann M, Creutzig U: Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML. Pediatr Blood Cancer; 2006 Oct 15;47(5):539-42
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  • [Title] Low efficacy of methotrexate in childhood acute myeloid leukemia (AML): single-agent therapeutic window study in relapsed AML.
  • BACKGROUND: The efficacy in pediatric acute myeloid leukemia (AML) of single-agent methotrexate (MTX) at a higher dose than previously applied, 1,000 mg/m2, given as a theoretically beneficial 36-hr continuous infusion, is unknown, but may be beneficial based on preclinical data.
  • PROCEDURE: We performed a therapeutic window study in children with first relapsed AML treated in four different countries.
  • By that time, another four patients had been enrolled, of which one patient with a late relapsed AML FAB type M7 showed a good response.
  • CONCLUSIONS: This study shows that single-agent MTX in the applied regimen in pediatric relapsed AML has limited efficacy.
  • However, it also demonstrates the feasibility of an international and therapeutic window phase II study in pediatric relapsed AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methotrexate / therapeutic use


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

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  • (PMID = 17284535.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096735; United States / NCI NIH HHS / CA / CA96735
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CDKN1A protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1885483
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68. 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


69. 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.
  • A 58-year-old woman presented with a 3-day history of fever and abdominal pain.
  • 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


70. Hiçsönmez G: The effect of steroid on myeloid leukemic cells: the potential of short-course high-dose methylprednisolone treatment in inducing differentiation, apoptosis and in stimulating myelopoiesis. Leuk Res; 2006 Jan;30(1):60-8
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  • [Title] The effect of steroid on myeloid leukemic cells: the potential of short-course high-dose methylprednisolone treatment in inducing differentiation, apoptosis and in stimulating myelopoiesis.
  • Several in vitro studies have shown that dexamethasone (Dex) and prednisolone can induce differentiation of some mouse and human myeloid leukemic cells to macrophages and granulocytes.
  • Based on in vitro experiments, we have shown that short-course (3-7 days) high-dose methylprednisolone (HDMP) (20-30 mg/kg/day) treatment can induce differentiation of myeloid leukemic cells in vivo in children with different subtypes of acute myeloblastic leukemia (AML) (AML-M1, -M2, -M3, -M4, -M7).
  • We have also shown that induction of apoptosis of myeloid leukemic cells with or without differentiation is possible by short-course HDMP treatment.
  • Addition of HDMP to mild cytotoxic chemotherapy (low-dose cytosine arabinoside (LD-Ara-c), weekly mitoxantrone and Ara-c or 6-thioguanine) increased the remission rate (87-89%) and improved the outcome of AML children.
  • We believe that the results of our 17-year clinical experience will provide important benefits to AML patients.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Apoptosis / drug effects. Cell Differentiation / drug effects. Leukemia, Myeloid, Acute / metabolism. Methylprednisolone / pharmacology. Myelopoiesis / drug effects

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  • (PMID = 15979702.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antigens, CD34; X4W7ZR7023 / Methylprednisolone
  • [Number-of-references] 111
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71. Bug G, Atta J, Klein SA, Hertenstein B, Bergmann L, Boehrer S, Mousset S, Hoelzer D, Martin H: High-dose melphalan is an effective salvage therapy in acute myeloid leukaemia patients with refractory relapse and relapse after autologous stem cell transplantation. Ann Hematol; 2005 Oct;84(11):748-54
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  • [Title] High-dose melphalan is an effective salvage therapy in acute myeloid leukaemia patients with refractory relapse and relapse after autologous stem cell transplantation.
  • In a pilot study high-dose melphalan (HD-Mel, 200 mg/m2) and autologous stem cell transplantation (ASCT) were administered to 14 patients (median age 52, range 29-60 years) with acute myeloid leukaemia (AML) in first relapse after a previous ASCT in first complete remission (n=11) or chemotherapy (n=3).
  • Our results highly encourage to further investigate HD-Mel and ASCT as a promising salvage regimen for relapsed AML patients for whom autologous peripheral blood stem cells are available.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Melphalan / therapeutic use. Salvage Therapy / methods. Stem Cell Transplantation

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  • (PMID = 16001243.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
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72. Faderl S, Verstovsek S, Cortes J, Ravandi F, Beran M, Garcia-Manero G, Ferrajoli A, Estrov Z, O'Brien S, Koller C, Giles FJ, Wierda W, Kwari M, Kantarjian HM: Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older. Blood; 2006 Jul 1;108(1):45-51
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  • [Title] Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older.
  • Outcome of patients with acute myeloid leukemia (AML) who are older than 60 years of age remains unsatisfactory, with low remission rates and poor overall survival.
  • We have previously established the activity of clofarabine plus cytarabine in AML relapse.
  • We have now conducted a phase 2 study of clofarabine plus cytarabine in patients aged 50 years or older with previously untreated AML.
  • Clofarabine was given at 40 mg/m2 as a 1-hour intravenous infusion for 5 days (days 2 to 6) followed 4 hours later by cytarabine at 1 g/m2/d as a 2-hour intravenous infusion for 5 days (days 1 to 5).
  • Of 60 patients, 29 (48%) had secondary AML, 30 (50%) had abnormal karyotypes (monosomy 5 and/or 7 in 15 [25%]), and 11 (21%) showed FLT3 abnormalities.
  • Clofarabine plus cytarabine has activity in adult AML, achieving a good CR rate.
  • Modifications of this combination in AML therapy of older patients warrant further evaluation.
  • [MeSH-major] Adenine Nucleotides / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Chromosome Aberrations. Drug Administration Schedule. Humans. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome


73. Marisavljevic D, Markovic O, Zivkovic R: An unusual case of smoldering AML with prolonged indolent clinical course and spontaneous remission in the terminal phase. Med Oncol; 2009 Dec;26(4):476-9
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  • [Title] An unusual case of smoldering AML with prolonged indolent clinical course and spontaneous remission in the terminal phase.
  • An unusual case of acute myeloblastic leukemia (AML) with indolent clinical course and spontaneous remission in the terminal phase is described.
  • A 63-year-old male has been diagnosed to suffer from AML, subtype M2.
  • Clinical course was slowly progressive ("smoldering" AML).
  • Five years from diagnosis patient exhibited spontaneous remission of the disease, accompanied with disappearance of del(6q) clone.
  • Additional curiosity in this case is the fact that patient's older brother died of acute lymphoblastic leukemia at the age of 71 years.
  • Possible mechanisms of spontaneous remission of AML and genetic predisposition for human leukemia are discussed with a review of the literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Neoplasm Recurrence, Local / pathology. Neoplasm Regression, Spontaneous

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  • (PMID = 19130323.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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74. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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75. 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


76. Kanemura N, Tsurumi H, Kasahara S, Hara T, Yamada T, Sawada M, Goto N, Kitagawa J, Shimizu M, Oyama M, Moriwaki H: Continuous drip infusion of low dose cytarabine and etoposide with granulocyte colony-stimulating factor for elderly patients with acute myeloid leukaemia ineligible for intensive chemotherapy. Hematol Oncol; 2008 Mar;26(1):33-8
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  • [Title] Continuous drip infusion of low dose cytarabine and etoposide with granulocyte colony-stimulating factor for elderly patients with acute myeloid leukaemia ineligible for intensive chemotherapy.
  • BACKGROUNDS AND OBJECTIVES: The optimal strategy for the management of elderly patients with acute myeloid leukaemia (AML) is still controversial.
  • We previously reported the effectiveness of low dose cytarabine (Ara-C) and etoposide (VP-16) (AV therapy) for those elderly AML patients ineligible for intensive chemotherapy.
  • PATIENTS AND METHODS: The eligibility for enrolment was AML patients according to the World Health Organization (WHO) criteria who were over 60 years of age and who had difficulty in tolerating intensive chemotherapy due to their poor performance status (PS) or some comorbidities.
  • They were given continuous drip infusion of Ara-C (20 mg/body) and VP-16 (50 mg/body) for 7-14 days, and were also simultaneously administered G-CSF (150 microg/m2) once daily.
  • CONCLUSION: AVG therapy was therefore found to be an effective and well-tolerated regimen for remission induction in elderly AML patients with poor PS or comorbidity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Monocytic, Acute / drug therapy

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  • (PMID = 17918772.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide
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77. Ruan GR, Li JL, Qin YZ, Li LD, Xie M, Chang Y, Zhang Y, Liu YR, Jiang B, Chen SS, Huang XJ: Nucleophosmin mutations in Chinese adults with acute myelogenous leukemia. Ann Hematol; 2009 Feb;88(2):159-66
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  • [Title] Nucleophosmin mutations in Chinese adults with acute myelogenous leukemia.
  • Recently, mutations in the nucleophosmin (NPM1) gene were detected in 50-60% of adult acute myelogenous leukemia (AML) patients, mainly with a normal karyotype.
  • In this study, we detected typical NPM1 mutations (types A, B, D) in untreated Chinese AML patients using real-time quantitative polymerase chain reaction (RQ-PCR) followed by sequence analysis.
  • The detection rate of NPM1 mutations in 220 AML patients was 16.4%, including 107 (14.2%) with the French-American-British (FAB) subtype M2, 43 (2.3%) with M3, and 52 (30.8%) with M4/M5.
  • Sequence analysis revealed that all the 36 positive cases were heterozygous for the mutation with 4-bp insertions at nt 959; the 36 cases included 29 (80.6%) cases with type A, four (11.1%) cases with type B, and one rare DD-3 mutation.
  • We also detected two new mutations, namely, CTCG and CAAG insertions, named BJ-01 and BJ-02, respectively.
  • The results demonstrated that RQ-PCR was a reliable and sensitive method for detecting NPM1 mutations, for screening AML, and for the quantitative analysis of minimal residual diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics


78. 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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79. Graf M, Reif S, Hecht K, Kroell T, Nuessler V, Schmetzer H: Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies. Eur J Haematol; 2005 Dec;75(6):477-84
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  • [Title] Expression of poliovirus receptor-related proteins PRR1 and PRR2 in acute myeloid leukemia: first report of surface marker analysis, contribution to diagnosis, prognosis and implications for future therapeutical strategies.
  • There is evidence to suggest, that those receptors could have a role in leukemia.
  • We have studied the expression of PRR molecules PRR1 and PRR2 on mononuclear bone marrow (BM) cells of 55 patients with acute myeloid leukemia (AML) at first diagnosis by FACS-analysis using directly Phycoerythrin-labeled markers (PRR1 clone R1.302.12; PRR2 clone R2.477.1) in combination with other Fluorescein conjugated antibodies to evaluate the blast phenotype in AML.
  • We could demonstrate, that on average 35% PRR1(+) or 45% PRR2(+) cells in AML were found.
  • Within FAB-types we observed a high PRR1 expression in cases with M3 and M4 and lowest expressions in M0 and M5; a high PRR2 expression was found in cases with M3, M4, M5 and M1 and lowest expressions in M0 and M2.
  • Moreover cut-off-values with a maximum probability for a significant differentiation between cases with higher or lower levels of these markers could be found: cases with >78% PRR1(+) and cases with >77% PRR2(+) cells were characterized by a tendency for longer relapse free survival times.
  • Qui-square analyses showed, that 3 of 4 cases with FAB-type M3 (P = 0.03) or a favorable karyotype (P = 0.04) were found in the group with >7% PRR1(+) cells, due to only few cases available a similar correlation, however, could not be found in cases with >78% PRR2(+) cells.
  • We can conclude, that blasts in AML regularly express PRR1 and PRR2.
  • Cases with a high expression of PRR1 or PRR2 are characterized by a more favorable prognosis.
  • [MeSH-major] Biomarkers, Tumor. Cell Adhesion Molecules. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Membrane Glycoproteins

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  • (PMID = 16313259.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / Membrane Glycoproteins; 0 / nectins
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80. Erikci AA, Ozturk A, Tekgunduz E, Sayan O: Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine. Clin Lymphoma Myeloma; 2009 Aug;9(4):E14-5
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  • [Title] Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine.
  • BACKGROUND: The association of acute leukemia and multiple myeloma (MM) has been usually described not only as a complication of chemotherapy but also in the absence of chemotherapy or together at the time of diagnosis.
  • Such leukemias are typically acute myeloid leukemia (AML).
  • CASE REPORT: We report a case of a 68-year-old female who developed AML 2 years after the diagnosis of light chain (kappa) myeloma.
  • The patient was treated with an anthracycline-lacking therapy consisting of etoposide 120 mg/m2, thioguanine 100 mg/m2 orally twice daily on 1-5 days, and cytarabine 40 mg/m2 subcutaneously on day 1 (ETC) because of poor cardiac performance.
  • This therapy might be a safe alternative in secondary leukemia especially for elderly patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Etoposide / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Multiple Myeloma / drug therapy. Thioguanine / therapeutic use


81. Zhu X, Ma Y, Liu D: Novel agents and regimens for acute myeloid leukemia: 2009 ASH annual meeting highlights. J Hematol Oncol; 2010;3:17
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  • [Title] Novel agents and regimens for acute myeloid leukemia: 2009 ASH annual meeting highlights.
  • Prognostic markers, such as NPM1, Flt3-ITD, and cytogenetic abnormalities have made it possible to formulate aggressive treatment plans for unfavorable acute myeloid leukemia (AML).
  • However, the long-term survival of AML with unfavorable factors remains unsatisfactory.
  • The latest data indicate that the standard dose of daunorubicin (DNR) at 45 mg/m2 is inferior to high dose 90 mg/m2 for induction therapy.
  • New agents, including the nucleoside analogues (clofarabine, sapacitabine, elacytarabine), FLT3 inhibitor (sorafenib), farnesyl-transferase inhibitor (tipifarnib), histone deacetylase inhibitor (vorinostat), lenalidomide, as well as DNA methyltransferase inhibitors (decitabine, azacitidine), were recently reported for AML treatment in the 2009 ASH annual meeting.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy


82. 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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83. Jung SH, Kim HC, Yu CS, Kim JC: Solitary preleukemic granulocytic sarcoma as a cause of small bowel obstruction. Gut Liver; 2007 Jun;1(1):82-6
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  • [Title] Solitary preleukemic granulocytic sarcoma as a cause of small bowel obstruction.
  • Granulocytic sarcoma is an extramedullary tumor composed of immature granulocytic cells.
  • These tumors usually occur simultaneously with or follow after the onset of acute myeloid leukemia (AML) or other myeloproliferative disorders.
  • Rarely, it is the first manifestation of AML which appears several months before the onset of leukemia.
  • Immunohistochemical studies showed that the neoplastic cells were of myeloid lineage positive for myeloperoxidase and leukocyte common antigen, but negative for CD3, 20, 56, 79a, and cytokeratin.
  • Initially, there was no evidence of blood or bone marrow involvement suggesting acute leukemia or other myeloproliferative disorders.
  • The findings were consistent with the diagnostic findings of solitary granulocytic sarcoma (preleukemic).
  • Sequentially, the patient developed FAB M2 acute myeloid leukemia.

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  • (PMID = 20485664.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2871656
  • [Keywords] NOTNLM ; Acute myeloid leukemia / Granulocytic sarcoma / Small bowel obstruction
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84. Jin J, Jiang DZ, Mai WY, Meng HT, Qian WB, Tong HY, Huang J, Mao LP, Tong Y, Wang L, Chen ZM, Xu WL: Homoharringtonine in combination with cytarabine and aclarubicin resulted in high complete remission rate after the first induction therapy in patients with de novo acute myeloid leukemia. Leukemia; 2006 Aug;20(8):1361-7
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  • [Title] Homoharringtonine in combination with cytarabine and aclarubicin resulted in high complete remission rate after the first induction therapy in patients with de novo acute myeloid leukemia.
  • To assess the efficacy and toxicity of HAA regimen (homoharritonine 4 mg/m2/day, days 1-3; cytarabine 150 mg/m2/day, days 1-7; aclarubicin 12 mg/m2/day, days 1-7) as an induction therapy in the treatment of de novo acute myeloid leukemia (AML), 48 patients with newly diagnosed AML, aged 35 (14-57) years, were entered into this clinical study.
  • This study suggested that HAA regimen might be a well-tolerable, effective induction regimen in young adult patients with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 16791270.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 6FG8041S5B / homoharringtonine; 74KXF8I502 / Aclarubicin
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85. Anwar Iqbal M, Al-Omar HM, Owaidah T, Al-Humaidan H, Bhuiyan ZA, Sahovic E: del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality. Eur J Haematol; 2006 Sep;77(3):245-50
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  • [Title] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.
  • OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.
  • In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.
  • RESULTS: A diagnosis of AML-M2 was confirmed in both patients by morphological and immunophenotyping studies.
  • CONCLUSION: To our knowledge, deletion 6p23 as a sole primary abnormality was reported in only one case.
  • The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16856925.001).
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins
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86. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
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87. Liu H, Qian WB, Mai WY, Meng HT, Tong HY, Tong Y, Mao LP, Huang J, Wang L, Jiang DZ, Jin J: [HAA regimen as induction chemotherapy for newly diagnosed acute myelogenous leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2008 Jan;29(1):9-12
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  • [Title] [HAA regimen as induction chemotherapy for newly diagnosed acute myelogenous leukemia].
  • OBJECTIVE: To analyse the outcome of newly diagnosed adult acute myeloid leukemia (AML) patients treated with HAA (homoharringtonine, cytarabine and aclarubicin) regimen and explore the efficacy and safety of this regimen.
  • Kaplan-Meier method was used to estimate relapse free survival (RFS) rate and the differences were compared with 2-sided log-rank test.
  • For the AML-M5 and AML-M /M2 patients the CR rate was 74% and 87% and 3 year RFS of CR patients was 75% and 37%, respectively.
  • CONCLUSION: HAA regimen is a safe, efficacious, and well-tolerable induction therapy for newly diagnosed AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18512308.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Harringtonines; 04079A1RDZ / Cytarabine; 6FG8041S5B / homoharringtonine; 74KXF8I502 / Aclarubicin
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88. Dai H, Xue Y, Pan J, Wu Y, Wang Y, Shen J, Zhang J: Two novel translocations disrupt the RUNX1 gene in acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):120-4
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  • [Title] Two novel translocations disrupt the RUNX1 gene in acute myeloid leukemia.
  • Translocations involving 21q22 are commonly observed in both de novo and therapy-related acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Here we report two novel translocations involving the RUNX1 gene: t(1;21)(q12;q22) in a 53-year-old woman with AML-M5b and t(11;21)(q13;q22) in a 65-year-old man with AML-M2.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic


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

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  • (PMID = 19465351.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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90. Mori M, Ohta M, Miyata A, Higashihara M, Oshimi K, Kimura H, Yagasaki F, Sunami K: Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG). Leuk Lymphoma; 2006 Oct;47(10):2062-9
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  • [Title] Treatment of acute myeloid leukemia patients aged more than 75 years: results of the E-AML-01 trial of the Japanese Elderly Leukemia and Lymphoma Study Group (JELLSG).
  • The feasibility and effects of combination chemotherapy for very elderly patients with acute myeloid leukemia was examined in 65 patients (including previous myelodysplastic syndrome) aged 76 years or morewith a performance status of 0 - 3.
  • Induction chemotherapy was performed with 30 mg/m2 daunorubicin on days 1 - 3, 150 mg/m2 behenoyl cytosine arabinoside on days 1 - 7, and 70 mg/m2 6-mercaptopurine with 300 mg allopurinol taken orally on days 1 - 7 (BHAC-DM).
  • BHAC-DM is feasible and effective for selected very elderly acute myeloid leukemia patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy

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  • (PMID = 17071477.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 9YVR68W306 / enocitabine
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91. Hegenbart U, Niederwieser D, Sandmaier BM, Maris MB, Shizuru JA, Greinix H, Cordonnier C, Rio B, Gratwohl A, Lange T, Al-Ali H, Storer B, Maloney D, McSweeney P, Chauncey T, Agura E, Bruno B, Maziarz RT, Petersen F, Storb R: Treatment for acute myelogenous leukemia by low-dose, total-body, irradiation-based conditioning and hematopoietic cell transplantation from related and unrelated donors. J Clin Oncol; 2006 Jan 20;24(3):444-53
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  • [Title] Treatment for acute myelogenous leukemia by low-dose, total-body, irradiation-based conditioning and hematopoietic cell transplantation from related and unrelated donors.
  • The study reported here assessed outcomes for patients with acute myeloid leukemia (AML) in different stages of their disease, who were not considered candidates for conventional hematopoietic cell transplantation (HCT) because of age and/or other known risk factors and were given minimal conditioning followed by HCT from related or unrelated donors.
  • PATIENTS AND METHODS: The present study included 122 patients with AML, who were conditioned with 2 Gy total-body irradiation (TBI) on day 0 with or without preceding fludarabine (30 mg/m2/d from days -4 to -2), and given postgrafting cyclosporine at 6.25 mg/kg twice daily from day -3 and mycophenolate mofetil at 15 mg/kg twice daily from day 0.
  • Cumulative incidences of acute graft-versus-host disease grades 2 to 4 at 6 months were 35% after related and 42% after unrelated HCT, respectively.
  • With a median follow-up of 44 months (range, 26 to 79 months), 51 patients were alive, of whom 48 were in complete remission (CR).
  • CONCLUSION: We conclude that HCT from related and unrelated donors after low-dose TBI is a promising treatment for elderly patients with AML.


92. Kelly J, Foot NJ, Conneally E, Enright H, Humphreys M, Saunders K, Neat MJ: 3'CBFbeta deletion associated with inv(16) in acute myeloid leukemia. Cancer Genet Cytogenet; 2005 Oct 15;162(2):122-6
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  • [Title] 3'CBFbeta deletion associated with inv(16) in acute myeloid leukemia.
  • Recent reports have shown that concomitant submicroscopic deletions can occur in association with chromosomal translocations/inversions in several leukemia subtypes.
  • Detectable by fluorescence in situ hybridization (FISH), these losses of sequence include deletion of the 5' region of the ABL gene and the 3' region of BCR in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), as well as the 5' region of ETO in acute myeloid leukemia (AML) French-American-British type M2 associated with t(8;21), 3'MLL in AML and ALL, and 3' core-binding factor beta (CBFbeta) in AML associated with inv(16).
  • We analyzed a series of 39 patients diagnosed with AML who had cytogenetically detectable inv(16)/t(16;16) by using a FISH probe for the CBFbeta region to determine the incidence of the 3'CBFbeta deletion.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 16. Core Binding Factor beta Subunit / genetics. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Chromosome Deletion. Female. Humans. In Situ Hybridization, Fluorescence. Male

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  • (PMID = 16213359.001).
  • [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 / CBFB protein, human; 0 / Core Binding Factor beta Subunit
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93. Minderman H, O'Loughlin KL, Smith PF, Pendyala L, Greco WR, Sweeney KG, Ford LA, Wetzler M, Baer MR: Sequential administration of irinotecan and cytarabine in the treatment of relapsed and refractory acute myeloid leukemia. Cancer Chemother Pharmacol; 2006 Jan;57(1):73-83
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  • [Title] Sequential administration of irinotecan and cytarabine in the treatment of relapsed and refractory acute myeloid leukemia.
  • PURPOSE: Based on reported synergy of the topoisomerase-I (topo-I) inhibitor irinotecan with antimetabolites, irinotecan and cytarabine (Ara-C) were administered sequentially to patients with acute myeloid leukemia (AML) refractory to or relapsed following high-dose Ara-C and anthracycline therapy.
  • EXPERIMENTAL DESIGN: In vitro synergy of irinotecan followed by Ara-C was confirmed in a human AML cell line as a basis for the clinical trial.
  • Irinotecan was administered daily for 5 days, with Ara-C 1 g/m2 12 h after each irinotecan dose.
  • Irinotecan was initiated at 5 mg/m2, and the dose was escalated by 5 mg/m2 increments in cohorts of three patients and in individual patients.
  • RESULTS: The irinotecan dose reached 15 mg/m2 in three-patient cohorts without reaching the maximum tolerated dose, and reached 30 mg/m2 in individual patients.
  • This combination is active in refractory AML and warrants further study.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Camptothecin / pharmacokinetics. Camptothecin / therapeutic use. Cytarabine / administration & dosage. Cytarabine / adverse effects. Cytarabine / pharmacokinetics. Cytarabine / therapeutic use. DNA Damage. DNA Topoisomerases, Type I / metabolism. DNA, Neoplasm / biosynthesis. Dose-Response Relationship, Drug. Drug Synergism. Female. HL-60 Cells. Humans. Male. Middle Aged. Recurrence

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  • (PMID = 16010591.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 89938; United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 04079A1RDZ / Cytarabine; 7673326042 / irinotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I; XT3Z54Z28A / Camptothecin
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94. 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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95. Cassileth PA, Lee SJ, Litzow MR, Miller KB, Stadtmauer EA, Tallman MS, Lazarus HM, Bennett JM, Paietta E, Dewald GW, Rowe JM, Eastern Cooperative Oncology Group: Intensified induction chemotherapy in adult acute myeloid leukemia followed by high-dose chemotherapy and autologous peripheral blood stem cell transplantation: an Eastern Cooperative Oncology Group trial (E4995). Leuk Lymphoma; 2005 Jan;46(1):55-61
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  • [Title] Intensified induction chemotherapy in adult acute myeloid leukemia followed by high-dose chemotherapy and autologous peripheral blood stem cell transplantation: an Eastern Cooperative Oncology Group trial (E4995).
  • The feasibility of intensified therapy in adults < 61-years-old with de novo acute myeloid leukemia (AML) was evaluated by adding high-dose cytarabine (HDAC) to conventional induction therapy and in post-remission therapy prior to peripheral blood stem cell transplantation (PBSCT).
  • Patients were treated with conventional induction therapy (daunorubicin days 1-3 and cytarabine days 1-7), followed by HDAC (2 gm/M2) every 12 h ( x 6) on days 8-10.
  • Patients in complete remission (CR) with HLA-matched siblings were assigned to allogeneic PBSCT; the others received two courses of HDAC (3 gm/M2 every 12 h on days 1, 3, and 5) given 1 month apart.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation

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  • (PMID = 15621781.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA07190; United States / NCI NIH HHS / CA / CA11083; United States / NCI NIH HHS / CA / CA13650; United States / NCI NIH HHS / CA / CA15488; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA66636
  • [Publication-type] Clinical Trial; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin; HDAC protocol
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96. Tomonaga M: [Nuclear abnormalities in Pelger-Huet anomaly; progress in blood cell morphology]. Rinsho Byori; 2005 Jan;53(1):54-60
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  • We compared neutrophil morphology between familial Pelger-Huet anomaly and so called pseudo-Pelger-Huet anomaly observed in patients with myelodysplastic syndromes(MDS) and acute myeloid leukemia(AML).
  • The neutrophils in MDS were much similar to those of the familial anomaly, but neutrophils of AML, such as t (8;21) M2-AML and t (15;17) M3-AML, showed more heterogeneous pattern in lobulation and chromatin-hypercondensation.
  • In conclusion, our morphological recognition of certain abnormality of cells shows an marked progression when genetic abnormality responsible for some of them are discovered, and often make us recognize a further heterogeneity in them.
  • We, hematologists and technicians, must be well prepared to report our own observation of an un-explained morphological abnormality.
  • [MeSH-minor] Base Sequence. Chromatin / metabolism. Chromatin Assembly and Disassembly. Humans. Lamin Type B / deficiency. Leukemia, Myeloid, Acute / blood. Mutation. Myelodysplastic Syndromes / blood. Receptors, Cytoplasmic and Nuclear / genetics

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  • (PMID = 15724491.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Chromatin; 0 / Lamin Type B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / lamin B receptor
  • [Number-of-references] 10
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97. Horácek JM, Pudil R, Tichý M, Jebavý L, Strasová A, Praus R, Zák P, Malý J: The use of biochemical markers in cardiotoxicity monitoring in patients treated for leukemia. Neoplasma; 2005;52(5):430-4
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  • [Title] The use of biochemical markers in cardiotoxicity monitoring in patients treated for leukemia.
  • The aim of the study was to monitor cardiotoxicity of induction chemotherapy in acute myeloid leukemia (AML) patients and to assess the potential for use of biochemical markers in early diagnostics of cardiotoxicity.
  • Fifteen consecutive adult patients with a newly diagnosed AML were studied.
  • All patients received induction chemotherapy containing Idarubicin (IDA) 3 x 12 mg/m2 and intermediate doses of Cytarabine (8 x 1.5 g/m2).
  • The mean baseline value of NT-proBNP in newly diagnosed AML patients was 129.7+/-59.6 pg/ml.
  • The mean NT-proBNP value increased after the first IDA infusion to 307.3+/-171.4 pg/ml (p=0.02).
  • In most of the patients, the second and the third IDA infusions were not associated with a further increase in the NT-proBNP value and levels after 2 and 4 weeks were not significantly different from the baseline.
  • Our results suggest that induction chemotherapy in AML (IDA 36 mg/m2 and intermediate doses of Cytarabine): 1. does not cause detectable damage of the myocyte structure, 2. is in all patients associated with acute neurohumoral activation (transient elevation of NT-proBNP) indicating acute subclinical cardiotoxicity, 3. may lead to congestive heart failure and NT-proBNP seems to be a promising early marker and predictor of this complication.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Biomarkers / blood. Heart Diseases / chemically induced. Idarubicin / adverse effects. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Creatine Kinase, MB Form / blood. Cytarabine / administration & dosage. Cytarabine / adverse effects. Echocardiography. Female. Humans. Male. Middle Aged. Natriuretic Peptide, Brain / blood. Peptide Fragments / blood. Troponin T / blood

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  • (PMID = 16151589.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Biomarkers; 0 / Peptide Fragments; 0 / Troponin T; 0 / pro-brain natriuretic peptide (1-76); 04079A1RDZ / Cytarabine; 114471-18-0 / Natriuretic Peptide, Brain; EC 2.7.3.2 / Creatine Kinase, MB Form; ZRP63D75JW / Idarubicin
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98. 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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99. 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


100. Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia. Leuk Res; 2005 May;29(5):557-64
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  • [Title] p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
  • Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with acute leukemia.
  • To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-cell acute lymphoblastic leukemia (PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
  • Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
  • Among 108 AML patients, p15 mRNA expression was significantly lower in the myeloid lineage (M1, M2, M3) than the monocytic lineage (M4, M5) (P = 0.0019).
  • Above all, the majority of M3 patients showed low p15 expression compared with M1 and M2 patients (P = 0.029).
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Lineage. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured

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  • (PMID = 15755508.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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