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1. Watt CD, Bagg A: Molecular diagnosis of acute myeloid leukemia. Expert Rev Mol Diagn; 2010 Nov;10(8):993-1012
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular diagnosis of acute myeloid leukemia.
  • The diagnosis and classification of acute myeloid leukemia is multifaceted, requiring the integration of a variety of laboratory findings, with genetic approaches now firmly established as a central component.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Molecular Diagnostic Techniques

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  • (PMID = 21080817.001).
  • [ISSN] 1744-8352
  • [Journal-full-title] Expert review of molecular diagnostics
  • [ISO-abbreviation] Expert Rev. Mol. Diagn.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
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2. Rowe D, Strain L, Lowe C, Jones G: A case of acute myeloid leukemia with inv(16)(p13q22) reveals a novel MYH11 breakpoint and a new CBF beta-MYH11 transcript variant. Haematologica; 2007 Oct;92(10):1433-4
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  • [Title] A case of acute myeloid leukemia with inv(16)(p13q22) reveals a novel MYH11 breakpoint and a new CBF beta-MYH11 transcript variant.
  • We present a case of acute myeloid leukemia (AML) with a cytogenetically typical inv(16)(p13q22), M4 morphology and eosinophilia.
  • However, studies revealed a CBF beta-MYH11 fusion transcript which did not correspond to any of the 10 known variants.
  • [MeSH-major] Chromosomes, Human, Pair 16 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Transcription, Genetic / genetics

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  • (PMID = 18024381.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion
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3. Wang Y, Fang M, Sun X, Sun J: Telomerase activity and telomere length in acute leukemia: correlations with disease progression, subtypes and overall survival. Int J Lab Hematol; 2010 Apr;32(2):230-8
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  • [Title] Telomerase activity and telomere length in acute leukemia: correlations with disease progression, subtypes and overall survival.
  • The progressive shortening of telomeres and the activation of telomerase are considered to be one of the important mechanisms in cellular immortalization and disease progression.
  • Bone marrow samples were collected from 148 patients with acute leukemia (AL).
  • Based on the stage of the disease, patients were divided into the newly diagnosed group, the relapsed group and the complete remission (CR) group. telomerase activity (TA) was examined by PCR-ELISA, and telomere length (TL) was examined by Southern blot analyses.
  • TA and TL were analyzed in relation to AL stage and subtype.
  • TA had no difference between acute nonlymphocytic leukemia (ANLL) group and acute lymphocytic leukemia (ALL) group.
  • But TA in group of subtype M3 was lower than other subtypes of ANLL.
  • Patients in late-stage disease had shorter TL and higher TA than those in early stages.
  • The shortened TL and elevated TA correlated with disease progression and relapse, and they may serve as prognostic factors for AL patients with poor outcome.
  • M3 subtype is special with relative lower TA and long-lasting survival than other subtypes.
  • [MeSH-major] Leukemia / metabolism. Leukemia / physiopathology. Telomerase / metabolism. Telomere / genetics
  • [MeSH-minor] Adult. Aged. Blotting, Southern. Disease Progression. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Reference Standards

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  • (PMID = 19614710.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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4. Arana-Yi C, Block AW, Sait SN, Ford LA, Barcos M, Baer MR: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine. Leuk Res; 2008 Jul;32(7):1043-8
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) have been reported only rarely following treatment of AML.
  • We report five patients treated for de novo AML who developed t-MDS/t-AML, all with chromosome 7 abnormalities, including -7, del(7)(q22q36) and del(7)(p11.22p22).
  • These cases further document t-MDS/t-AML as a complication of therapy for AML.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytarabine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / drug therapy


5. Tsimberidou AM, Keating MJ: Richter syndrome: biology, incidence, and therapeutic strategies. Cancer; 2005 Jan 15;103(2):216-28
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  • Richter's transformation denotes the development of high-grade non-Hodgkin lymphoma, prolymphocytic leukemia, Hodgkin disease, or acute leukemia in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma.
  • Therapeutic strategies include intensive chemotherapy, monoclonal antibodies, and stem cell transplantation.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Humans. Male. Prognosis. Risk Assessment. Severity of Illness Index. Stem Cell Transplantation / methods. Survival Analysis. Syndrome. Treatment Outcome

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  • [Copyright] (c) 2004 American Cancer Society.
  • (PMID = 15578683.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 159
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6. Tanaka-Harada Y, Kawakami M, Oka Y, Tsuboi A, Katagiri T, Elisseeva OA, Nishida S, Shirakata T, Hosen N, Fujiki F, Murao A, Nakajima H, Oji Y, Kanda Y, Kawase I, Sugiyama H: Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients with myeloid malignancies. Cancer Sci; 2010 Mar;101(3):594-600
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  • [Title] Biased usage of BV gene families of T-cell receptors of WT1 (Wilms' tumor gene)-specific CD8+ T cells in patients with myeloid malignancies.
  • WT1 (Wilms' tumor gene 1) protein is a potent pan-tumor-associated antigen (TAA) and WT1-specific cytotoxic T lymphocytes (WT1 tetramer(+) CD8(+) T cells) are spontaneously induced in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • We conducted a single-cell level comparative analysis of T-cell receptor beta-chain variable region (TCR-BV) gene families of a total of 1242 spontaneously induced WT1 tetramer(+) CD8(+) T cells in HLA-A*2402(+) patients with AML or MDS and those in healthy donors (HDs).
  • This is the first report of direct usage analysis of TCR-BV gene families of individual TAA-specific CD8(+) T cells at single-cell level.
  • Usage analysis using single-cell RT-PCR of TCR-BV gene families of individual FACS-sorted WT1 tetramer(+) CD8(+) T cells showed for the first time (i) that BVs 5, 6, 20, and 27 were commonly biased in both HDs and patients;.
  • (iii) that BV19 was commonly biased in the patients; and (iv) that BVs 7 and 28, BVs 9 and 15, and BVs 12 and 29 were specifically biased in HDs, AML, and MDS patients, respectively.
  • However, statistical analysis of similarity among HD, AML, and MDS of individual usage frequencies of 24 kinds of TCR-BV gene families indicated that the usage frequencies of TCR-BV gene families in AML and MDS patients reflect those in HDs.
  • These findings represent a novel insight for a better understanding of WT1-specific immune response.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Genes, T-Cell Receptor beta. Leukemia, Myeloid, Acute / immunology. Myelodysplastic Syndromes / immunology. WT1 Proteins / immunology


7. Cencic R, Carrier M, Trnkus A, Porco JA Jr, Minden M, Pelletier J: Synergistic effect of inhibiting translation initiation in combination with cytotoxic agents in acute myelogenous leukemia cells. Leuk Res; 2010 Apr;34(4):535-41
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  • [Title] Synergistic effect of inhibiting translation initiation in combination with cytotoxic agents in acute myelogenous leukemia cells.
  • We have previously shown that inhibition of translation initiation, using the small molecule inhibitor silvestrol, induces apoptosis in a pre-clinical murine lymphoma model when combined with daunorubicin.
  • Here we investigate the sensitivity of acute myelogenous leukemia (AML) cell lines to protein synthesis inhibition in combination with the standard cytotoxic agents daunorubicin, etoposide, and cytarabine.
  • Silvestrol shows synergy with standard-of-care agents in AML cell lines and synergizes with ABT-737, a small molecule inhibitor of Bcl-X(L) and Bcl-2.
  • The in vitro synergy between silvestrol and the cytotoxic drugs used in AML therapy provides a basis for in vivo evaluation of these combinations.

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 19726085.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM073855; Canada / Canadian Institutes of Health Research / / MOP-79385
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABT-737; 0 / Biphenyl Compounds; 0 / Cytotoxins; 0 / Nitrophenols; 0 / Peptide Initiation Factors; 0 / Piperazines; 0 / Protein Synthesis Inhibitors; 0 / Sulfonamides; 0 / Triterpenes; 0 / silvestrol; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS616104; NLM/ PMC4117193
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8. Zhou FL, Zhang WG, Wei YC, Meng S, Bai GG, Wang BY, Yang HY, Tian W, Meng X, Zhang H, Chen SP: Involvement of oxidative stress in the relapse of acute myeloid leukemia. J Biol Chem; 2010 May 14;285(20):15010-5
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  • [Title] Involvement of oxidative stress in the relapse of acute myeloid leukemia.
  • The aims of the present study were to determine the level of oxidative stress and the salient factors leading to the relapse of acute myeloid leukemia (AML).
  • Oxidative stress-related parameters and the expressions of specific genes were monitored in 102 cases of AML during a pretreatment period from a primary status to a relapse status.
  • Linear regression showed that a low T-AOC and up-regulated TRX expression were the independent factors correlated with relapse.
  • A strong association between oxidative stress and the incidence of disease relapse was observed, which has potential prognosis implications.
  • These results indicate that oxidative stress is a crucial feature of AML and probably affects the development and relapse of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Oxidative Stress

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  • (PMID = 20233720.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.17.3.2 / Xanthine Oxidase; EC 1.4.3.4 / Monoamine Oxidase; EC 3.5.4.4 / Adenosine Deaminase
  • [Other-IDs] NLM/ PMC2865279
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9. Stevens JM, Macdougall F, Jenner M, Oakervee H, Cavenagh J, Lister AT: Patterns of recruitment into acute myeloid leukaemia (AML) 15 and outcome for young patients with AML at a single referral centre. Br J Haematol; 2009 Apr;145(1):40-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of recruitment into acute myeloid leukaemia (AML) 15 and outcome for young patients with AML at a single referral centre.
  • This study assessed the recruitment to an acute myeloid leukaemia (AML) trial (AML15) in a single centre, evaluated whether outcome was influenced by trial entry and whether the trial population could be considered representative of all AML patients by retrospective comparison of patient characteristics, trial entry and outcome for 81 consecutive patients (<60 years).
  • All patients were considered for trial entry, however the trial was not offered to 12 (15%) patients.
  • Thus the overall survival estimates generated from large phase III trials may indicate that the outcome for patients with AML is better than the outcome experienced in the 'real' world.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase III as Topic. Leukemia, Myeloid, Acute / drug therapy. Patient Selection. Randomized Controlled Trials as Topic

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  • (PMID = 19210510.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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10. Ryningen A, Wergeland L, Glenjen N, Gjertsen BT, Bruserud O: In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8. Leuk Res; 2005 Feb;29(2):185-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro crosstalk between fibroblasts and native human acute myelogenous leukemia (AML) blasts via local cytokine networks results in increased proliferation and decreased apoptosis of AML cells as well as increased levels of proangiogenic Interleukin 8.
  • Interactions between native human acute myelogenous leukemia (AML) blasts and nonleukemic cells in the bone marrow microenvironment seem important both for disease development chemosensitivity.
  • Native human AML blasts from consecutive patients were cultured with normal human bone marrow stromal cells and two fibroblast lines (HFL1 and Hs27) separated by a semipermeable membrane.
  • This bidirectional crosstalk via the cytokine network between AML blasts and fibroblasts caused (i) increased proliferation, (ii) mediated antiapoptotic signalling and (iii) increased local levels of proangiogenic IL8.
  • [MeSH-major] Cell Communication. Cytokines / physiology. Fibroblasts / physiology. Interleukin-8 / biosynthesis. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / physiology. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Disease Progression. Female. Humans. Male. Middle Aged. Signal Transduction. Stromal Cells / physiology

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  • (PMID = 15607368.001).
  • [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 / Cytokines; 0 / Interleukin-8
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11. Martins C, Lacerda JF, Lourenço F, Carmo JA, Lacerda JM: Autologous stem cell transplantation in acute myeloid leukemia. Factors influencing outcome. A 13 year single institution experience. Acta Med Port; 2005 Sep-Oct;18(5):329-37
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  • [Title] Autologous stem cell transplantation in acute myeloid leukemia. Factors influencing outcome. A 13 year single institution experience.
  • We report our results of autologous stem cell transplantation (SCT) in patients with AML during the last 13 years.
  • Between August 1990 and December 2003, 42 patients with acute myeloid leukemia (AML) received an autologous SCT.
  • Patients were classified as standard risk if first complete remission (CR) was induced after one or two chemotherapy regimens and the white blood cell count at presentation was below 50,000/mL (n=12), while patients requiring more than two induction regimens to attain first CR and with CR2 ou more advanced disease and/or had a higher white blood cell count at presentation were defined as high risk (n=30).
  • The median patient age was 24 years (range, 2-56 years), and the median time interval from diagnosis to autologous SCT was 9 months (range 3-87 months).
  • The conditioning regimen for SCT consisted of busulfan (BU) 16 mg/kg and melfalan (MEL) 180 mg/m2 (BUMEL) in 17 (40%) patients and busulfan 16 mg/kg and VP-16 60 mg/kg (BUVP16) in 22 (52%) patients.
  • Three patients received a different conditioning regimen with BCNU 300 mg/m2, VP16 2 g/m2 and melphalan 160 mg/m2 (BEM).
  • Patients with FAB M3 subtype also had a superior OS than the other FAB subtypes (100% vs 44%, p=0.05).
  • In fact, the patients with standard risk had a superior OS and DFS than those with high risk disease (67% vs 23%, p=0.0004; and 50% vs 27%, p=0.01, respectively).
  • When patients with FAB M3 disease were excluded from the analysis, the group with standard risk continue to have a superior OS and DFS (67% vs 13%, p=0.008; and 50% vs 14%, p=0.02, respectively).
  • We conclude that autologous SCT is an effective treatment in AML with the possibility of long survivorship, particularly in patients with standard risk disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Transplantation Conditioning / methods. Transplantation, Autologous. Treatment Outcome


12. Neumann F, Gattermann N, Barthelmes HU, Haas R, Germing U: Levels of beta 2 microglobulin have a prognostic relevance for patients with myelodysplastic syndrome with regard to survival and the risk of transformation into acute myelogenous leukemia. Leuk Res; 2009 Feb;33(2):232-6
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  • [Title] Levels of beta 2 microglobulin have a prognostic relevance for patients with myelodysplastic syndrome with regard to survival and the risk of transformation into acute myelogenous leukemia.
  • The risk of AML evolution was higher in patients with B2M> or =2mg/dl.
  • Using multivariate analysis we found the B2M level at the time of diagnosis to be an independent prognostic parameter for survival and for the risk of developing AML in high-risk MDS patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / diagnosis. beta 2-Microglobulin / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis. Survival Rate. Young Adult


13. Sherborne AL, Houlston RS: What are genome-wide association studies telling us about B-cell tumor development? Oncotarget; 2010 Sep;1(5):367-72
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  • [Title] What are genome-wide association studies telling us about B-cell tumor development?
  • It has long been speculated that common genetic variation influences the development of B-cell malignancy, however until recently evidence for this assertion was lacking.
  • Recent GWAS of chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL) have identified novel disease genes for CLL and ALL and underscore the importance of polymorphic variation in B-cell development genes as determinants of leukemia risk.
  • [MeSH-major] B-Lymphocytes / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Gene Expression Regulation, Leukemic. Genetic Predisposition to Disease. Genome-Wide Association Study. Humans. Phenotype. Risk Assessment. Risk Factors

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  • (PMID = 21307401.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3157732
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14. Bunin NJ, Davies SM, Aplenc R, Camitta BM, DeSantes KB, Goyal RK, Kapoor N, Kernan NA, Rosenthal J, Smith FO, Eapen M: Unrelated donor bone marrow transplantation for children with acute myeloid leukemia beyond first remission or refractory to chemotherapy. J Clin Oncol; 2008 Sep 10;26(26):4326-32
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  • [Title] Unrelated donor bone marrow transplantation for children with acute myeloid leukemia beyond first remission or refractory to chemotherapy.
  • PURPOSE: Identify prognostic factors that influence outcome after unrelated donor bone marrow transplantation in children with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: Included are 268 patients (age <or= 18 years) with AML in second complete remission (n = 142), relapse (n = 90), or primary induction failure (n = 36) at transplantation.
  • RESULTS: In this analysis, the only risk factor that predicted leukemia recurrence and overall and leukemia-free survival was disease status at transplantation.
  • The 5-year probabilities of leukemia-free survival were 45%, 20%, and 12% for patients who underwent transplantation at second complete remission, relapse, and primary induction failure, respectively.
  • As expected, risk of acute but not chronic graft-versus-host disease (GVHD) was lower with T-cell-depleted bone marrow grafts; T-cell-depleted grafts were not associated with higher risks of leukemia recurrence.
  • We observed similar risks of leukemia relapse in patients with and without acute and chronic GVHD.
  • CONCLUSION: Children who underwent transplantation in remission had a superior outcome compared with children who underwent transplantation during relapse or persistent disease.
  • Nevertheless, 20% of children who underwent transplantation in relapse are long-term survivors, suggesting that unrelated donor bone marrow transplantation is an effective therapy in a significant proportion of children with recurrent or primary refractory AML.

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  • (PMID = 18779619.001).
  • [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 / U24 CA076518; United States / NCI NIH HHS / CA / U24-CA76518
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC2653120
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15. Rodríguez Pérez A, López Carrizosa MC, Villalón Blanco L, Samper Ots PM, Ortiz Cruz E: Granulocytic sarcoma of the right humerus in a non-leukaemia patient. Clin Transl Oncol; 2008 Nov;10(11):758-60
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  • [Title] Granulocytic sarcoma of the right humerus in a non-leukaemia patient.
  • Granulocytic sarcoma (GS), an uncommon solid extramedullary tumour, should be considered even in the absence of leukaemia, as delay in diagnosis and treatment worsens the prognosis.
  • We present a GS (single humeral bone lesion) in a non-leukaemia patient, treated with intensive AML (Acute Myeloid Leukaemia) chemotherapy and sequential radiotherapy, in complete response 26 months after diagnosis, confirmed by histopathology and without leukaemia progression.
  • [MeSH-major] Bone Neoplasms / diagnosis. Humerus / pathology. Sarcoma, Myeloid / diagnosis

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  • (PMID = 19015073.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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16. Metzner A, Precht C, Fehse B, Fiedler W, Stocking C, Günther A, Mayr GW, Jücker M: Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D. Gene Ther; 2009 Apr;16(4):570-3
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  • [Title] Reduced proliferation of CD34(+) cells from patients with acute myeloid leukemia after gene transfer of INPP5D.
  • Acute myeloid leukemia (AML) is a malignant disease characterized by deregulated proliferation of immature myeloid cells.
  • Constitutive activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is frequently detected in approximately 50-70% of AML patients.
  • After lentiviral-mediated gene transfer of INPP5D into CD34(+) cells derived from AML patients (n=12) the granulocyte macrophage-colony stimulating factor (GM-CSF)-dependent proliferation was reduced in all samples analyzed (average 86%; range 72-93%).
  • In addition, SHIP1 reduced the autonomous proliferation of CD34(+) cells from a patient with a secondary AML who had a very high peripheral blast count (300 x 10(9) l(-1)).
  • These data show that SHIP1 can effectively block GM-CSF-dependent and autonomous proliferation of AML cells.
  • [MeSH-major] Antigens, CD34 / blood. Leukemia, Myeloid, Acute / pathology. Phosphoric Monoester Hydrolases / genetics
  • [MeSH-minor] Cell Proliferation / drug effects. Gene Transfer Techniques. Genetic Vectors. Humans. Lentivirus / genetics. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Ribonucleosides / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19148132.001).
  • [ISSN] 1476-5462
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ribonucleosides; 2421HMY9N6 / triciribine; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.56 / inositol-polyphosphate 5-phosphatase
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17. Stasi R, Evangelista ML, Buccisano F, Venditti A, Amadori S: Gemtuzumab ozogamicin in the treatment of acute myeloid leukemia. Cancer Treat Rev; 2008 Feb;34(1):49-60
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  • [Title] Gemtuzumab ozogamicin in the treatment of acute myeloid leukemia.
  • Gemtuzumab ozogamicin (GO) is a chemotherapeutic agent that consists of a humanized anti-CD33 antibody (hP67.6) linked to N-acetyl-calicheamicin 1,2-dimethyl hydrazine dichloride, a potent enediyne antitumor antibiotic.
  • GO was approved conditionally by the Federal Drug Administration in May 2000 as single-agent therapy for first recurrence of acute myeloid leukemia (AML) in patients over the age of 60 years who are unfit for conventional cytotoxic therapy.
  • GO monotherapy at the dose of 9 mg/m(2) is complicated with hepatic veno-occlusive disease in approximately 5% of cases, particularly prior to or following stem cell transplantation.
  • GO has shown remarkable activity in acute promyelocytic leukemia, particularly for the elimination of minimal residual disease.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Humans. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 17942233.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab
  • [Number-of-references] 77
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18. Patel VB, Singh R, Connolly C, Kasprowicz V, Zumla A, Ndungu T, Dheda K: Comparison of a clinical prediction rule and a LAM antigen-detection assay for the rapid diagnosis of TBM in a high HIV prevalence setting. PLoS One; 2010 Dec 22;5(12):e15664
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  • [Title] Comparison of a clinical prediction rule and a LAM antigen-detection assay for the rapid diagnosis of TBM in a high HIV prevalence setting.
  • BACKGROUND/OBJECTIVE: The diagnosis of tuberculous meningitis (TBM) in resource poor TB endemic environments is challenging.
  • The accuracy of current tools for the rapid diagnosis of TBM is suboptimal.
  • We sought to develop a clinical-prediction rule for the diagnosis of TBM in a high HIV prevalence setting, and to compare performance outcomes to conventional diagnostic modalities and a novel lipoarabinomannan (LAM) antigen detection test (Clearview-TB®) using cerebrospinal fluid (CSF).
  • METHODS: Patients with suspected TBM were classified as definite-TBM (CSF culture or PCR positive), probable-TBM and non-TBM.
  • There were 39, 55 and 54 patients in the definite, probable and non-TBM groups, respectively.
  • The LAM sensitivity and specificity (95%CI) was 31% (17;48) and 94% (85;99), respectively (cut-point ≥ 0.18).
  • LAM positivity was associated with HIV co-infection and low CD4 T cell count (CD4<200 vs. >200 cells/µl; p = 0.03).
  • When LAM was combined with the clinical-prediction-rule, the sensitivity increased significantly (p<0.001) to 63% (47;68) and specificity remained high at 93% (82;98).
  • CONCLUSIONS: Despite its modest sensitivity the LAM ELISA is an accurate rapid rule-in test for TBM that has incremental value over smear-microscopy.
  • The rule-in value of LAM can be further increased by combination with a clinical-prediction rule, thus enhancing the rapid diagnosis of TBM in HIV-infected persons with advanced immunosuppression.

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  • [Cites] Int J Tuberc Lung Dis. 2009 Oct;13(10):1253-9 [19793430.001]
  • (PMID = 21203513.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / D43 TW000231; United States / FIC NIH HHS / TW / D43TW00231
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens; 0 / Lipopolysaccharides; 0 / lipoarabinomannan
  • [Other-IDs] NLM/ PMC3008727
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19. George P, Bali P, Annavarapu S, Scuto A, Fiskus W, Guo F, Sigua C, Sondarva G, Moscinski L, Atadja P, Bhalla K: Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. Blood; 2005 Feb 15;105(4):1768-76
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  • [Title] Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3.
  • Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3.
  • In the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-Abl with the T315I mutation, treatment with the combination attenuated the levels of the mutant Bcr-Abl and induced apoptosis.
  • Finally, cotreatment with LBH589 and 17-AAG also induced more apoptosis of IM-resistant primary CML-BC and acute myeloid leukemia (AML) cells (with activating mutation of FLT-3) than treatment with either agent alone.
  • [MeSH-major] Blast Crisis / metabolism. Enzyme Inhibitors / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors. Hydroxamic Acids / analogs & derivatives. Hydroxamic Acids / pharmacology. Leukemia, Myeloid / metabolism. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Rifabutin / analogs & derivatives. Rifabutin / pharmacology
  • [MeSH-minor] Acute Disease. Apoptosis / drug effects. Benzamides. Benzoquinones. Cell Line, Tumor. Drug Combinations. Drug Synergism. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Gene Deletion. Gene Expression Regulation. Humans. Imatinib Mesylate. Indoles. K562 Cells. Lactams, Macrocyclic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / pharmacology. Point Mutation. Polyubiquitin / metabolism. Proteasome Endopeptidase Complex / metabolism. Pyrimidines / pharmacology. fms-Like Tyrosine Kinase 3

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  • (PMID = 15514006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95188
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Benzoquinones; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Indoles; 0 / Lactams, Macrocyclic; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 120904-94-1 / Polyubiquitin; 1W306TDA6S / Rifabutin; 4GY0AVT3L4 / tanespimycin; 8A1O1M485B / Imatinib Mesylate; 9647FM7Y3Z / panobinostat; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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20. Us T, Ozune L, Kasifoglu N, Akgun Y: The investigation of parvovirus B19 infection in patients with haematological disorders by using PCR and ELISA techniques. Braz J Infect Dis; 2007 Jun;11(3):327-30
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  • The purpose of the study was to investigate the frequency of parvovirus B19 infections in patients with diagnosis of haematological disorders.
  • B19 infection was established in 3 of 11 patients with chronic myeloid leukemia, in 3 of 11 acute myeloid leukemia, in 2 of 11 patients with multiple myeloma, in 3 of 8 patients with Hodgkin's lymphoma, in 5 of 10 patients with non-Hodgkin's lymphoma, in 1 of 6 patients with myelodysplastic syndrome, in 4 of 11 patients with chronic lymphocytic leukemia, and in 2 of 11 patients with acute lymphocytic leukemia.
  • [MeSH-major] Hematologic Diseases / virology. Parvoviridae Infections / virology. Parvovirus B19, Human
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antibodies, Viral / blood. Chronic Disease. DNA, Viral / analysis. Enzyme-Linked Immunosorbent Assay. Female. Hodgkin Disease / virology. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. Leukemia / virology. Lymphoma, Non-Hodgkin / virology. Male. Middle Aged. Polymerase Chain Reaction. Prospective Studies

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  • (PMID = 17684634.001).
  • [ISSN] 1413-8670
  • [Journal-full-title] The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
  • [ISO-abbreviation] Braz J Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / DNA, Viral; 0 / Immunoglobulin G; 0 / Immunoglobulin M
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21. Meshinchi S, Arceci RJ: Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia. Oncologist; 2007 Mar;12(3):341-55
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  • [Title] Prognostic factors and risk-based therapy in pediatric acute myeloid leukemia.
  • Acute myeloid leukemia (AML) has posed significant therapeutic challenges to pediatric oncologists.
  • Despite intensive therapy, half of the children with AML relapse and die from their disease.
  • Efforts to identify risk factors in AML are directed toward defining populations who may benefit from alternative therapies.
  • Patients at lower risk for relapse may benefit from treatment de-escalation, sparing them adverse side effects.
  • Management of high-risk patients may prove more difficult, as the nearly myeloablative nature of AML therapy leaves little room for therapy escalation short of stem cell transplantation.
  • This review evaluates prognostic factors in pediatric AML and discusses the feasibility of using these factors in risk-adapted therapy regimens.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / therapeutic use. Child. Humans. Neoplasm Recurrence, Local. Prognosis. Risk Assessment. Risk Factors. Stem Cell Transplantation

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  • (PMID = 17405900.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 133
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22. Fuh B, Lurito J, Grossi M, Daeschner C, Russo S: Bilateral internal carotid artery occlusions in a pediatric patient with refractory acute myeloid leukemia. Pediatr Blood Cancer; 2010 May;54(5):770-2
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  • [Title] Bilateral internal carotid artery occlusions in a pediatric patient with refractory acute myeloid leukemia.
  • Thromboembolism is a well-known complication of cancer including acute myeloid leukemia (AML) especially in patients with high myeloblast counts.
  • We report the case of a 3-year-old male with refractory AML who developed spontaneous bilateral internal carotid artery occlusion with diffuse cerebral infarcts.
  • [MeSH-major] Carotid Artery, Internal. Carotid Stenosis / etiology. Cerebral Infarction / etiology. Leukemia, Myeloid, Acute / complications

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  • (PMID = 20052773.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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23. Giles FJ, Borthakur G, Ravandi F, Faderl S, Verstovsek S, Thomas D, Wierda W, Ferrajoli A, Kornblau S, Pierce S, Albitar M, Cortes J, Kantarjian H: The haematopoietic cell transplantation comorbidity index score is predictive of early death and survival in patients over 60 years of age receiving induction therapy for acute myeloid leukaemia. Br J Haematol; 2007 Feb;136(4):624-7
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  • [Title] The haematopoietic cell transplantation comorbidity index score is predictive of early death and survival in patients over 60 years of age receiving induction therapy for acute myeloid leukaemia.
  • The haematopoietic cell transplantation comorbidity index (HCTCI) predicts nonrelapse mortality and overall survival (OS) post-stem cell transplantation.
  • HCTCI scores were assessed in 177 patients over 60 years of age receiving acute myeloid leukaemia (AML) induction therapy.
  • The HCTCI score is predictive of early death rates and OS in older patients receiving AML induction therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Severity of Illness Index
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Epidemiologic Methods. Female. Hematopoietic Stem Cell Transplantation. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Prognosis. Treatment Outcome

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  • (PMID = 17223919.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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24. Tseng MY, Chen YC, Lin YY, Chu SJ, Tsai SH: Simultaneous bilateral central retinal vein occlusion as the initial presentation of acute myeloid leukemia. Am J Med Sci; 2010 Apr;339(4):387-9
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  • [Title] Simultaneous bilateral central retinal vein occlusion as the initial presentation of acute myeloid leukemia.
  • Ocular involvement is not uncommon in patients with leukemia; however, bilateral CRVO as a complication of acute myeloid leukemia has rarely been reported.
  • Here, we report a patient who had simultaneous bilateral CRVO as the initial presentation of acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / diagnosis. Retinal Vein Occlusion / complications. Retinal Vein Occlusion / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male

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  • (PMID = 20186040.001).
  • [ISSN] 1538-2990
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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25. Burnett AK, Milligan D, Prentice AG, Goldstone AH, McMullin MF, Hills RK, Wheatley K: A comparison of low-dose cytarabine and hydroxyurea with or without all-trans retinoic acid for acute myeloid leukemia and high-risk myelodysplastic syndrome in patients not considered fit for intensive treatment. Cancer; 2007 Mar 15;109(6):1114-24
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  • [Title] A comparison of low-dose cytarabine and hydroxyurea with or without all-trans retinoic acid for acute myeloid leukemia and high-risk myelodysplastic syndrome in patients not considered fit for intensive treatment.
  • BACKGROUND: The survival of older patients with acute myeloid leukemia has not improved.
  • Few clinical trials have been available for older patients who are not considered fit for an intensive chemotherapy approach.
  • METHODS: Between December 1998 and November 2003, as part of National Cancer Research Institute Acute Myeloid Leukemia 14 Trial, 217 patients, who were deemed unfit for intensive chemotherapy were randomized to receive low-dose cytarabine (Ara-C) (20 mg twice daily for 10 days) or hydroxyurea with or without all-trans retinoic acid (ATRA).
  • Patients who had adverse cytogenetics did not benefit.
  • Toxicity scores or supportive care requirements did not differ between the treatment arms.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Cytarabine / administration & dosage. Cytarabine / adverse effects. Female. Humans. Hydroxyurea / administration & dosage. Hydroxyurea / adverse effects. Male. Middle Aged. Risk. Survival. Treatment Outcome. Tretinoin / administration & dosage. Tretinoin / adverse effects


26. Sahu GR, Mishra R, Nagpal JK, Das BR: Notice of retraction. Alteration of p73 in acute myelogenous leukemia. Am J Hematol; 2008 Aug;83(8):691
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  • [Title] Notice of retraction. Alteration of p73 in acute myelogenous leukemia.

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  • [RetractionOf] Sahu GR, Mishra R, Nagpal JK, Das BR. Am J Hematol. 2005 May;79(1):1-7 [15849769.001]
  • (PMID = 18615454.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Retraction of Publication
  • [Publication-country] United States
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27. Cellai C, Laurenzana A, Bianchi E, Sdelci S, Manfredini R, Vannucchi AM, Caporale R, Balliu M, Mannelli F, Ferrari S, Bosi A, Miniati D, Cocco PL, Veronneau S, Stankova J, Paoletti F: Mechanistic insight into WEB-2170-induced apoptosis in human acute myelogenous leukemia cells: the crucial role of PTEN. Exp Hematol; 2009 Oct;37(10):1176-1185.e21
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  • [Title] Mechanistic insight into WEB-2170-induced apoptosis in human acute myelogenous leukemia cells: the crucial role of PTEN.
  • OBJECTIVE: This study aimed to investigate the mechanisms of action of WEB-2170, an inverse agonist of platelet-activating factor receptor, capable of inducing apoptosis in human acute myelogenous leukemia (AML) cells.
  • MATERIAL AND METHODS: Gene expression profiling followed by cytofluorimetric, morphologic, and biologic analyses were used to monitor WEB-2170 effects in AML cell lines (ie, NB4, KG1, NB4-MR4, THP1, and U937) and blasts from patients with different AML (M0-M5) subtypes.
  • We have found that WEB-2170 triggered apoptosis in NB4, KG1, and NB4-MR4 cells where PTEN was expressed, but not in THP1 and U937 cells where PTEN was absent.
  • CONCLUSION: We demonstrated that WEB-2170 is a powerful antileukemic agent with interesting translational opportunities to treat AML and described mechanisms of drug-induced intrinsic and extrinsic apoptosis both in AML cell lines and blasts from AML patients by addressing PTEN as the master regulator of the whole process.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Azepines / pharmacology. Leukemia, Myeloid / pathology. Neoplasm Proteins / physiology. PTEN Phosphohydrolase / physiology. Triazoles / pharmacology
  • [MeSH-minor] Acute Disease. Adult. Aged. Cell Line, Tumor / drug effects. Female. G0 Phase / drug effects. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / physiology. Humans. Male. Middle Aged. Neoplastic Stem Cells / drug effects. Neoplastic Stem Cells / pathology. Phosphorylation / drug effects. Polymerase Chain Reaction. Protein Processing, Post-Translational / drug effects. Protein Transport / drug effects. RNA Interference. RNA, Small Interfering / pharmacology. Young Adult


28. Montesinos JJ, Sánchez-Valle E, Flores-Figueroa E, Martínez-Jaramillo G, Flores-Guzmán P, Miranda-Peralta E, Gutiérrez-Romero M, Mayani H: Deficient proliferation and expansion in vitro of two bone marrow cell populations from patients with acute myeloid leukemia in response to hematopoietic cytokines. Leuk Lymphoma; 2006 Jul;47(7):1379-86
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  • [Title] Deficient proliferation and expansion in vitro of two bone marrow cell populations from patients with acute myeloid leukemia in response to hematopoietic cytokines.
  • One has previously characterized two different hematopoietic cell populations (obtained by negative-selection) from normal bone marrow.
  • One has also characterized the chronic myeloid leukemia (CML) counterparts of these two populations and demonstrated functional deficiencies in terms of their growth in culture.
  • In keeping with this line of research, the goal of the present study was to obtain the same two populations (Populations I and II) from acute myeloid leukemia (AML) bone marrow and to characterize their biological behavior under the same culture conditions.
  • The results demonstrated that AML-derived Populations I and II were unable to proliferate in culture conditions that allowed significant proliferation of Populations I and II from normal marrow.
  • Population I from AML also showed a deficient expansion capacity; in contrast, Population II cells were able to expand to a similar extent to the one observed for Population II from normal marrow.
  • Both normal and AML populations were highly sensitive to the inhibitory effects of TNF-alpha; interestingly, whereas in normal fractions TNF-alpha showed a more pronounced inhibitory effect on more mature cells (Population I), this cytokine inhibited proliferation and expansion of AML Populations I and II in a similar degree.
  • It is noteworthy that the functional deficiencies observed in AML cells were even more pronounced than those previously reported for cultures of CML cells.
  • [MeSH-major] Bone Marrow / metabolism. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Cytokines / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Cell Culture Techniques / methods. Cell Proliferation. Culture Media, Serum-Free. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Male. Middle Aged. Stem Cells / metabolism

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  • (PMID = 16923572.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Culture Media, Serum-Free; 0 / Cytokines; EC 3.2.2.5 / Antigens, CD38
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29. 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.
  • Only one case each with an NPM1 mutation was detected in four M0, seven M1, five M6, and two M7 cases.
  • Further, 38.9% (14/36) patients with NPM1 mutations simultaneously exhibited internal tandem duplications in the FLT3 gene, and 66.7% (22/33) patients did not express CD34.
  • 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


30. Venizelos ID, Klonizakis I, Vlahaki E, Haralambidou S, Tatsiou Z, Ioannidou E: Skin relapse of acute myeloid leukemia associated with trisomy 8. Acta Dermatovenerol Alp Pannonica Adriat; 2007 Jun;16(2):77-80
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  • [Title] Skin relapse of acute myeloid leukemia associated with trisomy 8.
  • Acute myeloid leukemia (AML) is a morphologically diverse group of hematopoietic malignancies characterized by proliferation of immature cells that arise in the myeloid progenitor cells of the bone marrow.
  • It shows cutaneous lesions relatively rarely.
  • An association of AML with skin involvement and trisomy 8 has rarely been reported.
  • We present the case of a 74-year-old woman that presented with fatigue, nausea, dyspnea, and night sweats.
  • Accordingly, a diagnosis of AML involving the skin was made.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / pathology. Skin Neoplasms / pathology. Trisomy

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  • (PMID = 17992463.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
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31. Aref S, El-Sherbiny M, Azmy E, Goda T, Selim T, El-Refaie M, Emaad T: Elevated serum endostatin levels is associated with favorable outcome in acute myeloid leukemia. Indian J Hematol Blood Transfus; 2008 Mar;24(1):1-6
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  • [Title] Elevated serum endostatin levels is associated with favorable outcome in acute myeloid leukemia.
  • The levels and the prognostic relevance of serum endostatin in AML patient is not fully clear.
  • AIM: To evaluate serum levels of endostatin in acute myeloid leukemia patients before chemotherapy and after achieving complete remission and to correlate endostatin levels with patients outcome.
  • MATERIALS AND METHODS: Serum samples from 30 adult patients (22 males and 8 females, median age 37, range 19-66 years) with AML had been taken before chemotherapy was administered.
  • RESULTS: Endostatin serum levels were not significantly different in the pretreatment AML patients as compared to that in normal controls (P>0.05).
  • In AML patients the baseline endostatin levels were significantly lower than at CR (P=0.001).
  • No significant correlation were detected between pretreatment serum endostatin levels and age, peripheral blood white cell counts, platelet counts, bone marrow blast cell counts, blast cell distribution ratio.
  • The prognostic value of sE was also evaluated by dividing AML patients into high and low sE groups using the 75 percentile sE levels of the patients group as cutoff.
  • CONCLUSIONS: Elevated endostatin levels at AML diagnosis is a good prognostic marker for patients' outcome.

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  • (PMID = 23100932.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453162
  • [Keywords] NOTNLM ; AML / Angiogenesis / Endostatin / Prognosis
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32. Hack CE, Haber LT, Maier A, Shulte P, Fowler B, Lotz WG, Savage RE Jr: A Bayesian network model for biomarker-based dose response. Risk Anal; 2010 Jul;30(7):1037-51
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  • A Bayesian network model was developed to integrate diverse types of data to conduct an exposure-dose-response assessment for benzene-induced acute myeloid leukemia (AML).
  • The network approach was used to evaluate and compare individual biomarkers and quantitatively link the biomarkers along the exposure-disease continuum.
  • The network-derived benchmark concentration was approximately an order of magnitude lower than that from the usual exposure concentration versus response approach, which suggests that the presence of more information in the low-dose region (where changes in biomarkers are detectable but effects on AML mortality are not) helps inform the description of the AML response at lower exposures.
  • This work provides a quantitative approach for linking changes in biomarkers of effect both to exposure information and to changes in disease response.
  • Such linkage can provide a scientifically valid point of departure that incorporates precursor dose-response information without being dependent on the difficult issue of a definition of adversity for precursors.
  • [MeSH-minor] Air Pollutants / toxicity. Dose-Response Relationship, Drug. Humans. Leukemia, Myeloid, Acute / chemically induced. Monte Carlo Method

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  • (PMID = 20412521.001).
  • [ISSN] 1539-6924
  • [Journal-full-title] Risk analysis : an official publication of the Society for Risk Analysis
  • [ISO-abbreviation] Risk Anal.
  • [Language] eng
  • [Grant] United States / PHS HHS / / GS-10F-0369N
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants; 0 / Biomarkers; J64922108F / Benzene
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33. Marcucci G, Mrózek K, Ruppert AS, Maharry K, Kolitz JE, Moore JO, Mayer RJ, Pettenati MJ, Powell BL, Edwards CG, Sterling LJ, Vardiman JW, Schiffer CA, Carroll AJ, Larson RA, Bloomfield CD: Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study. J Clin Oncol; 2005 Aug 20;23(24):5705-17
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  • [Title] Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study.
  • PURPOSE: Because both t(8;21) and inv(16) disrupt core binding factor (CBF) in acute myeloid leukemia (AML) and confer relatively favorable prognoses, these cytogenetic groups are often treated similarly.
  • PATIENTS AND METHODS: We analyzed 144 consecutive adults with t(8;21) and 168 with inv(16) treated on Cancer and Leukemia Group B front-line studies.
  • RESULTS: With a median follow-up of 6.4 years, for CBF AML as a whole, the CR rate was 88%, 5-year OS was 50% and CIR was 53%.
  • Unexpectedly, race was an important predictor for t(8;21) AML, in that nonwhites failed induction more often (odds ratio = 5.7; P = .006) and had shorter OS than whites when certain secondary cytogenetic abnormalities were present.
  • For inv(16) AML, secondary cytogenetic abnormalities (especially +22) and male sex predicted better outcome.
  • CONCLUSION: When the prognostic impact of race, secondary cytogenetic abnormalities, sex, and response to salvage treatment is considered, t(8;21) and inv(16) AMLs seem to be distinct clinical entities and should be stratified and reported separately.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Aged. Aziridines / administration & dosage. Benzoquinones / administration & dosage. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Prognosis. Proportional Hazards Models. Prospective Studies. Remission Induction. Statistics, Nonparametric. Survival Analysis

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  • (PMID = 16110030.001).
  • [ISSN] 0732-183X
  • [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 / CA101140; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / K08-CA90469; United States / NCI NIH HHS / CA / P30-CA16058
  • [Publication-type] 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 / Aziridines; 0 / Benzoquinones; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; FQL5EUP13W / diaziquone; ZS7284E0ZP / Daunorubicin
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34. LaFiura KM, Edwards H, Taub JW, Matherly LH, Fontana JA, Mohamed AN, Ravindranath Y, Ge Y, Children's Oncology Group: Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group. Oncogene; 2008 Aug 21;27(36):4933-42
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  • [Title] Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group.
  • t(8;21)(q22;q22) results in the AML1-ETO (A1E) fusion gene and is a common cytogenetic abnormality in acute myeloid leukemia (AML).
  • By RT-PCR amplifications and DNA sequencing, numerous in-frame and out-of-frame AML1b-ETO and AML1c-ETO transcripts were identified in 13 pediatric t(8;21) AMLs, likely resulting from alternate splicing, internal deletions and/or breakpoint region insertions involving both the AML1 (RUNX1) and ETO regions.
  • These structure alterations were found in AML1c-ETO but not AML1b-ETO transcripts in two adult t(8;21) AMLs.
  • When transfected into HeLa cells, only AML1b, and not the in-frame A1E forms, transactivated the GM-CSF promoter.

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  • (PMID = 18469864.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / CA30969; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / P30 CA022453; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA92308
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS505499; NLM/ PMC3763903
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35. Zebisch A, Czernilofsky AP, Keri G, Smigelskaite J, Sill H, Troppmair J: Signaling through RAS-RAF-MEK-ERK: from basics to bedside. Curr Med Chem; 2007;14(5):601-23
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  • Strategies, which aim at inhibiting hyperactive signaling molecules, appear conceptually straight forward, but their translation into clinical practice has been hampered by many setbacks.
  • Understanding structure, function and regulation of this intracellular pathway as well as its crosstalk with other signaling activities in the cell will be essential to ensure reasonable usage of new therapeutic possibilities.
  • Signaling aberrations and signal transduction therapies will be discussed exemplary for two types of hematological neoplasia, acute myeloid leukemia (AML) and the myelodysplastic syndromes (MDS).

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  • (PMID = 17346150.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / W 1101
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.11.1 / raf Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 3.6.1.- / GTP-Binding Proteins
  • [Number-of-references] 202
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36. Dick JE: Acute myeloid leukemia stem cells. Ann N Y Acad Sci; 2005 Jun;1044:1-5
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  • [Title] Acute myeloid leukemia stem cells.
  • The concept that only a subpopulation of rare cancer stem cells (CSCs) is responsible for maintenance of the neoplasm emerged nearly 50 years ago; however, conclusive proof for the existence of a CSC was obtained only relatively recently.
  • The evidence for the existence of CSCs was first derived from the study of human acute myeloid leukemia (AML), largely because of the availability of quantitative stem cell assays for the leukemic stem cell (LSC).
  • These studies showed that only rare cells within the leukemic clone had the capacity to initiate AML growth after transplant into NOD/SCID mice, establishing the hierarchical organization of AML.
  • These findings have important implications for our understanding of the leukemogenic process as well as the design of more effective therapies to eliminate AML based on eradication of the LSCs.
  • [MeSH-major] Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Animals. Humans. Neoplastic Stem Cells / classification. Neoplastic Stem Cells / pathology. Neoplastic Stem Cells / transplantation


37. Lemez P, Urbánek V: Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients. Neoplasma; 2005;52(5):398-401
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  • [Title] Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients.
  • The aim was to follow-up gonadal functions in long-term survivors of acute myeloid leukemias (AML) after intensive chemotherapy based on high-doses of cytosine arabinoside (Ara-C) and anthracyclines in the study UHKT-911.
  • Adult patients were treated with at least 3 cycles of chemotherapy including 1-3 courses of Ara-C 10 x 2000 mg/m2/12 h and daunorubicin (DNR) 2 x 45 mg/m2/d.
  • The semen of a 49-year-old patient contained normal numbers of spermatozoa with decreased velocity when examined 1 year after chemotherapy but 4 years later exhibited oligoasthenozoospermia.
  • The patient received 4 cycles of Ara-C and DNR plus one cycle with etoposide 350 mg/m2 and mitoxantrone 30 mg/m2.
  • Semen examination of two patients 55- and 59-year-old showed permanent oligoasthenozoospermia with only sporadic progressively motile spermatozoa which might not be compatible with fertilization by sexual intercourse.
  • They received the same chemotherapy including cumulative doses of etoposide 500 mg/m2 and mitoxantrone 36 mg/m2.
  • Permanent amenorrhea developed in two women (42- and 46-year-old) during chemotherapy with DNR, Ara-C, etoposide, and mitoxantrone which was not the case in three women (29-40 years old) treated without etoposide and mitoxantrone.
  • Intensive chemotherapy with high-doses of Ara-C and DNR plus one cycle of etoposide and mitoxantrone may cause permanent gonadal dysfunction in middle-aged patients with AML.
  • [MeSH-major] Amenorrhea / chemically induced. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / drug therapy. Spermatozoa / drug effects
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Transplantation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Oligospermia / chemically induced. Sperm Motility / drug effects

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  • (PMID = 16151584.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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38. Polakova K, Bandzuchova E, Sabty FA, Mistrik M, Demitrovicova L, Russ G: Activation of HLA-G expression by 5-aza-2 - deoxycytidine in malignant hematopoetic cells isolated from leukemia patients. Neoplasma; 2009;56(6):514-20
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  • [Title] Activation of HLA-G expression by 5-aza-2 - deoxycytidine in malignant hematopoetic cells isolated from leukemia patients.
  • Human leukocyte antigen - G (HLA-G) is a non-classical HLA class I antigen with restricted distribution in normal tissues.
  • Recently it was demonstrated that DNA methyltransferase inhibitor 5-aza-2 - deoxycytidine (AdC) induces/enhances HLA-G transcription in many leukemia cell lines of different origin.
  • Here we investigated the effect of AdC on HLA-G expression in malignant hematopoetic cells isolated from patients with acute myeloid leukemia (AML) and chronic lymphocytic leukemia (B-CLL).
  • Nevertheless treatment with 5-aza-2 - deoxycytidine enhanced HLA-G transcription and concomitantly HLA-G protein synthesis in some leukemia cells.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Azacitidine / analogs & derivatives. Gene Expression Regulation, Leukemic / drug effects. HLA Antigens / metabolism. Hematopoietic Stem Cells / pathology. Histocompatibility Antigens Class I / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Blotting, Western. DNA Methylation. DNA Modification Methylases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. HLA-G Antigens. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cell Transplantation

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  • (PMID = 19728760.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / RNA, Messenger; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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39. Tadmor T, Vadazs Z, Dar H, Laor R, Attias D: Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-. J Pediatr Hematol Oncol; 2006 Aug;28(8):544-6
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  • [Title] Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-.
  • Hemophagocytic syndrome (HS) is a severe and acute proliferative process of histiocytes, often associated with infection or malignancy.
  • No consistent clonal abnormality has been reported in HS.
  • We report a case of a child presented with HS, who progressed later to acute myeloid leukemia (AML)-M4, associated with a clonal evolution, from normal to a complex karyotype consisting of t [7:17] and deletions in chromosomes 7, 17, and 5.
  • This is the second report of involvement of 7q rearrangement in a child with HS that has progressed to AML.
  • Additional studies are required to establish the association reported here, between HS with progression to AML and chromosome rearrangements that involve chromosome 7q.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / genetics
  • [MeSH-minor] Acute Disease. Child, Preschool. Fatal Outcome. Humans. Male. Remission Induction. Treatment Outcome

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  • (PMID = 16912598.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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40. Palamarchuk A, Zanesi N, Aqeilan RI, Efanov A, Maximov V, Santanam U, Hagan JP, Croce CM, Pekarsky Y: Tal1 transgenic expression reveals absence of B lymphocytes. Cancer Res; 2006 Jun 15;66(12):6014-7
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  • TAL1 oncogene encodes a helix-loop-helix transcription factor, Tal1, which is required for blood cell development, and its activation is a frequent event in T-cell acute lymphoblastic leukemia.
  • To investigate the function of Tal1 in B cells, we generated Emu-TAL1 transgenic mouse line, expressing Tal1 in mouse B-cell lineage.
  • Fluorescence-activated cell sorting (FACS) analysis of lymphocytes isolated from spleens of five out of five founders reveals complete absence of IgM- or CD19-expressing cells.
  • Analysis of the recombination status of IgH genes revealed the presence of D-J but absence or drastic reduction of V-D-J rearrangements.

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  • (PMID = 16778172.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Immunoglobulin Heavy Chains; 0 / Proto-Oncogene Proteins; 135471-20-4 / TAL1 protein, human
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41. Braess J, Spiekermann K, Staib P, Grüneisen A, Wörmann B, Ludwig WD, Serve H, Reichle A, Peceny R, Oruzio D, Schmid C, Schiel X, Hentrich M, Sauerland C, Unterhalt M, Fiegl M, Kern W, Buske C, Bohlander S, Heinecke A, Baurmann H, Beelen DW, Berdel WE, Büchner T, Hiddemann W: Dose-dense induction with sequential high-dose cytarabine and mitoxantone (S-HAM) and pegfilgrastim results in a high efficacy and a short duration of critical neutropenia in de novo acute myeloid leukemia: a pilot study of the AMLCG. Blood; 2009 Apr 23;113(17):3903-10
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  • [Title] Dose-dense induction with sequential high-dose cytarabine and mitoxantone (S-HAM) and pegfilgrastim results in a high efficacy and a short duration of critical neutropenia in de novo acute myeloid leukemia: a pilot study of the AMLCG.
  • Dose density during early induction has been demonstrated to be one of the prime determinants for treatment efficacy in acute myeloid leukemia (AML).
  • The German AML Cooperative Group has therefore piloted a dose-dense induction regimen sequential high-dose AraC and mitoxantrone followed by pegfilgrastim (S-HAM) in which 2 induction cycles are applied over 11 to 12 days instead of 25 to 29 days as used in conventional double induction, thereby increasing dose density 2-fold.
  • Of 172 de novo AML patients (excluding acute promyelocytic leukemia), 61% reached a complete remission, 22% a complete remission with incomplete peripheral recovery, 7% had persistent leukemia, 10% died (early death) resulting in an overall response rate of 83%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Mitoxantrone / therapeutic use. Neutropenia / chemically induced

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  • (PMID = 19131552.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3A58010674 / pegfilgrastim; BZ114NVM5P / Mitoxantrone; PVI5M0M1GW / Filgrastim
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42. Huang Y, Li WJ, Wei CX, Zhou Z, Nie B: [Expression of HoxA10 in acute leukemia and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):959-63
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  • [Title] [Expression of HoxA10 in acute leukemia and its significance].
  • To investigate the expression of HoxA(10) mRNA in acute leukemia patients and its significance, HoxA(10) level was detected by reverse transcription polymerase chain reaction (RT-PCR) in 50 patients with acute leukemias, 7 healthy volunteers and 3 patients with ITP (idiopathic thrombocytopenic purpura).
  • The regularity of the expression of HoxA(10) gene in acute leukemia and the relationship between HoxA(10) level and the prognosis of leukemia was explored.
  • The results showed that HoxA(10) was expressed in all types of acute myelogenous leukemia; HoxA(10) message was also observed in acute lymphoblastic leukemia patients and part of control groups.
  • 3 normal donors were found not to express HoxA(10).
  • The level of HoxA(10) mRNA of acute myelogenous leukemia patients was significantly higher than that of acute lymphoblastic leukemia patients and controls (P < 0.01).
  • HoxA(10) gene appeared to be more strongly expressed in AML-M(1) and -M(2) subtypes than in AML-M(4) and -M(5) subtypes, and the gene was notable high expressed in acute promyelocytic leukemia.
  • The level of HoxA(10) of 9 non-responsive patients was higher than that of 8 remission patients, but there was no significant difference between them (P = 0.258).
  • HoxA(10) was overexpressed in acute myelogenous leukemia.
  • It is concluded that HoxA(10) is a major transcription factor regulating hematopoiesis and a mark to differentiate lymphoid leukemia and myelogenous leukemia, but not a specific gene of cancer.
  • The level of HoxA(10) is related with load of leukemic cells and curative effect, and can affect occurrence and development of leukemia in combination with many cytokines, HoxA(10) may facilitate the leukemia progression with another cofactors.

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  • (PMID = 16403259.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 140441-81-2 / HOXA10 protein, human
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43. Wykrzykowska JJ, Carrozza J, Laham RJ: Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting. J Invasive Cardiol; 2006 Aug;18(8):E217-20
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  • [Title] Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting.
  • Of the type-A dissections in the International Registry of Aortic Dissections (IRAD), 27% were caused by coronary interventions.
  • [MeSH-major] Aneurysm, Dissecting / therapy. Aortic Aneurysm / therapy. Coronary Aneurysm / therapy. Coronary Disease / therapy. Stents

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  • (PMID = 16877790.001).
  • [ISSN] 1557-2501
  • [Journal-full-title] The Journal of invasive cardiology
  • [ISO-abbreviation] J Invasive Cardiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Dawson MA, Avery S, McQuilten ZK, Bailey MJ, Shortt J, Polizzotto MN, Wood EM, Cole-Sinclair MF: Blood transfusion requirements for patients undergoing chemotherapy for acute myeloid leukemia how much is enough? Haematologica; 2007 Jul;92(7):996-7
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  • [Title] Blood transfusion requirements for patients undergoing chemotherapy for acute myeloid leukemia how much is enough?
  • Although essential in the management of AML, there is little information quantitating transfusion requirements for these patients.
  • We evaluated 111 consecutive adults treated for AML, showing that approximately 150 blood donors are required to adequately cater for a single patient's complete therapy with little variation for age, prognostic group or intensity of treatment.
  • [MeSH-major] Blood Transfusion / utilization. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols. Blood Donors / supply & distribution. Humans. Middle Aged

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  • (PMID = 17606456.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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45. Leslie M, Case MC, Hall AG, Coulthard SA: Expression levels of asparagine synthetase in blasts from children and adults with acute lymphoblastic leukaemia. Br J Haematol; 2006 Mar;132(6):740-2
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  • [Title] Expression levels of asparagine synthetase in blasts from children and adults with acute lymphoblastic leukaemia.
  • L-asparaginase is active in the treatment of acute lymphoblastic leukaemia (ALL) through the depletion of serum asparagine.
  • Here we report that median asparagine synthetase (AS) mRNA levels were higher in acute myeloid leukaemia (AML) than ALL blasts in both children and adults, with intermediate levels in normal peripheral blood mononuclear cells (NPBMC).
  • NPBMC versus child ALL (Tukeys multiple comparison test, P < 0.05); child ALL versus child AML (P < 0.001) and adult ALL versus adult AML (P < 0.01) were all significant and support the hypothesis that selectivity to treatment with l-asparaginase is due, at least in part, to lower AS expression.
  • [MeSH-major] Aspartate-Ammonia Ligase / analysis. Lymphocytes / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Line, Tumor. Child. Child, Preschool. Female. Humans. Infant. Leukemia, Myeloid / enzymology. Leukocytes, Mononuclear / enzymology. Male. Middle Aged. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 16487174.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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46. Wandroo F, Stableforth P, Hasan Y: Aspergillus brain abscess in a patient with acute myeloid leukaemia successfully treated with voriconazole. Clin Lab Haematol; 2006 Apr;28(2):130-3
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  • [Title] Aspergillus brain abscess in a patient with acute myeloid leukaemia successfully treated with voriconazole.
  • [MeSH-major] Aspergillosis / drug therapy. Aspergillus fumigatus. Brain Abscess / drug therapy. Central Nervous System Fungal Infections / drug therapy. Leukemia, Erythroblastic, Acute / drug therapy. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 16630219.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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47. Hatfield K, Øyan AM, Ersvaer E, Kalland KH, Lassalle P, Gjertsen BT, Bruserud Ø: Primary human acute myeloid leukaemia cells increase the proliferation of microvascular endothelial cells through the release of soluble mediators. Br J Haematol; 2009 Jan;144(1):53-68
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  • [Title] Primary human acute myeloid leukaemia cells increase the proliferation of microvascular endothelial cells through the release of soluble mediators.
  • Bone marrow angiogenesis is suggested to play a role in the pathogenesis of acute myeloid leukaemia (AML) and endothelial cells may mediate chemosensitivity.
  • This study investigated in vitro endothelial effects of coculture of microvascular endothelial cells (MVEC) with AML cells derived from 33 consecutive AML patients.
  • A proliferation assay showed that (i) AML cells from the majority of patients examined increased endothelial cell proliferation, while cytokine neutralizing experiments had divergent effects on proliferation and (ii) the angiopoietin/Tie2 system was important for growth of AML cells, and angiopoietin-1 induced phosphorylation of signal transducers and activators of transcription (STAT) proteins in AML cells.
  • Finally, gene expression profiling of MVEC cocultured with AML cells was conducted in non-contact cultures.
  • Microarray analysis revealed that the majority of significantly expressed genes could be categorized into gene ontology terms involved in transcription, cellular organization and intracellular signalling.
  • Our study indicates a role for the leukaemic-endothelium crosstalk in leukaemogenesis with enhancement of endothelial cell growth and increased AML cell proliferation possibly mediated by angiopoietin-1 and the STAT signalling pathway.
  • [MeSH-major] Angiopoietin-1 / metabolism. Endothelial Cells / pathology. Leukemia, Myeloid, Acute / pathology. STAT Transcription Factors / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Cell Proliferation. Chemokine CXCL10 / genetics. Chemokine CXCL11 / genetics. Chemokine CXCL9 / genetics. Coculture Techniques. Female. Gene Expression Profiling. Humans. Interleukin-8 / genetics. Lung / blood supply. Male. Microcirculation. Middle Aged. Molecular Sequence Data. Neovascularization, Pathologic. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Up-Regulation

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  • (PMID = 19016730.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Chemokine CXCL10; 0 / Chemokine CXCL11; 0 / Chemokine CXCL9; 0 / Interleukin-8; 0 / STAT Transcription Factors
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48. Ozdogu H, Boga C, Kizilkilic E, Kozanoglu I, Karakus S, Sahin FI, Unalan D, Haberal M: The first 2 years of clinical experience with peripheral blood stem cell transplantation for various hematological malignancies: results from a single Baskent University Center. Transplant Proc; 2007 May;39(4):1257-60
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  • [Title] The first 2 years of clinical experience with peripheral blood stem cell transplantation for various hematological malignancies: results from a single Baskent University Center.
  • Autologous stem cell transplantation is the current standard approach for patients with multiple myeloma and relapsed or refractory lymphoma.
  • Nonmyeloablative allogeneic stem cell transplantation has been applied worldwide.
  • Seven evaluable patients younger than 65 years old with stage II/III multiple myeloma were treated with high-dose melphalan therapy (140 mg/m(2)) plus autologous peripheral blood stem cell transplantation.
  • At a median follow-up of 10 months, all patients remained disease-free.
  • Four patients with acute myeloblastic leukemia underwent nonmyeloablative allogeneic peripheral stem cell transplantation.
  • All patients received fully matched blood from a related donor 2 days after chemotherapy in conjunction with graft-versus-host disease prophylaxis.
  • All other patients in remission remained with >90% donor cell engraftment.
  • These patients are disease-free at 13, 10, and 2 months.
  • [MeSH-major] Hematologic Neoplasms / therapy. Peripheral Blood Stem Cell Transplantation / methods. Transplantation Conditioning / methods. Transplantation, Autologous
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Communicable Disease Control. Cyclosporine / therapeutic use. Female. Hematopoietic Stem Cell Mobilization. Humans. Immunosuppressive Agents / therapeutic use. Male. Melphalan / therapeutic use. Middle Aged. Mitoxantrone / therapeutic use. Patient Selection. Treatment Outcome

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  • (PMID = 17524948.001).
  • [ISSN] 0041-1345
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; BZ114NVM5P / Mitoxantrone; Q41OR9510P / Melphalan
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49. Ciurea SO, Andersson BS: Busulfan in hematopoietic stem cell transplantation. Biol Blood Marrow Transplant; 2009 May;15(5):523-36
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  • [Title] Busulfan in hematopoietic stem cell transplantation.
  • The development of intravenous busulfan (Bu) and its incorporation in the preparative regimens for allogeneic stem cell transplantation has changed transplantation for myelogenous malignancies.
  • Bypassing the oral route to achieve 100% bioavailability translated into improved control over drug administration, with increased safety and reliability of generating therapeutic Bu levels, maximizing antileukemic efficacy.
  • Bu-nucleoside analog-based conditioning chemotherapy, thus far represented by fludarabine (Flu), is becoming the conditioning chemotherapy regimen of choice for patients with acute myelogenous leukemia (AML) at many transplant centers.
  • The use of busulfan Bu-based conditioning is extending rapidly also to hematopoietic stem cell transplantation (HSCT) for lymphoid malignancies, genetic diseases, and umbilical cord blood transplantation.

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  • (PMID = 19361744.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; G1LN9045DK / Busulfan
  • [Number-of-references] 115
  • [Other-IDs] NLM/ NIHMS111769; NLM/ PMC4261695
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50. Lal D, Park JA, Demock K, Marinaro J, Perez AM, Lin MH, Tian L, Mashtare TJ, Murphy M, Prey J, Wetzler M, Fetterly GJ, Wang ES: Aflibercept exerts antivascular effects and enhances levels of anthracycline chemotherapy in vivo in human acute myeloid leukemia models. Mol Cancer Ther; 2010 Oct;9(10):2737-51
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  • [Title] Aflibercept exerts antivascular effects and enhances levels of anthracycline chemotherapy in vivo in human acute myeloid leukemia models.
  • The efficacy of aflibercept alone and in combination with doxorubicin was evaluated in human VEGF-expressing acute myeloid leukemia (AML) cell lines and primary cells xenotransplanted into immunodeficient mice.
  • Aflibercept reduced primary VEGF/VEGFR-positive AML colony formation growth in vitro and inhibited AML xenograft growth up to 93% in association with antiangiogenic and antiproliferative effects, hypoxia, and VEGF sequestration in multiple models.
  • High VEGF-A expression by AML cells promoted in vivo xenograft growth and aflibercept sensitivity.
  • Aflibercept therapy slowed disease progression in two systemic human AML xenograft models and reduced peripheral leukemia disease in a primary relapsed AML model in NOD/SCID/IL2Rγnull mice.
  • Sequential aflibercept followed by doxorubicin resulted in progressive anthracycline accumulation in marrow and extramedullary AML sites and resulted in 2-fold higher drug levels 24 hours after administration.
  • These data suggest that inefficient drug delivery by leukemia-associated vasculature may mediate chemoresistance and support further clinical evaluation of combination aflibercept and anthracycline therapy in refractory/relapsed AML patients.
  • [MeSH-major] Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Recombinant Fusion Proteins / pharmacology

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  • (PMID = 20924124.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA016156
  • [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 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Recombinant Fusion Proteins; 15C2VL427D / aflibercept; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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51. Kojima K, Konopleva M, Samudio IJ, Ruvolo V, Andreeff M: Mitogen-activated protein kinase kinase inhibition enhances nuclear proapoptotic function of p53 in acute myelogenous leukemia cells. Cancer Res; 2007 Apr 1;67(7):3210-9
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  • [Title] Mitogen-activated protein kinase kinase inhibition enhances nuclear proapoptotic function of p53 in acute myelogenous leukemia cells.
  • Activation of the Raf/MEK/ERK pathway and inactivation of wild-type p53 by Mdm2 overexpression are frequent molecular events in acute myelogenous leukemia (AML).
  • We investigated the interaction of Raf/MEK/ERK and p53 pathways after their simultaneous blockades using a selective small-molecule antagonist of Mdm2, Nutlin-3a, and a pharmacologic MEK-specific inhibitor, PD98059.
  • We found that PD98059, which itself has minimal apoptogenic activity, acts synergistically with Nutlin-3a to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13.
  • In accordance with the activation of transcription-dependent apoptosis, PD98059 treatment promoted the translocation of p53 from the cytoplasm to the nucleus in OCI-AML-3 cells, in which p53 primarily initiates transcription-independent apoptosis when cells are treated with Nutlin-3a alone.
  • [MeSH-major] Apoptosis / physiology. Leukemia, Myeloid, Acute / enzymology. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / enzymology. Cell Nucleus / physiology. Drug Synergism. Fatty Acids, Unsaturated / pharmacology. Flavonoids / pharmacology. Humans. Imidazoles. Piperazines. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors. Transcription, Genetic. raf Kinases / metabolism

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  • (PMID = 17409429.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P01 CA55164
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Fatty Acids, Unsaturated; 0 / Flavonoids; 0 / Imidazoles; 0 / Piperazines; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; 87081-35-4 / leptomycin B; EC 2.7.11.1 / raf Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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52. Wei Y, Kadia T, Tong W, Zhang M, Jia Y, Yang H, Hu Y, Viallet J, O'Brien S, Garcia-Manero G: The combination of a histone deacetylase inhibitor with the BH3-mimetic GX15-070 has synergistic antileukemia activity by activating both apoptosis and autophagy. Autophagy; 2010 Oct;6(7):976-8
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  • [Title] The combination of a histone deacetylase inhibitor with the BH3-mimetic GX15-070 has synergistic antileukemia activity by activating both apoptosis and autophagy.
  • We analyzed the cellular and molecular effects of two different histone deacetylase inhibitors (HDACi), MGCD0103 and vorinostat, in combination with GX15-070, a BH3-mimetic, in acute myeloid leukemia (AML) cell lines and primary AML cells, and demonstrated that the combination has a synergistic antileukemia effect.
  • We observed that in addition to apoptosis, autophagy also accounts for the observed nonapoptotic decrease of cell viability.
  • These findings reveal that for this specific combination, autophagy plays a positive role in inducing cytotoxicity, and that the involved ER signaling networks, as well as their clinical relevance, should be further studied in both preclinical and clinical trials of leukemia and other malignancies.
  • [MeSH-major] Apoptosis / drug effects. Autophagy / drug effects. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / drug therapy. Pyrroles
  • [MeSH-minor] BH3 Interacting Domain Death Agonist Protein / metabolism. Benzamides / pharmacology. Benzamides / therapeutic use. Cell Line, Tumor / drug effects. Drug Synergism. Humans. Hydroxamic Acids / pharmacology. Hydroxamic Acids / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use

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  • (PMID = 20729640.001).
  • [ISSN] 1554-8635
  • [Journal-full-title] Autophagy
  • [ISO-abbreviation] Autophagy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Benzamides; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Pyrimidines; 0 / Pyrroles; 0 / obatoclax; 58IFB293JI / vorinostat; A6GWB8T96J / mocetinostat
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53. Jacobi A, Thieme S, Lehmann R, Ugarte F, Malech HL, Koch S, Thiede C, Müller K, Bornhäuser M, Ryser M, Brenner S: Impact of CXCR4 inhibition on FLT3-ITD-positive human AML blasts. Exp Hematol; 2010 Mar;38(3):180-90
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  • [Title] Impact of CXCR4 inhibition on FLT3-ITD-positive human AML blasts.
  • OBJECTIVE: Internal tandem duplication (ITD) mutations of the FLT3 receptor are associated with a high incidence of relapse in acute myeloid leukemia (AML).
  • Expression of the CXCR4 receptor in FLT3-ITD-positive AML is correlated with poor outcome, and inhibition of CXCR4 was shown to sensitize AML blasts toward chemotherapy.
  • The aim of this study was to evaluate the impact of FLT3-ITD on cell proliferation and CXCR4-dependent migration in human hematopoietic progenitor cells and to investigate their response to CXCR4 inhibition.
  • MATERIALS AND METHODS: We used primary blasts from patients with FLT3-ITD or FLT3 wild-type AML.
  • Cocultivation of FLT3-ITD-positive AML blasts or hematopoietic progenitor cells on bone marrow stromal cells resulted in a strong proliferation advantage and increased early cobblestone area-forming cells compared to FLT3-wild-type AML blasts.
  • Addition of the CXCR4 inhibitor AMD3100 to the coculture significantly reduced both cobblestone area-forming cells and proliferation of FLT3-ITD-positive cells, but did not affect FLT3-wild-type cells-highlighting the critical interaction between CXCR4 and FLT3-ITD.
  • CONCLUSION: CXCR4 inhibition to decrease cell proliferation and to control the leukemic burden may provide a novel therapeutic strategy in patients with advanced FLT3-ITD-positive AML.

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  • [Copyright] Copyright 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20035824.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / Z01 AI000988; United States / Intramural NIH HHS / / Z01 AI000988-02; United States / Intramural NIH HHS / / ZIA AI000988-03; United States / Intramural NIH HHS / / ZIA AI000988-04
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Heterocyclic Compounds; 0 / Receptors, CXCR4; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins; 155148-31-5 / JM 3100; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS762780; NLM/ PMC4777334
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54. Tsai DE, Luger SM, Andreadis C, Vogl DT, Kemner A, Potuzak M, Goradia A, Loren AW, Perl AE, Schuster SJ, Porter DL, Stadtmauer EA, Goldstein SC, Thompson JE, Swider C, Bagg A, Mato AR, Carroll M: A phase I study of bexarotene, a retinoic X receptor agonist, in non-M3 acute myeloid leukemia. Clin Cancer Res; 2008 Sep 1;14(17):5619-25
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  • [Title] A phase I study of bexarotene, a retinoic X receptor agonist, in non-M3 acute myeloid leukemia.
  • PURPOSE: Bexarotene is a retinoic X receptor agonist that has been shown in vitro to inhibit growth and induce differentiation of myeloid leukemic cell lines.
  • We therefore conducted a phase I dose escalation study to assess the maximum tolerated dose, toxicities, and activity of bexarotene in patients with non-M3 acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: We enrolled patients with active non-M3 AML who had either relapsed or refractory disease or were not eligible for standard cytotoxic chemotherapy.
  • Cohorts of three to six patients received escalating doses of daily oral bexarotene ranging from 100 to 400 mg/m(2) until evidence of disease progression or unacceptable adverse events occurred.
  • Three patients with relapsed AML survived >1 year while taking bexarotene.
  • Leukemic blast differentiation was suggested by the presence of the leukemic cytogenetic abnormality in mature circulating granulocytes and the occurrence of differentiation syndrome.
  • Bexarotene is well tolerated in patients with non-M3 AML and has evidence of antileukemic activity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Retinoid X Receptors / antagonists & inhibitors. Tetrahydronaphthalenes / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Male. Maximum Tolerated Dose. Middle Aged

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  • [CommentIn] Clin Cancer Res. 2008 Sep 1;14(17):5311-3 [18765520.001]
  • (PMID = 18765556.001).
  • [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
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; A61RXM4375 / bexarotene
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55. Pearce DJ, Taussig D, Zibara K, Smith LL, Ridler CM, Preudhomme C, Young BD, Rohatiner AZ, Lister TA, Bonnet D: AML engraftment in the NOD/SCID assay reflects the outcome of AML: implications for our understanding of the heterogeneity of AML. Blood; 2006 Feb 01;107(3):1166-73
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  • [Title] AML engraftment in the NOD/SCID assay reflects the outcome of AML: implications for our understanding of the heterogeneity of AML.
  • We explored why 51% of 59 acute myeloid leukemia (AML) patients were unable to initiate leukemia in NOD/SCID mice.
  • Increasing the cell dose, using more permissive recipients, and alternative tissue sources did not cause AML engraftment in most previously nonengrafting AML samples.
  • Homing of AML cells to the marrow was the same between engrafters and nonengrafters.
  • The only variable that was related to engraftment ability was the karyotypically defined risk stratification of individual AML cases.
  • Of interest, follow-up of younger patients with intermediate-risk AML revealed a significant difference in overall survival between NOD/SCID engrafting and nonengrafting AMLs.
  • Hence, the ability of AML to engraft in the NOD/SCID assay seems to be an inherent property of AML cells, independent of homing, conditioning, or cell frequency/source, which is directly related to prognosis.
  • Our results suggest an important difference between leukemic initiating cells between engrafting and nonengrafting AML cases that correlates with treatment response.
  • [MeSH-major] Biological Assay. Graft Survival. Leukemia, Myeloid, Acute. Neoplastic Stem Cells. Stem Cell Transplantation

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  • (PMID = 16234360.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United States / NHLBI NIH HHS / HL / HL-64856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1895911
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56. Shabbir M, Stuart R: Lestaurtinib, a multitargeted tyrosine kinase inhibitor: from bench to bedside. Expert Opin Investig Drugs; 2010 Mar;19(3):427-36
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  • IMPORTANCE OF THE FIELD: Internal tandem duplication of the fms-like tyrosine kinase 3 (FLT3) gene (FLT3-ITD) is a common recurring mutation in acute myeloid leukemia (AML) with normal karyotype, and the presence of FLT3-ITD confers a poor prognosis on this large subgroup of AML patients.
  • AREAS COVERED IN THIS REVIEW: An extensive literature search was conducted that included published articles and abstracts on the preclinical and clinical development of this agent spanning the last decade.
  • TAKE HOME MESSAGE: Lestaurtinib is a multi targeted tyrosine kinase inhibitor which has been shown to potently inhibit FLT3 at nanomolar concentrations in preclinical studies, leading to its rapid development as a potential targeted agent for treatment of AML.
  • Currently, Phase II and Phase III studies are underway aiming to establish the future of this agent as a treatment option for patients with FLT3-ITD AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carbazoles / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20141349.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Protein Kinase Inhibitors; DO989GC5D1 / lestaurtinib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 63
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57. Bhayat F, Das-Gupta E, Hubbard R: Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study. BMC Cancer; 2010;10:514
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  • [Title] Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study.
  • BACKGROUND: We have previously shown that in the UK mortality in people with Acute Myeloid Leukaemia (AML) was nearly 50% greater among the most socio-economically deprived.
  • The aim of this study was to determine whether AML patients from lower socioeconomic classes had a lower chance of receiving a bone marrow transplant.
  • METHODS: Using Hospital Episode Statistics (HES) data, we identified all incident cases of AML admitted to UK hospitals between 1998 and 2007.
  • We calculated the number of bone marrow transplantations undertaken in AML patients, stratifying our results by gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity.
  • We used logistic regression to calculate odds ratios for bone marrow transplantation, adjusting for gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity score.
  • RESULTS: We identified a total of 23 910 incident cases of AML over this 10-year time period, of whom 1 140 (4.8%) underwent BMT.
  • Bone marrow transplantation declined with increasing socioeconomic deprivation (p for trend < 0.001) such that people in the most deprived socioeconomic quintile were 40% less likely to have a transplant than those in the most advantaged group (Odds Ratio 0.60, 95% confidence interval 0.49, 0.73), even after adjusting for gender, age at diagnosis, year of diagnosis and co-morbidity.
  • CONCLUSION: This large cohort study demonstrates that AML patients from lower socioeconomic classes are less likely to undergo bone marrow transplantation than their better off counter-parts.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy


58. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
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  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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59. Li L, Han W, Gu Y, Qiu S, Lu Q, Jin J, Luo J, Hu X: Honokiol induces a necrotic cell death through the mitochondrial permeability transition pore. Cancer Res; 2007 May 15;67(10):4894-903
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  • [Title] Honokiol induces a necrotic cell death through the mitochondrial permeability transition pore.
  • Previous reports have shown that honokiol induces apoptosis in numerous cancer cell lines and showed preclinical efficacies against apoptosis-resistant B-cell chronic lymphocytic leukemia and multiple myeloma cells from relapse-refractory patients.
  • Here, we show that honokiol can induce a cell death distinct from apoptosis in HL60, MCF-7, and HEK293 cell lines.
  • The death was characterized by a rapid loss of integrity of plasma membrane without externalization of phosphatidyl serine.
  • The broad caspase inhibitor z-VAD-fmk failed to prevent this cell death.
  • Consistently, caspase activation and DNA laddering were not observed.
  • The death was paralleled by a rapid loss of mitochondrial membrane potential, which was mechanistically associated with the mitochondrial permeability transition pore regulated by cyclophilin D (CypD) based on the following evidence: (a) cyclosporin A, an inhibitor of CypD (an essential component of the mitochondrial permeability transition pore), effectively prevented honokiol-induced cell death and loss of mitochondrial membrane potential;.
  • (b) inhibition of CypD by RNA interference blocked honokiol-induced cell death;.
  • (c) CypD up-regulated by honokiol was correlated with the death rates in HL60, but not in K562 cells, which underwent apoptosis after being exposed to honokiol.
  • We further showed that honokiol induced a CypD-regulated death in primary human acute myelogenous leukemia cells, overcame Bcl-2 and Bcl-X(L)-mediated apoptotic resistance, and was effective against HL60 cells in a pilot in vivo study.
  • To the best of our knowledge, this is the first report to document an induction of mitochondrial permeability transition pore-associated cell death by honokiol.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Biphenyl Compounds / pharmacology. Lignans / pharmacology. Mitochondrial Membrane Transport Proteins / physiology. Neoplasms / drug therapy. Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Apoptosis Inducing Factor / metabolism. Cell Death / drug effects. Cell Line, Tumor. Cell Nucleus / metabolism. Cyclophilins / metabolism. Female. HL-60 Cells. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Male. Membrane Potential, Mitochondrial / drug effects. Middle Aged. Mitochondria / drug effects. Mitochondria / metabolism. Mitochondria / physiology. Necrosis. Reactive Oxygen Species / metabolism

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  • (PMID = 17510419.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AIFM1 protein, human; 0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Inducing Factor; 0 / Biphenyl Compounds; 0 / Lignans; 0 / Mitochondrial Membrane Transport Proteins; 0 / Reactive Oxygen Species; 0 / mitochondrial permeability transition pore; 11513CCO0N / honokiol; EC 5.2.1.- / Cyclophilins; EC 5.2.1.8 / PPID protein, human
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60. Sollars VE, Pequignot E, Rothstein JL, Buchberg AM: Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes. Mamm Genome; 2006 Aug;17(8):808-21
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  • [Title] Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes.
  • The myeloid progenitor cell compartment (MPC) exhibits pronounced expansion in human myeloid leukemias.
  • It is becoming more apparent that progression of myelodysplastic syndromes and myeloproliferative diseases to acute myelogenous leukemia is the result of defects in progenitor cell maturation.
  • The MPC of bone marrow was analyzed in mice using a cell culture assay for measuring the relative frequency of proliferative myeloid progenitors.
  • The SWR/J and FVB/J strains show consistently low frequencies of myeloid progenitors, while the DBA/2J and SJL/J inbred strains show consistently high frequencies of myeloid progenitors within the bone marrow compartment.
  • Given the importance of this cell compartment in leukemia progression and the soon to be released genomic sequence of 15 mouse strains, these differences may provide a valuable tool for research into leukemia.
  • [MeSH-major] Cell Proliferation. Genetic Predisposition to Disease. Leukemia / genetics. Myeloid Progenitor Cells / metabolism
  • [MeSH-minor] Animals. Bone Marrow / growth & development. Cell Size. Chromosomes, Mammalian. Cytokines / metabolism. Flow Cytometry. Linkage Disequilibrium. Male. Mice. Mice, Inbred Strains. Stem Cells

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  • (PMID = 16897342.001).
  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA09678
  • [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 / Cytokines
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61. Lim AY, Gaffney K, Scott DG: Methotrexate-induced pancytopenia: serious and under-reported? Our experience of 25 cases in 5 years. Rheumatology (Oxford); 2005 Aug;44(8):1051-5
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  • Pancytopenia was defined as white blood cell count (WBC) <3.5 x 10(9)/l, haemoglobin (Hb) <11 g/dl and platelet count <130 x 10(9)/l.
  • There were seven deaths (28% mortality), five from sepsis and two from acute myeloid leukaemia.

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  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):361-2; author reply 363-4 [16332953.001]
  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):362-3; author reply 363-4 [16332952.001]
  • [CommentIn] Rheumatology (Oxford). 2006 Mar;45(3):361; author reply 363-4 [16332954.001]
  • (PMID = 15901903.001).
  • [ISSN] 1462-0324
  • [Journal-full-title] Rheumatology (Oxford, England)
  • [ISO-abbreviation] Rheumatology (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; YL5FZ2Y5U1 / Methotrexate
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62. Jóhannsdóttir IM, Hjermstad MJ, Moum T, Wesenberg F, Hjorth L, Schrøder H, Lähteenmäki P, Jónmundsson G, Loge JH: Social outcomes in young adult survivors of low incidence childhood cancers. J Cancer Surviv; 2010 Jun;4(2):110-8
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  • The study objective was to assess social outcomes in early adulthood after successful treatment for childhood acute myeloid leukemia (AML), Wilms tumor (WT) and infratentorial astrocytoma (IA).
  • METHODS: Nordic patients treated for AML, WT and IA from 1985 to 2001 identified from a database administered by NOPHO (Nordic Society of Paediatric Haematology and Oncology) were invited to participate in a postal survey.
  • [MeSH-major] Astrocytoma / psychology. Infratentorial Neoplasms / psychology. Leukemia, Myeloid, Acute / psychology. Social Behavior. Survivors / psychology. Wilms Tumor / psychology

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  • (PMID = 20082150.001).
  • [ISSN] 1932-2267
  • [Journal-full-title] Journal of cancer survivorship : research and practice
  • [ISO-abbreviation] J Cancer Surviv
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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63. Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E: Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia. Pediatr Blood Cancer; 2006 Feb;46(2):266
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  • [Title] Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
  • [MeSH-major] Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage. Leukemia, Myeloid, Acute / complications


64. Nishizawa M, Hirayama F, Matsuyama N, Tada K, Kaneko H, Watanabe M, Miura Y, Tsudo M: [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate]. Rinsho Ketsueki; 2009 Jan;50(1):16-22
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  • [Title] [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate].
  • We report a fatal case of transfusion-related acute lung injury (TRALI) with anti-leukocyte antibodies detected both in the patient's serum and in the causative red cell concentrate (RC-M.A.P).
  • A 41-year-old Japanese woman diagnosed as having acute myeloid leukemia (AML, M2) developed TRALI caused by RC-M.A.P 15 days after the start of induction therapy for AML.
  • [MeSH-major] Acute Lung Injury / etiology. Autoantibodies / blood. Erythrocyte Transfusion / adverse effects. HLA Antigens / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes / immunology

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  • (PMID = 19225224.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / HLA Antigens
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65. Mishra P, Kumar R, Mahapatra M, Sharma S, Dixit A, Chaterjee T, Choudhry DR, Saxena R, Choudhry VP: Tuberculosis in acute leukemia: a clinico-hematological profile. Hematology; 2006 Oct;11(5):335-40
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  • [Title] Tuberculosis in acute leukemia: a clinico-hematological profile.
  • We studied 130 consecutive cases of acute leukemia over a 2-year period and identified 9 cases (6.9%) with active tuberculosis (TB).
  • Eight patients with TB had acute myeloid leukemia (AML).
  • Patients with AML were more likely to develop TB as compared to patients with acute lymphoblastic leukemia (ALL) despite the wider use of steroids and radiotherapy in ALL protocols {OR 4.41 (CI 0.53-36.44)}.
  • On the whole, TB did not cause any undue delay in chemotherapy and did not flare up during subsequent chemotherapy cycles.
  • However it is not a commonly described infection in acute leukemia and a high index of suspicion is warranted especially in areas endemic for TB.
  • [MeSH-major] Leukemia / complications. Tuberculosis / etiology
  • [MeSH-minor] Acute Disease. Adult. Antitubercular Agents / therapeutic use. Female. Humans. Incidence. Leukemia, Myeloid. Male. Neutropenia. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • (PMID = 17607583.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antitubercular Agents
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66. Kamel AM, El-Sharkawy N, Yassin D, Shaaban K, Hussein H, Sidhom I, Abo El-Naga S, Ameen M, El-Hattab O, Aly El-Din NH: P-gp expression and Rh 123 efflux assay have no impact on survival in Egyptian pediatric acute lymphoblastic leukemia patients. J Egypt Natl Canc Inst; 2005 Sep;17(3):165-72
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  • [Title] P-gp expression and Rh 123 efflux assay have no impact on survival in Egyptian pediatric acute lymphoblastic leukemia patients.
  • PURPOSE: In a previous work we have studied MDR status in terms of P-glycoprotein (P-gp) expression and Rhodamine 123 efflux assay in Egyptian acute leukemia patients.
  • We have reported results comparable to the literature as regards ANLL both in pediatric and adult cases.
  • MATERIAL AND METHODS: A total of 108 cases were studied including 80 ALL and 28 ANLL.
  • ANLL cases included 18 male and 10 female with an age range of 6m to 18 yrs and a median of 8 yrs.
  • MDR expression and function were correlated to age, Hb, TLC, CD34 expression, immunophenotype and DNA index in ALL, FAB subtypes in ANLL as well as to CR, DFS and EFS in ALL.
  • In ANLL P-gp expression was encountered in 47.6% of cases, while positive Rh123 efflux assay was encountered in 75% of cases.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. P-Glycoprotein / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Rhodamine 123

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  • (PMID = 16799654.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123
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67. Ustun C: Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia. J Laparoendosc Adv Surg Tech A; 2007 Apr;17(2):213-5
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  • [Title] Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia.
  • The management of acute myelogenous leukemia is often complicated by infections due to neutropenia, but the appendix is not a common site of infection in adult patients with acute myelogenous leukemia.
  • The diagnosis of acute appendicitis may be delayed or even missed because of the lack of characteristic signs and symptoms associated with acute appendicitis in neutropenic patients.
  • The case presented here is of a 33-year-old Hispanic man with acute myelogenous leukemia who developed severe diffuse acute abdominal pain with positive signs of rebound tenderness, fever, and hypotension ten days after receiving reinduction chemotherapy.
  • The patient was at his nadir, with a white blood cell count of 0.2 x 10(9)/L, platelet count of 20 x 10(9)/L, and hemoglobin of 7 g/dL.
  • A computed tomography scan of the abdomen was suspicious for acute appendicitis.
  • [MeSH-major] Appendicitis / surgery. Leukemia, Myeloid, Acute / complications

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  • (PMID = 17484650.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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68. Kern W, Haferlach T: [Quantification of minimal residual disease by multiparameter flow cytometry in acute myeloid leukemia. From diagnosis to prognosis]. Med Klin (Munich); 2005 Jan 15;100(1):54-9
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  • [Title] [Quantification of minimal residual disease by multiparameter flow cytometry in acute myeloid leukemia. From diagnosis to prognosis].
  • Today, multiparameter flow cytometry allows the simultaneous assessment of up to five surface and cytoplasmic antigens in different cell populations from peripheral blood and bone marrow samples.
  • In the setting of diagnosing acute myeloid leukemias (AML) this method is used not only to subclassify AML and separate it from acute lymphoblastic and biphenotypic leukemias but also for the identification of leukemia-associated aberrant immunophenotypes (LAIPs).
  • Since these LAIPs are defined individually for each patient, leukemic bone marrow cells can be detected during the course of treatment using the LAIP allowing the quantification of minimal residual disease (MRD) which is not detectable by cytomorphology.
  • Due to its close correlation with the course of the disease and with the risk of relapse the MRD represents an important prognostic parameter which is increasingly used for stratification of therapy in clinical trials.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis

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  • (PMID = 15654545.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Epitopes; EC 3.1.3.48 / Antigens, CD45
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69. Uzunhan Y, Cadranel J, Boissel N, Gardin C, Arnulf B, Bergeron A: [Lung involvement in lymphoid and lympho-plasmocytic proliferations (except lymphomas)]. Rev Mal Respir; 2010 Jun;27(6):599-610
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  • [Transliterated title] Les manifestations pulmonaires spécifiques des hémopathies myéloïdes aiguës et des hémopathies lymphoïdes et lymphoplasmocytaires. Partie II : les manifestations pulmonaires spécifiques des hémopathies lymphoïdes et lymphoplasmocytaires (hors lymphomes).
  • INTRODUCTION - BACKGROUND: The non infectious pulmonary manifestations occurring in lymphoplasmocytic proliferations others than lymphomas are poorly understood and have rarely been the object of dedicated publications.
  • VIEWPOINTS: The purpose of this work is to review the literature of the various specific lung manifestations occurring during these malignant haematological diseases.
  • We will also consider acute lymphoblastic leukaemia, chronic lymphocytic leukaemia and hairy cell leukaemia, as well as malignant plasmocytic disorders such as myeloma, POEMS syndrome and Waldenström's macroglobulinaemia.
  • CONCLUSION: During the course of lymphoplasmocytic diseases, lung manifestations are variable and sometimes require invasive techniques for definitive diagnosis.
  • [MeSH-major] Lung Diseases / etiology. Lymphoproliferative Disorders / complications
  • [MeSH-minor] Humans. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Multiple Myeloma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Waldenstrom Macroglobulinemia / complications

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  • [Copyright] Copyright 2010 SPLF. Published by Elsevier Masson SAS. All rights reserved.
  • (PMID = 20610075.001).
  • [ISSN] 1776-2588
  • [Journal-full-title] Revue des maladies respiratoires
  • [ISO-abbreviation] Rev Mal Respir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
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70. Long J, Parkin B, Ouillette P, Bixby D, Shedden K, Erba H, Wang S, Malek SN: Multiple distinct molecular mechanisms influence sensitivity and resistance to MDM2 inhibitors in adult acute myelogenous leukemia. Blood; 2010 Jul 8;116(1):71-80
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  • [Title] Multiple distinct molecular mechanisms influence sensitivity and resistance to MDM2 inhibitors in adult acute myelogenous leukemia.
  • The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel therapeutic approaches are needed to improve outcomes.
  • Given that the fraction of AML with mutated p53 is small ( approximately 10%), it appears rational to study MDM2 inhibitors as therapy for AML.
  • Here, we report results of a detailed characterization of sensitivity and resistance to treatment ex vivo with the MDM2 inhibitor MI219 in AML blasts from 109 patients.
  • In line with previous observations, all AML cases with mutated p53 were resistant to MI219.
  • Importantly, approximately 30% of AML cases with unmutated p53 also demonstrated primary resistance to MI219.
  • Analysis of potential mechanisms associated with MI219 resistance in AML blasts with wild-type p53 uncovered distinct molecular defects, including low or absent p53 protein induction after MDM2 inhibitor treatment or external irradiation.
  • Finally, analysis of very sensitive AML cases uncovered a strong and significant association with mutated Flt3 status (Flt3-ITD), which for the first time identified a clinically high-risk group of AML that may particularly benefit from MDM2 inhibitor treatment.

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  • (PMID = 20404136.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA136537; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / 1R01 CA136537-01; United States / NCRR NIH HHS / RR / UL1RR024986; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCRR NIH HHS / RR / UL1 RR024986
  • [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 / Imidazoles; 0 / Indoles; 0 / MDM4 protein, human; 0 / MI-63 compound; 0 / Nuclear Proteins; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Spiro Compounds; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2904583
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71. Qadir M, O'Loughlin KL, Fricke SM, Williamson NA, Greco WR, Minderman H, Baer MR: Cyclosporin A is a broad-spectrum multidrug resistance modulator. Clin Cancer Res; 2005 Mar 15;11(6):2320-6
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  • PURPOSE: Overexpression of the multidrug resistance proteins P-glycoprotein (Pgp), multidrug resistance protein (MRP-1), breast cancer resistance protein (BCRP), and lung resistance protein (LRP) is associated with treatment failure in acute myeloid leukemia (AML) and other malignancies.
  • The Pgp modulator cyclosporin A has shown clinical efficacy in AML, whereas its analogue PSC-833 has not.
  • EXPERIMENTAL DESIGN: We studied the effects of cyclosporin A and PSC-833 on in vitro drug retention and cytotoxicity in resistant cell lines overexpressing Pgp, MRP-1, and BCRP and on nuclear-cytoplasmic drug distribution and cytotoxicity in cells overexpressing LRP.
  • Moreover, cyclosporin A enhanced nuclear distribution of doxorubicin in 8226/MR20 cells, which also express LRP, and increased doxorubicin cytotoxicity 12-fold without an effect on cellular doxorubicin content, consistent with expression of wild-type BCRP, which does not efflux doxorubicin.
  • Cyclosporin A also enhanced nuclear doxorubicin distribution in a second cell line with LRP overexpression, HT1080/DR4.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Antibiotics, Antineoplastic / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Nucleus / metabolism. Cells, Cultured. Cytoplasm / metabolism. Doxorubicin / metabolism. HL-60 Cells / drug effects. HL-60 Cells / metabolism. Humans. Kidney / drug effects. Kidney / metabolism. Mitoxantrone / metabolism. Neoplasm Proteins / metabolism. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 15788683.001).
  • [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 / NCI NIH HHS / CA / P30 CA 16056; United States / NCI NIH HHS / CA / R21 CA 98457; United States / NCI NIH HHS / CA / T32 CA 09072-28
  • [Publication-type] 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 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 80168379AG / Doxorubicin; 83HN0GTJ6D / Cyclosporine; BZ114NVM5P / Mitoxantrone
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72. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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73. Raza A, Mehdi M, Mumtaz M, Ali F, Lascher S, Galili N: Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia. Cancer; 2008 Oct 1;113(7):1596-604
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  • [Title] Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia.
  • Many patients will either not respond or will have only limited and/or brief responses to single-agent therapy.
  • Eventually, 30% of patients with MDS will progress and develop acute myeloid leukemia (AML).
  • METHODS: 5-Azacytidine (AZA) and thalidomide were administered to 40 patients with MDS or AML.
  • AZA was given at a dose of 75 mg/m2 subcutaneously for 5 of 28 days together with thalidomide starting at a dose of 50 mg per day and increasing to 100 mg per.
  • Six patients had refractory anemia (RA), 2 patients had RA with ringed sideroblasts, 10 patients had RA with excess blasts (RAEB), 1 patient had RAEB in transformation, 4 patients had chronic myelomonocytic leukemia, 1 patient had chronic idiopathic myelofibrosis, and 16 patients had AML.
  • RESULTS: A hematologic improvement (HI) was observed in 15 of 36 patients (42%), stable disease was observed in 5 of 36 patients (14%), and 10 of 36 patients (28%) had disease progression.
  • It was noteworthy that 9 of 14 patients with AML had a history of prior MDS, 2 of 9 patients achieved a CR, 4 of 9 patients had HI (HI-E and bilineage HI), and 1 patient had stable disease and was continuing treatment.
  • CONCLUSIONS: The current findings indicated that a combination of low-dose AZA and thalidomide was well tolerated and was effective therapy for the treatment of patients with MDS and AML arising from prior MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Azacitidine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Thalidomide / administration & dosage


74. 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).
  • Among these cases, three-way breakpoints 18p11.3 and 2q11.2 have not been previously reported.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic


75. Tessema M, Länger F, Bock O, Seltsam A, Metzig K, Hasemeier B, Kreipe H, Lehmann U: Down-regulation of the IGF-2/H19 locus during normal and malignant hematopoiesis is independent of the imprinting pattern. Int J Oncol; 2005 Feb;26(2):499-507
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  • In order to elucidate the contribution of H19 and IGF-2 to leukemogenesis, the mRNA expression level of both genes were quantitated in bone marrow biopsies and peripheral blood samples from normal (n=98), chronic myelomonocytic leukemia (CMML, n=43), chronic myelogenous leukemia (CML, n=40) and, acute myelogenous leukemia (AML, n=32) cases.
  • This down-regulation was not accompanied by changes in methylation of the differentially methylated region (DMR).
  • No correlations between imprinting status (mono- versus biallelic expression), quantitative mRNA expression levels and course of disease were found for the IGF-2 gene.
  • The data suggest a disturbed regulation of the IGF-2/H19 locus in myeloid leukemias which is not caused by loss of imprinting.
  • [MeSH-minor] Alleles. Biopsy. Bone Marrow Cells / metabolism. DNA Methylation. DNA, Complementary / metabolism. Genotype. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Models, Genetic. RNA, Long Noncoding. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15645136.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / H19 long non-coding RNA; 0 / RNA, Long Noncoding; 0 / RNA, Messenger; 0 / RNA, Untranslated; 67763-97-7 / Insulin-Like Growth Factor II
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76. Paupert J, Mansat-De Mas V, Demur C, Salles B, Muller C: Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features. Cell Cycle; 2008 Apr 15;7(8):1047-53
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  • [Title] Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features.
  • The metalloprotease 9 (MMP-9), a known mediator of tumour invasion, is secreted as a 92 kDa pro-form but a non-secreted variant of 85 Kda has been described.
  • We previously showed that the DNA repair protein Ku interacts at the cell surface of leukaemia cell lines with the 85 Kda pro-form of MMP-9 and these Ku/MMP-9 complexes regulates cell invasion, highlighting their importance in haematological malignancies.
  • We demonstrate here that all samples of acute myeloid leukaemia (AML) blasts purified from bone marrow of 16 affected patients express the 85 Kda form of MMP-9.
  • However, only AML that display monocytic lineage markers (AML4/5) express this form at the cell surface with co-expression of the membrane associated form of Ku.
  • Blocking antibodies directed against Ku or MMP-9 specifically inhibited cell invasion of those expressing Ku/MMP-9 on the cell surface.
  • The membrane form of Ku might represent an important factor in the exposition to the cell surface of this specific MMP-9 pro-form in AML with monocytic features.
  • These results might have important functional significance in the occurrence of extra-medullar infiltrates of leukaemia cells that occurs frequently during the onset of monocyte-related AML sub-types.
  • [MeSH-major] DNA Helicases / metabolism. Leukemia, Myeloid, Acute / metabolism. Matrix Metalloproteinase 9 / metabolism. Membrane Proteins / metabolism. Monocytes / metabolism. Neoplasm Invasiveness / physiopathology
  • [MeSH-minor] Adult. Aged. Blotting, Western. Cell Line, Tumor. Female. Humans. Male. Middle Aged

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  • (PMID = 18414048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / XRCC5 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.4.- / DNA Helicases
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77. Zhang Y, He Q, Huang XJ, Jiang H, Yang SM, Lu J, Qing YZ, Shi Y, Dang H, Qiu JY, Lu DP: [Cytogenetic study on eosinophilia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):454-7
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  • The aim of study was to investigate the importance of chromosome aberration in differential diagnosis of eosinophilia and the chromosomal aberrations involved in patients with clonal eosinophilia.
  • Combining clinical, hematological and cytogenetical data, the 5 patients were diagnosed as acute myeloid leukemia with eosinophilia, chronic eosinophilic leukemia, 8p11 myeloproliferative syndrome, chronic myeloid leukemia in acute phase and acute myeloid leukemia-M(4Eo) respectively.
  • In conclusion, cytogenetical detection is very important in differential diagnosis of clonal eosinophilic disorders and chronic eosinophilic leukemia, which is suggested to be done routinely in clinic.

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  • (PMID = 17605843.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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78. Kuiken C, Yusim K, Boykin L, Richardson R: The Los Alamos hepatitis C sequence database. Bioinformatics; 2005 Feb 1;21(3):379-84
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  • AVAILABILITY: The HCV website can be accessed via http://hcv.lanl.gov and http://hcv-db.org.

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  • (PMID = 15377502.001).
  • [ISSN] 1367-4803
  • [Journal-full-title] Bioinformatics (Oxford, England)
  • [ISO-abbreviation] Bioinformatics
  • [Language] eng
  • [Grant] United States / PHS HHS / / 04-2085
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Viral Proteins
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79. Kang LC, Dunphy CH: Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes. Arch Pathol Lab Med; 2006 Feb;130(2):153-7
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  • [Title] Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes.
  • CONTEXT: MIC2 ("thymus leukemia") antigen has been shown to be expressed by T cells and monocytes, as well as B cells and granulocyte-lineage cells.
  • It is most intensely expressed by the most immature thymus T-lineage cells and is more intensely expressed by CD34-positive/CD33-positive myeloid cells (compared to more mature myeloid cells) and the earliest CD34-positive/CD10-positive B-cell precursor cells (compared to cells of later B-cell precursor stages).
  • CD99 (MIC2) is characteristically expressed in precursor B- and T-cell lymphoblastic lymphomas/leukemias, as well as in Ewing sarcoma/primitive neuroectodermal tumors (ES/PNET).
  • It has also been shown to be expressed in a few terminal deoxynucleotidyl transferase (TdT)-positive myeloid processes, but has been uniformly negative in TdT-negative myeloid processes.
  • A more recent study showed that 43% of acute myeloid leukemias (AMLs) and 55% of chloromas express CD99, concluding that CD99 is commonly expressed in AML and rarely seen in myeloproliferative disorders, myelodysplastic syndromes, or normal bone marrow.
  • Although this study speculated that MIC2 expression was probably not limited to TdT-positive AML, there was no comparison with TdT reactivity in this study.
  • OBJECTIVE: Since AML and high-grade myelodysplastic syndrome may occasionally be difficult to distinguish morphologically from acute lymphoblastic leukemia and ES/ PNET, we undertook a study to analyze MIC2 expression in conjunction with TdT reactivity in distinguishing AML or high-grade myelodysplastic syndrome from acute lymphoblastic leukemia and ES/PNET.
  • DESIGN: We studied bone marrow core and clot paraffin specimens from AML (classified according to criteria of the World Health Organization; n = 49), myelodysplastic syndromes (n = 4), precursor B-cell acute lymphoblastic leukemia (n = 4), ES/PNET (n = 1), and normal bone marrow (n = 3) with MIC2 (CD99) and TdT immunohistochemistry.
  • RESULTS: Overall, CD99 was expressed in 24 (49%) of 49 AML cases, including all (11/11) TdT-positive cases.
  • CD99 was expressed in all subtypes of AML except M5.
  • Expression of TdT was limited to a subset of AML-M0, -M1, -M2, and -M4, and AML with multilineage dysplasia.
  • CONCLUSIONS: In contrast to a previous study, CD99 expression was not restricted to TdT-positive hematologic proliferations.
  • In particular, the CD99-positive M3 and M7 AMLs were TdT negative.
  • An M5 AML may likely be excluded based on a uniform TdT-negative/CD99-negative immunophenotype.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow / metabolism. Cell Adhesion Molecules / metabolism. DNA Nucleotidylexotransferase / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Neuroectodermal Tumors, Primitive / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retrospective Studies. Sarcoma, Ewing / diagnosis

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  • (PMID = 16454553.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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80. Yoneda K, Morii T, Nieda M, Tsukaguchi N, Amano I, Tanaka H, Yagi H, Narita N, Kimura H: The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy. Leuk Res; 2005 Feb;29(2):147-52
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  • [Title] The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy.
  • In this study, we assessed the Valpha24+ NKT cell numbers in peripheral blood (PB) from 30 healthy donors and 70 patients with haematopoietic malignancy including chronic myelogenous leukemia (CML), malignant lymphoma (ML), acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • Here, we demonstrated that PB Valpha24+ NKT cell numbers were significantly decreased in all the patients with haematopoietic malignancy in comparison with that in healthy donors (P < 0.005).
  • In particular CD4- CD8- Valpha24+ NKT cell numbers were more significantly decreased in the patients with haematopoietic malignancy (P < 0.0001).
  • [MeSH-major] Hematologic Neoplasms / blood. Killer Cells, Natural / cytology. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Antigens, CD8 / biosynthesis. Flow Cytometry. Humans. Lymphocyte Count. Lymphocytes / cytology. Lymphocytes / immunology. Survival Analysis

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  • (PMID = 15607362.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Receptors, Antigen, T-Cell, alpha-beta
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81. Dekel B, Metsuyanim S, Garcia AM, Quintero C, Sanchez MJ, Izraeli S: Organ-injury-induced reactivation of hemangioblastic precursor cells. Leukemia; 2008 Jan;22(1):103-13
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  • Early in mammalian development, the stem cell leukemia (SCL/TAL1) gene and its distinct 3' enhancer (SCL 3'En) specify bipotential progenitor cells that give rise to blood and endothelium, thus termed hemangioblasts.
  • Here, we demonstrate that cells expressing the SCL 3'En in the adult kidney are comprised of CD45+CD31- hematopoietic cells, CD45-CD31+ endothelial cells and CD45-CD31- interstitial cells.
  • Creation of bone marrow chimeras of SCL 3'En transgenic mice into wild-type hosts shows that all three types of SCL 3'En-expressing cells in the adult kidney can originate from the bone marrow.
  • Ischemia/reperfusion injury to the adult kidney of SCL 3'En transgenic mice results in the intrarenal elevation of SCL and FLK1 mRNA levels and of cells expressing hem-endothelial progenitor markers (CD45, CD34, c-Kit and FLK1).
  • Furthermore, analysis of SCL 3'En in the ischemic kidneys reveals an increase in the abundance of SCL 3'En-expressing cells, predominantly within the CD45 (+) hematopoietic fraction and to a lesser extent in the CD45 (-) fraction.
  • Our results suggest organ-injury-induced reactivation of bone marrow-derived hemangioblasts and possible local angioblastic progenitors expressing SCL and SCL 3'En.
  • [MeSH-major] Endothelium, Vascular / cytology. Hematopoietic Stem Cells / metabolism. Kidney Diseases / metabolism. Reperfusion Injury / metabolism. Vascular Endothelial Growth Factor Receptor-2 / genetics

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  • (PMID = 17898790.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Flt1 protein, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.1.3.48 / Antigens, CD45
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82. Müller AM, Duque J, Shizuru JA, Lübbert M: Complementing mutations in core binding factor leukemias: from mouse models to clinical applications. Oncogene; 2008 Oct 2;27(44):5759-73
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  • [Title] Complementing mutations in core binding factor leukemias: from mouse models to clinical applications.
  • A great proportion of acute myeloid leukemias (AMLs) display cytogenetic abnormalities including chromosomal aberrations and/or submicroscopic mutations.
  • These abnormalities significantly influence the prognosis of the disease.
  • Core binding factor (CBF) leukemias denote AMLs with chromosomal aberrations disrupting one of the CBF transcription factor genes; the most common examples are translocation t(8;21) and inversion inv(16), which result in the generation of the AML1-ETO and CBFbeta-MYH11 fusion proteins, respectively.
  • However, in murine models, these alterations alone do not suffice to generate full-blown leukemia, but rather, complementary events are required.
  • In fact, a substantial proportion of primary CBF leukemias display additional activating mutations, mostly of the receptor tyrosine kinase (RTK) c-KIT.
  • Here, we present a concise review on complementing mutations in CBF leukemias including pathophysiology, mouse models, and clinical implications.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / diagnosis. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Genetic Complementation Test. Mice. Prognosis

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  • (PMID = 18604246.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 118
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83. Karp JE, Blackford A, Smith BD, Alino K, Seung AH, Bolaños-Meade J, Greer JM, Carraway HE, Gore SD, Jones RJ, Levis MJ, McDevitt MA, Doyle LA, Wright JJ: Clinical activity of sequential flavopiridol, cytosine arabinoside, and mitoxantrone for adults with newly diagnosed, poor-risk acute myelogenous leukemia. Leuk Res; 2010 Jul;34(7):877-82
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  • [Title] Clinical activity of sequential flavopiridol, cytosine arabinoside, and mitoxantrone for adults with newly diagnosed, poor-risk acute myelogenous leukemia.
  • In a Phase II study, flavopiridol 50 mg/m(2) was given by 1-h infusion daily x 3 beginning day 1 followed by 2 g/m(2)/72 h ara-C beginning day 6 and 40 mg/m(2) mitoxantrone on day 9 (FLAM) to 45 adults with newly diagnosed acute myelogenous leukemia (AML) with multiple poor-risk features.
  • Median OS and DFS are not reached (67% alive 12.5-31 months, 58% in CR 11.4-30 months), with median follow-up 22 months.

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 19962759.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P30 CA06973-44; United States / NCI NIH HHS / CA / U01 CA069854; United States / NCRR NIH HHS / RR / M01-RR0052; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / CA069854-05; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCI NIH HHS / CA / U01 CA069854-05
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Piperidines; 0 / Polyamines; 04079A1RDZ / Cytarabine; 45AD6X575G / alvocidib; 63CZ7GJN5I / Allopurinol; 9YCX42I8IU / Sevelamer; BZ114NVM5P / Mitoxantrone
  • [Other-IDs] NLM/ NIHMS158765; NLM/ PMC2875369
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84. Kudo K, Kojima S, Tabuchi K, Yabe H, Tawa A, Imaizumi M, Hanada R, Hamamoto K, Kobayashi R, Morimoto A, Nakayama H, Tsuchida M, Horibe K, Kigasawa H, Tsukimoto I, Japanese Childhood AML Cooperative Study Group: Prospective study of a pirarubicin, intermediate-dose cytarabine, and etoposide regimen in children with Down syndrome and acute myeloid leukemia: the Japanese Childhood AML Cooperative Study Group. J Clin Oncol; 2007 Dec 1;25(34):5442-7
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  • [Title] Prospective study of a pirarubicin, intermediate-dose cytarabine, and etoposide regimen in children with Down syndrome and acute myeloid leukemia: the Japanese Childhood AML Cooperative Study Group.
  • PURPOSE: To evaluate a less intensive chemotherapeutic regimen specifically designed for patients with Down syndrome (DS) and acute myeloid leukemia (AML), and to determine the prognostic factors for event-free survival.
  • PATIENTS AND METHODS: Seventy-two patients with AML-DS were treated with remission induction chemotherapy consisting of pirarubicin (25 mg/m2/d for 2 days), cytarabine (100 mg/m2/d for 7 days), and etoposide (150 mg/m2/d for 3 days).
  • Prophylaxis for CNS leukemia was not included.
  • RESULTS: All but two patients were younger than 4 years, and 67 of the 72 patients (93%) were diagnosed as acute megakaryoblastic leukemia (AMKL).
  • CONCLUSION: A less intensive chemotherapeutic regimen produces excellent outcomes in standard-risk AML-DS patient.
  • Risk-oriented therapy should be considered for future trials in AML-DS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Down Syndrome / complications. Leukemia, Megakaryoblastic, Acute / drug therapy
  • [MeSH-minor] Child. Child, Preschool. Cytarabine / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Etoposide / administration & dosage. Female. Humans. Infant. Male. Prospective Studies. Treatment Outcome


85. Slovak ML, Smith DD, Bedell V, Hsu YH, O'Donnell M, Forman SJ, Gaal K, McDaniel L, Schultz R, Ballif BC, Shaffer LG: Assessing karyotype precision by microarray-based comparative genomic hybridization in the myelodysplastic/myeloproliferative syndromes. Mol Cytogenet; 2010;3:23
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  • RESULTS: We performed an exploratory study on 30 cases of MDS, myeloproliferative neoplasia (MPN) or evolving acute myeloid leukemia (AML) (% bone marrow blasts ≤ 30%, range 0-30%, median, 8%) by aCGH, using a genome-wide bacterial artificial chromosome (BAC) microarray.
  • Cryptic 344-kb RUNX1 deletions were found in three patients at time of AML transformation.
  • CONCLUSIONS: The detection of previously known and unknown genomic alterations suggests that aCGH has considerable promise for identification of both recurring microscopic and submicroscopic genomic imbalances that contribute to myeloid disease pathogenesis and progression.

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  • (PMID = 21078186.001).
  • [ISSN] 1755-8166
  • [Journal-full-title] Molecular cytogenetics
  • [ISO-abbreviation] Mol Cytogenet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3000833
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86. Birtwistle J, Hayden RE, Khanim FL, Green RM, Pearce C, Davies NJ, Wake N, Schrewe H, Ride JP, Chipman JK, Bunce CM: The aldo-keto reductase AKR1C3 contributes to 7,12-dimethylbenz(a)anthracene-3,4-dihydrodiol mediated oxidative DNA damage in myeloid cells: implications for leukemogenesis. Mutat Res; 2009 Mar 9;662(1-2):67-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The aldo-keto reductase AKR1C3 contributes to 7,12-dimethylbenz(a)anthracene-3,4-dihydrodiol mediated oxidative DNA damage in myeloid cells: implications for leukemogenesis.
  • Other studies have demonstrated the oxidative activation of polycyclic aromatic hydrocarbon (PAH) procarcinogens by AKR1C3 in cell-free systems.
  • Quantitative RT-PCR identified AKR1C3 as the predominant AKR1C isoform expressed in acute myeloid leukemia (AML).
  • Exposure of K562 and KG1a myeloid cell lines to the known AKR1C3 substrate 7,12-dimethylbenz(a)anthracene-3,4-dihydrodiol (7,12-DMBA-3,4-diol) resulted in both single strand DNA breaks and oxidative DNA damage as measured using conventional and FPG-modified comet assays respectively.
  • Knockdown of AKR1C3 did not alter single strand DNA breaks following 7,12-DMBA-3,4-diol exposure but significantly decreased oxidative DNA damage.
  • A similar interrelationship between AKR1C3 activity and 7,12-DMBA-3,4-diol mediated oxidative DNA damage but not single strand breaks was observed in KG1a cells.
  • Since K562 cells are a model of AML blast crisis of chronic myeloid leukemia (CML) the data presented here identify AKR1C3 as a novel mediator of carcinogen-induced initiation of leukemia, as a novel regulator of erythroid differentiation and paradoxically as a potential new target in the treatment of CML.
  • [MeSH-major] 3-Hydroxysteroid Dehydrogenases / metabolism. 9,10-Dimethyl-1,2-benzanthracene / analogs & derivatives. DNA Damage. Hydroxyprostaglandin Dehydrogenases / metabolism. Leukemia, Myeloid, Acute / enzymology. Oxidative Stress
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Gene Expression Regulation, Leukemic. Gene Knockdown Techniques. Glycophorin / metabolism. Hemoglobins / metabolism. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Stem Cells / metabolism

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  • (PMID = 19162045.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glycophorin; 0 / Hemoglobins; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; 72617-60-8 / 7,12-dimethylbenz(a)anthracene-3,4-dihydrodiol; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases
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87. Tohyama K, Shiga S, Itose Y, Uchihashi K, Ohkura M, Takahashi K, Itoh M, Ichiyama S, Hamaguchi Y: Improved detection of minimal acute myeloid leukemia cells by the use of the combined parameters of XE-2100 hematology analyzer. Cytometry B Clin Cytom; 2005 Jul;66(1):18-24
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  • [Title] Improved detection of minimal acute myeloid leukemia cells by the use of the combined parameters of XE-2100 hematology analyzer.
  • BACKGROUND: For the diagnosis and therapy of acute leukemia, it is important to detect a small number of leukemic cells precisely.
  • Although several automated hematology analyzers that carry blast-detecting programs have been developed, they do not exert sufficient detection sensitivity to exceed the sensitivity of manual eye counting method.
  • A small number of leukemic myeloblasts was detected at the better sensitivity than the eye counting method in the clinical course of the patients with acute myeloid leukemia.
  • CONCLUSIONS: The daily practical use of this blast multi-scoring program will surely contribute to sensitive, objective, and real-time evaluation of the control of acute myeloid leukemia with a low cost.
  • [MeSH-major] Hematologic Tests / methods. Hematology / methods. Leukemia, Myeloid / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Erythrocyte Count / instrumentation. Erythrocyte Count / methods. Female. Humans. Leukocyte Count / instrumentation. Leukocyte Count / methods. Male. Middle Aged. Platelet Count / instrumentation. Platelet Count / methods. Sensitivity and Specificity

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15800879.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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88. Bayona C, Lassaletta A, Pérez A, Sevilla J, Albi G, Villa JR, Madero L: [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia]. An Pediatr (Barc); 2007 Sep;67(3):278-9
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  • [Title] [Fatal hemoptysis secondary to invasive pulmonary aspergillosis in a girl with acute myeloblastic leukemia].
  • [Transliterated title] Hemoptisis fatal secundaria a aspergilosis pulmonar invasiva en una paciente con leucemia mieloblástica aguda.
  • [MeSH-major] Aspergillosis / complications. Hemoptysis / etiology. Leukemia, Myeloid, Acute / complications. Lung Diseases, Fungal / complications

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  • (PMID = 17785168.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
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89. Suzukawa K, Shimizu S, Nemoto N, Takei N, Taki T, Nagasawa T: Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21). Int J Hematol; 2005 Jul;82(1):38-41
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  • [Title] Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21).
  • More than 40 genes have been reported as translocation partners of the mixed lineage leukemia gene (MLL) in hematologic malignancies.
  • On the other hand, there is only 1 report of an MLL-AF17 fusion transcript in acute myeloid leukemia (AML).
  • Here we describe a 40-year-old man with a diagnosis of AML involving t(11;17)(q23;q21).
  • Although the previously reported form of the MLL-AF17 fusion transcript was not detected by reverse transcriptase-polymerase chain reaction (PCR) analysis, a novel form of an MLL-AF17 fusion transcript joining MLL exon 6 to AF17 exon 9 was detected by complementary DNA panhandle PCR.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic / genetics. Chromosome Breakage. Histone-Lysine N-Methyltransferase. Humans. Leucine Zippers. Male. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 16105757.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLL-AF17 fusion protein, human; 0 / MLLT6 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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90. Konoplev S, Rassidakis GZ, Estey E, Kantarjian H, Liakou CI, Huang X, Xiao L, Andreeff M, Konopleva M, Medeiros LJ: Overexpression of CXCR4 predicts adverse overall and event-free survival in patients with unmutated FLT3 acute myeloid leukemia with normal karyotype. Cancer; 2007 Mar 15;109(6):1152-6
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  • [Title] Overexpression of CXCR4 predicts adverse overall and event-free survival in patients with unmutated FLT3 acute myeloid leukemia with normal karyotype.
  • BACKGROUND: CXC chemokine receptor 4 (CXCR4) expression in acute myeloid leukemia (AML) is reported to correlate with FLT3 gene mutation and poorer prognosis.
  • The prognostic significance of CXCR4 expression in patients with AML that have a normal karyotype and no evidence of FLT3 gene mutations was examined.
  • METHODS: The prognostic significance of CXCR4 expression in 122 AML patients with normal karyotype and no evidence of FLT3 gene mutation treated at our institution between 1997 and 2003 was analyzed.
  • Sixty-six patients died, including 9 with no evidence of disease.
  • CONCLUSIONS.: The results suggest that CXCR4 expression is associated with poor prognosis in AML patients with an unmutated FLT3 gene.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Receptors, CXCR4 / analysis. Receptors, CXCR4 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Immunohistochemistry. Karyotyping. Male. Middle Aged. Mutation. Prognosis. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17315232.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, CXCR4; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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91. Chen HC, Hu WX, Liu QX, Li WK, Chen FZ, Rao ZZ, Liu XF, Luo YP, Cao YF: Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility. Eur J Cancer Prev; 2008 Jun;17(3):251-8
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  • [Title] Genetic polymorphisms of metabolic enzymes CYP1A1, CYP2D6, GSTM1 and GSTT1 and leukemia susceptibility.
  • The genetic polymorphisms of biotransformation phase I enzymes, cytochrome P450 (CYP1A1 and CYP2D6), and phase II enzymes, glutathione S-transferase (GSTM1 and GSTT1), were analyzed in 204 healthy persons and 348 leukemia patients, who suffered from also acute lymphoblastic leukemia (ALL), acute nonlymphoblastic leukemia (ANLL) chronic myelogenous leukemia (CML), from the Han ethnic group in Changsha City of Hunan Province of China.
  • Our results showed that the frequencies of polymorphisms of CYP1A1, CYP2D6 and GSTT1 among the groups including acute lymphoblastic leukemia, ANLL, chronic myelogenous leukemia and healthy control have no significant differences.
  • The variation of GSTM1-null genotype alone correlated with the development of ANLL.
  • The combined genotypes of GSTM1-null with GSTT1-null, or GSTM1-null with CYP1A1 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant and CYP2D6 heterozygous mutant, or GSTM1-null with CYP1A1 heterozygous mutant, CYP2D6 heterozygous mutant and GSTT1-null were found in individuals with high risk of ANLL.
  • All these findings suggest that GSTM1-null genotype alone or in coordination with the relevant genotypes of other metabolic enzymes might be susceptibility factors in the etiology of ANLL.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Glutathione Transferase / genetics. Leukemia / genetics. Polymorphism, Single Nucleotide
  • [MeSH-minor] Case-Control Studies. DNA Mutational Analysis. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Risk Factors

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  • (PMID = 18414197.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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92. Advances in the biology and therapy of acute myelogenous leukemia. Selection of keynote addresses from the Acute Leukemia Forum 2007. March 23, 2007. San Francisco, California, USA. Best Pract Res Clin Haematol; 2008 Mar;21(1):1-98
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  • [Title] Advances in the biology and therapy of acute myelogenous leukemia. Selection of keynote addresses from the Acute Leukemia Forum 2007. March 23, 2007. San Francisco, California, USA.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 18561374.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Congresses; Overall
  • [Publication-country] England
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93. Jaroslav P, Martina H, Jirí S, Hana K, Petr S, Tomás K, Julius M, Cedrik H: Expression of cyclins D1, D2, and D3 and Ki-67 in Leukemia. Leuk Lymphoma; 2005 Nov;46(11):1605-1612
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  • [Title] Expression of cyclins D1, D2, and D3 and Ki-67 in Leukemia.
  • Cyclins are very important components of the cell cycle machinery because their levels regulate cell proliferation.
  • We studied the expression of the positive cell cycle regulators (D cyclins) and the cell proliferation marker (Ki-67) in human acute myeloid (AML), chronic myeloid (CML), acute lymphoblastic (ALL) and chronic lymphocytic (CLL) leukemia [mainly by comparative reverse transcription polymerase chain reaction (RT-PCR)].
  • Significant differences were found in the expression of cyclin D1, which was the highest in leukocytes (CD19 + ) of CLL patients whereas lower expression was found in CML, AML and ALL patients and normal bone marrow and peripheral blood leukocytes (P < 0.001).
  • Expression of the proliferative marker Ki-67 was high in CML, ALL and AML cells and low in CD19-positive CLL cells.
  • We did not find any significant relationship between cyclin D1 expression in cells of CML and AML patients and their clinical outcome.
  • [MeSH-major] Cyclins / genetics. Gene Expression Regulation, Neoplastic. Leukemia / pathology
  • [MeSH-minor] Acute Disease. Cell Proliferation. Cyclin D1 / analysis. Cyclin D1 / genetics. Cyclin D2. Cyclin D3. Gene Expression Profiling. Humans. Ki-67 Antigen / analysis. Ki-67 Antigen / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16334487.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / CCND3 protein, human; 0 / Cyclin D2; 0 / Cyclin D3; 0 / Cyclins; 0 / Ki-67 Antigen; 136601-57-5 / Cyclin D1
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94. McCubrey JA, Steelman LS, Chappell WH, Abrams SL, Wong EW, Chang F, Lehmann B, Terrian DM, Milella M, Tafuri A, Stivala F, Libra M, Basecke J, Evangelisti C, Martelli AM, Franklin RA: Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. Biochim Biophys Acta; 2007 Aug;1773(8):1263-84
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  • [Title] Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance.
  • Even in the absence of obvious genetic mutations, this pathway has been reported to be activated in over 50% of acute myelogenous leukemia and acute lymphocytic leukemia and is also frequently activated in other cancer types (e.g., breast and prostate cancers).
  • Although both of these pathways are commonly thought to have anti-apoptotic and drug resistance effects on cells, they display different cell lineage specific effects.
  • For example, Raf/MEK/ERK is usually associated with proliferation and drug resistance of hematopoietic cells, while activation of the Raf/MEK/ERK cascade is suppressed in some prostate cancer cell lines which have mutations at PTEN and express high levels of activated Akt.
  • Raf/MEK/ERK may promote cell cycle arrest in prostate cells and this may be regulated by p53 as restoration of wild-type p53 in p53 deficient prostate cancer cells results in their enhanced sensitivity to chemotherapeutic drugs and increased expression of Raf/MEK/ERK pathway.
  • Thus in advanced prostate cancer, it may be advantageous to induce Raf/MEK/ERK expression to promote cell cycle arrest, while in hematopoietic cancers it may be beneficial to inhibit Raf/MEK/ERK induced proliferation and drug resistance.
  • Thus the Raf/MEK/ERK pathway has different effects on growth, prevention of apoptosis, cell cycle arrest and induction of drug resistance in cells of various lineages which may be due to the presence of functional p53 and PTEN and the expression of lineage specific factors.

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  • (PMID = 17126425.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098195-05; United States / NCI NIH HHS / CA / R01 CA098195-05; United States / PHS HHS / / R01098195
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.11.1 / raf Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
  • [Number-of-references] 196
  • [Other-IDs] NLM/ NIHMS28626; NLM/ PMC2696318
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95. Shali W, Hélias C, Fohrer C, Struski S, Gervais C, Falkenrodt A, Leymarie V, Lioure B, Raby P, Herbrecht R, Lessard M: Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH. Cancer Genet Cytogenet; 2006 Jul 15;168(2):133-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.
  • We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or acute myeloid leukemias (t-AML) observed for 6 years.
  • These cases were classified into three groups according to the primary diagnosis.
  • Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/AML.
  • A considerable proportion of recurrent balanced translocations characterized t-AML secondary to therapy.
  • After treatment for lymphomas and chronic myeloproliferative diseases, there were more complex unbalanced abnormalities than the control group.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


96. McComb T, Sudesh V, Richardson M: Volume Bragg grating stabilized spectrally narrow Tm fiber laser. Opt Lett; 2008 Apr 15;33(8):881-3
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  • A Tm-doped large mode area (LMA) silica fiber laser has been locked to a stable wavelength of 2,053.9 nm using a volume Bragg grating (VBG).
  • Although this laser had modest output (approximately 5W) and slope efficiency (41%), this new approach to spectrally limiting the output of LMA fiber lasers is inherently extendable to kilowatt powers, opening up several applications including high-power pulsed fiber lasers and spectral beam combining.

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  • (PMID = 18414564.001).
  • [ISSN] 0146-9592
  • [Journal-full-title] Optics letters
  • [ISO-abbreviation] Opt Lett
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. Jenkins C, Hewamana S, Gilkes A, Neelakantan S, Crooks P, Mills K, Pepper C, Burnett A: Nuclear factor-kappaB as a potential therapeutic target for the novel cytotoxic agent LC-1 in acute myeloid leukaemia. Br J Haematol; 2008 Dec;143(5):661-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear factor-kappaB as a potential therapeutic target for the novel cytotoxic agent LC-1 in acute myeloid leukaemia.
  • Nuclear factor-kappaB (NF-kappaB) has been implicated in a number of malignancies and has been suggested to be a potential molecular target in the treatment of leukaemia.
  • This study demonstrated the constitutive activation of NF-kappaB in human myeloid blasts and a clear correlation between NF-kappaB expression and in vitro cytoprotection.
  • High NF-kappaB expression was found in many of the poor prognostic acute myeloid leukaemia (AML) subtypes, such as French-American-British classification M0 and M7, and the poor cytogenetic risk group.
  • The in vitro effects of LC-1, a novel dimethylamino-parthenolide analogue, were assessed in 62 primary untreated AML samples.
  • LC-1 was found to be cytotoxic to AML cells in a dose-dependent manner, mediated through the induction of apoptosis.
  • The median drug concentration necessary to kill 50% of the cells was 4.5 micromol/l for AML cells, compared with 12.8 micromol/l for normal marrow cells.
  • Consequently, LC-1 treatment provides a proof of principle for the use of NF-kappaB inhibitors in the treatment of AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. NF-kappa B / antagonists & inhibitors. Sesquiterpenes / therapeutic use

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  • (PMID = 19036014.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / LC-1 compound; 0 / NF-kappa B; 0 / Sesquiterpenes
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98. Owen CJ, Toze CL, Koochin A, Forrest DL, Smith CA, Stevens JM, Jackson SC, Poon MC, Sinclair GD, Leber B, Johnson PR, Macheta A, Yin JA, Barnett MJ, Lister TA, Fitzgibbon J: Five new pedigrees with inherited RUNX1 mutations causing familial platelet disorder with propensity to myeloid malignancy. Blood; 2008 Dec 1;112(12):4639-45
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  • [Title] Five new pedigrees with inherited RUNX1 mutations causing familial platelet disorder with propensity to myeloid malignancy.
  • Familial platelet disorder with propensity to myeloid malignancy (FPD/AML) is an autosomal dominant syndrome characterized by platelet abnormalities and a predisposition to myelodysplasia (MDS) and/or acute myeloid leukemia (AML).
  • The disorder, caused by inherited mutations in RUNX1, is uncommon with only 14 pedigrees reported.
  • We screened 10 families with a history of more than one first degree relative with MDS/AML for inherited mutations in RUNX1.
  • Germ- line RUNX1 mutations were identified in 5 pedigrees with a 3:2 predominance of N-terminal mutations.
  • Several affected members had normal platelet counts or platelet function, features not previously reported in FPD/AML.
  • The median incidence of MDS/AML among carriers of RUNX1 mutation was 35%.
  • Individual treatments varied but included hematopoietic stem cell transplantation from siblings before recognition of the inherited leukemogenic mutation.
  • Transplantation was associated with a high incidence of complications including early relapse, failure of engraftment, and posttransplantation lymphoproliferative disorder.
  • Given the small size of modern families and the clinical heterogeneity of this syndrome, the diagnosis of FPD/AML could be easily overlooked and may be more prevalent than previously recognized.
  • Therefore, it would appear prudent to screen young patients with MDS/AML for RUNX1 mutation, before consideration of sibling hematopoietic stem cell transplantation.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid / genetics. Pedigree
  • [MeSH-minor] Adolescent. Adult. Aged. Child. DNA Mutational Analysis. Disease Progression. Family. Female. Hematopoietic Stem Cell Transplantation / contraindications. Humans. Male. Middle Aged. Mutation / physiology. Young Adult


99. Napper JM, Sollars VE: 17-N-Allylamino-17-demethoxygeldanamycin induces a diverse response in human acute myelogenous cells. Leuk Res; 2010 Nov;34(11):1493-500
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  • [Title] 17-N-Allylamino-17-demethoxygeldanamycin induces a diverse response in human acute myelogenous cells.
  • The goal of this study was to ascertain the specific effects of 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG) treatment in human acute myelogenous leukemia (AML).
  • Four human leukemia cell lines were treated with varying doses of 17-AAG followed by analysis of toxicity, apoptosis, proliferation, and cell cycle.
  • Cell cycle analysis revealed that the cells accumulate in G2/M phase within 96 h of treatment, although the effect was not equivalent among the cell lines. p21, p53 expression and MDR1 activity were among the possible mechanisms uncovered for the differing responses.
  • Exploiting these differences may allow for more effective combinatory treatments in patients with AML.

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20646760.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / 5P20RR020180; United States / NCI NIH HHS / CA / R03 CA129790; United States / NCI NIH HHS / CA / 1R03 CA129790; United States / NCRR NIH HHS / RR / P20 RR016477; United States / NCRR NIH HHS / RR / 5P20RR016477; United States / NCRR NIH HHS / RR / P20 RR020180
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Benzoquinones; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Lactams, Macrocyclic; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Tumor Suppressor Protein p53; 4GY0AVT3L4 / tanespimycin
  • [Other-IDs] NLM/ NIHMS209678; NLM/ PMC2946448
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100.