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1. Ragusa M, Avola G, Angelica R, Barbagallo D, Guglielmino MR, Duro LR, Majorana A, Statello L, Salito L, Consoli C, Camuglia MG, Di Pietro C, Milone G, Purrello M: Expression profile and specific network features of the apoptotic machinery explain relapse of acute myeloid leukemia after chemotherapy. BMC Cancer; 2010;10:377
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  • [Title] Expression profile and specific network features of the apoptotic machinery explain relapse of acute myeloid leukemia after chemotherapy.
  • BACKGROUND: According to the different sensitivity of their bone marrow CD34+ cells to in vitro treatment with Etoposide or Mafosfamide, Acute Myeloid Leukaemia (AML) patients in apparent complete remission (CR) after chemotherapy induction may be classified into three groups: (i) normally responsive;.
  • This inversely correlates with in vivo CD34+ mobilization and, interestingly, also with the prognosis of the disease: patients showing a good mobilizing activity are resistant to chemotherapy and subject to significantly higher rates of Minimal Residual Disease (MRD) and relapse than the others.
  • METHODS: To investigate the molecular bases of the differential chemosensitivity of bone marrow hematopoietic stem cells (HSC) in CR AML patients, and the relationship between chemosensitivity, mobilizing activity and relapse rates, we analyzed their AM expression profile by performing Real Time RT-PCR of 84 AM genes in CD34+ pools from the two extreme classes of patients (i.e., chemoresistant and highly chemosensitive), and compared them with normal controls.
  • Interestingly, our analysis of the AM network showed that the dysregulated genes in these patients are characterized by high network centrality (i.e., high values of betweenness, closeness, radiality, stress) and high involvement in drug response.
  • CONCLUSIONS: AM genes represent critical nodes for the proper execution of cell death following pharmacological induction in patients.
  • We propose that their dysregulation (either due to inborn or de novo genomic mutations selected by treatment) could cause a relapse in apparent CR AML patients.
  • Based on this, AM profiling before chemotherapy and transplantation could identify patients with a predisposing genotype to MRD and relapse: accordingly, they should undergo a different, specifically tailored, therapeutic regimen and should be carefully checked during the post-treatment period.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis. Biomarkers, Tumor / genetics. Bone Marrow Cells / metabolism. Drug Resistance, Neoplasm / genetics. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Antigens, CD34 / metabolism. Cell Movement. Cohort Studies. Female. Humans. Male. Middle Aged. Neoplasm, Residual / drug therapy. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Oligonucleotide Array Sequence Analysis. Prospective Studies. RNA, Messenger / genetics. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20642818.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2914706
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2. 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.
  • The activities of adenosine deaminase and xanthine oxidase were higher in the relapse condition, whereas those of glutathione peroxidase, monoamine oxidase, and superoxide dismutase, and the total antioxidant capacity (T-AOC) were lower in the primary condition and in controls.
  • Of particular note, levels of advanced oxidation protein products, malondialdehyde, and 8-hydroxydeoxyguanosine were also significantly higher in relapse patients.
  • Furthermore, real-time PCR with SYBR Green revealed that the expression levels of human thioredoxin (TRX) and indoleamine 2,3-dioxygenase were increased in relapse patients.
  • 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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3. Kim WI, Matise I, Diers MD, Largaespada DA: RAS oncogene suppression induces apoptosis followed by more differentiated and less myelosuppressive disease upon relapse of acute myeloid leukemia. Blood; 2009 Jan 29;113(5):1086-96
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  • [Title] RAS oncogene suppression induces apoptosis followed by more differentiated and less myelosuppressive disease upon relapse of acute myeloid leukemia.
  • To study the oncogenic role of the NRAS oncogene (NRAS(G12V)) in the context of acute myeloid leukemia (AML), we used a Vav promoter-tetracycline transactivator (Vav-tTA)-driven repressible TRE-NRAS(G12V) transgene system in Mll-AF9 knock-in mice developing AML.
  • Conditional repression of NRAS(G12V) expression greatly reduced peripheral white blood cell (WBC) counts in leukemia recipient mice and induced apoptosis in the transplanted AML cells correlated with reduced Ras/Erk signaling.
  • We conclude that, in AML induced by an Mll-AF9 transgene, NRAS(G12V) expression contributes to acute leukemia maintenance by suppressing apoptosis and reducing differentiation of leukemia cells.

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  • (PMID = 18952898.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / U01 CA84221
  • [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 / Mllt3 protein, mouse; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2635074
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4. 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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  • OBJECTIVE: Internal tandem duplication (ITD) mutations of the FLT3 receptor are associated with a high incidence of relapse in acute myeloid leukemia (AML).
  • 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.

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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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5. Lancet JE, Karp JE: Novel postremission strategies in adults with acute myeloid leukemia. Curr Opin Hematol; 2009 Mar;16(2):105-11
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  • [Title] Novel postremission strategies in adults with acute myeloid leukemia.
  • PURPOSE OF REVIEW: Given the high rates of relapse in acute myeloid leukemia (AML), there is tremendous opportunity for the development of new therapeutic strategies in the postremission state.
  • Unfortunately, the currently available modalities for postremission therapy, namely chemotherapy, have proven largely ineffective in changing the natural history of AML.
  • The challenges to overcome therapeutic failure in the minimal residual disease status may relate to an incomplete understanding of the mechanisms and cell populations that are directly related to disease relapse as well as suboptimal ability to identify patients at highest risk for relapse.
  • RECENT FINDINGS: Being a heterogeneous disease, relapsed AML is unlikely to emanate from one predominant mechanism; instead, there are likely multiple biologic factors at play that allow for clinical relapse to occur.
  • These factors likely include multidrug resistance proteins, aberrant signal transduction pathways, survival of leukemia stem cells, microenvironmental interactions, and immune tolerance.

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  • [CommentIn] Curr Opin Hematol. 2009 Mar;16(2):63 [19468265.001]
  • (PMID = 19468272.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCRR NIH HHS / RR / RR000052-466559; United States / NCRR NIH HHS / RR / M01 RR000052-466559
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 64
  • [Other-IDs] NLM/ NIHMS187903; NLM/ PMC2861990
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6. Giles F, Vey N, DeAngelo D, Seiter K, Stock W, Stuart R, Boskovic D, Pigneux A, Tallman M, Brandwein J, Kell J, Robak T, Staib P, Thomas X, Cahill A, Albitar M, O'Brien S: Phase 3 randomized, placebo-controlled, double-blind study of high-dose continuous infusion cytarabine alone or with laromustine (VNP40101M) in patients with acute myeloid leukemia in first relapse. Blood; 2009 Nov 5;114(19):4027-33
Hazardous Substances Data Bank. CYTARABINE .

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  • [Title] Phase 3 randomized, placebo-controlled, double-blind study of high-dose continuous infusion cytarabine alone or with laromustine (VNP40101M) in patients with acute myeloid leukemia in first relapse.
  • An international, randomized (2:1), double-blind, placebo-controlled study was conducted to compare complete remission (CR) rates and overall survival (OS) in patients with first relapse acute myeloid leukemia (AML) treated with laromustine and high-dose cytarabine (HDAC) versus HDAC/placebo.
  • [MeSH-major] Cytarabine / administration & dosage. Hydrazines / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Sulfonamides / administration & dosage

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  • [CommentIn] Blood. 2010 Jan 14;115(2):430 [20075171.001]
  • (PMID = 19710500.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00112554
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hydrazines; 0 / Sulfonamides; 04079A1RDZ / Cytarabine; 14J2G0U3NQ / laromustine
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7. Mesters RM, Padró T, Bieker R, Steins M, Kreuter M, Göner M, Kelsey S, Scigalla P, Fiedler W, Büchner T, Berdel WE: Stable remission after administration of the receptor tyrosine kinase inhibitor SU5416 in a patient with refractory acute myeloid leukemia. Blood; 2001 Jul 1;98(1):241-3
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  • [Title] Stable remission after administration of the receptor tyrosine kinase inhibitor SU5416 in a patient with refractory acute myeloid leukemia.
  • Herein is described the successful treatment of a 65-year-old woman with SU5416, in second relapse of acute myeloid leukemia (AML) and refractory toward standard chemotherapy regimens.
  • This is the first report of a stable remission achieved after administration of the RTK inhibitor SU5416 in a patient with AML relapse.
  • [MeSH-major] Indoles / administration & dosage. Leukemia, Myeloid / drug therapy. Pyrroles / administration & dosage
  • [MeSH-minor] Acute Disease. Angiogenesis Inhibitors / administration & dosage. Antineoplastic Agents / administration & dosage. Bone Marrow Cells / chemistry. Endothelium, Vascular / chemistry. Endothelium, Vascular / cytology. Female. Humans. Immunohistochemistry. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / drug effects. Receptor Protein-Tyrosine Kinases / metabolism. Receptors, Growth Factor / drug effects. Receptors, Growth Factor / metabolism. Receptors, Vascular Endothelial Growth Factor. Remission Induction / methods

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  • (PMID = 11418488.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / Receptors, Growth Factor; 71IA9S35AJ / Semaxinib; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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8. Styczynski J, Wysocki M: Ex vivo drug resistance in childhood acute myeloid leukemia on relapse is not higher than at first diagnosis. Pediatr Blood Cancer; 2004 Feb;42(2):195-9
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  • [Title] Ex vivo drug resistance in childhood acute myeloid leukemia on relapse is not higher than at first diagnosis.
  • Relapsed pediatric patients with acute myeloid leukemia (AML) have a poor clinical prognosis.
  • The aim of this study was the analysis of the ex vivo drug resistance profile on relapse in childhood AML in comparison to newly diagnosed AML.
  • Finally, ex vivo drug resistance of 20 relapsed samples were compared with that of 60 de novo AML, including 9 matched pairs.
  • Up to 18 drugs were tested for each patient.
  • No significant differences between drug resistance at diagnosis and at relapse in AML was found, neither for the whole groups of patients, nor for matched pairs only.
  • Possibly, relatively good sensitivity of myeloblasts on relapse was found against melphalan, thiotepa, 4-HOO-ifosfamide, and cladribine.
  • In summary, cellular drug resistance in childhood AML at relapse is not higher than at first diagnosis.
  • These observations suggest that other, than cellular drug resistance, factors play a key role in therapy failure of relapsed childhood AML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Leukemia, Myeloid / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Cell Division / drug effects. Child. Child, Preschool. Cytogenetic Analysis. Drug Screening Assays, Antitumor. Female. Humans. Infant. Infant, Newborn. Male

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 14752887.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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9. Martner A, Thorén FB, Aurelius J, Söderholm J, Brune M, Hellstrand K: Immunotherapy with histamine dihydrochloride for the prevention of relapse in acute myeloid leukemia. Expert Rev Hematol; 2010 Aug;3(4):381-91
Hazardous Substances Data Bank. HISTAMINE .

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  • [Title] Immunotherapy with histamine dihydrochloride for the prevention of relapse in acute myeloid leukemia.
  • Most patients with acute myeloid leukemia (AML) achieve complete remission (CR) after induction chemotherapy.
  • HDC reduces myeloid cell-derived suppression of anti-leukemic lymphocytes, and aims to unravel a therapeutic benefit of IL-2 in AML by improving natural killer and T-cell activation.
  • A randomized Phase III trial with 320 AML patients in CR demonstrated a significant reduction of relapse risk after immunotherapy with HDC plus low-dose IL-2 in the post-consolidation phase.
  • HDC is the first approved therapeutic to target the state of immunosuppression in AML; further development in this area may comprise supplementary or alternative counter-suppressive agents with the aim to improve the efficacy of cancer immunotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Histamine / therapeutic use. Immunotherapy. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 21083028.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-2; 820484N8I3 / Histamine
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10. Unal S, Cakir M, Kuşkonmaz B, Cetin M, Tuncer AM: Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia. Turk J Pediatr; 2009 Jan-Feb;51(1):69-71
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  • [Title] Successful treatment with gemtuzumab ozogamicin monotherapy in a pediatric patient with resistant relapse of acute myeloid leukemia.
  • There are few therapeutic options in relapsed or refractory acute myeloid leukemia patients.
  • Herein, we present a 15-year-old acute myeloid leukemia patient who was resistant at relapse and could achieve remission with gemtuzumab ozogamicin at a total dose of 9 mg/m2, divided into three doses and delivered to hematopoietic stem-cell transplantation; however, the patient relapsed in a short time without application of transplantation.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19378895.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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11. van Stijn A, Kok A, van der Pol MA, Feller N, Roemen GM, Westra AH, Ossenkoppele GJ, Schuurhuis GJ: A flow cytometric method to detect apoptosis-related protein expression in minimal residual disease in acute myeloid leukemia. Leukemia; 2003 Apr;17(4):780-6
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  • [Title] A flow cytometric method to detect apoptosis-related protein expression in minimal residual disease in acute myeloid leukemia.
  • Minimal residual disease (MRD) cells are thought to be responsible for the persistence and relapse of acute myeloid leukemia (AML).
  • Flow cytometric MRD detection by the establishment of a leukemia-associated phenotype (LAP) at diagnosis can be used in 80% of AML patients, allowing detection and functional characterization of MRD in follow-up bone marrow.
  • Firstly, validation of this assay using Western blot analysis in five leukemia cell lines showed a significant correlation (R=0.70: P<0.0001).
  • The flow cytometric protocol thus enables analysis of apoptosis-related proteins at different stages of the disease, which will lead to a better understanding of the role of apoptosis resistance in the emergence of MRD in AML.
  • [MeSH-major] Apoptosis. Flow Cytometry / methods. Gene Expression Profiling / methods. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / pathology. Neoplasm Proteins / analysis. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blotting, Western. Bone Marrow / pathology. Cell Membrane Permeability / drug effects. Genes, bcl-2. Humans. K562 Cells. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm, Residual. Saponins / pharmacology. Specimen Handling. Tumor Cells, Cultured. U937 Cells. bcl-2-Associated X Protein. bcl-X Protein

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  • (PMID = 12682637.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Saponins; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
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12. Owonikoko T, Agha M, Balassanian R, Smith R, Raptis A: Gemtuzumab therapy for isolated extramedullary AML relapse following allogeneic stem-cell transplant. Nat Clin Pract Oncol; 2007 Aug;4(8):491-5
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  • [Title] Gemtuzumab therapy for isolated extramedullary AML relapse following allogeneic stem-cell transplant.
  • BACKGROUND: A 19-year-old male with primary refractory acute myeloid leukemia received salvage therapy with mitoxantrone and cytarabine combination.
  • Ten months following repeat transplant, the patient presented with an increasing number of extramedullary sites of biopsy-proven disease relapse (i.e. cranial and peripheral nerves, tongue, abdominal wall and chest wall).
  • DIAGNOSIS: Isolated extramedullary relapse of acute myeloid leukemia after stem-cell transplant.
  • MANAGEMENT: Primary leukemia treatment with idarubicin, cytarabine, etoposide, dexamethasone, tioguanine on protocol and salvage therapy with mitoxantrone and cytarabine combination for primary refractory disease.
  • A matched-unrelated-donor stem-cell transplant for consolidation and donor-lymphocyte infusions were performed, followed by repeat unrelated-donor transplant for leukemia relapse in the marrow, radiation therapy and gemtuzumab ozogamicin for multiple sites of extramedullary leukemia relapse.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Neoplasm Recurrence, Local / drug therapy. Sarcoma, Myeloid / drug therapy

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  • (PMID = 17657254.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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13. Kaur B, Gottardo NG, Keil AD, Hallam LA, Baker DL: A rare case of adenoviral fulminant hepatic necrosis after chemotherapy. Pediatr Hematol Oncol; 2002 Jul-Aug;19(5):361-71
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  • The authors report a rare case of fulminant adenoviral hepatic necrosis occurring after chemotherapy in a patient with a second relapse of acute myeloid leukemia.
  • A 10-year-old girl with relapsed acute myeloid leukemia after allogeneic bone marrow transplant underwent re-induction chemotherapy with high-dose cytosine arabinoside and amsacrine.
  • During induction she developed diarrhea and a marked coagulopathy, followed by fulminant hepatic failure and acute pre-renal failure.
  • Adenovirus type 5 was cultured from ante mortem clinical samples and detected by polymerase chain reaction in postmortem samples of heart blood, lung, trachea, spleen, and liver.
  • [MeSH-major] Adenovirus Infections, Human / etiology. Hepatitis, Viral, Human / etiology. Leukemia, Myeloid, Acute / drug therapy. Liver / pathology

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  • (PMID = 12078868.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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14. Grier DD, Eskew A, White T, McLean TW: An unusual case of acute myeloid leukemia: late isolated testicular relapse followed by isolated central nervous system relapse. Pediatr Blood Cancer; 2010 Dec 1;55(6):1231-3
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  • [Title] An unusual case of acute myeloid leukemia: late isolated testicular relapse followed by isolated central nervous system relapse.
  • Testicular relapse of acute myeloid leukemia without bone marrow involvement is a rare event.
  • We describe a case of an 18-year-old male who had an isolated testicular relapse 86 months (7.2 years) from original diagnosis.
  • Fluorescence in situ hybridization and immunohistochemistry were used to establish the diagnosis of a relapse rather than a new leukemic process.
  • This patient had a 7.2-year period between original diagnosis and the testicular relapse of acute myeloid leukemia.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Leukemia, Myeloid, Acute / surgery. Neoplasm Recurrence, Local / diagnosis. Testicular Neoplasms / drug therapy

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  • (PMID = 20589624.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin
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15. Takahashi T, Tsukuda H, Kimura H, Yoshimoto M, Tsujisaki M: Extramedullary relapse of AML with t(9;11)(p22;q23) associated with clonal evolution from trisomy 8 into tetrasomy 8. Intern Med; 2010;49(5):447-51
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  • [Title] Extramedullary relapse of AML with t(9;11)(p22;q23) associated with clonal evolution from trisomy 8 into tetrasomy 8.
  • This report describes a patient with extramedullary relapse of acute myeloid leukemia (AML) without involving bone marrow.
  • A 57-year-old man was diagnosed as having acute monoblastic leukemia with t(9;11)(p22;q23) and trisomy 8.
  • Aspiration from the forearm showed leukemic relapse, and fluorescence in situ hybridization (FISH) revealed that the majority of the cells had 11q23 anomaly and tetrasomy 8.
  • Bone marrow or meningeal relapse was not observed.
  • To our knowledge, this is the first case report of clonal evolution associated with the development of myeloid sarcoma as a relapse in AML.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / genetics. Trisomy / genetics
  • [MeSH-minor] Chromosome Aberrations. Drug Therapy. Forearm. Humans. Male. Middle Aged. Recurrence. Thigh

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  • (PMID = 20190481.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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16. Sumi M, Ichikawa N, Nasu K, Shimizu I, Ueki T, Ueno M, Kobayashi H: Gemtuzumab ozogamicin-induced long-term remission in a woman with acute myelomonocytic leukemia and bone marrow relapse following allogeneic transplantation. Int J Hematol; 2009 Dec;90(5):643-7
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  • [Title] Gemtuzumab ozogamicin-induced long-term remission in a woman with acute myelomonocytic leukemia and bone marrow relapse following allogeneic transplantation.
  • A 56-year-old woman with acute myelomonocytic leukemia underwent myeloablative allogeneic hematopoietic stem cell transplantation (allo-SCT) from a matched unrelated donor in her first complete remission (CR).
  • On day 58, she showed grade II acute GVHD, but this resolved spontaneously.
  • On day 140, she developed hematological relapse with 40.2% marrow infiltration of CD33-positive blasts.
  • Although transfusion-dependent pancytopenia persisted for 8 months after GO administration, bone marrow examination revealed the recovery of normal hematopoietic cells with 0.8% blasts.
  • Although the standard treatment for acute myeloid leukemia relapse after allo-SCT still remains to be established, GO may be a promising option.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelomonocytic, Acute / drug therapy. Salvage Therapy / methods

  • Genetic Alliance. consumer health - Acute Myelomonocytic Leukemia.
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  • (PMID = 19904520.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 93NS566KF7 / gemtuzumab
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17. Giles F, Verstovsek S, Faderl S, Vey N, Karp J, Roboz G, Khan KD, Cooper M, Bilgrami SF, Ferrant A, Daenen S, Karsten V, Cahill A, Albitar M, Kantarjian H, O'Brien S, Feldman E: A phase II study of cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients with very high risk relapsed acute myeloid leukemia. Leuk Res; 2006 Dec;30(12):1591-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients with very high risk relapsed acute myeloid leukemia.
  • Cloretazine (VNP40101M) is a sulfonylhydrazine alkylating agent with significant anti-leukemia activity.
  • A multicenter phase II study of cloretazine was conducted in patients with first relapse of acute myeloid leukemia (AML) following an initial complete remission (CR) of less than 12 months.
  • Median overall survival (2.3 months) in the study cohort was directly comparable to that of 233 matched patients treated with other single agents.
  • [MeSH-major] Hydrazines / administration & dosage. Leukemia, Myeloid / drug therapy. Sulfonamides / administration & dosage
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cohort Studies. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Recurrence. Remission Induction. Risk Factors. Survival Rate. Treatment Outcome

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
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  • (PMID = 16574225.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Letter; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydrazines; 0 / Sulfonamides; 14J2G0U3NQ / laromustine
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18. Specchia G, Pastore D, Carluccio P, Spinosa G, Giannoccaro M, Rizzi R, Mestice A, Liso V: Gemtuzumab ozogamicin with cytarabine and mitoxantrone as a third-line treatment in a poor prognosis group of adult acute myeloid leukemia patients: a single-center experience. Ann Hematol; 2007 Jun;86(6):425-8
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemtuzumab ozogamicin with cytarabine and mitoxantrone as a third-line treatment in a poor prognosis group of adult acute myeloid leukemia patients: a single-center experience.
  • We analyzed the safety and efficacy of gemtuzumab ozogamicin (GO) combined with cytarabine and mitoxantrone in the treatment of 21 patients with acute myeloid leukemia (11 refractory and 10 in second relapse).
  • In our experience, the addition of GO to mitoxantrone and cytarabine is feasible in refractory or second relapse acute myeloid leukemia patients but yields a low response rate when used as a third-line treatment.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal, Humanized. Cytarabine / administration & dosage. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Palliative Care / methods. Remission Induction. Salvage Therapy / methods. Survival Analysis

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Hazardous Substances Data Bank. CYTARABINE .
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  • (PMID = 17364181.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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19. Tempescul A, Ianotto JC, Eveillard JR, Guillerm G, Berthou C, Marion V, De Braekeleer M: High-dose melphalan followed by a second bone marrow transplantation in early relapse of acute myeloid leukemia after bone marrow transplantation in children. Ann Hematol; 2008 Jun;87(6):503-4
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose melphalan followed by a second bone marrow transplantation in early relapse of acute myeloid leukemia after bone marrow transplantation in children.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Melphalan / therapeutic use






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