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1. Ohtsuka Y, Manabe A, Kawasaki H, Hasegawa D, Zaike Y, Watanabe S, Tanizawa T, Nakahata T, Tsuji K: RAS-blocking bisphosphonate zoledronic acid inhibits the abnormal proliferation and differentiation of juvenile myelomonocytic leukemia cells in vitro. Blood; 2005 Nov 1;106(9):3134-41
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  • [Title] RAS-blocking bisphosphonate zoledronic acid inhibits the abnormal proliferation and differentiation of juvenile myelomonocytic leukemia cells in vitro.
  • Juvenile myelomonocytic leukemia (JMML) is a clonal myeloproliferative/myelodysplastic disorder of early childhood with a poor prognosis.
  • The current result offers a novel approach to therapy in JMML.
  • [MeSH-major] Cell Differentiation / drug effects. Diphosphonates / pharmacology. Imidazoles / pharmacology. Leukemia, Myelomonocytic, Acute / pathology. Leukemia, Myelomonocytic, Chronic / pathology. Phosphates / pharmacology. ras Proteins / antagonists & inhibitors
  • [MeSH-minor] Adolescent. Bone Marrow / drug effects. Cell Proliferation / drug effects. Flow Cytometry. Humans. Tumor Cells, Cultured

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  • (PMID = 16046524.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Imidazoles; 0 / Phosphates; 6XC1PAD3KF / zoledronic acid; EC 3.6.5.2 / ras Proteins
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2. Iversen PO, Emanuel PD, Sioud M: Targeting Raf-1 gene expression by a DNA enzyme inhibits juvenile myelomonocytic leukemia cell growth. Blood; 2002 Jun 1;99(11):4147-53
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  • [Title] Targeting Raf-1 gene expression by a DNA enzyme inhibits juvenile myelomonocytic leukemia cell growth.
  • Juvenile myelomonocytic leukemia (JMML) is an aggressive childhood disorder with few therapeutic options.
  • The DNA enzyme efficiently catabolized mRNA-Raf-1 with subsequent inhibition of JMML cell growth, suggesting its potential as a mechanism-based therapy in this fatal leukemia.
  • [MeSH-major] DNA-Directed DNA Polymerase / metabolism. Gene Expression Regulation, Neoplastic. Leukemia, Myelomonocytic, Acute / pathology. Proto-Oncogene Proteins c-raf / genetics
  • [MeSH-minor] Bone Marrow Cells / cytology. Bone Marrow Cells / drug effects. Breast Neoplasms. Cell Division. DNA Primers. Enzyme Activation. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Transcription, Genetic. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 12010819.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA80916
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Tumor Necrosis Factor-alpha; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.7.7 / DNA-Directed DNA Polymerase
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3. Arceci RJ, Sande J, Lange B, Shannon K, Franklin J, Hutchinson R, Vik TA, Flowers D, Aplenc R, Berger MS, Sherman ML, Smith FO, Bernstein I, Sievers EL: Safety and efficacy of gemtuzumab ozogamicin in pediatric patients with advanced CD33+ acute myeloid leukemia. Blood; 2005 Aug 15;106(4):1183-8
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  • [Title] Safety and efficacy of gemtuzumab ozogamicin in pediatric patients with advanced CD33+ acute myeloid leukemia.
  • This open-label, dose-escalation study evaluated the safety and efficacy of single-agent gemtuzumab ozogamicin, a humanized anti-CD33 antibody-targeted chemotherapeutic agent, for pediatric patients with multiple relapsed or primary refractory acute myeloid leukemia (AML).
  • One patient treated at 9 mg/m2 developed veno-occlusive disease (VOD) of the liver and defined the dose-limiting toxicity.
  • Thirteen patients underwent hematopoietic stem-cell transplantation less than 3.5 months after the last dose of gemtuzumab ozogamicin; 6 (40%) developed VOD.
  • Mean multidrug resistance-protein-mediated drug efflux was significantly lower in the leukemic blasts of patients achieving remission (P < .005).
  • Further studies in combination with standard induction therapy for childhood AML are warranted.
  • [MeSH-major] Aminoglycosides / administration & dosage. Aminoglycosides / toxicity. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / toxicity. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Leukemia, Myeloid / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Acute Disease. Adolescent. Antibodies, Monoclonal, Humanized. Blast Crisis. Child. Child, Preschool. Drug Resistance. Female. Hematopoietic Stem Cell Transplantation. Hepatic Veno-Occlusive Disease / chemically induced. Humans. Hyperbilirubinemia / chemically induced. Infant. Male. Maximum Tolerated Dose. Remission Induction / methods. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 15886328.001).
  • [ISSN] 0006-4971
  • [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 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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4. Hijiya N, Metzger ML, Pounds S, Schmidt JE, Razzouk BI, Rubnitz JE, Howard SC, Nunez CA, Pui CH, Ribeiro RC: Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):63-9
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  • [Title] Severe cardiopulmonary complications consistent with systemic inflammatory response syndrome caused by leukemia cell lysis in childhood acute myelomonocytic or monocytic leukemia.
  • BACKGROUND: Life-threatening pulmonary complications that coincide with cell lysis during early chemotherapy and that mimic systemic inflammatory response syndrome (SIRS) have been reported in patients with acute myeloid leukemia (AML).
  • Severe SIRS was significantly more common in myelomonocytic or monocytic AML (M4/M4eo/M5) than in other subtypes (P = 0.010) and significantly more common in M4eo than in M4/M5 (P = 0.008).
  • Among 112 cases for which information was available, leukocyte reduction was significantly greater in patients with M4/M4eo/M5 than among others during the first 4 days of chemotherapy (P = 0.015).
  • CONCLUSIONS: Patients with M4/M4eo/M5 AML, especially M4eo, experience life-threatening cardiopulmonary complications of tumor lysis that meet the criteria for severe SIRS.
  • [MeSH-major] Cell Death. Leukemia, Monocytic, Acute / complications. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / complications. Leukemia, Myelomonocytic, Acute / drug therapy. Systemic Inflammatory Response Syndrome / etiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Humans. Male. Retrospective Studies. Risk Factors

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15368547.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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5. Flotho C, Kratz C, Niemeyer CM: Targeting RAS signaling pathways in juvenile myelomonocytic leukemia. Curr Drug Targets; 2007 Jun;8(6):715-25
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  • [Title] Targeting RAS signaling pathways in juvenile myelomonocytic leukemia.
  • Juvenile myelomonocytic leukemia (JMML) is a rapidly fatal myeloproliferative disorder of early childhood for which no effective treatment other than hematopoietic stem cell transplantation is currently available.
  • Hence, targeting RAS or its interactors on a molecular level is a promising strategy in the development of novel rational therapies for this menacing disease.
  • Here we give an overview of current concepts on the pathogenesis of JMML, present important aspects of cellular RAS biology that can be exploited for pharmacologic manipulation, and discuss mouse models that have greatly advanced our understanding of the role RAS plays in JMML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Child. Disease Models, Animal. Humans. Mice. ras Proteins / drug effects. ras Proteins / metabolism

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  • (PMID = 17584027.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.6.5.2 / ras Proteins
  • [Number-of-references] 97
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6. Niemeyer CM, Kratz C: Juvenile myelomonocytic leukemia. Curr Treat Options Oncol; 2003 Jun;4(3):203-10
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  • [Title] Juvenile myelomonocytic leukemia.
  • Juvenile myelomonocytic leukemia is an aggressive neoplasia of early childhood.
  • In the absence of an HLA-matched family donor, early SCT from an unrelated donor will be the treatment of choice for most children.
  • With clear evidence of a graft-versus-leukemia effect and a high post-transplant relapse rate, outcome of SCT will depend, in part, on the management of immunosuppression during the procedure.
  • The impact of pretransplant cytoreductive treatment, such as intensive chemotherapy, splenectomy, or 13-cis retinoic acid, is unclear.
  • Hypersensitivity for granulocyte-macrophage colony-stimulating factor and pathologic activation of the Ras/MAPK pathway play an important role in the pathophysiology of juvenile myelomonocytic leukemia and will provide the opportunity for several novel therapy approaches.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute. Leukemia, Myelomonocytic, Chronic
  • [MeSH-minor] Child, Preschool. Combined Modality Therapy. Hematopoietic Stem Cell Transplantation. Humans. Infant

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  • (PMID = 12718797.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 41
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7. Wuchter C, Ruppert V, Schrappe M, Dörken B, Ludwig WD, Karawajew L: In vitro susceptibility to dexamethasone- and doxorubicin-induced apoptotic cell death in context of maturation stage, responsiveness to interleukin 7, and early cytoreduction in vivo in childhood T-cell acute lymphoblastic leukemia. Blood; 2002 Jun 1;99(11):4109-15
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  • [Title] In vitro susceptibility to dexamethasone- and doxorubicin-induced apoptotic cell death in context of maturation stage, responsiveness to interleukin 7, and early cytoreduction in vivo in childhood T-cell acute lymphoblastic leukemia.
  • Within childhood T-cell acute lymphoblastic leukemia (T-ALL), patients with a cortical (CD1a(+)) immunophenotype have been identified as a subgroup with favorable outcome in the acute lymphoblastic leukemia-Berlin-Frankfurt-Münster (ALL-BFM), Cooperative study group for childhood acute lymphoblastic leukemia (COALL) and Pediatric Oncology Group studies.
  • We investigated in leukemic samples of children with T-ALL (n = 81) whether the different in vivo therapy response could be linked to differential in vitro susceptibility to apoptotic cell death.
  • When compared to cortical T-ALL, mature (CD1a(-), surface CD3(+)) T-ALL were significantly more resistant to doxorubicin, and immature, pro-/pre-T-ALL were more resistant to both drugs (P <.05).
  • Apoptosis-related parameters (Bax, Bcl-2, CD95, and CD95-induced apoptosis) did not account for differential susceptibility to drug-induced apoptosis.
  • Analysis of clinical data showed that in vitro susceptibility to dexamethasone (but not to doxorubicin) closely correlated with early in vivo therapy response characterized by percentages of blast cells in bone marrow on day 15 (r(s) = -0.46, P =.001).
  • Taken together, the in vitro assessment of drug-induced apoptosis revealed maturation-dependent differences within childhood T-ALL.
  • The enhanced sensitivity to both drugs in cortical T-ALL might account for the better in vivo treatment response of this prognostically favorable T-ALL subgroup.
  • [MeSH-major] Antigens, CD / analysis. Apoptosis / drug effects. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Interleukin-7 / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antigens, CD1 / analysis. Antigens, CD2 / analysis. Antigens, CD34 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Child. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Neoplasm Staging. Sialic Acid Binding Ig-like Lectin 3. Tumor Cells, Cultured

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  • (PMID = 12010814.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD1; 0 / Antigens, CD2; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD1a antigen; 0 / CD33 protein, human; 0 / Interleukin-7; 0 / Sialic Acid Binding Ig-like Lectin 3; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin
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8. Orsino A, Schneider R, DeVeber G, Grant R, Massicotte P, Canning P, Carcao M: Childhood acute myelomonocytic leukemia (AML-M4) presenting as catastrophic antiphospholipid antibody syndrome. J Pediatr Hematol Oncol; 2004 May;26(5):327-30
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  • [Title] Childhood acute myelomonocytic leukemia (AML-M4) presenting as catastrophic antiphospholipid antibody syndrome.
  • : The authors describe a 15-year-old girl presenting with a cerebral ischemic stroke as the first manifestation of catastrophic antiphospholipid antibody syndrome secondary to acute myeloid leukemia (AML).
  • Despite treatment with anticoagulants, therapeutic plasma exchange, and chemotherapy, the patient developed multiorgan thromboses and failure, eventually culminating in death.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / etiology. Leukemia, Myelomonocytic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Antibodies, Antiphospholipid / blood. Catastrophic Illness. Diagnosis, Differential. Fatal Outcome. Female. Humans. Stroke / etiology. Thrombosis / etiology. Treatment Failure


9. Pui CH, Schrappe M, Ribeiro RC, Niemeyer CM: Childhood and adolescent lymphoid and myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2004;:118-45
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  • [Title] Childhood and adolescent lymphoid and myeloid leukemia.
  • Remarkable progress has been made in the past decade in the treatment and in the understanding of the biology of childhood lymphoid and myeloid leukemias.
  • With contemporary improved risk assessment, chemotherapy, hematopoietic stem cell transplantation and supportive care, approximately 80% of children with newly diagnosed acute lymphoblastic leukemia and 50% of those with myeloid neoplasm can be cured to date.
  • Ching-Hon Pui describes certain clinical and biologic features that still have prognostic and therapeutic relevance in the context of contemporary treatment programs.
  • He emphasizes that treatment failure in some patients is not due to intrinsic drug resistance of leukemic cells but is rather caused by suboptimal drug dosing due to host compliance, pharmacodynamics, and pharmacogenetics.
  • Finally, he contends that with optimal risk-directed systemic and intrathecal therapy, cranial irradiation may be omitted in all patients, regardless of the presenting features.
  • Martin Schrappe performs detailed analyses of the prognostic impact of presenting age, leukocyte count, sex, immunophenotype, genetic abnormality, early treatment response, and in vitro drug sensitivity/resistance in childhood acute lymphoblastic leukemia, based on the large database of the Berlin-Frankfurt-Münster consortium.
  • He also succinctly summarizes the important treatment components resulting in the improved outcome of children and young adolescents with this disease.
  • He describes the treatment approach that led to the improved outcome of adolescent patients, a finding that may be applied to young adults in the second and third decade of life.
  • Finally, he believes that treatment reduction under well-controlled clinical trials is feasible in a subgroup of patients with excellent early treatment response as evidenced by minimal residual disease measurement during induction and consolidation therapy.
  • Raul Ribeiro describes distinct morphologic and genetic subtypes of acute myeloid leukemia.
  • The finding of essentially identical gene expression profiling by DNA microarray in certain specific genetic subtypes of childhood and adult acute myeloid leukemia suggests a shared leukemogenesis.
  • He then describes the principles of treatment as well as the efficacy and toxicity of various forms of postremission therapy, emphasizing the need of tailoring therapy to both the disease and the age of the patient.
  • Early results suggest that minimal residual disease measurement can also improve the risk assessment in acute myeloid leukemia, and that cranial irradiation can be omitted even in those with central-nervous-system leukemia at diagnosis.
  • Charlotte Niemeyer describes a new classification of myelodysplastic and myeloproliferative diseases in childhood, which has greatly facilitated the diagnosis of myelodysplastic syndromes and juvenile myelomonocytic leukemia.
  • The recent discovery of somatic mutations in PTPN11 has improved the understanding of the pathobiology and the diagnosis of juvenile myelomonocytic leukemia.
  • She then describes the various treatment approaches for both juvenile myelomonocytic leukemia and myelodysplastic syndromes in the US and Europe, emphasizing the differences between childhood and adult cases for the latter group of diseases.
  • She also raises some controversial issues regarding treatment that will require well-controlled international clinical trials to address.

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  • (PMID = 15561680.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-71907; United States / NCI NIH HHS / CA / CA-71970; United States / NCI NIH HHS / CA / CA-78224; United States / NCI NIH HHS / CA / CA20180; United States / NIGMS NIH HHS / GM / GM-61374; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Journal Article; 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.; Review
  • [Publication-country] United States
  • [Number-of-references] 157
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10. Woods WG, Barnard DR, Alonzo TA, Buckley JD, Kobrinsky N, Arthur DC, Sanders J, Neudorf S, Gold S, Lange BJ: Prospective study of 90 children requiring treatment for juvenile myelomonocytic leukemia or myelodysplastic syndrome: a report from the Children's Cancer Group. J Clin Oncol; 2002 Jan 15;20(2):434-40
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  • [Title] Prospective study of 90 children requiring treatment for juvenile myelomonocytic leukemia or myelodysplastic syndrome: a report from the Children's Cancer Group.
  • PURPOSE: We report the first large prospective study of children with myelodysplastic syndrome (MDS) and juvenile myelomonocytic leukemia (JMML) treated in a uniform fashion on Children's Cancer Group protocol 2891.
  • PATIENTS AND METHODS: Ninety children with JMML, various forms of MDS, or acute myeloid leukemia (AML) with antecedent MDS were treated with a five-drug induction regimen (standard or intensive timing).
  • All other patients were randomized between autologous BMT and aggressive nonmyeloablative chemotherapy.
  • For patients achieving remission, long-term survivors were found in those receiving either allogeneic BMT or chemotherapy.
  • CONCLUSION: Childhood subtypes of MDS and JMML represent distinct entities with distinct clinical outcomes.
  • Children with a history of MDS who present with AML do well with AML-type therapy.
  • Patients with RA or RAEB respond poorly to AML induction therapy.
  • The optimum treatment for JMML remains unknown.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelomonocytic, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


11. Korthof ET, Snijder PP, de Graaff AA, Lankester AC, Bredius RG, Ball LM, Lie JL, Vossen JM, Egeler RM: Allogeneic bone marrow transplantation for juvenile myelomonocytic leukemia: a single center experience of 23 patients. Bone Marrow Transplant; 2005 Mar;35(5):455-61
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  • [Title] Allogeneic bone marrow transplantation for juvenile myelomonocytic leukemia: a single center experience of 23 patients.
  • Juvenile myelomonocytic leukemia (JMML) is a childhood leukemia for which allogeneic BMT is the only curative therapy.
  • At our pediatric stem cell transplantation unit, we performed 26 BMTs in 23 children (age 0.5-12.7 years).
  • Nine of these patients died, one achieved a second remission following acute nonlymphatic leukemia chemotherapy (duration to date 5.3 years).
  • Together with a trend towards less relapse in patients with graft-versus-host-disease and in patients transplanted with matched unrelated donors, this suggests a graft-versus-leukemia effect of allogeneic BMT in JMML.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myelomonocytic, Chronic / therapy
  • [MeSH-minor] Child. Child, Preschool. Female. Graft vs Host Disease. Graft vs Leukemia Effect. Histocompatibility. Humans. Infant. Lymphocyte Depletion. Male. Multivariate Analysis. Recurrence. Retrospective Studies. Risk Factors. Survival Analysis. Transplantation Conditioning / methods. Transplantation Conditioning / mortality. Transplantation, Homologous. Treatment Outcome

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  • [CommentIn] Bone Marrow Transplant. 2005 Sep;36(5):453-4; author reply 454 [15968292.001]
  • (PMID = 15654356.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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12. Wójcik D, Pietras W, Ussowicz M, Chybicka A: [What to improve in approach to diagnose and treat pediatric myelodysplastic syndromes and juvenile myelomonocytic leukemia in Poland?]. Przegl Lek; 2006;63(1):29-30
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  • [Title] [What to improve in approach to diagnose and treat pediatric myelodysplastic syndromes and juvenile myelomonocytic leukemia in Poland?].
  • [Transliterated title] Jak poprawić diagnostyke i leczenie dzieciecych zespołów mielodysplastycznych i młodzieńczej białaczki mielomonocytowej w Polsce?
  • Chemotherapy is generally, not useful in childhood MDS.
  • With a few exceptions hematopoieitic stem cell transplantation (HSCT) is the only curative treatment for children with MDS.
  • Successful management of the disease needs to be run on a basis of cooperative efforts between clinicians and scientists involved in pediatric MDS.
  • This includes need for centralized update and morphologic re-evaluation of all patients in the country as well as appointments on a regular basis for all individuals involved in treatment of MDS for quality control.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Leukemia, Myelomonocytic, Acute / therapy. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Female. Humans. Male. Poland / epidemiology. Retrospective Studies. Treatment Outcome


13. Bachmann PS, Lock RB: In vivo models of childhood leukemia for preclinical drug testing. Curr Drug Targets; 2007 Jun;8(6):773-83
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  • [Title] In vivo models of childhood leukemia for preclinical drug testing.
  • The number of new anti-cancer drugs emerging for clinical trials in humans far exceeds the availability of pediatric acute leukemia patients to be entered into clinical trials.
  • Therefore, preclinical testing of new agents for the treatment of childhood acute leukemia is essential to ensure that the most promising drugs are prioritized to enter clinical trials.
  • Historically, the murine system has been central to modeling human leukemia in vivo.
  • A greater knowledge of the molecular lesions underlying particular subtypes of leukemia has led to the generation of genetically engineered murine models, generally involving the knockin or knockout of certain genes and fusion genes at their normal genetic locus.
  • However, the most predominant in vivo models for preclinical drug testing have been human leukemia xenografts.
  • Successful engraftment of all subtypes of acute lymphoblastic leukemia, most subtypes of acute myeloid leukemia as well as juvenile myelomonocytic leukemia, chronic myeloid leukemia and chronic lymphocytic leukemia have been described in various immune-deficient murine hosts.
  • Preclinical testing of novel therapeutics in vivo will likely identify the most promising new agents to enter clinical trials, and will allow their future use to be optimized in combination with other novel and conventional chemotherapeutics.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Evaluation, Preclinical / methods. Drug Screening Assays, Antitumor / methods. Leukemia / drug therapy

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  • (PMID = 17584033.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 154
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14. Yalman N, Sarper N, Devecioğlu O, Anak S, Eryilmaz E, Can M, Yenilmez H, Ağaoğlu L, Gedikoğlu G: Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia. Turk J Pediatr; 2000 Jul-Sep;42(3):198-204
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  • [Title] Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia.
  • The prognosis of relapsed acute leukemia or chronic leukemia in acute blast crisis is poor and new chemotherapeutic regimens could be useful for these patients.
  • Six relapsed acute lymphoblastic leukemia (ALL), nine relapsed acute myeloblastic leukemia (AML), one chronic myelomonocytic leukemia (CMML) and one chronic myeloid leukemia (CML) in acute blast crisis between three to 18 years (median 10 years) received fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) chemotherapy (CT).
  • The regimen was ineffective in B-cell ALL as in acute blastic crisis of CMML and CML.
  • FLAG-IDA appears to be a myelotoxic therapy for relapsed or poor risk leukemia in a developing country.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy / methods. Vidarabine / analogs & derivatives

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  • (PMID = 11105617.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] TURKEY
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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15. Okada S, Hongo T, Yamada S, Watanabe C, Fujii Y, Ohzeki T, Horikoshi Y, Ito T, Yazaki M, Komada Y, Tawa A: In vitro efficacy of l-asparaginase in childhood acute myeloid leukaemia. Br J Haematol; 2003 Dec;123(5):802-9
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  • [Title] In vitro efficacy of l-asparaginase in childhood acute myeloid leukaemia.
  • To explore the potential efficacy of l-asparaginase treatment in acute myeloid leukaemia (AML) patients, we studied the in vitro resistance of French-American-British (FAB) subtypes of childhood AML to l-asparaginase using a methyl-thiazol-tetrazolium assay.
  • We tested leukaemic cells obtained from 177 common acute lymphoblastic leukaemia (cALL) and 228 AML children at diagnosis.
  • The median LD70asp among each FAB subtype of AML was 0.76 (M0), 0.46 (M1), 10.00 (M2), 10.00 (M3), 1.18 (M4), 1.35 (M5) and 10.00 (M7).
  • Type M3 samples had the highest LD70asp.
  • The LD70asp of the M2 samples was significantly higher than that of the M1, M4 and M5 samples.
  • In conclusion, cells from AML types M1, M4 and M5 were relatively sensitive to l-asparaginase, and M1 cells were as sensitive as those of cALL, suggesting that l-asparaginase treatment may be effective for these subtypes of AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Asparaginase / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Age Factors. Analysis of Variance. Child. Child, Preschool. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Humans. Infant. Lethal Dose 50. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Lymphocyte Count. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sex Factors

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  • (PMID = 14632770.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
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16. Shah M, Agarwal B: Recent advances in management of acute myeloid leukemia (AML). Indian J Pediatr; 2008 Aug;75(8):831-7
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  • [Title] Recent advances in management of acute myeloid leukemia (AML).
  • Acute myeloid leukemia (AML) is the most common childhood malignancy.
  • A number of chromosomal abnormalities are used to predict outcome and stratify therapeutic risk groups in children with AML.
  • This article aims to review the recent development in diagnosis, treatment and monitoring of AML.
  • Better understanding of the molecular pathogenesis of AML has led to the development of target-specific therapies.
  • Some of the new classes of drugs include monoclonal antibody directed against the CD33 antigen, farnesyltransferase inhibitors (FTI), and FMSlike tyrosine kinase 3 (FLT3) inhibitors.
  • The role of allogenic SCT, particularly whether it should be done during first CR or reserved for second remission, remains the most controversial issue in pediatric AML.
  • There is a need of collaboration with international pediatric cooperative oncology groups and definitive clinical trials in order to establish use of these newer molecules in pediatric populations.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use. Leukemia, Myeloid, Acute / therapy. Neoplasm, Residual / drug therapy
  • [MeSH-minor] Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Child. Child, Preschool. Humans. Prognosis. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. fms-Like Tyrosine Kinase 3 / antagonists & inhibitors. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 18769895.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunologic Factors; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 43
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17. Laatiri MA, Chehata S, Amouri A, Bouaouina N, Chatti S, Saad A, Ennabli S: [Childhood acute myeloblastic leukemias. Report of 21 cases]. Tunis Med; 2000 Mar;78(3):167-71
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  • [Title] [Childhood acute myeloblastic leukemias. Report of 21 cases].
  • Between 1989 and 1996, 21 cases with acute non lymphoblastic leukemia (11 males and 10 females) were diagnosed in our institution.
  • The 3-year survival rate was 20% and the relapse-free-survival rate was 12% confirming the worse prognosis of this leukemia when treated with standard chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Monocytic, Acute / diagnosis. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / diagnosis. Leukemia, Myelomonocytic, Acute / drug therapy

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  • (PMID = 11026819.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] TUNISIA
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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18. Hall PD, Razzouk BI, Willoughby TE, McLean TW, Frankel AE: The majority of children and adolescents with acute myeloid leukemia have detectable anti-DT388-GMCSF IgG concentrations, but at concentrations that should not preclude in vivo activity. J Pediatr Hematol Oncol; 2002 Oct;24(7):521-6
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  • [Title] The majority of children and adolescents with acute myeloid leukemia have detectable anti-DT388-GMCSF IgG concentrations, but at concentrations that should not preclude in vivo activity.
  • PURPOSE: As a novel approach for the treatment of acute myeloid leukemia (AML), the authors are developing a fusion toxin (DT(388)-GMCSF) consisting of a truncated diphtheria toxin (DT(388)) linked to human granulocyte-macrophage colony-stimulating factor (GMCSF).
  • A critical step in the development of DT(388)-GMCSF for clinical use in childhood and adolescent AML is to determine whether children and adolescents have preexisting antibodies to DT(388)-GMCSF due to childhood immunizations against diphtheria toxoid.
  • PATIENTS AND METHODS: Sera from 33 children and adolescents with AML and one with juvenile myelomonocytic leukemia were collected.
  • Anti-DT(388)-GMCSF antibody concentrations were detected by an enzymoimmunoassay and by an in vitro bioassay.
  • RESULTS: Thirty of 34 (88%) children and adolescents had detectable anti-DT(388)-GMCSF IgG antibody concentrations.
  • There was no difference between the anti-DT(388)-GMCSF IgG concentrations in these children and adolescents with AML and in 43 adults with AML.
  • Preliminary results of the phase 1 trial of DT -GMCSF in adults with AML indicate that patients with baseline anti-DT(388)-GMCSF IgG concentrations of less than 2 microg/mL can achieve circulating DT(388)-GMCSF concentrations and can exhibit antileukemic activity.
  • Twenty-three of 34 (67.6%) children and adolescents had anti-DT(388)-GMCSF IgG concentrations less than 2 microg/mL.
  • CONCLUSIONS: Despite routine diphtheria toxoid vaccinations, most children and adolescents with AML do not have anti-DT -GMCSF IgG concentrations that preclude in vivo activity of DT -GMCSF.
  • [MeSH-major] Diphtheria Toxin / immunology. Granulocyte-Macrophage Colony-Stimulating Factor / immunology. Immunoglobulin G / immunology. Leukemia, Myeloid, Acute / immunology. Recombinant Fusion Proteins / immunology

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  • (PMID = 12368687.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DTctGMCSF protein, recombinant; 0 / Diphtheria Toxin; 0 / Diphtheria Toxoid; 0 / Immunoglobulin G; 0 / Recombinant Fusion Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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19. Ambati S, Chamyan G, Restrepo R, Escalon E, Fort J, Pefkarou A, Khatib ZA, Dehner LP: Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):433-5
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  • [Title] Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia.
  • A child with acute pre-B cell lymphoblastic leukemia underwent haploidentical bone marrow transplantation (BMT) after first relapse.
  • Approximately 8 months after the BMT, he developed a soft tissue mass overlying a defect in the left frontal bone.
  • He received chemotherapy with vinblastine, prednisone, 6-mercaptopurine and methotrexate and has been in remission for over 4 years.
  • Only one previous example of acute lymphoblastic leukemia in childhood has been reported with R-D disease.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Graft vs Host Disease / etiology. Histiocytosis, Sinus / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Histiocytes. Humans. Male. Remission Induction. S100 Proteins

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18493991.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / S100 Proteins
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20. Shenoy S, Smith FO: Hematopoietic stem cell transplantation for childhood malignancies of myeloid origin. Bone Marrow Transplant; 2008 Jan;41(2):141-8
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  • [Title] Hematopoietic stem cell transplantation for childhood malignancies of myeloid origin.
  • Myeloid malignancies in children include de novo acute/chronic myeloid leukemia (AML/CML) and secondary malignancy due to genetic predisposition or previous therapy.
  • Generations of clinical trials for childhood myeloid disorders have resulted in improved disease characterization and outcome, and defined therapeutic strategies combining chemotherapy, biologic response modifiers and immunotherapy.
  • With advancement in molecular genetics and the development of sensitive techniques to detect response, residual disease and relapse, therapy can be tailored in a risk-based manner using clinical and biological/molecular parameters and several 'good-risk' myeloid malignancies enjoy high cure rates with targeted therapy.
  • However, hematopoietic stem cell transplant remains the best method of treatment intensification for poor-risk disorders such as relapsed/secondary AML, myelodysplastic syndrome and juvenile myelomonocytic leukemia.
  • Indications for transplant and outcomes of previous clinical studies, and novel transplant strategies designed to improve safety and efficacy of the procedure are reviewed.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy
  • [MeSH-minor] Child. Child, Preschool. Humans. Infant. Myelodysplastic Syndromes / therapy. Risk Factors. Survival Analysis. Transplantation Conditioning / methods

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  • (PMID = 18176616.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 48
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21. Yabe M, Sako M, Yabe H, Osugi Y, Kurosawa H, Nara T, Tokuyama M, Adachi S, Kobayashi C, Yanagimachi M, Ohtsuka Y, Nakazawa Y, Ogawa C, Manabe A, Kojima S, Nakahata T, Japanese Childhood MDS Study Group: A conditioning regimen of busulfan, fludarabine, and melphalan for allogeneic stem cell transplantation in children with juvenile myelomonocytic leukemia. Pediatr Transplant; 2008 Dec;12(8):862-7
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  • [Title] A conditioning regimen of busulfan, fludarabine, and melphalan for allogeneic stem cell transplantation in children with juvenile myelomonocytic leukemia.
  • Five patients developed acute GVHD and two developed chronic GVHD.
  • [MeSH-major] Busulfan / administration & dosage. Immunosuppressive Agents / therapeutic use. Leukemia, Myelomonocytic, Juvenile / drug therapy. Melphalan / administration & dosage. Stem Cell Transplantation / methods. Vidarabine / analogs & derivatives

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  • (PMID = 18397212.001).
  • [ISSN] 1399-3046
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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22. Zülfikar B: Two patients with haemophilia and acute leukaemia. Haemophilia; 2002 Sep;8(5):698-702
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two patients with haemophilia and acute leukaemia.
  • Acute leukaemia is the commonest form of malignancy in childhood.
  • Of a total of 440 people with haemophilia registered with our society, two were diagnosed with acute leukaemia last year.
  • The first case involved a 14-year-old boy with moderate haemophilia A, who developed acute lymphoblastic leukaemia (ALL) [French-American-British (FAB) classification L2].
  • The second subject was a 16-year-old boy who had moderately severe haemophilia A with no previous family history, and developed acute nonlymphocytic (myelomonocytic) leukaemia (FAB-M4).
  • Both patients received conventional chemotherapy and this report discusses the potential problems in management of such cases, including diagnosis and administration of chemotherapy in subjects with a pre-existing haemorrhagic disorder.
  • Extensive cutaneous and mucosal bleeding, as well as bleeds in joints previously affected by haemarthrosis and alterations of haematological values were all initially suggestive of the development of inhibitors against factor VIII, but the appearance of blasts in the peripheral blood and bone marrow led to the definitive diagnosis.
  • The risk of bleeding, due to the combination of both leukaemia and the consequences of the chemotherapy, was overcome by the administration of coagulation factor concentrates (daily initially followed by prophylactic doses after successful induction of remission in both patients).
  • [MeSH-major] Developing Countries. Hemophilia A / complications. Leukemia, Myelomonocytic, Acute / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Cost of Illness. Fatal Outcome. HIV Seronegativity. Humans. Immunosuppressive Agents / therapeutic use. Male. Turkey

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  • (PMID = 12199682.001).
  • [ISSN] 1351-8216
  • [Journal-full-title] Haemophilia : the official journal of the World Federation of Hemophilia
  • [ISO-abbreviation] Haemophilia
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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23. Ning ZQ, Li J, Arceci RJ: Activating mutations of c-kit at codon 816 confer drug resistance in human leukemia cells. Leuk Lymphoma; 2001 May;41(5-6):513-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activating mutations of c-kit at codon 816 confer drug resistance in human leukemia cells.
  • An improved understanding of how leukemia cells grow and become resistant to treatment remains critical for developing more effective therapies.
  • We have identified activating mutations of c-kit at codon 816 (Asp(816) ) from a revertant of the cytokine-dependent acute myeloid leukemia (AML) cell line, MO7e (D816H), and de novo childhood AML (D816N).
  • Following transduction of the mutant c-kit cDNAs, MO7e cells acquire a growth advantage and resistance to apoptosis in response to chemotherapeutic drugs and ionizing radiation, in addition to cytokine-independent survival.
  • These results suggest a potentially important role of Asp(816) mutations of c-kit in both malignant cell proliferation and resistance to therapy.
  • [MeSH-major] Leukemia / drug therapy. Leukemia / pathology. Leukemia, Myelomonocytic, Acute / pathology. Mutation. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / pharmacology
  • [MeSH-minor] Amino Acid Substitution. Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis / genetics. Apoptosis / radiation effects. Cell Division / drug effects. Cell Division / genetics. Child. Codon / genetics. Cytokines / pharmacology. Drug Resistance, Neoplasm / genetics. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Stem Cell Factor / drug effects. Transduction, Genetic. Transplantation, Heterologous. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / radiation effects

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  • (PMID = 11378569.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Codon; 0 / Cytokines; 0 / Stem Cell Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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24. Ng SM, Ariffin WA, Lin HP, Chan LL, Chin YM: Clinical features and treatment outcome of children with myeloid antigen coexpression in B-lineage acute lymphoblastic leukemia: a study of 151 Malaysian children. J Trop Pediatr; 2000 Apr;46(2):73-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical features and treatment outcome of children with myeloid antigen coexpression in B-lineage acute lymphoblastic leukemia: a study of 151 Malaysian children.
  • The purpose of the study was to evaluate the incidence of myeloid antigen coexpression and its prognostic significance in childhood acute lymphoblastic leukemia (ALL) in Malaysia.
  • Presenting features and treatment outcome of 39 B-lineage ALL patients with myeloid antigen coexpression (My+B) were compared with 112 B-lineage ALL patients without myeloid antigen coexpression (My-B) for similarity in demographic, clinical and laboratory features and their treatment outcome.
  • My+B and My-B patients were treated with a uniform treatment protocol.
  • Treatment outcome were not significant between the two groups.
  • This study demonstrates that myeloid antigen coexpression is fairly common and constitutes 23 per cent of childhood ALL within the Malaysian population and that it is not an adverse risk factor in childhood ALL.
  • [MeSH-major] Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antigen Presentation / drug effects. B-Lymphocytes / classification. B-Lymphocytes / immunology. Biomarkers / analysis. Cell Lineage. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Immunophenotyping. Infant. Male. Survival Rate. Treatment Outcome

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  • (PMID = 10822932.001).
  • [ISSN] 0142-6338
  • [Journal-full-title] Journal of tropical pediatrics
  • [ISO-abbreviation] J. Trop. Pediatr.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers
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25. Hiçsönmez G, Cetin M, Yenicesu I, Olcay L, Koç A, Aktaş D, Tunçbilek E, Tuncer M: Evaluation of children with myelodysplastic syndrome: importance of extramedullary disease as a presenting symptom. Leuk Lymphoma; 2001 Aug;42(4):665-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Three patients with juvenile myelomonocytic leukemia (JMML) and 2 patients with chronic myelomonocytic leukemia (CMML) presented with pleural effusion.
  • Since high-dose methylprednisolone (HDMP, 20-30 mg/kg/day) has been shown to induce differentiation and apoptosis of myeloid leukemic cells in children with different morphological subtypes of acute myeloid leukemia in vivo and in vitro, 25 children with de novo MDS were treated with combined HDMP and cytotoxic chemotherapy.
  • Dramatic improvement of EMD and decrease in blast cells both in the peripheral blood and bone marrow were obtained following administration of short-course HDMP treatment alone as observed in children with AML.
  • In conclusion EMD can be a presenting finding in childhood MDS as observed in adults.
  • In addition, the beneficial effect of HDMP combined with more intensive chemotherapy should be explored as alternative therapy in children with MDS not suitable for bone marrow transplantation.
  • [MeSH-major] Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adolescent. Anti-Inflammatory Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Leukemia, Myelomonocytic, Chronic / diagnosis. Leukemia, Myelomonocytic, Chronic / drug therapy. Male. Methylprednisolone / administration & dosage. Prospective Studies. Remission Induction. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / drug therapy. Treatment Outcome


26. Yang CP, Hung JJ, Jaing TH, Lin KH, Lin DT, Lu MY, Liang DC, Chen SH, Liu HC, Hsiao CC, Shu SG, Chen JS, Chang TT, Chiou SS, Hsieh YL, Lin MT, Lee MT, Peng CT, Cheng SN, Chen RL, Chen BW, Lin KS: Treatment results of the TPOG-NHL92 protocols for childhood non-Hodgkin's lymphomas in Taiwan: a report from the Taiwan Pediatric Oncology Group (TPOG). Acta Paediatr Taiwan; 2000 Jul-Aug;41(4):193-204

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment results of the TPOG-NHL92 protocols for childhood non-Hodgkin's lymphomas in Taiwan: a report from the Taiwan Pediatric Oncology Group (TPOG)
  • A nation-wide chemotherapeutic trial for childhood non-Hodgkin's lymphoma (NHL) was conducted by the Taiwan Pediatric Oncology Group (TPOG).
  • Four TPOG-NHL92 protocols based on stage and histology were activated in 1992: TPOG-92LD (treatment duration: 8 months) was used for localized (stages I/II) NHL with any histology, 92LB (2 years), 92SNC (5 months), and 92LC (1 year) for advanced (stages III/IV) lymphoblastic (LB), small non-cleaved cell (SNC), and large cell (LC) lymphoma, respectively.
  • There were 54 (27.3%) patients with LB, 94 (47.5%) with SNC including B-cell acute lymphoblastic leukemia (B-ALL), and 50 (25.2%) with LC.
  • There were 176 patients eligible for evaluation of treatment results.
  • As of August 31, 1999, 26 patients relapsed, six died during remission, one patient developed secondary acute myelomonocytic leukemia, and 105 patients remained in continuous remission with a median remission duration of 49 months.
  • We concluded that following the strategy of stratification of therapy, only disease stages had prognostic significance in this study.
  • More efforts are needed to improve our treatment results.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy

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  • [CommentIn] Acta Paediatr Taiwan. 2000 Jul-Aug;41(4):175-6 [11021000.001]
  • (PMID = 11021005.001).
  • [ISSN] 1608-8115
  • [Journal-full-title] Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi
  • [ISO-abbreviation] Acta Paediatr Taiwan
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
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27. Anagnostopoulos C, Jadwat Y, Wood NH, Meyerov R, Lemmer J, Bouckaert M, Feller L: A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo. SADJ; 2007 Oct;62(9):390, 392-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A report of oral extramedullary acute myeloid leukaemia (AML) in an 8-year-old girl with newly diagnosed AML-M4Eo.
  • Acute myeloid leukaemia (AML), characterized by proliferation of immature neoplastic myeloid cells, is uncommon in childhood.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / pathology. Mouth Neoplasms / pathology
  • [MeSH-minor] Bone Marrow Neoplasms / pathology. Child. Diagnosis, Differential. Eosinophilia / pathology. Fatal Outcome. Female. Humans. Immunophenotyping / methods. Sepsis / drug therapy

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  • (PMID = 18260548.001).
  • [ISSN] 1029-4864
  • [Journal-full-title] SADJ : journal of the South African Dental Association = tydskrif van die Suid-Afrikaanse Tandheelkundige Vereniging
  • [ISO-abbreviation] SADJ
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] South Africa
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28. Stam RW, Hubeek I, den Boer ML, Buijs-Gladdines JG, Creutzig U, Kaspers GJ, Pieters R: MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia. Leukemia; 2006 Jan;20(1):179-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia.
  • [MeSH-major] Cytarabine / therapeutic use. Drug Resistance, Neoplasm / genetics. Gene Rearrangement. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Cell Proliferation / drug effects. Drug Screening Assays, Antitumor. Histone-Lysine N-Methyltransferase. Humans. In Vitro Techniques. Models, Biological






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