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Items 1 to 24 of about 24
1. 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.
  • 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.
  • 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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2. 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).
  • 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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3. 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.
  • Bisphosphonate zoledronic acid (ZOL), a RAS-blocking compound, suppressed colony formation from bone marrow (BM) cells of 8 patients with JMML and 5 healthy control subjects without and with GM-CSF (10 ng/mL), respectively, in a dose-dependent manner in clonal culture.
  • [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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4. Gulen H, Basarir F, Hakan N, Ciftdogan DY, Tansug N, Onag A: Premature labor and leukoerythroblastosis in a newborn with parvovirus B19 infection. Haematologica; 2005 Nov;90 Suppl:ECR38
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  • The etiological factors observed in leukoerythroblastosis occurring during neonatal and early childhood period are congenital-postnatal viral infections, juvenile myelomonocytic leukemia and osteopetrosis.
  • It is reported that it can be observed following hematologic malignancies especially juvenile myelomonocytic leukemia, acute infections, hemolytic anemia, osteopetrosis, myelofibrosis, neuroblastoma and taking certain medicines.

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  • (PMID = 16266929.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Viral; 0 / Immunoglobulin G; 0 / Immunoglobulin M
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5. 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
  • [MeSH-minor] Animals. Animals, Genetically Modified. Child. Disease Models, Animal. Disease-Free Survival. Humans. Mice. Mice, Knockout. Neoplasm Transplantation. Recurrence

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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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6. Roman E, Cooney E, Harrison L, Militano O, Wolownik K, Hawks R, Foley S, Satwani P, Unal E, Bhatia M, Bradley B, Del Toro G, George D, Garvin J, van de Ven C, Cairo MS: Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia. Clin Cancer Res; 2005 Oct 1;11(19 Pt 2):7164s-7170s
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  • [Title] Preliminary results of the safety of immunotherapy with gemtuzumab ozogamicin following reduced intensity allogeneic stem cell transplant in children with CD33+ acute myeloid leukemia.
  • PURPOSE: Myeloablative allogeneic stem cell transplantation (SCT) has been successful in the treatment of childhood acute myeloid leukemia (AML), but may be associated with significant toxicity and recurrent disease.
  • Targeted immunotherapy with gemtuzumab ozogamicin has been shown to be safe, well tolerated in children, and, as a single agent, gemtuzumab ozogamicin has induced responses in 30% of patients with recurrent CD33+ AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation / methods

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  • (PMID = 16203817.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL07968
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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7. 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.
  • TNF-alpha plays a permissive role, being dependent upon GM-CSF to induce JMML cell proliferation.
  • 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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8. Yagi T, Hibi S, Takanashi M, Kano G, Tabata Y, Imamura T, Inaba T, Morimoto A, Todo S, Imashuku S: High frequency of Ikaros isoform 6 expression in acute myelomonocytic and monocytic leukemias: implications for up-regulation of the antiapoptotic protein Bcl-XL in leukemogenesis. Blood; 2002 Feb 15;99(4):1350-5
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  • [Title] High frequency of Ikaros isoform 6 expression in acute myelomonocytic and monocytic leukemias: implications for up-regulation of the antiapoptotic protein Bcl-XL in leukemogenesis.
  • While studying Ikaros proteins in childhood acute myeloid leukemia (AML), Ikaros isoform 6 (Ik6) expression was detected in 7 of 10 cases of M4 and M5 leukemia, but in none of the remaining French-American-British subtypes (M2, 8 cases; M7, 6 cases).
  • To clarify the function of Ik6 in developing blood cells, this isoform was transiently transfected into an Ik2(+), interleukin-3 (IL-3)-dependent 32D murine myeloid precursor cell line and studied the expression of Bcl-2 family proteins in relation to in vitro cell growth, using a tetracycline-inducible TREx system.
  • Up-regulation of Bcl-XL, but not of other Bcl-2 family proteins, was associated with the suppression of functional Ik2 by Ik6 in a dominant-negative fashion.
  • Thus, the pathogenesis of myelomonocytic/monocytic AML may involve aberrant regulation of apoptosis due to unscheduled expression of the Ik6 isoform.
  • [MeSH-major] DNA-Binding Proteins. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Transcription Factors / physiology
  • [MeSH-minor] Adolescent. Animals. Apoptosis / drug effects. Blood Cells / metabolism. Blood Cells / pathology. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. COS Cells. Cell Transformation, Neoplastic / chemically induced. Cell Transformation, Neoplastic / metabolism. Child. Child, Preschool. Female. Gene Expression / drug effects. Gene Expression Regulation. Hematopoiesis / drug effects. Humans. Ikaros Transcription Factor. Infant. Male. Mice. Protein Isoforms / genetics. Protein Isoforms / pharmacology. Protein Isoforms / physiology. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Transfection. Tumor Cells, Cultured. Up-Regulation / drug effects. bcl-X Protein

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  • [CommentIn] Blood. 2002 Aug 15;100(4):1511-2; 1512-3 [12184276.001]
  • [CommentIn] Blood. 2002 Nov 1;100(9):3436-7 [12412579.001]
  • (PMID = 11830486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 0 / Zfpn1a1 protein, mouse; 0 / bcl-X Protein; 148971-36-2 / Ikaros Transcription Factor
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9. 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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  • [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.
  • Although stimulation of mutant c-kit-bearing MO7e cells with stem cell factor (SCF), a ligand for c-Kit, does not have a significant effect on cell proliferation, SCF further inhibits apoptosis induced by cytotoxic agents.
  • [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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10. 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.
  • 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.
  • 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.
  • 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.
  • In Section IV, Dr.
  • 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.
  • Together with the findings of mutations in RAS and NF1 in the other patients, she suggests that pathological activation of RAS-dependent pathways plays a central role in the leukemogenesis of this disease.
  • 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.

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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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11. 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).
  • Results were compared with patients with de novo AML.
  • Remission rates for patients with RAEB in transformation (RAEB-T) (69%) or antecedent MDS (81%) were similar to de novo AML (77%).
  • Actuarial survival rates at 6 years were as follows: JMML, 31% +/- 26%; RA and RAEB, 29% +/- 16%; RAEB-T, 30% +/- 18%; antecedent MDS, 50% +/- 25%; and de novo AML, 45% +/- 3%.
  • 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.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelomonocytic, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


12. 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.
  • The RAS proteins function as fundamental signaling switches that control normal cell growth and differentiation.
  • Deregulated activation of RAS-dependent signaling pathways constitutes a potent mechanism of malignant cell transformation.
  • 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.
  • 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.
  • In addition, we review recent approaches to develop agents that interfere with the RAS network at the level of the granulocyte-macrophage colony-stimulating factor receptor, posttranslational RAS processing (prenylation and endoprotease cleavage), RAF serine/threonine kinase, MEK mitogen-activated protein kinase, and target of rapamycin activity.
  • Preclinical and clinical data of these pharmaceuticals in JMML and other myeloid malignancies is discussed.
  • [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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13. 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).
  • METHODS: We reviewed the records of patients with de novo AML, excluding M3 and Down syndrome, treated at our institution between 1991 and 2002 to determine the prevalence of severe SIRS with grade 3/4 pulmonary complications and to identify AML subtypes associated with severe SIRS.
  • 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

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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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14. Chang YH, Jou ST, Lin DT, Lu MY, Lin KH: Second allogeneic hematopoietic stem cell transplantation for juvenile myelomonocytic leukemia: case report and literature review. J Pediatr Hematol Oncol; 2004 Mar;26(3):190-3
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  • [Title] Second allogeneic hematopoietic stem cell transplantation for juvenile myelomonocytic leukemia: case report and literature review.
  • Juvenile myelomonocytic leukemia (JMML) is a rare clonal myeloproliferative disease in young childhood.
  • A 5-year-old girl with JMML, who had experienced a relapse after the first transplant, did not respond to donor lymphocyte infusion and withdrawal of immune-suppressing agents.
  • Detailed reports from the English literature since 1988 relating to a total of 13 JMML patients undergoing a second transplant were reviewed.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelomonocytic, Acute / therapy

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  • (PMID = 15125612.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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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. 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.
  • It is not cost-effective; dose modifications or a regimen without IDA may be tried if there is an available marrow donor.
  • [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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17. 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.
  • 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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18. 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].
  • [Transliterated title] Leucémies aiguës myéloblastiques de l'enfant. A propos de 21 cas.
  • 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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19. 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
  • [MeSH-minor] Administration, Oral. Child. Child, Preschool. Female. History, Ancient. Humans. Male. Pilot Projects. Remission Induction. Transplantation Conditioning / methods. Transplantation, Homologous / methods

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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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20. 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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  • [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.
  • 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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21. 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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  • [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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22. 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

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  • [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.
  • Stages I, II, III, and IV (including B-ALL) of the disease comprised 5%, 10%, 43%, and 42% of cases, respectively.
  • 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.
  • The 7-year EFS for stages I/II, III, and IV of the disease was 73%, 68.9%, and 50.3% (P = 0.0212), respectively.
  • [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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23. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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.
  • In conclusion EMD can be a presenting finding in childhood MDS as observed in adults.
  • [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


24. 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
Hazardous Substances Data Bank. CYTARABINE .

  • [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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