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1. Mukiibi JM, Nyirenda CM, Adewuyi JO, Mzula EL, Magombo ED, Mbvundula EM: Leukaemia at Queen Elizabeth Central Hospital in Blantyre, Malawi. East Afr Med J; 2001 Jul;78(7):349-54
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  • An overview of the problems encountered in the management of leukaemia in developing countries especially those in sub-Saharan Africa are highlighted.
  • RESULTS: Of the 95 leukaemia patients diagnosed during the study period, childhood (0-15 years) leukaemia occurred in 27 (28.4%) patients while adulthood (above 15 years) leukaemia accounted for 68 (71.6%) patients.
  • The main leukaemia types were: acute lymphoblastic leukaemia (ALL) 14 (14.7%), acute myeloblastic leukaemia (AML) 25 (26.3%), chronic myeloid (granulocytic) leukaemia (CML) 32 (33.7%), chronic lymphocytic (lymphatic) leukaemia (CLL) 22 (23.2%) and hairy cell leukaemia (HCL) two (2.1%) patients.
  • Abdominal swelling (87.5%) due to splenomegaly (81.3%) were the main clinical features in the CML group whereas lymphadenopathy (63.6%) followed by splenomegaly (59.1%) were the dominant presenting features in CLL.
  • Haematologically, although leucocytosis characterised both acute and chronic leukaemias, most cases of acute leukaemia presented with more severe anaemia (Hb < 7 g/dl) and marked thrombocytopenia (Platelet count < 50 x 10(9)/l) than the chronic leukaemias.
  • While there is need to increase diagnostic awareness among clinicians and laboratory staff, the severe chronic shortage of cytotoxic drugs and lack of supportive care facilities commonly encountered in developing countries should be realistically addressed through cost-sharing, cost recovery, adequate government subvention and donations from charitable organisations.
  • [MeSH-major] Leukemia / epidemiology

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  • (PMID = 11957257.001).
  • [ISSN] 0012-835X
  • [Journal-full-title] East African medical journal
  • [ISO-abbreviation] East Afr Med J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Kenya
  • [Number-of-references] 18
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2. Styczynski J, Wysocki M, Balwierz W, Kowalczyk JR: Dexrazoxane has no impact on sensitivity of childhood leukemic blasts to daunorubicin. Leukemia; 2002 May;16(5):820-5
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  • [Title] Dexrazoxane has no impact on sensitivity of childhood leukemic blasts to daunorubicin.
  • The sensitivity to DEX, DNR and their combination was tested by the MTT assay in human promyelocytic leukemia HL-60, the erythroid blast crisis CML K562 cell lines and in 45 children with ALL and AML.
  • In conclusion, it seems that DEX possibly has no impact on the sensitivity of childhood leukemic blasts to DNR, however, has weak cytotoxic properties itself.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Daunorubicin / pharmacology. Drug Resistance, Neoplasm. Leukemia / pathology. Razoxane / pharmacology
  • [MeSH-minor] Adolescent. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Survival / drug effects. Child. Child, Preschool. Drug Interactions. Flow Cytometry. HL-60 Cells. Humans. Infant. K562 Cells. Tumor Cells, Cultured / drug effects

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  • [ErratumIn] Leukemia 2002 Nov;16(11):2346
  • (PMID = 11986942.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5AR83PR647 / Razoxane; ZS7284E0ZP / Daunorubicin
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3. Anuchapreeda S, Thanarattanakorn P, Sittipreechacharn S, Tima S, Chanarat P, Limtrakul P: Inhibitory effect of curcumin on MDR1 gene expression in patient leukemic cells. Arch Pharm Res; 2006 Oct;29(10):866-73
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  • When patients with cancers are treated with chemotherapeutic agents a long time, some of the cancer cells develop the multidrug resistance (MDR) phenotype.
  • MDR cancer cells are characterized by the overexpression of multidrug resistance1(MDR1) gene which encodes P-glycoprotein (Pgp), a surface protein of tumor cells that functions to produce an excessive efflux and thereby an insufficient intracellular concentration of chemotherapeutic agents.
  • The leukemic cells were collected from 78 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period from July 2003 to February 2005.
  • There were 61 cases of acute lymphoblastic leukemia (ALL), 14 cases of acute myeloblastic leukemia (AML), and 3 cases of chronic myelocytic leukemia (CML).
  • Curcumin affected the MDR1 gene expression in 5 of 11 relapsed cases (45%), 10 of 26 cases of drug maintenance (38%), 7 of 18 cases of completed treatment (39%), and 11 of 23 cases of new patients (48%).
  • Thus, curcumin treatment may provide a lead for clinical treatment of leukemia patients in the future.
  • [MeSH-major] Curcumin / pharmacology. Gene Expression Regulation, Leukemic / drug effects. Genes, MDR / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Age Factors. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Bone Marrow / drug effects. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Survival / drug effects. Child, Preschool. Female. Humans. Infant. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid / blood. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / genetics. RNA, Messenger / isolation & purification. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured

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  • (PMID = 17121181.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; IT942ZTH98 / Curcumin
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4. Hawkins LM, Jayanthan AA, Narendran A: Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity. Pediatr Res; 2005 Mar;57(3):430-7
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  • [Title] Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) on pediatric acute lymphoblastic leukemia (ALL) with respect to Bcr-Abl status and imatinib mesylate sensitivity.
  • Acute lymphoblastic leukemia (ALL) with Bcr-Abl translocation is one of the most difficult to treat and deadly diseases in children.
  • Recently, the geldanamycin family of antibiotics has been found to induce apoptosis in many malignant cells, including adult CML and AML.
  • We describe experiments in which 17-allylamino-17-demethoxygeldanamycin (17-AAG) was evaluated in the context of Bcr-Abl and resistance to imatinib mesylate.
  • Pediatric ALL cell lines with varying Bcr-Abl status and imatinib mesylate sensitivity were generated and their growth inhibition by 17-AAG was studied in vitro.
  • Western blots were used to follow the changes in proteins that correlate with cell survival.
  • Results show that apoptosis was induced in all lines with an increased 50% inhibitory concentration (IC50) for Bcr-Abl positive but imatinib mesylate-resistant cells.
  • A decrease in p53, survivin, Her2/neu, and WT1 was seen in cells that expressed these proteins.
  • With some notable exceptions, when combined with 17-AAG, the IC50 of most of the common chemotherapeutic agents decreased.
  • We describe an experimental approach to investigate the complex interaction between Bcr-Abl status, imatinib mesylate sensitivity, and 17-AAG in pediatric ALL.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Genes, abl. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Rifabutin / analogs & derivatives
  • [MeSH-minor] Adult. Apoptosis / drug effects. Benzamides. Benzoquinones. Cell Line, Tumor. Cell Survival / drug effects. Child. Drug Therapy, Combination. Humans. Imatinib Mesylate. Lactams, Macrocyclic. Protein Kinase Inhibitors / metabolism. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use


5. Lavu EK, Vince JD, Kiromat M, Oswyn G, Golpak P, Tefuarani N: Leukaemia in children in Papua New Guinea: an unusual pattern. Ann Trop Paediatr; 2003 Dec;23(4):265-71
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  • Only 34 (31%) of the children were diagnosed with acute lymphoblastic leukaemia (ALL) compared with 54 (49%) children with acute myeloid leukaemia (AML).
  • There was no evidence of an early childhood peak of ALL.
  • Only eight (22%) of those diagnosed with ALL were classified as type L1.
  • Our figures reflect a relative absence of the common (cALL) cell type in early childhood leukaemia and support the role of infection and its effect on the immune system in the aetiology of childhood leukaemia.
  • Our data also revealed an unusually high proportion of chronic myeloid leukaemia (CML).
  • [MeSH-major] Leukemia / epidemiology
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Female. Humans. Incidence. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / mortality. Male. Papua New Guinea / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Sex Distribution

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  • (PMID = 14738574.001).
  • [ISSN] 0272-4936
  • [Journal-full-title] Annals of tropical paediatrics
  • [ISO-abbreviation] Ann Trop Paediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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6. Tse KF, Novelli E, Civin CI, Bohmer FD, Small D: Inhibition of FLT3-mediated transformation by use of a tyrosine kinase inhibitor. Leukemia; 2001 Jul;15(7):1001-10
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  • FLT3 is a member of the type III receptor tyrosine kinase (RTK) family.
  • Aberrant expression of the FLT3 gene has been documented in both adult and childhood leukemias including AML, ALL and CML.
  • In transfected Ba/F3 cells, AG1296 selectively and potently inhibited autophosphorylation of FL-stimulated wild-type and constitutively activated FLT3.
  • Several proteins phosphorylated by the activated FLT3 signaling pathway, including STAT 5A, STAT 5B and CBL, were no longer phosphorylated when these cells were treated with AG1296.
  • The activity against FLT3 suggests a potential therapeutic application for AG1296 or similar drugs in the treatment of leukemias involving deregulated FLT3 tyrosine kinase activity and as a tool for studying the biology of FLT3.
  • [MeSH-major] Cell Transformation, Neoplastic / drug effects. Enzyme Inhibitors / pharmacology. Milk Proteins. Proto-Oncogene Proteins / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Tyrphostins / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line. DNA-Binding Proteins / metabolism. Dose-Response Relationship, Drug. Humans. Mice. Phosphorylation. STAT5 Transcription Factor. Trans-Activators / metabolism. Tyrosine / metabolism. fms-Like Tyrosine Kinase 3

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  • (PMID = 11455967.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA70970
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / Tyrphostins; 146535-11-7 / 6,7-dimethoxy-3-phenylquinoxaline; 42HK56048U / Tyrosine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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7. Gassas A, Doyle JJ, Weitzman S, Freedman MH, Hitzler JK, Sharathkumar A, Dror Y: A basic classification and a comprehensive examination of pediatric myeloproliferative syndromes. J Pediatr Hematol Oncol; 2005 Apr;27(4):192-6
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  • Based on the predominant proliferating cell lineage, the authors established a classification system for childhood MPS.
  • Primary MPS was classified into granulocytic proliferation--chronic myelogenous leukemia (CML); monocytic--juvenile myelomonocytic leukemia (JMML); megakaryocytic--essential thrombocythemia (ET), familial thrombocytosis, transient myeloproliferative disorder of Down syndrome (TMD); erythrocytic--polycythemia vera, familial erythrocytosis; fibroblastic--idiopathic myelofibrosis (IMF); eosinophilic--idiopathic hypereosinophilic syndrome (IHES); and mast cells--mastocytosis.
  • Secondary MPS was classified as non-clonal proliferation (eg, infections, drugs, toxins, autoimmune, non-hematologic neoplasm, and trauma), and these were excluded from the study.
  • Significant proportions of cases of childhood MPS (60%) were unique to the pediatric population and not seen in adults.
  • The most common disorders were JMML (n = 31), TMD of Down syndrome (n = 30), and CML (n = 30); the other disorders were rare: four cases of ET, two of IMF, two of IHES, two of mastocytosis, and one primary erythrocytosis.
  • MPS in children is different from adult-type MPS in terms of biology, categories, classification, and prognosis.

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  • [CommentIn] J Pediatr Hematol Oncol. 2006 Oct;28(10):700-1 [17023836.001]
  • (PMID = 15838389.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Meta-Analysis
  • [Publication-country] United States
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8. Balwierz W, Pawińska K, Skoczeń S, Klekawka T, Strojny W, Niezgoda A: [Perspectives in the use of imatinib in the treatment of childhood cancers]. Przegl Lek; 2004;61 Suppl 2:95-9
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  • [Title] [Perspectives in the use of imatinib in the treatment of childhood cancers].
  • Introduction of novel diagnostic methods and multimodal therapy has resulted in about 70% probability of cure of childhood neoplasms.
  • However, treatment results of some neoplastic diseases in children, including chronic myelogenous leukemia (CML) still remain unsatisfactory.
  • With introduction of new drugs that selectively inhibit mechanisms of maturation and proliferation of cancer cells, new hope has arisen.
  • In our paper we present the mechanism of action of imatinib, the tyrosine kinase inhibitor which was employed in the treatment of CML and gastrointestinal stromal tumors.
  • Currently, there are several ongoing studies assessing the efficacy of this novel drug in the therapy of brain tumors, neuroblastoma, lung and prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Brain Neoplasms / drug therapy. Child. Clinical Trials as Topic. Drug Resistance, Neoplasm. Female. Gastrointestinal Neoplasms / drug therapy. Humans. Imatinib Mesylate. Lung Neoplasms / drug therapy. Male. Neuroblastoma / drug therapy. Prostatic Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 15686056.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 36
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9. Anuchapreeda S, Limtrakul P, Thanarattanakorn P, Sittipreechacharn S, Chanarat P: Inhibitory effect of curcumin on WT1 gene expression in patient leukemic cells. Arch Pharm Res; 2006 Jan;29(1):80-7
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  • Wilms' tumor1 (WT1) protein is highly expressed in leukemic blast cells of myeloid and lymphoid origin.
  • The leukemic cells were collected from 70 childhood leukemia patients admitted at Maharaj Nakorn Chiang Mai Hospital, Chiang Mai, Thailand, in the period July 2003 to February 2005.
  • There were 58 cases of acute lymphoblastic leukemia (ALL), 10 cases of acute myeloblastic leukemia (AML), and 2 cases of chronic myelocytic leukemia (CML).
  • It affected the WT1 gene expression in 4 of 8 relapsed cases (50%), 12 of 24 cases of drug maintenance (50%), 7 of 16 cases of completed treatment (44%), and 12 of 22 cases of new patients (54%).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Genes, Wilms Tumor / drug effects. Leukemia / drug therapy. Leukemia / genetics
  • [MeSH-minor] Adolescent. Cell Line, Tumor. Child. Child, Preschool. Electrophoresis, Polyacrylamide Gel. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Infant. K562 Cells. Male. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tetrazolium Salts. Thiazoles

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  • (PMID = 16491848.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
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10. Apperley J: CML in pregnancy and childhood. Best Pract Res Clin Haematol; 2009 Sep;22(3):455-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CML in pregnancy and childhood.
  • The appropriate management of children with CML has also been radically changed by the advent of imatinib.
  • Data relating to the efficacy and safety of second generation tyrosine kinase inhibitors in childhood is entirely absent and transplant remains the first choice for patients failing imatinib and perhaps also for young patients with sub-optimal responses.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / adverse effects. Pregnancy Complications, Neoplastic / chemically induced. Pyrimidines / adverse effects
  • [MeSH-minor] Abnormalities, Drug-Induced / etiology. Adult. Age Factors. Benzamides. Child. Female. Fetal Diseases / chemically induced. Humans. Imatinib Mesylate. Male. Maternal-Fetal Exchange. Pregnancy. Treatment Outcome. Young Adult

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  • (PMID = 19959094.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 119
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11. Suttorp M, Millot F: Treatment of pediatric chronic myeloid leukemia in the year 2010: use of tyrosine kinase inhibitors and stem-cell transplantation. Hematology Am Soc Hematol Educ Program; 2010;2010:368-76
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  • [Title] Treatment of pediatric chronic myeloid leukemia in the year 2010: use of tyrosine kinase inhibitors and stem-cell transplantation.
  • Allogeneic hematopoietic stem cell transplantation (allo-SCT) remains the only proven cure for chronic myeloid leukemia (CML), a rare malignancy in childhood.
  • With the excellent results induced by the tyrosine kinase inhibitor (TKI) imatinib in adults in the last decade, the appropriate management of children with CML has also changed radically, and only a minority are now transplanted as a front-line treatment.
  • Data on pediatric experiences with imatinib in CML from controlled trials remain very limited, but this review of available data describes the role of imatinib in children with CML, addressing:.
  • 2) pharmacokinetics in childhood;.
  • 5) the timing of allo-SCT in children; and 6) treatment of CML relapse after allo-SCT.
  • Because the characteristics of CML in children seem to overlap extensively with what is described in adult internal medicine, most answers and pediatric algorithms are adapted from the treatment of CML in adults.
  • Today in 2010, allo-SCT in children should be postponed until CML becomes refractory to imatinib.
  • The approach for young patients with suboptimal responses is unclear because data on the efficacy and safety of second-generation TKIs in childhood are almost entirely missing.






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