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1. Adamson PC: Imaging in early phase childhood cancer trials. Pediatr Radiol; 2009 Feb;39 Suppl 1:S38-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imaging in early phase childhood cancer trials.
  • Advances made in the treatment of childhood malignancies during the last four decades have resulted in overall cure rates of approximately 80%, but progress has slowed significantly during the last 10 years, underscoring the need for more effective and less toxic agents.
  • Current research is focused on development of molecularly targeted agents, an era ushered in with the discovery of imatinib mesylate for the treatment of chronic myelogenous leukemia.
  • Parallel to the initial advances made in molecularly targeted agents has been the development of a spectrum of novel imaging modalities.
  • Future goals for imaging in childhood cancer research thus include (1) patient identification based on target identification or other biologic characteristics of the tumor, (2) assessing pharmacokinetic-pharmacodynamic (PK-PD) effects, and (3) predictive value with an early indication of patient benefit.
  • Development and application of novel imaging modalities for children with cancer can serve to streamline development of molecularly targeted agents.
  • [MeSH-major] Neoplasms / diagnosis. Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Benzamides. Child. Clinical Trials as Topic. Humans. Imatinib Mesylate. Piperazines / pharmacokinetics. Piperazines / therapeutic use. Positron-Emission Tomography. Pyrimidines / pharmacokinetics. Pyrimidines / therapeutic use. Signal Transduction / drug effects. Tomography, X-Ray Computed

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  • (PMID = 19083226.001).
  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 32
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2. Bhattacharjee H, Carbrey J, Rosen BP, Mukhopadhyay R: Drug uptake and pharmacological modulation of drug sensitivity in leukemia by AQP9. Biochem Biophys Res Commun; 2004 Sep 24;322(3):836-41
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  • [Title] Drug uptake and pharmacological modulation of drug sensitivity in leukemia by AQP9.
  • Leukemia is the most common childhood cancer.
  • Trisenox, the active ingredient of which is trivalent arsenic, is the first line of treatment for acute promyelocytic leukemia.
  • Since drug action usually requires uptake of the drug, it is of importance to determine the transport system responsible for Trisenox uptake.
  • In this study we report to show that AQP9 expression modulates the drug sensitivity of leukemic cells.
  • AQP9 was transfected into the chronic myelogenous leukemia cell line K562.
  • The promyelocytic leukemia cell line HL60 treated with vitamin D showed higher expression of AQP9 and hypersensitivity to Trisenox and Sb(III).
  • Trisenox hypersensitivity results from increased expression of AQP9 drug uptake system.
  • The possibility of using pharmacological agents to increase expression of AQP9 gene delivers the promise of new therapies for the treatment of leukemia.
  • Thus, drug hypersensitivity can be correlated with increased expression of the drug uptake system.
  • This is the first demonstration that AQP9 can modulate drug sensitivity in cancer.
  • [MeSH-minor] Arsenicals / pharmacokinetics. Biological Transport. Cloning, Molecular. HL-60 Cells. Humans. K562 Cells. Kinetics. Oxides / pharmacokinetics. Recombinant Proteins / metabolism. Transfection. Vitamin D / pharmacology

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  • (PMID = 15336539.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM 52216
  • [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 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Ion Channels; 0 / Oxides; 0 / Recombinant Proteins; 1406-16-2 / Vitamin D; S7V92P67HO / arsenic trioxide
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3. Hosoya Y, Lefor A, Hirashima Y, Nokubi M, Yamaguti T, Jinbu Y, Muroi K, Nakazawa M, Yasuda Y: Successful treatment of esophageal squamous cell carcinoma in a patient with Fanconi anemia. Jpn J Clin Oncol; 2010 Aug;40(8):805-10
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  • Fanconi anemia is a congenital syndrome characterized by hypoplasia of bone marrow and the development of aplastic anemia in childhood, followed by myelodysplastic syndrome and acute myelogenous leukemia in later life.
  • Hematologic findings returned to normal, but chronic graft-versus-host disease persisted.
  • Reduced doses of alkylating agents and radiotherapy are used in patients with Fanconi anemia.


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4. Kawaguchi H, Taketani T, Hongo T, Park MJ, Koh K, Ida K, Kobayashi M, Takita J, Taki T, Yoshino H, Bessho F, Hayashi Y: In vitro drug resistance to imatinib and mutation of ABL gene in childhood Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia. Leuk Lymphoma; 2005 Feb;46(2):273-6
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  • [Title] In vitro drug resistance to imatinib and mutation of ABL gene in childhood Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia.
  • Imatinib, the ABL kinase inhibitor, is used not only for Philadelphia chromosome-positive (Ph + ) chronic myelogenous leukemia, but also for Ph + acute lymphoblastic leukemia (ALL), although resistance to the drug tends to develop in an early stage of the clinical course.
  • We describe a childhood refractory Ph + ALL patient in whom progressive resistance to imatinib was correlated with the appearance of a mutation in the BCR-ABL kinase domain and in vitro drug resistance to imatinib as determined by the methyl-thiazol-tetrazolium (MTT) assay.
  • A missense mutation of T to C (Y253H) of the ABL gene was identified in the resistant clone, suggesting that this mutation may play an etiological role in the rapid loss of drug sensitivity.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Genes, abl / genetics. Mutation, Missense. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cell Survival / drug effects. Child. Humans. Imatinib Mesylate. Male. Philadelphia Chromosome


5. Pogorzała M, Styczyński J, Jankowska K, Kurylak A, Wysocki M: [Imatinib mesylate in treatment of childhood chronic myeloid leukaemia. Preliminary report]. Med Wieku Rozwoj; 2006 Jul-Sep;10(3 Pt 1):603-12
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  • [Title] [Imatinib mesylate in treatment of childhood chronic myeloid leukaemia. Preliminary report].
  • THE AIM of this preliminary study was to estimate the efficacy and adverse events of imatinib, a selective tyrosine kinase inhibitor, in children with chronic myeloid leukaemia.
  • One child with chronic myeloid leukaemia diagnosed at blast crisis demonstrated resistance to imatinib therapy.
  • CONCLUSIONS: Imatinib seems to be an efficient and well tolerated drug in children with chronic myeloid leukaemia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Benzamides. Child. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Imatinib Mesylate. Male. Remission Induction. Research Design. Treatment Outcome

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  • (PMID = 17317891.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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6. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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7. 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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8. Hongo T, Okada S, Inoue N, Yamada S, Yajima S, Watanabe C, Fujii Y, Horikoshi Y: Two groups of Philadelphia chromosome-positive childhood acute lymphoblastic leukemia classified by pretreatment multidrug sensitivity or resistance in in vitro testing. Int J Hematol; 2002 Oct;76(3):251-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two groups of Philadelphia chromosome-positive childhood acute lymphoblastic leukemia classified by pretreatment multidrug sensitivity or resistance in in vitro testing.
  • The development of effective chemotherapy is imperative for children with Philadelphia chromosome-positive (Ph) acute lymphoblastic leukemia (ALL) because of the poor prognosis of this condition.
  • Initial cellular drug resistance is thought to be an important cause of induction failure and early relapse.
  • Sixteen children (5.8%) had Ph-positive results of cytogenetic analysis.
  • We examined in vitro drug resistance to 14 agents and found that leukemic cells in Ph ALL were significantly more resistant than were cells in non-Ph ALL to melphalan, bleomycin, etoposide, mitoxantrone, L-asparaginase, and vinblastine.
  • With the prednisolone, L-asparaginase, and vincristine (PAV) combination of drugs, 10 of the 16 Ph patients with ALL (62.5%) showed relative resistance (RR) (sensitivity to only 1 or to none of the 3 drugs) at initiation of treatment.
  • These 10 patients experienced significantly poorer event-free survival (EFS) than did the 6 patients with supersensitivity (SS) (defined as sensitivity to all 3 or to 2 of the 3 drugs, P = .019).
  • Leukemic cells from RR patients were found to be multiresistant to 12 drugs with 2.0- to 58.4-fold RR compared with cells from SS patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Cell Survival. Child. Child, Preschool. Disease-Free Survival. Drug Screening Assays, Antitumor. Female. Humans. Infant. Male. Prognosis


9. Liu CY, Hsu YH, Pan PC, Wu MT, Ho CK, Su L, Xu X, Li Y, Christiani DC, Kaohsiung Leukemia Research Group: Maternal and offspring genetic variants of AKR1C3 and the risk of childhood leukemia. Carcinogenesis; 2008 May;29(5):984-90
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  • [Title] Maternal and offspring genetic variants of AKR1C3 and the risk of childhood leukemia.
  • The aldo-keto reductase 1C3 (AKR1C3) gene located on chromosome 10p15-p14, a regulator of myeloid cell proliferation and differentiation, represents an important candidate gene for studying human carcinogenesis.
  • In a prospectively enrolled population-based case-control study of Han Chinese conducted in Kaohsiung in southern Taiwan, a total of 114 leukemia cases and 221 controls <20 years old were recruited between November 1997 and December 2005.
  • The present study set out to evaluate the association between childhood leukemia and both maternal and offspring's genotypes.
  • After correcting for multiple comparisons, we observed that risk of developing childhood leukemia is significantly associated with rs10508293 polymorphism on intron 4 of the AKR1C3 gene in both offspring alone and in the combined maternal and offspring genotypes (nominal P < 0.0001, permutation P < 0.005).
  • The maternal methylenetetrahydrofolate reductase A1298C polymorphism was found to be an effect modifier of the maternal intron 4 polymorphism of the AKR1C3 gene (rs10508293) and the childhood leukemia risk.
  • In conclusion, this study suggests that AKR1C3 polymorphisms may be important predictive markers for childhood leukemia susceptibility.

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  • (PMID = 18339682.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES00002; United States / NIEHS NIH HHS / ES / ES09723
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
  • [Other-IDs] NLM/ PMC2902386
  • [Investigator] Chang TT; Lin SF; Chiou SS; Jang RC; Hsiao HH; Liu TC; Lin PC; Hsiao CC; Sheen JM; Kuo CY; Wang MC; Huang CH; Huang CB; Wong YC; Wu HB; Lin SJ; Sun YM; Hsieh KS; Chang YH
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10. Uren A, Toretsky JA: Pediatric malignancies provide unique cancer therapy targets. Curr Opin Pediatr; 2005 Feb;17(1):14-9
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  • PURPOSE OF REVIEW: Improving overall survival and reducing morbidity are major goals of childhood cancer research.
  • This review explores an old idea that increased survival in childhood cancer can be achieved by inhibiting specific cancer targets.
  • Tumor-specific translocation-generated fusion proteins appear to be ideal tumor-specific therapeutic targets.
  • This review will describe advances in aspects of target identification, potential for small molecule screening, and the evolution of clinical resistance to this new generation of pharmaceuticals.
  • RECENT FINDINGS: Advances in molecular biology have identified new protein targets along with increased understanding of the biologic role of these proteins.
  • Ewing sarcoma family of tumors research has benefited from new target discovery and enhanced biologic understanding of the EWS-FLI1 fusion protein.
  • Patients with chronic myeloid leukemia have benefited from the discovery of the BCR-ABL kinase inhibitor imatinib mesylate (Gleevec), thus showing how a molecular therapeutic target can be inactivated for improved therapy.
  • This review also describes how patients with synovial sarcoma might benefit from future therapy directed towards the SYT-SSX family of fusion proteins.

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  • (PMID = 15659957.001).
  • [ISSN] 1040-8703
  • [Journal-full-title] Current opinion in pediatrics
  • [ISO-abbreviation] Curr. Opin. Pediatr.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA088004-08; United States / NCI NIH HHS / CA / R01 CA088004; United States / NCI NIH HHS / CA / CA88004; United States / NCI NIH HHS / CA / R01 CA088004-08
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETV6-NTRK3 fusion protein, human; 0 / EWS-FLI fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS; 0 / SYT-SSX fusion protein; 0 / Transcription Factors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 61
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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.


13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. Schrappe M, Reiter A, Ludwig WD, Harbott J, Zimmermann M, Hiddemann W, Niemeyer C, Henze G, Feldges A, Zintl F, Kornhuber B, Ritter J, Welte K, Gadner H, Riehm H: Improved outcome in childhood acute lymphoblastic leukemia despite reduced use of anthracyclines and cranial radiotherapy: results of trial ALL-BFM 90. German-Austrian-Swiss ALL-BFM Study Group. Blood; 2000 Jun 1;95(11):3310-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved outcome in childhood acute lymphoblastic leukemia despite reduced use of anthracyclines and cranial radiotherapy: results of trial ALL-BFM 90. German-Austrian-Swiss ALL-BFM Study Group.
  • Trial ALL-BFM 90 was designed to improve outcome in patients with childhood acute lymphoblastic leukemia (ALL) by using a reduced treatment regimen.
  • Patients were stratified into a standard-risk group (SRG), a medium-risk group (MRG), both defined by adequate early treatment response; and a high-risk group (HRG), defined by inadequate response to the cytoreductive prednisone prephase, induction failure, or Philadelphia-chromosome-positive ALL.
  • Four treatment modifications were evaluated: dose intensification in induction by a more rapid drug sequence; administration of L-asparaginase during consolidation therapy in the MRG (randomized); enforced consolidation by rotational elements in the HRG; and reduction in the dose of anthracyclines and use of only 12-Gy preventive cranial radiotherapy in the MRG and HRG, with the aim of avoiding toxicity.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Asparaginase / administration & dosage. Brain Neoplasms / prevention & control. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Immunophenotyping. Infant. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiotherapy. Male. Prognosis. Regression Analysis. Survival Analysis. Time Factors. Treatment Outcome

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  • (PMID = 10828010.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; EC 3.5.1.1 / Asparaginase
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