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1. Oliveira GA, Costa ES, Freitas MS, Dutra FF, Maia SF, Guerra MC, Tabernero MD, Borojevic R, Otazu IB, Silva JL: Positive response to imatinib mesylate therapy for childhood chronic myeloid leukemia. Braz J Med Biol Res; 2010 Jun;43(6):580-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Positive response to imatinib mesylate therapy for childhood chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is rare in the pediatric population, accounting for 2-3% of childhood leukemia cases, with an annual incidence of one case per million children.
  • The low toxicity profile of imatinib mesylate has led to its approval as a front-line therapy in children for whom interferon treatment has failed or who have relapsed after allogeneic transplantation.
  • We describe the positive responses of 2 children (case 1 - from a 7-year-old male since May 2005; case 2 - from a 5-year-old female since June 2006) with Philadelphia-positive chromosome CML treated with imatinib (300 mg/day, orally) for up to 28 months, as evaluated by morphological, cytogenetic, and molecular approaches.
  • Our patients are alive, are in the chronic phase, and are in continuous morphological complete remission.

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  • (PMID = 20396859.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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2. Kolb EA, Pan Q, Ladanyi M, Steinherz PG: Imatinib mesylate in Philadelphia chromosome-positive leukemia of childhood. Cancer; 2003 Dec 15;98(12):2643-50
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  • [Title] Imatinib mesylate in Philadelphia chromosome-positive leukemia of childhood.
  • BACKGROUND: Initial treatment for adult patients with Philadelphia chromosome-positive (Ph[+]) chronic myelogenous leukemia (CML) now includes imatinib mesylate.
  • METHODS: In the current series, the authors report 5 consecutive patients ages 20 months to 12 years with Ph+ leukemia who were treated with imatinib and evaluated for a response using cytogenetics, fluorescent in situ hybridization (FISH), and real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) on serial bone marrow aspirations.
  • RESULTS: After the initiation of imatinib therapy, all 4 patients with CML were found to have no detectable Ph chromosome by cytogenetics (median of 198 days of imatinib therapy; range, 138-346 days), FISH (median of 285 days of imatinib therapy; range, 138-366 days), and real-time RT-PCR (median of 287 days of imatinib therapy; range, 224-366 days).
  • One patient with Ph+ acute mixed lineage leukemia achieved a morphologic disease remission with standard chemotherapy, but within 10 months had increasing Ph positivity in consecutive bone marrow aspirations.
  • Imatinib was added to the intensive leukemia therapy, and within 26 days there were no detectable Ph+ cells in the bone marrow.
  • CONCLUSIONS: Imatinib mesylate was found to be effective in inducing undetectable residual disease in a small cohort of pediatric patients with Ph+ leukemia.
  • Further studies of the use of imatinib in childhood Ph+ malignancies are needed.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Child. Child, Preschool. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Infant. Male. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Risk Factors. Survival Rate. Treatment Outcome

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  • [Copyright] Copyright 2003 American Cancer Society.
  • (PMID = 14669284.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 34
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3. Haltrich I, Kost-Alimova M, Kovács G, Kriván G, Dobos M, Imreh S, Fekete G: [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia]. Magy Onkol; 2005;49(2):141-7
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  • [Title] [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia].
  • [Transliterated title] A "3q21q26-szindróma" azonosítása sokpontos interfázis-FISH vizsgálattal gyermekkori myeloid leukaemiában.
  • Cytogenetic syndrome involving bands 3q21 and 3q26, known as "3q21q26 syndrome" has been observed in adult patients with acute myelogenous leukemia (0.5-2%), chronic myelogenous leukemia in blast crisis (20%), myelodysplastic syndromes and myeloproliferative disorders.
  • In the present study bone marrow samples from two boys (12 and 16 years), diagnosed with CML and AML respectively, were investigated using conventional cytogenetic methods, interphase "multipoint" fluorescence in situ hybridization (FISH), dual color-FISH and multiplex FISH.
  • The "multipoint" FISH analysis identified in de novo childhood AML case an inv(3)(q21q26) and a complex 3q rearrangement including inversion and duplication in the CML case.
  • The affected patients were resistant to conventional chemotherapy and had a short survival.
  • This syndrome is very rare in de novo childhood AML, and simultaneous presence of 3q inversion and duplication, to our knowledge, has not yet been identified in hematological malignancies.
  • The results of our study emphasize the importance of classical and modern cytogenetic analysis in the diagnosis of hematologic malignancies, because in the majority of cases they can provide additional diagnostic information for the clinicians in deciding the best therapeutic approach, precise classification and prognosis of the disease.
  • [MeSH-major] Chromosomes, Human, Pair 3. Gene Rearrangement. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16249810.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
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4. Singh N, Bakhshi S: Imatinib-induced dental hyperpigmentation in childhood chronic myeloid leukemia. J Pediatr Hematol Oncol; 2007 Mar;29(3):208-9
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  • [Title] Imatinib-induced dental hyperpigmentation in childhood chronic myeloid leukemia.
  • [MeSH-major] Gingival Diseases / chemically induced. Hyperpigmentation / chemically induced. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / adverse effects. Pyrimidines / adverse effects. Tooth Diseases / chemically induced
  • [MeSH-minor] Adolescent. Benzamides. Female. Humans. Imatinib Mesylate. Treatment Outcome


5. 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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  • [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.
  • Among all 2178 patients (</= 18 years of age), the 6-year event-free survival (EFS) rate (+/- SE) was 78% +/- 1%, with a median observation time of 4.8 years.
  • L-asparaginase did not improve outcome in the MRG: the event-free interval was 83% +/- 2% with L-asparaginase (n = 528) and 81% +/- 2% without it (n = 557).
  • The rates of isolated central nervous system relapse in the MRG and HRG were 0.8% and 1.6%, respectively; thus, the 12-Gy preventive cranial radiotherapy regimen apparently provided sufficient central nervous system prophylaxis.
  • 001) was based on fewer recurrences among patients in the MRG with B-cell-precursor ALL, indicating an advantage of more condensed induction therapy.
  • [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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6. Balaji R, Ramachandran K, Nair M, Kusumakumari P: Chemotherapy-induced posterior reversible encephalopathy syndrome in childhood chronic myeloid leukemia. A case report and review of the literature. Neuroradiol J; 2009 May 15;22(2):204-8

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  • [Title] Chemotherapy-induced posterior reversible encephalopathy syndrome in childhood chronic myeloid leukemia. A case report and review of the literature.
  • Contrast enhanced computed tomography (CT) of the brain revealed bilateral symmetric subcortical hypodense lesions in the parieto-occipital regions.
  • Transient DWI hyperintensities seen in cortical watershed areas corresponding to the hyperintense foci in FLAIR imaging are suggestive of foci of vasogenic edema secondary to vasospasm in highly ischemia-sensitive cerebral tissue.

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  • (PMID = 24207042.001).
  • [ISSN] 1971-4009
  • [Journal-full-title] The neuroradiology journal
  • [ISO-abbreviation] Neuroradiol J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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7. Laningham FH, Kun LE, Reddick WE, Ogg RJ, Morris EB, Pui CH: Childhood central nervous system leukemia: historical perspectives, current therapy, and acute neurological sequelae. Neuroradiology; 2007 Nov;49(11):873-88
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  • [Title] Childhood central nervous system leukemia: historical perspectives, current therapy, and acute neurological sequelae.
  • INTRODUCTION: During the past three decades, improvements in the treatment of childhood leukemia have resulted in high cure rates, particularly for acute lymphoblastic leukemia (ALL).
  • Unfortunately, successful therapy has come with a price, as significant morbidity can result from neurological affects which harm the brain and spinal cord.
  • The expectation and hope is that chemotherapy, as a primary means of CNS therapy, will result in acceptable disease control with less CNS morbidity than has been observed with combinations of chemotherapy and radiotherapy over the past several decades.
  • METHODS AND RESULTS: In this review we discuss the poignant, historical aspects of CNS leukemia therapy, outline current methods of systemic and CNS leukemia therapy, and present imaging findings we have encountered in childhood leukemia patients with a variety of acute neurological conditions.
  • A major objective of our research is to understand the neuroimaging correlates of acute and chronic effects of cancer and therapy.
  • Specific features related to CNS leukemia and associated short-term toxicities, both disease- and therapy-related, are emphasized in this review with the specific neuroimaging findings.
  • Specific CNS findings are similarly important when treating acute myelogenous leukemia (AML), and details of leukemic involvement and toxicities are also presented in this entity.
  • CONCLUSION: Despite contemporary treatment approaches which favor the use of chemotherapy (including intrathecal therapy) over radiotherapy in the treatment of CNS leukemia, children still occasionally experience morbid neurotoxicity.
  • Specific neuroimaging findings frequently indicate a need to alter antileukemia therapy.
  • It is important to appreciate that intrathecal and high doses of systemic chemotherapy are not innocuous and are associated with acute, specific, recognizable, and often serious neurological consequences.

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  • (PMID = 17924103.001).
  • [ISSN] 0028-3940
  • [Journal-full-title] Neuroradiology
  • [ISO-abbreviation] Neuroradiology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090246-05; United States / NCI NIH HHS / CA / R01 CA090246; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / R01 CA090246-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Number-of-references] 39
  • [Other-IDs] NLM/ NIHMS49119; NLM/ PMC2386669
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8. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • It results in juxtaposition of the 5' part of the BCR gene on chromosome 22 to the 3' part of the ABL1 gene (previously ABL) on chromosome 9.
  • CML is clinically characterized by three distinct phases: chronic, accelerated, and blast phase.
  • Blast crisis is characterized by the rapid expansion of a population of differentiation arrested blast cells (myeloid or lymphoid cells population), with secondary chromosomal abnormalities present.
  • We report a case of myeloid blast crisis of CML resistant to imatinib mesylate and chemotherapy.
  • By use of cytogenetic, fluorescence in situ hybridization, and comparative genomic hybridization methods, we identified a cluster of BCR-ABL amplification on inverted duplication of the Ph chromosome with t(3;21)(q26;q22) and increased genomic levels of the RUNX1 gene (previously AML1).
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • Our study indicated that the progenitor of CML was BCR-ABL dependent through the amplification of Ph chromosome as a mechanism of resistance to imatinib therapy.
  • The coexistence of BCR-ABL and t(3;21)(q26;q22) with RUNX1 rearrangement might play a pivotal role in the CML blast transformation.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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9. Matsuyama T, Horibe K, Kato K, Kojima SS: Bone marrow transplantation for children with acute myelogenous leukaemia in the first complete remission. Eur J Cancer; 2000 Feb;36(3):368-75
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  • [Title] Bone marrow transplantation for children with acute myelogenous leukaemia in the first complete remission.
  • Of 52 children aged 9 months to 16 years old with acute myelogenous leukaemia (AML) in first complete remission undergoing bone marrow transplantation at our institution, 31 received allogeneic transplants (allo-BMT) and 21 received autologous transplants (ABMT).
  • Initial induction and consolidation chemotherapy were not uniform.
  • Conditioning included chemotherapy (n=43: 4 x 4 mg/kg of busulfan and 3 x 60 to 70 mg/m(2) of melphalan) or total body irradiation (12 Gy) plus chemotherapy (n=9).
  • Amongst allograft cases, acute or chronic GVHD developed in 7 patients each (23%).
  • Although the presented data are based on a retrospective evaluation, we consider BMT for childhood AML during first complete remission an effective treatment for eradicating leukaemia.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 10708939.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
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10. Yalman N, Sarper N, Devecioğlu O, Anak S, Eryilmaz E, Can M, Yenilmez H, Ağaoğlu L, Gedikoğlu G: Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia. Turk J Pediatr; 2000 Jul-Sep;42(3):198-204
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  • [Title] Fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) for the treatment of relapsed or poor risk childhood acute leukemia.
  • The prognosis of relapsed acute leukemia or chronic leukemia in acute blast crisis is poor and new chemotherapeutic regimens could be useful for these patients.
  • Six relapsed acute lymphoblastic leukemia (ALL), nine relapsed acute myeloblastic leukemia (AML), one chronic myelomonocytic leukemia (CMML) and one chronic myeloid leukemia (CML) in acute blast crisis between three to 18 years (median 10 years) received fludarabine, cytarabine, G-CSF and idarubicin (FLAG-IDA) chemotherapy (CT).
  • The regimen was ineffective in B-cell ALL as in acute blastic crisis of CMML and CML.
  • FLAG-IDA appears to be a myelotoxic therapy for relapsed or poor risk leukemia in a developing country.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy / methods. Vidarabine / analogs & derivatives

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  • (PMID = 11105617.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] TURKEY
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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11. Apperley J: CML in pregnancy and childhood. Best Pract Res Clin Haematol; 2009 Sep;22(3):455-74
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  • [Title] CML in pregnancy and childhood.
  • Children born to men who are actively taking imatinib at the time of conception appear healthy and current advice is not to discontinue treatment.
  • The appropriate management of children with CML has also been radically changed by the advent of imatinib.
  • The features of the disease at presentation, the natural history and the response to therapy seem to be identical in children to that seen in adults.
  • 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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12. 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.
  • In neoplastic diseases in which treatment results remain poor, intensification of treatment components (chemotherapy, radiotherapy) did not succeed in improving the treatment results.
  • In recent years no improvement was made in gene therapy.
  • 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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13. 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

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  • (PMID = 15621812.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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14. de Figueiredo AF, Mkrtchyan H, Liehr T, Soares Ventura EM, de Jesus Marques-Salles T, Santos N, Ribeiro RC, Abdelhay E, Macedo Silva ML: A case of childhood acute myeloid leukemia AML (M5) with a neocentric chromosome neo(1)(qter--&gt;q23 approximately 24::q23 approximately 24--&gt;q43--&gt;neo--&gt;q43--&gt;qter) and tetrasomy of chromosomes 8 and 21. Cancer Genet Cytogenet; 2009 Sep;193(2):123-6
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  • [Title] A case of childhood acute myeloid leukemia AML (M5) with a neocentric chromosome neo(1)(qter-->q23 approximately 24::q23 approximately 24-->q43-->neo-->q43-->qter) and tetrasomy of chromosomes 8 and 21.
  • Hyperdiploidy is rarely observed in childhood acute myeloid leukemia (AML).
  • Little is known about the prognostic significance of these chromosomal abnormalities in childhood AML.
  • In the actual case, complete remission was achieved after chemotherapy, which continued for 7 months.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics


15. Adamson PC: Imaging in early phase childhood cancer trials. Pediatr Radiol; 2009 Feb;39 Suppl 1:S38-41
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  • [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.
  • Since imatinib's introduction into the clinic, an increasing number of tyrosine kinase inhibitors have been developed and entered into clinical trials and practice.
  • 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.
  • [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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16. 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.
  • During imatinib therapy myalgia, ostealgia and mild myelosuppression were observed.
  • 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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17. 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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  • [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.
  • Of these, the SS subgroup of Ph ALL patients may be curable with chemotherapy and stem cell transplantation.
  • For EFS improvement in the RR group, it may be necessary to use a new chemotherapy approach from initiation.
  • [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


18. 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;.
  • 4) early monitoring of treatment efficacy in an attempt to avoid failure;.
  • 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.


19. Limsuwan A, Pakakasama S, Rochanawutanon M, Hong-eng S: Pulmonary arterial hypertension after childhood cancer therapy and bone marrow transplantation. Cardiology; 2006;105(3):188-94
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  • [Title] Pulmonary arterial hypertension after childhood cancer therapy and bone marrow transplantation.
  • According to the Third World Symposium on Pulmonary Arterial Hypertension (PAH), chemotherapy is considered to be one of the possible risk factors for patients developing PAH.
  • However, to date, no literature has sufficiently addressed the risk, natural history, and effective treatment of this condition.
  • We report our experience on how early diagnosis, detailed monitoring of disease course, and appropriate treatment application have led to a successful outcome of PAH management in childhood after cancer therapy.
  • Our report reaffirmed the fact that PAH is now a recognized complication of chemotherapy and bone marrow transplantation for leukemia.
  • Combined pulmonary vasodilator treatment has a beneficial effect in improving the patient's condition and functional status as suggested by initial acute pulmonary vasodilator testing.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Bone Marrow Transplantation / adverse effects. Hypertension, Pulmonary / etiology
  • [MeSH-minor] Adolescent. Benzamides. Cyclophosphamide / adverse effects. Cytarabine / adverse effects. Female. Humans. Hyperplasia / etiology. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Piperazines / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Pyrimidines / adverse effects. Vasodilator Agents / therapeutic use


20. Paulino AC, Fowler BZ: Secondary neoplasms after radiotherapy for a childhood solid tumor. Pediatr Hematol Oncol; 2005 Mar;22(2):89-101
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  • [Title] Secondary neoplasms after radiotherapy for a childhood solid tumor.
  • This study was conducted to determine the outcome of patients who develop a second neoplasm after radiotherapy (RT) for a childhood solid tumor.
  • The medical records and radiotherapy charts were reviewed to determine if the patient developed a secondary neoplasm after treatment for malignancy.
  • Twenty-three (5.4%) patients developed a secondary neoplasm.
  • The types of initial solid tumors treated with RT were Ewing sarcoma in 6, Wilms tumor in 6, medulloblastoma in 5, neuroblastoma in 3, and other in 3.
  • Median RT dose was 45 Gy (range, 12.3 to 60 Gy) using 4 MV in 9, 1.25 MV in 8, 250 KV in 4, and 6 MV photons in 1 patient.
  • Fourteen had chemotherapy.
  • For the 14 malignant neoplasms, the median time interval from initial tumor to second malignancy was 10.1 years.
  • The 14 second malignant neoplasms (SMN) were osteosarcoma in 3, breast carcinoma in 2, melanoma in 2, malignant fibrous histiocytoma in 1, dermatofibrosarcoma in 1, leiomyosarcoma in 1, mucoepidermoid carcinoma in 1, colon cancer in 1, chronic myelogenous leukemia in 1, and basal cell carcinoma in 1.
  • The 14 benign neoplasms appeared at a median time of 16.9 years and included cervical intraepithelial neoplasia in 3, osteochondroma in 3, thyroid adenoma in 1, duodenal adenoma in 1, lipoma in 1, cherry angioma in 1, uterine leiomyoma in 1, ovarian cystadenofibroma in 1, and giant cell tumor in 1.

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  • (PMID = 15804994.001).
  • [ISSN] 0888-0018
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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21. Yokota S, Okamoto T: [The minimal residual disease (MRD) in hematological malignancies]. Gan To Kagaku Ryoho; 2001 Jun;28(6):762-8
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  • Molecular genetic and cytoimmunological markers have been applied for the detection of minimal residual disease (MRD) in hematological malignancies.
  • These markers include surface markers or rearranged T-cell receptor and immunoglobulin genes in the lymphoid malignancies and fused genes associated with chromosomal translocations such as BCR-ABL in t(9;22) or PML-RAR alpha in t(15;17) in myeloid malignancies.
  • By examining a large number of patients, it has been shown that the MRD in the early phase of chemotherapy has a correlation with the prognosis of childhood ALL.
  • Based on these observations, a new strategy of chemotherapy in which the post-remission therapy is modified based on the MRD results has begun.
  • The diagnosis of MRD will be used as an important routine examination in chemotherapy for leukemia/lymphoma patients.
  • [MeSH-major] Leukemia / diagnosis. Lymphoma / diagnosis. Neoplasm, Residual / diagnosis
  • [MeSH-minor] Adult. Child, Preschool. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Translocation, Genetic

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  • (PMID = 11432342.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 12
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22. Walther JU, Pohl I, Rausch A, Fuehrer M: Proliferation studies on chromosome preparations of bone marrow in hematological disease. Oncol Rep; 2006 Oct;16(4):893-9
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  • The disorders studied were: Acute lymphoblastic leukemia (ALL) (N=107), chronic myeloid leukemia (CML) (N=166) and aplastic anemia in childhood (AA) (N=39).
  • The most important findings include: i) ALL: Immunological subtypes can be differentiated according to their proliferation profile; there is a striking difference between childhood and adult ALL in proliferation activity; most importantly initial proliferation is much higher in patients who will relapse than in those with stable remission.
  • ii) CML: Philadelphia-positive CML shows proliferation activities quite distinct from Philadelphia-negative CML; however there is only a small change in the proliferative activity from the chronic phase to the accelerated phase or blast crisis.
  • iii) AA: Very low proliferation scores rise quickly to near normal levels during immunosuppressive therapy in most patients.
  • Higher levels at diagnosis are associated with a faster and better response to therapy.
  • In conclusion, assessment of the proliferative activity in cytogenetic preparations made from bone marrow samples of patients with haematological disease may add valuable information as to diagnostic sub-groups and clinical course and may contribute to therapeutic decisions.
  • [MeSH-major] Bone Marrow Cells / cytology. Chromosomes / ultrastructure. Hematologic Neoplasms / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 16969511.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
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23. Cazzaniga G, Lanciotti M, Rossi V, Di Martino D, Aricò M, Valsecchi MG, Basso G, Masera G, Micalizzi C, Biondi A: Prospective molecular monitoring of BCR/ABL transcript in children with Ph+ acute lymphoblastic leukaemia unravels differences in treatment response. Br J Haematol; 2002 Nov;119(2):445-53
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  • [Title] Prospective molecular monitoring of BCR/ABL transcript in children with Ph+ acute lymphoblastic leukaemia unravels differences in treatment response.
  • Children with Philadelphia-chromosome-positive (Ph+) acute lymphoblastic leukaemia (ALL) represent a subgroup at very high risk for treatment failure, despite intensive chemotherapy.
  • However, recent retrospective studies showed that Ph+ childhood ALL is a heterogeneous disease with regard to treatment response.
  • We have prospectively monitored, by reverse transcription polymerase chain reaction (RT-PCR) during follow-up, the presence of the BCR/ABL fusion transcript in Ph+ ALL children diagnosed in the Italian multicentre Associazione Italiana Ematologia Oncologia Pediatrica ALL-AIEOP-95 therapy protocol.
  • To our knowledge, this is the first report on the evaluation of minimal residual disease (MRD) in childhood Ph+ ALL prospectively enrolled in an intensive, Berlin-Frankfurt-Munster (BFM)-type treatment protocol.
  • Twenty were good responders to the pre-phase of prednisone/intrathecal methotrexate treatment (PGR) and seven were poor responders (PPR).
  • Within the PPR group, the RT-PCR monitoring constantly showed positivity for the BCR/ABL fusion transcript and all the patients died of disease progression.
  • In contrast, highly sensitive qualitative RT-PCR monitoring revealed heterogeneity within the PGR group of Ph+ childhood ALL patients.
  • Three different subgroups could be defined, according to the clearance of Ph+ cells within the first 5 months of treatment.
  • This provides useful information on the capability of chemotherapy to reduce the leukaemic clone, with prognostic implications.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Neoplasm, Residual / genetics
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Male. Methotrexate / administration & dosage. Prednisone / administration & dosage. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. METHOTREXATE .
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  • (PMID = 12406084.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate
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24. Kiyotani C, Kiyokawa N, Mori T: [Clinical problems in the treatment of myeloid leukemia in childhood]. Nihon Rinsho; 2009 Oct;67(10):1991-6
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical problems in the treatment of myeloid leukemia in childhood].
  • As for childhood AML, intensification of chemotherapy and advance in supportive care have contributed toward the patient survival.
  • In addition to prevent early death, we have to develop a risk classification and appropriate therapies with updated genomics, especially for the intermediate risk group which has much diversity.
  • Also, new treatment strategies utilizing various molecular-targeted therapies are required.
  • For childhood CML, the possibilities of unknown risks which accompanied by life-long imatinib treatment should be considered.
  • Comparing SCT and imatinib, We need to make an original treatment guideline for child CML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy

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  • (PMID = 19860203.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 15
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25. Dölken G: Detection of minimal residual disease. Adv Cancer Res; 2001;82:133-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of minimal residual disease.
  • A high percentage of patients with leukemia, lymphoma, and solid tumors achieve a complete clinical remission after initial treatment, but the majority of these patients will finally relapse from residual tumor cells detectable in clinical remission only by the most sensitive methods.
  • Depending on the underlying malignant disease and therapeutic treatment, the presence of residual tumor cells in an individual patient may herald relapse, but a long-term stable situation or slowly vanishing tumor cells are also possible.
  • Molecular monitoring of residual leukemia and lymphoma cells by quantitative PCR techniques has provided important information about the effectiveness of treatment and the risk of recurrent disease as shown by minimal residual disease (MRD) analysis in patients with various malignant diseases.
  • Such diseases include childhood acute lymphoblastic leukemia, after induction therapy; acute promyelocytic leukemia, during and after chemotherapy; and chronic myelogenous leukemia, during treatment with alpha-interferon and after allogeneic bone marrow transplantation.
  • Evaluation of the predictive value of the detection of MRD has to take into account its evolution and course, the pathogenesis, biology, and natural course of the underlying malignant disease, the molecular genetic lesion, and finally, the type of treatment.
  • Quantification of minimal residual cells by the recently developed real-time quantitative PCR technique will surely have a major impact on our therapeutic strategies for patients with leukemia, lymphomas, and solid tumors.
  • Based on quantitative PCR data, the terms molecular remission and molecular relapse have to be exactly defined and validated in prospective clinical trials to assess the biological and clinical significance of MRD in various types of malignancies.

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  • (PMID = 11447762.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 326
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26. 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
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of esophageal squamous cell carcinoma in a patient with Fanconi anemia.
  • 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.
  • Esophageal cancer developed at age 35.
  • Invasion of the bronchus and aorta by the tumor was suspected on computed tomography.
  • After two courses of chemotherapy with cisplatin (total dose, 100 mg) and 5-fluorouracil (5000 mg) plus radiotherapy (30 Gy), Grade 3 diarrhea and bone marrow suppression developed, and treatment was discontinued.
  • After resolution of toxicity, a good response to the neoadjuvant therapy was seen on computed tomography scan, and a subtotal esophagectomy was performed which demonstrated a complete response in the resected specimen.
  • However, tongue cancer developed at age 40 years, and hemiglossectomy was performed.
  • However, the optimal dosage of chemoradiotherapy and the treatment strategy for esophageal cancer in patients with Fanconi anemia remain unclear, and outcomes are generally extremely poor.
  • In this patient, esophageal cancer associated with Fanconi anemia responded well to multidisciplinary therapy.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Esophageal Neoplasms / therapy. Fanconi Anemia / complications
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Bone Marrow Transplantation. Child. Cisplatin / administration & dosage. Combined Modality Therapy. Esophagectomy. Female. Fluorouracil / administration & dosage. Humans. Neoplasm Staging. Radiotherapy Dosage. Tomography, X-Ray Computed. Tongue Neoplasms / pathology. Tongue Neoplasms / secondary






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