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1. Kantarjian H, Talpaz M, O'Brien S, Giles F, Faderl S, Verstovsek S, Garcia-Manero G, Shan J, Rios MB, Champlin R, de Lima M, Cortes J: Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience. Cancer; 2005 May 15;103(10):2099-108
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  • [Title] Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience.
  • BACKGROUND: The effect of imatinib mesylate on survival in the accelerated phase of chronic myelogenous leukemia (CML) is unknown.
  • The objectives of this study were to update the long-term experience with imatinib in patients who had accelerated-phase CML and to compare outcomes with historic experience.
  • METHODS: The outcomes of 176 patients who received treatment with imatinib were reviewed and compared with the outcomes of 213 historic control patients with accelerated-phase CML who received treatment with interferon-alpha or with other modalities.
  • This may have implications in relation to subsequent therapy, because, according to the outcomes of patients who underwent allogeneic transplantation in accelerated phase at the authors' institution and from literature reports, the estimates of 5-year survival were 25-30%.
  • CONCLUSIONS: The current results suggest that imatinib improved survival compared with other therapies in patients with accelerated-phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Anemia / chemically induced. Benzamides. Bone Marrow Transplantation. Cohort Studies. Cytogenetic Analysis. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Hemoglobins / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Longitudinal Studies. Male. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 15830345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hemoglobins; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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2. le Coutre P, Ottmann OG, Giles F, Kim DW, Cortes J, Gattermann N, Apperley JF, Larson RA, Abruzzese E, O'Brien SG, Kuliczkowski K, Hochhaus A, Mahon FX, Saglio G, Gobbi M, Kwong YL, Baccarani M, Hughes T, Martinelli G, Radich JP, Zheng M, Shou Y, Kantarjian H: Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia. Blood; 2008 Feb 15;111(4):1834-9
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  • [Title] Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.
  • Patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia (CML-AP) have very limited therapeutic options.
  • Nilotinib is a highly selective BCR-ABL tyrosine kinase inhibitor.
  • This phase 2 trial was designed to characterize the efficacy and safety of nilotinib (400 mg twice daily) in this patient population with hematologic response (HR) as primary efficacy endpoint.
  • In conclusion, nilotinib is an effective and well-tolerated treatment in imatinib-resistant and -intolerant CML-AP.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Blood Cell Count. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Mutation. Safety

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  • (PMID = 18048643.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00384228
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 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
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3. Oki Y, Kantarjian HM, Gharibyan V, Jones D, O'brien S, Verstovsek S, Cortes J, Morris GM, Garcia-Manero G, Issa JP: Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia. Cancer; 2007 Mar 1;109(5):899-906
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  • [Title] Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia.
  • BACKGROUND: Resistance to imatinib is a frequent clinical problem in advanced phase chronic myelogenous leukemia (CML).
  • A Phase II study was performed on low-dose decitabine, a DNA methyltransferase inhibitor, in combination with imatinib in patients with CML in accelerated phase (AP) and myeloid blastic phase (BP).
  • The hematologic response rate was higher in patients without BCR-ABL kinase mutations (10 of 19, 53%) than in those with mutations (1 of 7, 14%).
  • CONCLUSIONS: Combination therapy with decitabine and imatinib is well tolerated and active in advanced phase CML without BCR-ABL kinase mutations.

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  • (PMID = 17236224.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-62202; United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 776B62CQ27 / decitabine; 8A1O1M485B / Imatinib Mesylate; M801H13NRU / Azacitidine
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4. Shah NP: Advanced CML: therapeutic options for patients in accelerated and blast phases. J Natl Compr Canc Netw; 2008 Mar;6 Suppl 2:S31-S36
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  • [Title] Advanced CML: therapeutic options for patients in accelerated and blast phases.
  • Tyrosine kinase inhibitor (TKI) therapy has impacted the natural course of chronic myelogenous leukemia (CML), because patients diagnosed as having chronic-phase disease can experience long-lasting responses.
  • However, for patients with advanced CML (accelerated and blast phases), the efficacy of all current therapies is reduced.
  • For patients with accelerated-phase CML, imatinib, dasatinib, and nilotinib have been shown to produce meaningful rates of hematologic and cytogenetic response.
  • Imatinib and dasatinib are also approved for blast-phase CML.
  • Moreover, because fewer mechanisms appear to exist for secondary resistance to dasatinib and nilotinib, reducing the potential for disease to escape TKI therapy, these agents may result in improved longer-term outcomes.
  • However, BCR-ABL-independent pathways may also become more important, indicating that other therapeutic targets may also have a future role in managing patients with advanced CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Blast Crisis / pathology. Clinical Trials as Topic. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / genetics. Humans

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  • (PMID = 18397679.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 33
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5. Altintas A, Cil T, Kilinc I, Kaplan MA, Ayyildiz O: Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report. J Neurooncol; 2007 Aug;84(1):103-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by a reciprocal translocation between chromosomes 9 and 22.
  • Imatinib mesylate is a potent and selective inhibitory of the BCR/ABL tyrosine kinase.
  • Imatinib is a first choice of treatment of chronic phase CML.
  • It has also shown activity in patients with CML in accelerated or blastic phases.
  • Herein, we report a patient with CML in accelerated phase that developed central nervous system disease while on imatinib mesylate therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / secondary. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Sarcoma, Myeloid / drug therapy


6. Nakazato T, Suzuki K, Mihara A, Sanada Y, Kakimoto T: [Successful induction of complete cytogenetic response with low-dose imatinib mesylate in an accelerated phase chronic myelogenous leukemia patient who developed severe bone marrow aplasia following standard-dose imatinib mesylate therapy]. Gan To Kagaku Ryoho; 2010 Mar;37(3):539-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful induction of complete cytogenetic response with low-dose imatinib mesylate in an accelerated phase chronic myelogenous leukemia patient who developed severe bone marrow aplasia following standard-dose imatinib mesylate therapy].
  • Bone marrow appearance was consistent with CML-AP, and t (9;22) (q34;q11) was detected on karyotyping.
  • Bone marrow biopsy showed severe bone marrow aplasia with no morphological evidence of disease progression.
  • This case also suggests that low-dose imatinib would be tolerable and effective for some CML patients who are intolerant of a standard dose of imatinib.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow / drug effects. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / administration & dosage. Piperazines / adverse effects. Pyrimidines / administration & dosage. Pyrimidines / adverse effects

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  • (PMID = 20332700.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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7. Cohen MH, Johnson JR, Pazdur R: U.S. Food and Drug Administration Drug Approval Summary: conversion of imatinib mesylate (STI571; Gleevec) tablets from accelerated approval to full approval. Clin Cancer Res; 2005 Jan 1;11(1):12-9
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  • [Title] U.S. Food and Drug Administration Drug Approval Summary: conversion of imatinib mesylate (STI571; Gleevec) tablets from accelerated approval to full approval.
  • Imatinib mesylate (Gleevec, Novartis Pharmaceuticals East Manruer, NJ) received accelerated approval on May 10, 2001 for the treatment of patients with chronic myeloid leukemia (CML) in (a) chronic phase after failure of IFN-alpha therapy, (b) accelerated phase, and (c) blast crisis.
  • The accelerated approval was accompanied by a postmarketing commitment by Novartis Pharmaceuticals to continue patient follow-up to determine duration of treatment response and survival.
  • The present review, based on a safety and efficacy report submitted on December 20, 2002, summarizes data applicable to the conversion of these three CML indications to full approval status.
  • RESULTS: Chronic phase CML: Five hundred thirty-two chronic phase CML patients who had not benefited from prior IFN therapy were treated at a starting imatinib mesylate dose of 400 mg p.o. qd; dose escalation to 800 mg p.o. qd was allowed.
  • Patients had received a median of 14 months of IFN therapy at doses > or =25 million IU/wk and were all in late chronic phase, with a median time from diagnosis of 32 months.
  • After 2 years of treatment, an estimated 85.4% of patients were free of progression to accelerated phase or blast crisis, and the estimated overall survival was 90.8% (95% confidence interval, 88.3-93.2).
  • Accelerated phase CML: Patients enrolled totaled 293: 235 with CML accelerated phase, 48 with relapsed/refractory acute lymphocytic leukemia, 2 with relapsed/refractory acute myelocytic leukemia, and 8 with relapsed/refractory CML in lymphoid blast crisis.
  • The median survival in the advanced leukemia population (acute lymphocytic leukemia, acute myelocytic leukemia, and lymphoid blast crisis) was only 5 months, and only two patients are still on treatment.
  • Blast crisis CML: A total of 260 patients were recruited.
  • CONCLUSIONS: The results confirm those of the interim analysis and suggest that imatinib mesylate represents an effective therapeutic agent for the treatment of patients with CML in chronic phase after failure of IFN-alpha therapy, in blast crisis, and in accelerated phase.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 15671523.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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8. Guilhot F, Apperley J, Kim DW, Bullorsky EO, Baccarani M, Roboz GJ, Amadori S, de Souza CA, Lipton JH, Hochhaus A, Heim D, Larson RA, Branford S, Muller MC, Agarwal P, Gollerkeri A, Talpaz M: Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. Blood; 2007 May 15;109(10):4143-50
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  • [Title] Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase.
  • Treatment options are limited for patients with imatinib-resistant or -intolerant accelerated phase chronic myeloid leukemia (CML-AP).
  • Dasatinib is a novel, potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC-family kinases that showed marked efficacy in a phase 1 trial of patients with imatinib-resistant CML.
  • Results are presented for 107 patients with CML-AP with imatinib-resistance or -intolerance from a phase 2, open-label study further evaluating dasatinib efficacy and safety.
  • Response rates for the 60% of patients with baseline BCR-ABL mutations did not differ from the total population.
  • In summary, dasatinib induced significant hematologic and cytogenetic responses in patients with imatinib resistance or intolerance, was well tolerated, and may represent a potent new therapeutic option for CML-AP.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Blood Cell Count. Cytogenetic Analysis. Dasatinib. Disease Progression. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Point Mutation. Protein-Tyrosine Kinases / genetics. Treatment Outcome


9. Luk'ianova AS, Pien'kovs'ka-Hrelia B, Masliak ZV: [Complex cytogenetic aberrations in a patient with chronic myeloid leukemia: a case report]. Tsitol Genet; 2009 May-Jun;43(3):48-54
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  • [Title] [Complex cytogenetic aberrations in a patient with chronic myeloid leukemia: a case report].
  • In this article is presented a case of multiple chromosomal aberrations in a patient with CML accelerated phase.
  • Our data suggested that detected changes can be correlated with previous treatment regimens and the influence of these changes on progression of disease is discussed.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics


10. Kumar L: Chronic myelogenous leukaemia (CML): an update. Natl Med J India; 2006 Sep-Oct;19(5):255-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myelogenous leukaemia (CML): an update.
  • The management of chronic myelogenous leukaemia (CML) has undergone a major change over the past 5 years.
  • All newly diagnosed patients of CML are candidates for imatinib mesylate therapy.
  • Almost 95% of patients with early chronic phase CML achieve complete haematological remission (CHR) and nearly 80% achieve complete cytogenetic response (CGR; 0% Philadelphia [Ph] chromosome-positive metaphases).
  • For patients with advanced CML (accelerated phase and blast crisis), achievement of CHR and major (complete and partial) CGR occurs in 25%-37% and 10%-30% of patients, respectively.
  • Most investigators agree that patients who fail to achieve CHR by 12 weeks, have partial cytogenetic response (< 35% Ph-positive metaphases) at 12 months, have CGR by 18 months, who relapse after initial response to imatinib, and those with a high Sokal score or in an advanced phase of CML should be considered for allogeneic stem cell transplantation (SCT).
  • Despite Ph negativity with imatinib treatment, most patients continue to remain BCR-ABL positive on molecular studies, and require treatment indefinitely.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17203680.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 87
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11. Apperley JF, Cortes JE, Kim DW, Roy L, Roboz GJ, Rosti G, Bullorsky EO, Abruzzese E, Hochhaus A, Heim D, de Souza CA, Larson RA, Lipton JH, Khoury HJ, Kim HJ, Sillaber C, Hughes TP, Erben P, Van Tornout J, Stone RM: Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial. J Clin Oncol; 2009 Jul 20;27(21):3472-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial.
  • PURPOSE Patients with chronic myelogenous leukemia in accelerated phase (CML-AP) that is resistant or intolerant to imatinib have limited therapeutic options.
  • Dasatinib, a potent inhibitor of BCR-ABL and SRC-family kinases, has efficacy in patients with CML-AP who have experienced treatment failure with imatinib.
  • We now report follow-up data from the full patient cohort of 174 patients enrolled onto a phase II trial to provide a more complete assessment of the efficacy and safety of dasatinib in this population.
  • PATIENTS AND METHODS Patients with imatinib-resistant (n = 161) or -intolerant (n = 13) CML-AP received dasatinib 70 mg orally twice daily.
  • Responses were achieved irrespective of imatinib status (resistant or intolerant), prior stem-cell transplantation, or the presence of prior BCR-ABL mutation.
  • CONCLUSION Dasatinib is effective in patients with CML-AP after imatinib treatment failure.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. Treatment Failure
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Dasatinib. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome. Young Adult


12. Kantarjian H, le Coutre P, Cortes J, Pinilla-Ibarz J, Nagler A, Hochhaus A, Kimura S, Ottmann O: Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance. Cancer; 2010 Jun 1;116(11):2665-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.
  • BACKGROUND: : INNO-406, a dual v-abl Abelson murine leukemia viral oncogene homolog (Abl)/v-yes-1 Yamaguchi sarcoma viral-related oncogene homolog (Lyn) tyrosine kinase inhibitor (TKI), has demonstrated specific Lyn kinase inhibitory activity with no or limited activity against other sarcoma (Src) family member kinases.
  • Several breakpoint cluster region (Bcr)-Abl kinase domain mutations are sensitive to INNO-406 in vitro, including mutations that involve a phenylalanine-to-leucine or phenylalanine-to-valine substitution at codon 317 (F317L and F317V, respectively).
  • In the current study, the authors evaluated the use of INNO-406 in patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) after imatinib resistance or intolerance.
  • Of 31 patients with CML in chronic phase who received INNO-406, the major cytogenetic response rate was 19%.
  • No responses were observed in patients who had CML in accelerated phase, CML in blastic phase, or Ph-positive ALL.
  • CONCLUSIONS: : INNO-406 had anti-CML efficacy in a heavily pretreated study population.
  • On the basis of the classic determinations of both DLT and MTD, the recommended phase 2 dose of oral INNO-406 was 240 mg twice daily.

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  • [Copyright] (c) 2010 American Cancer Society.
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Haematologica. 2008 Sep;93(9):1389-93 [18603549.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] Oncologist. 2004;9(3):259-70 [15169981.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1321-31 [15215876.001]
  • [Cites] Cancer Chemother Rep. 1966 May;50(4):219-44 [4957125.001]
  • [Cites] J Natl Compr Canc Netw. 2005 Nov;3(6):757-68 [16316612.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1061-6 [16642048.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Ann Intern Med. 2006 Dec 19;145(12):913-23 [17179059.001]
  • [Cites] Blood. 2007 Jan 1;109(1):306-14 [16954504.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2171-81 [17431887.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:371-5 [18024653.001]
  • [Cites] Haematologica. 2008 Feb;93(2):186-92 [18223278.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):980-3 [18191450.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Sep;8(9):1387-98 [18759691.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3948-54 [16105974.001]
  • (PMID = 20310049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632-070007; United States / NCI NIH HHS / CA / CA100632-070007; United States / NCI NIH HHS / CA / P01CA049639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA049639
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS189694; NLM/ PMC2876208
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13. Borthakur G, Kantarjian H, Daley G, Talpaz M, O'Brien S, Garcia-Manero G, Giles F, Faderl S, Sugrue M, Cortes J: Pilot study of lonafarnib, a farnesyl transferase inhibitor, in patients with chronic myeloid leukemia in the chronic or accelerated phase that is resistant or refractory to imatinib therapy. Cancer; 2006 Jan 15;106(2):346-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study of lonafarnib, a farnesyl transferase inhibitor, in patients with chronic myeloid leukemia in the chronic or accelerated phase that is resistant or refractory to imatinib therapy.
  • BACKGROUND: Lonafarnib (SCH66336) is a nonpeptidomimetic farnesyl transferase inhibitor that has demonstrated significant preclinical activity against chronic myelogenous leukemia (CML) cells and in CML animal models.
  • METHODS: In the current study, the efficacy of lonafarnib was investigated in patients with CML in the chronic or accelerated phase that was resistant or intolerant to imatinib.
  • Thirteen patients with CML in the chronic (n = 6 patients) or accelerated (n = 7 patients) phase were treated with lonafarnib at a dose of 200 mg orally twice daily.
  • The median age of the patients was 62 years (range, 38-80 yrs) and the median time from the diagnosis of CML to therapy with lonafarnib was 5 years (range, 0.3-13 yrs).
  • One patient in the accelerated phase of CML returned to the chronic phase, a response that lasted for 3 months.
  • Another patient with chronic phase disease had lowering of the leukocyte count without the need for hydroxyurea and normalization of the differential count that lasted for 5 months.
  • CONCLUSIONS: Single-agent lonafarnib appears to have clinical activity in a small proportion of patients with CML refractory to imatinib.
  • [MeSH-major] Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperidines / therapeutic use. Pyridines / therapeutic use

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  • (PMID = 16342165.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Piperidines; 0 / Pyridines; 0 / Pyrimidines; 193275-84-2 / lonafarnib; 8A1O1M485B / Imatinib Mesylate; EC 2.5.1.29 / Farnesyltranstransferase
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14. Gratwohl A, Heim D: Current role of stem cell transplantation in chronic myeloid leukaemia. Best Pract Res Clin Haematol; 2009 Sep;22(3):431-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current role of stem cell transplantation in chronic myeloid leukaemia.
  • Haematopoietic stem cell transplantation (HSCT) has seen considerable ups and downs in its role for patients with chronic myeloid leukaemia (CML).
  • It has provided the first proof of the principle for cure and has confirmed the concept of successful immunotherapy of leukaemia.
  • CML became the most frequent indication for an allogeneic HSCT worldwide.
  • The frequency of HSCT declined rapidly when the specific BCR/ABL tyrosine kinase inhibitor (TKI) imatinib appeared.
  • Risk assessment of both, disease risk and transplant risk, has become standard.
  • Allogeneic HSCT remains the first-line approach for patients with CML in accelerated phase or blast crisis.
  • It is the best option for all patients with failed second-line TKIs, with mutations T315I or with progressive disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 19959092.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 74
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15. Dutcher JP, Lee S, Gallagher RE, Makary AZ, Hines JD, Londer H, Farnen JP, Bennett JM, Paietta E, Rowe JM, Goloubeva O, Wiernik PH, Eastern Cooperative Oncology Group: Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993). Leuk Lymphoma; 2005 Mar;46(3):377-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993).
  • The aims of this study were to evaluate the safety and efficacy of all-trans retinoic acid (ATRA) in the treatment of the accelerated and blastic phase of chronic myeloid leukemia (CML) and to evaluate in vitro correlates of biological activity.
  • ATRA was administered in an intermittent schedule to patients with CML in the accelerated or blastic phases for a 6 week induction period, which was continued if there was evidence of clinical response or stable disease.
  • Laboratory correlative studies were performed prior to treatment and at intervals during treatment to evaluate effects on maturation and differentiation, and on CML progenitor cell growth by assessment of colony-forming cells (CFC).
  • ATRA demonstrated clinical and hematological activity in 5 of 18 patients with the accelerated phase of CML, and there was evidence of a biological effect in laboratory studies of 3 of the 5 patients' progenitor cells.
  • Combination therapy with other differentiating agents may be useful in this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Tretinoin / administration & dosage
  • [MeSH-minor] Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytogenetic Analysis. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Recombinant Proteins. Survival Analysis. Time Factors

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  • (PMID = 15621827.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 11083; United States / NCI NIH HHS / CA / CA 14548; United States / NCI NIH HHS / CA / CA 14958; United States / NCI NIH HHS / CA / CA 23318; United States / NCI NIH HHS / CA / CA 66636; United States / NCI NIH HHS / CA / CA21115
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 76543-88-9 / interferon alfa-2a
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16. Li X, Yang J, Chen X, Liu J, Li H, Zheng J, He Y, Chen Z, Huang S: A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript. Cancer Genet Cytogenet; 2007 Jul 15;176(2):166-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.
  • The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.
  • However, our knowledge about its therapeutic effect on CML patients with rare BCR/ABL fusion transcripts e19a2(u-bcr) remains sparse.
  • Here, we report on two CML patients with e19a2 transcripts who rapidly progressed into the accelerated phase, further confirming the possibility that 19a2 might be associated with an unfavorable prognosis in CML.
  • [MeSH-major] Gene Expression Regulation, Leukemic / drug effects. Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Disease Progression. Exons. Female. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Time Factors. Translocation, Genetic. Treatment Outcome

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  • (PMID = 17656262.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate
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17. Rosti G, Castagnetti F, Gugliotta G, Palandri F, Martinelli G, Baccarani M: Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'. Leuk Lymphoma; 2010 Apr;51(4):583-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'.
  • Imatinib has revolutionized the treatment of patients with chronic myeloid leukemia (CML).
  • Dasatinib, approved in 2006 for the treatment of patients with CML in all phases who experience imatinib resistance or intolerance, has displayed significant efficacy, with a 2-year follow-up showing durable hematologic and cytogenetic responses, as well as prolonged progression-free and overall survival.
  • Nilotinib was approved in 2007 for the treatment of patients with CML in chronic phase or CML in accelerated phase, resistant or intolerant to prior therapy including imatinib, based on strong efficacy as well as a favorable safety profile.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20302388.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Number-of-references] 30
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18. Kantarjian H, Cortes J, Kim DW, Dorlhiac-Llacer P, Pasquini R, DiPersio J, Müller MC, Radich JP, Khoury HJ, Khoroshko N, Bradley-Garelik MB, Zhu C, Tallman MS: Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up. Blood; 2009 Jun 18;113(25):6322-9
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  • [Title] Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up.
  • Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.
  • Studies have demonstrated the benefits of dasatinib 70 mg twice daily in patients with accelerated-phase chronic myeloid leukemia intolerant or resistant to imatinib.
  • A phase 3 study compared the efficacy and safety of dasatinib 140 mg once daily with the current twice-daily regimen.
  • Here, results from the subgroup with accelerated-phase chronic myeloid leukemia (n = 317) with a median follow-up of 15 months (treatment duration, 0.03-31.15 months) are reported.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Dasatinib. Drug Resistance, Neoplasm. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Fusion Proteins, bcr-abl / genetics. Gastrointestinal Diseases / chemically induced. Genes, abl. Heart Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Piperazines / adverse effects. Piperazines / pharmacology. Young Adult


19. Zhang Y, Jiang Q, Qiu JY, Chen SS, Jiang B, Huang XJ: [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment]. Zhonghua Nei Ke Za Zhi; 2007 Aug;46(8):648-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment].
  • OBJECTIVE: To investigate the change of Philadelphia chromosome-positive clone with secondary chromosomal aberrations after imatinib mesylate (IM) treatment in patients with chronic myeloid leukemia (CML) and its relation with prognosis.
  • METHODS: 37 cases of CML in accelerated phase and blastic phase were collected and chromosome specimens of bone marrow cells were prepared by with 24-hour culture.
  • The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations showed the following 4 types of change; amplification, no change, decrease and complete remission after treatment with IM.
  • 2 of the 24 cases in CML in accelerated phase gained complete cytogenetic response (CCyR) and 2 of the 13 in blastic phase did so.
  • CONCLUSION: The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations may drop in some CML patients after IM treatment and the patients may gain CCyR with accompanied prolonged survival.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17967235.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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20. Palandri F, Castagnetti F, Alimena G, Testoni N, Breccia M, Luatti S, Rege-Cambrin G, Stagno F, Specchia G, Martino B, Levato L, Merante S, Liberati AM, Pane F, Saglio G, Alberti D, Martinelli G, Baccarani M, Rosti G: The long-term durability of cytogenetic responses in patients with accelerated phase chronic myeloid leukemia treated with imatinib 600 mg: the GIMEMA CML Working Party experience after a 7-year follow-up. Haematologica; 2009 Feb;94(2):205-12
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  • [Title] The long-term durability of cytogenetic responses in patients with accelerated phase chronic myeloid leukemia treated with imatinib 600 mg: the GIMEMA CML Working Party experience after a 7-year follow-up.
  • BACKGROUND: Imatinib mesylate is the first line treatment for chronic myeloid leukemia.
  • The advent of imatinib increased survival significantly in patients in an advanced phase of the disease.
  • DESIGN AND METHODS: A phase 2 multicenter trial of the use of imatinib 600 mg/daily in patients with accelerated phase chronic myeloid leukemia was sponsored and promoted by the Italian Cooperative Study Group on Chronic Myeloid Leukemia in 2001.
  • One hundred and seven patients (96%) returned to chronic phase and 79 patients (71%) achieved a complete hematologic response.
  • CONCLUSIONS: Imatinib may induce durable responses, associated with prolonged survival, in patients with accelerated phase chronic myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage

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  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Cancer. 2000 Oct 15;89(8):1647-58 [11042556.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1928-37 [11877262.001]
  • [Cites] Blood. 2002 May 15;99(10):3530-9 [11986204.001]
  • [Cites] Blood. 2002 May 15;99(10):3547-53 [11986206.001]
  • [Cites] Clin Cancer Res. 2002 Jul;8(7):2167-76 [12114417.001]
  • [Cites] Haematologica. 2003 Nov;88(11):1213-20 [14607749.001]
  • [Cites] Blood. 1968 Sep;32(3):445-59 [4970948.001]
  • [Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]
  • [Cites] Cancer. 1988 Apr 1;61(7):1441-6 [3162181.001]
  • [Cites] Science. 1990 Feb 16;247(4944):824-30 [2406902.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6649-53 [2204061.001]
  • [Cites] J Clin Oncol. 1992 May;10(5):772-8 [1569449.001]
  • [Cites] J Clin Oncol. 1996 Jan;14(1):196-203 [8558198.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Clin Cancer Res. 1998 Jul;4(7):1661-72 [9676840.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] Nature. 2005 Jun 30;435(7046):1267-70 [15988530.001]
  • [Cites] Cancer. 2006 Mar 15;106(6):1306-15 [16463391.001]
  • [Cites] Haematologica. 2006 Apr;91(4):513-21 [16533723.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1421-3 [16601247.001]
  • [Cites] Blood. 2007 May 15;109(10):4143-50 [17264298.001]
  • [Cites] J Clin Oncol. 2008 Jan 1;26(1):106-11 [18165644.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1834-9 [18048643.001]
  • [Cites] Haematologica. 2008 May;93(5):770-4 [18367490.001]
  • [CommentIn] Haematologica. 2009 May;94(5):743-4 [19407320.001]
  • (PMID = 19144656.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2635408
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21. Bryant BJ, Alperin JB, Elghetany MT: Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia. Am J Hematol; 2007 Feb;82(2):150-4
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  • [Title] Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia.
  • Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML).
  • They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder.
  • Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia.
  • Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia.
  • This is the first case report of paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed CML.
  • The CBC revealed a leukocyte count of 238,300/microl and a differential consistent with CML.
  • Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML.
  • Although extramedullary blast crises herald the accelerated phases in approximately 10% of CML cases, megakaryoblastic blast transformation of CML accounts for less than 3% of these cases.
  • The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation. Paraplegia / pathology. Spinal Cord Compression / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Combined Modality Therapy. Female. Humans. Middle Aged. Splenic Neoplasms / diagnosis. Splenic Neoplasms / pathology. Splenic Neoplasms / secondary. Splenic Neoplasms / therapy

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17019692.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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22. Basak G, Torosian T, Snarski E, Niesiobedzka J, Majewski M, Gronkowska A, Urbanowska E, Jedrzejczak W: Hematopoietic stem cell transplantation for T315I-mutated chronic myelogenous leukemia. Ann Transplant; 2010 Apr-Jun;15(2):68-70
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  • [Title] Hematopoietic stem cell transplantation for T315I-mutated chronic myelogenous leukemia.
  • BACKGROUND: The T315I mutation of BCR/ABL gene is known to produce complete resistance of chronic myelogenous leukemia (CML) to all currently available BCR/ABL inhibitors.
  • However, evidence on efficiency of this treatment modality in CML with T315I mutation is lacking.
  • CASE REPORT: A 25-year-old patient was diagnosed with Philadelphia chromosome positive CML in accelerated phase.
  • Moreover, despite escalation of imatinib dosage, the disease relapsed after further 3 months of treatment.
  • Molecular studies revealed T315I mutation of BCR/ABL gene.
  • The course of transplantation was complicated by staphylococcal sepsis, grade I skin acute GvHD and limited chronic skin GVHD.
  • CONCLUSIONS: The clinical course of this case supports the idea that allogeneic hematopoietic transplantation is a viable treatment option for patients with CML bearing T315I mutation.
  • [MeSH-major] Genes, abl. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Mutation, Missense
  • [MeSH-minor] Adult. Amino Acid Substitution. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Humans. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Accelerated Phase / genetics. Leukemia, Myeloid, Accelerated Phase / therapy. Male. Protein Kinase Inhibitors / pharmacology. Remission Induction. Transplantation, Homologous

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  • (PMID = 20657522.001).
  • [ISSN] 2329-0358
  • [Journal-full-title] Annals of transplantation
  • [ISO-abbreviation] Ann. Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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23. Yu HH, Lu MY, Lin DT, Lin KH, Tang JL, Jou ST: Pathological fracture as a manifestation of extramedullary blastic crisis in chronic myelogenous leukemia: report of one case. Acta Paediatr Taiwan; 2006 May-Jun;47(3):150-4
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  • [Title] Pathological fracture as a manifestation of extramedullary blastic crisis in chronic myelogenous leukemia: report of one case.
  • A three-year-old girl with chronic myelogenous leukemia (CML) experienced a pathological fracture of her femur after a demonstrated osteolytic bone lesion.
  • Extramedullary disease (EMD) was diagnosed following the histologic findings of a biopsy of the osteolytic lesion.
  • This was the youngest patient to have been reported in English literature of Philadelphia chromosome positive (Ph+) CML with isolated bony EMD and pathological fracture.
  • Treatment with a tyrosine kinase inhibitor, imatinib mesylate (Gleevec), in bone marrow accelerated phase of CML was failed to reverse the progression of blastic transformation, neither in the extramedullary bone lesion nor in the bone marrow.
  • [MeSH-major] Blast Crisis / complications. Femoral Fractures / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 17078470.001).
  • [ISSN] 1608-8115
  • [Journal-full-title] Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi
  • [ISO-abbreviation] Acta Paediatr Taiwan
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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24. Etienne G, Milpied B, Réa D, Rigal-Huguet F, Tulliez M, Nicolini FE, French Intergroup of CML (Fi-LMC group): [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)]. Bull Cancer; 2010 Aug;97(8):997-1009
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  • [Title] [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)].
  • [Transliterated title] Recommandations du groupe Fi-LMC pour la gestion des effets indésirables du traitement par nilotinib (Tasigna) au cours de la leucémie myéloïde chronique.
  • Nilotinib (Tasigna) is a second-generation BCR-ABL kinase inhibitor, recently introduced and used for the treatment of chronic or accelerated phase CML patients, intolerant or resistant to imatinib.
  • This treatment represents and important step forward for the disease control of such patients but can lead to side effects, sometimes serious, which can limit its optimal use.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects

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  • (PMID = 20529767.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Practice Guideline
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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25. Ohmachi K, Ogiya D, Morita F, Kojima M, Tsuboi K, Tazume K, Komatsu M, Hayama N, Kumaki N, Ogawa Y, Ando K: Secondary pulmonary alveolar proteinosis in a patient with chronic myeloid leukemia in the accelerated phase. Tokai J Exp Clin Med; 2008 Dec;33(4):146-9
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  • [Title] Secondary pulmonary alveolar proteinosis in a patient with chronic myeloid leukemia in the accelerated phase.
  • Pulmonary alveolar proteinosis (PAP) is a rare respiratory disease the character of which is accumulation of protein consisting of surfactant in alveolar spaces.
  • PAP sometimes complicates with hematological malignancies, especially myeloid leukemia.
  • We experienced a case of PAP with chronic myeloid leukemia (CML).
  • 41 years old woman having CML for nine years developed PAP, and was treated by bronchoalveolar lavage and imatinib.
  • We consider that we should try to treat to improve respiratory status not only PAP but also hematological disease.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Pulmonary Alveolar Proteinosis / etiology

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  • (PMID = 21318986.001).
  • [ISSN] 2185-2243
  • [Journal-full-title] The Tokai journal of experimental and clinical medicine
  • [ISO-abbreviation] Tokai J. Exp. Clin. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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26. Voglová J, Maisnar V, Beránek M, Chrobák L: [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase]. Vnitr Lek; 2006 Sep;52(9):819-22
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  • [Title] [Combination of imatinib and anagrelide in treatment of chronic myeloid leukemia in blastic phase].
  • [Transliterated title] Kombinace imatinibu s anagrelidem v lécbe blastického zvratu chronické myeloidní leukemie.
  • Chronic myeloid leukemia in blast phase (BP) is resistant to chemotherapy and majority of patients die within 6 months.
  • Inhibitor Bcr-Abl tyrosine kinase imatinib mesylate dramatically improved outcome of patients in chronic phase (CP) and is also effective in BP of CML.
  • High platelet counts are often observed at diagnosis or in the subsequent course of the CML in about 25% of patients.
  • Anagrelide selectively reduces circulating platelets and is used in treatment of thrombocythemia in chronic myeloproliferative disorders.
  • Efficacy and safety of combination imatinib mesylate with anagrelide was demonstrated in chronic and accelerated phase of CML.
  • 51-year-old white man with CML presented in blast phase was followed for 4 years.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / administration & dosage. Platelet Aggregation Inhibitors / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Quinazolines / administration & dosage. Thrombocytosis / drug therapy


27. Quintás-Cardama A, Kantarjian H, Garcia-Manero G, O'Brien S, Faderl S, Estrov Z, Giles F, Murgo A, Ladie N, Verstovsek S, Cortes J: Phase I/II study of subcutaneous homoharringtonine in patients with chronic myeloid leukemia who have failed prior therapy. Cancer; 2007 Jan 15;109(2):248-55
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  • [Title] Phase I/II study of subcutaneous homoharringtonine in patients with chronic myeloid leukemia who have failed prior therapy.
  • Intravenous HHT has demonstrated activity in patients with chronic myeloid leukemia (CML) after failure with interferon.
  • METHODS: A Phase I study was completed of subcutaneous (s.c.
  • ) HHT in patients with CML in accelerated or blast phases and demonstrated efficacy and good tolerance at the same doses used by intravenous (i.v.) administration.
  • The cohort was then expanded to treated at the MTD to include patients in late chronic phase CML after imatinib failure.
  • The 2 patients with BCR-ABL kinase domain mutations at the start of therapy with HHT had a CG response and in both instances the mutations became undetectable.
  • CONCLUSIONS: Subcutaneous HHT is well tolerated and may have clinical activity in patients with CML after imatinib failure.
  • [MeSH-major] Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • [ErratumIn] Cancer. 2007 Jun 15;109(12):2625. Dosage error in article text
  • (PMID = 17154172.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Benzamides; 0 / Harringtonines; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 6FG8041S5B / homoharringtonine; 8A1O1M485B / Imatinib Mesylate
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28. Giles FJ, Abruzzese E, Rosti G, Kim DW, Bhatia R, Bosly A, Goldberg S, Kam GL, Jagasia M, Mendrek W, Fischer T, Facon T, Dünzinger U, Marin D, Mueller MC, Shou Y, Gallagher NJ, Larson RA, Mahon FX, Baccarani M, Cortes J, Kantarjian HM: Nilotinib is active in chronic and accelerated phase chronic myeloid leukemia following failure of imatinib and dasatinib therapy. Leukemia; 2010 Jul;24(7):1299-301
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  • [Title] Nilotinib is active in chronic and accelerated phase chronic myeloid leukemia following failure of imatinib and dasatinib therapy.
  • Nilotinib is a highly selective Bcr-Abl inhibitor approved for imatinib-resistant chronic myeloid leukemia (CML).
  • Nilotinib and dasatinib, a multi-targeted kinase inhibitor also approved for second-line therapy in CML, have different patterns of kinase selectivity, pharmacokinetics, and cell uptake and efflux properties, and thus patients may respond to one following failure of the other.
  • An international phase II study of nilotinib was conducted in CML patients (39 chronic phase (CP), 21 accelerated phase (AP)) after failure of both imatinib and dasatinib.
  • Median times from diagnosis of CP or AP to nilotinib therapy were 89 and 83 months, respectively.
  • Of 17 evaluable patients with CML-AP, 5 (29%) had a confirmed hematological response and 2 (12%) a MCyR.
  • Median overall survival for both populations has not been reached, and the estimated 18-month survival rate in CML-CP was 86% and that at 12 months for CML-AP was 80%.
  • Nilotinib is an effective therapy in CML-CP and -AP following failure of both imatinib and dasatinib therapy.
  • [MeSH-major] Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use

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  • [Cites] Blood. 2007 Jan 15;109(2):497-9 [16990591.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2242-9 [17496200.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):3881-8 [18559609.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1054-61 [19282833.001]
  • [Cites] Leukemia. 2010 Apr;24(4):855-7 [20147980.001]
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):6041-51 [19884523.001]
  • [Cites] Leukemia. 2010 Jan;24(1):6-12 [19798095.001]
  • [Cites] J Clin Oncol. 2010 Jan 20;28(3):363-5 [20008612.001]
  • [Cites] Leukemia. 2010 Mar;24(3):658-60 [20010623.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1698-707 [19474800.001]
  • (PMID = 20520639.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095684; United States / NCI NIH HHS / CA / R01 CA095684-08
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS264403; NLM/ PMC3078756
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29. Mauro MJ: Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia. Cancer Control; 2009 Apr;16(2):108-21
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  • [Title] Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia.
  • BACKGROUND: Research into chronic myeloid leukemia (CML) is increasingly focused on the problem of imatinib failure.
  • Dasatinib and nilotinib are both active in chronic- and accelerated-phase CML, including patients with imatinib-resistant or intolerant disease.
  • METHODS: This paper reviews advances in tailoring tyrosine kinase inhibition therapy according to patient risk profiles as well as hematologic, cytogenetic, and molecular responses, BCR-ABL mutation status, and emerging predictive factors.
  • CONCLUSIONS: Treatment for CML should be individualized and, when resistance to imatinib can be predicted, therapy should be modified so that patients do not progress beyond chronic phase and respond as promptly and deeply as required to maximally reduce risk.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / genetics

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  • (PMID = 19337197.001).
  • [ISSN] 1526-2359
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
  • [Number-of-references] 118
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30. Keam SJ: Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia. BioDrugs; 2008;22(1):59-69
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  • [Title] Dasatinib: in chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • Dasatinib is a small-molecule inhibitor of multiple tyrosine kinases, including BCR-ABL, SRC, c-KIT, ephrin A receptor and platelet-derived growth factor-beta receptor kinases, at nanomolar concentrations.
  • In vitro, dasatinib is 325-fold more potent than imatinib against cells expressing wild-type BCR-ABL.
  • The efficacy and tolerability of oral dasatinib has been established in the START phase II trials in adults with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph-positive ALL) who were intolerant or resistant to imatinib, and optimal dasatinib dosage regimens were identified in phase III randomized trials.
  • In patients with chronic phase CML, the major cytogenetic response rate in the START-C trial (median follow-up 15.2 months) was 59% with dasatinib, and in the randomized START-R trial (median follow-up 15 months), was greater with dasatinib than with high-dose imatinib (52% vs 33%).
  • Major hematologic response rates with dasatinib were 63% in patients with accelerated phase CML (follow-up > or =9 months; START-A trial), 34% in patients with myeloid blast phase CML and 35% in those with lymphoid blast phase CML (follow-up > or =12 months; START-B and START-L trials), and 41% in patients with Ph-positive ALL (follow-up > or =12 months; START-L trial).
  • Based on phase III results, a once-daily dasatinib regimen is considered optimal in chronic phase CML (starting dosage 100 mg once daily), while a twice-daily regimen continues to be recommended in accelerated phase, myeloid blast phase or lymphoid blast phase CML and Ph-positive ALL (starting dosage 70 mg twice daily).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage
  • [MeSH-minor] Animals. Controlled Clinical Trials as Topic. Dasatinib. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


31. Qazilbash MH, Qu Z, Hosing C, Couriel D, Donato M, Giralt S, Champlin R: Rituximab-induced acute liver failure after an allogeneic transplantation for chronic myeloid leukemia. Am J Hematol; 2005 Sep;80(1):43-5
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  • [Title] Rituximab-induced acute liver failure after an allogeneic transplantation for chronic myeloid leukemia.
  • We report our experience with a 21-year-old female with accelerated-phase chronic myeloid leukemia who underwent allogeneic hematopoietic stem cell transplantation from a matched, unrelated donor.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Liver Failure, Acute / chemically induced


32. Chen ZC, You Y, Zhu XM, Li QB, Li WM, Zou P: [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate]. Zhonghua Nei Ke Za Zhi; 2007 Dec;46(12):1003-6
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  • [Title] [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].
  • OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).
  • METHODS: 120 patients diagnosed as CML with positive Ph chromosome were treated with IM 400 mg/d for CML in chronic phase (CP) (n = 90) or 600 mg/d for CML in accelerated or blastic phase (AP or BP) (n = 30) once daily.
  • Hematological, cytogenetic and molecular effects of IM on the disease process of these patients were evaluated with blood and marrow cells morphology examination, G-band conventional cytogenetics analysis for Ph chromosome and PCR assay for BCR/ABL gene.
  • (1) In CML-CP patients, after a follow-up of 9 ( range 3-42) months, cumulative complete hematological response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMR) rates were 73.3%, 66.7% and 54.4%, which was not influenced by prior treatment of interferon.
  • CMR was better when time from diagnosis to treatment with IM was < or = 6 months (P < 0.05).
  • It is significant that the time to first CHR and time to first CCyR were related with the time to first CCyR and the time to first negative BCR/ ABL, respectively (both P < 0.05), while there was no relation between the time to first CHR and the time to first negative BCR/ABL (P > 0.05). (2) CHR, CCyR and CMR rates of the patients with progressive course (AP and BP) were 43.3%, 25.9% and 25.0%, respectively.
  • CONCLUSION: IM can lead to considerable hematological, cytogenetic and molecular response rates in CML, especially CML-CP patients, with minor tolerable side effects.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome

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  • (PMID = 18478917.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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33. Druker BJ, Guilhot F, O'Brien SG, Gathmann I, Kantarjian H, Gattermann N, Deininger MW, Silver RT, Goldman JM, Stone RM, Cervantes F, Hochhaus A, Powell BL, Gabrilove JL, Rousselot P, Reiffers J, Cornelissen JJ, Hughes T, Agis H, Fischer T, Verhoef G, Shepherd J, Saglio G, Gratwohl A, Nielsen JL, Radich JP, Simonsson B, Taylor K, Baccarani M, So C, Letvak L, Larson RA, IRIS Investigators: Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med; 2006 Dec 7;355(23):2408-17
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  • [Title] Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
  • BACKGROUND: The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase.
  • Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase.
  • For 5 years, we followed patients with CML who received imatinib as initial therapy.
  • METHODS: We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events.
  • An estimated 7% of patients progressed to accelerated-phase CML or blast crisis, and the estimated overall survival of patients who received imatinib as initial therapy was 89% at 60 months.
  • Patients who had a complete cytogenetic response or in whom levels of BCR-ABL transcripts had fallen by at least 3 log had a significantly lower risk of disease progression than did patients without a complete cytogenetic response (P<0.001).
  • CONCLUSIONS: After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients. (ClinicalTrials.gov number, NCT00006343 [ClinicalTrials.gov]. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Cytarabine / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / blood. Humans. Imatinib Mesylate. Interferon-alpha / administration & dosage. Kaplan-Meier Estimate. Male. Survival Analysis. Survival Rate. Treatment Outcome


34. Fausel CA: Novel treatment strategies for chronic myeloid leukemia. Am J Health Syst Pharm; 2006 Dec 1;63(23 Suppl 8):S15-20; quiz S21-2
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  • [Title] Novel treatment strategies for chronic myeloid leukemia.
  • PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma.
  • Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.
  • SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants.
  • Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.
  • Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.
  • Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials.
  • CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.
  • [MeSH-major] Drug Therapy / methods. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy

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  • (PMID = 17106016.001).
  • [ISSN] 1079-2082
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 23
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35. Krejci M, Mayer J, Doubek M, Brychtova Y, Pospisil Z, Racil Z, Dvorakova D, Lengerova M, Horky O, Koristek Z, Dolezal T, Vorlicek J: Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia. Bone Marrow Transplant; 2006 Oct;38(7):483-91
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  • [Title] Clinical outcomes and direct hospital costs of reduced-intensity allogeneic transplantation in chronic myeloid leukemia.
  • A reduced-intensity conditioning allogeneic stem cell transplantation was given to 19 patients (aged 15-59 years) in the first chronic phase and one patient in the accelerated phase with chronic myeloid leukemia (CML) after a regimen consisting of fludarabine (Flu), busulfan (Bu) and ATG Fresenius.
  • The incidence of acute and chronic graft-versus-host disease (GvHD) was 55 and 75%, respectively.
  • Flu+Bu+ATG is a low-toxicity regimen for patients with CML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / economics. Hospital Costs / statistics & numerical data. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Busulfan / administration & dosage. Czech Republic. Female. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Philadelphia Chromosome. Retrospective Studies. Survival Analysis. Transplantation, Homologous / economics. Transplantation, Homologous / methods. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives


36. DeAngelo DJ, Attar EC: Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice. Leuk Lymphoma; 2010 Mar;51(3):363-75
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  • [Title] Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.
  • The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).
  • The mechanisms underlying resistance are multifactorial and may include mutations in the kinase domain of BCR-ABL, increased production of BCR-ABL, or activation of BCR-ABL-independent pathways.
  • Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.
  • Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.
  • Nilotinib, an analogue of imatinib, is approved for the treatment of imatinib-resistant or -intolerant patients with chronic or accelerated phase CML.
  • Both agents have shown significant clinical activity in patients with imatinib-resistant or -intolerant CML, and their approval represents a major advancement in the treatment options available.
  • The presence of certain disease characteristics (e.g. specific BCR-ABL mutations) or patient comorbidities may facilitate more effective treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


37. Jabbour E, Cortés JE, Kantarjian H: Optimizing treatment with Bcr-Abl tyrosine kinase inhibitors in Philadelphia chromosome-positive chronic myeloid leukemia: focus on dosing schedules. Clin Lymphoma Myeloma; 2008 Mar;8 Suppl 3:S75-81
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  • [Title] Optimizing treatment with Bcr-Abl tyrosine kinase inhibitors in Philadelphia chromosome-positive chronic myeloid leukemia: focus on dosing schedules.
  • Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia chromosome (Ph), a genetic aberration that codes for bcrabl, which plays a key role in disease pathophysiology.
  • Dose-escalated imatinib (800 mg daily) has shown some limited activity in patients with imatinib-resistant CML, but the development of second-generation tyrosine kinase inhibitors has broadened the treatment options.
  • Dasatinib has demonstrated activity in all phases of CML and Ph+ acute lymphocytic leukemia and is approved for the treatment of adults in this setting.
  • Recent phase III data have demonstrated that, in patients with chronic-phase CML, dasatinib 100 mg once daily is equally effective, with improved tolerability, compared with the previously approved 70-mg twice-daily dose.
  • Nilotinib, which has been recently approved, has increased potency for Brc-Abl compared with imatinib and has demonstrated activity in patients with imatinib-resistant and -intolerant chronic- and accelerated-phase CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Dasatinib. Fusion Proteins, bcr-abl. Humans

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  • (PMID = 19254884.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 51
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38. Notari M, Neviani P, Santhanam R, Blaser BW, Chang JS, Galietta A, Willis AE, Roy DC, Caligiuri MA, Marcucci G, Perrotti D: A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation. Blood; 2006 Mar 15;107(6):2507-16
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  • [Title] A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation.
  • Altered mRNA translation is one of the effects exerted by the BCR/ABL oncoprotein in the blast crisis phase of chronic myelogenous leukemia (CML).
  • Here, we report that in BCR/ABL+ cell lines and in patient-derived CML blast crisis mononuclear and CD34+ cells, p210(BCR/ABL) increases expression and activity of the transcriptional-inducer and translational-regulator heterogeneous nuclear ribonucleoprotein K (hnRNP K or HNRPK) in a dose- and kinase-dependent manner through the activation of the MAPK(ERK1/2) pathway.
  • Furthermore, HNRPK down-regulation and interference with HNRPK translation-but not transcription-regulatory activity impairs cytokine-independent proliferation, clonogenic potential, and in vivo leukemogenic activity of BCR/ABL-expressing myeloid 32Dcl3 and/or primary CD34+ CML-BC patient cells.
  • Mechanistically, we demonstrate that decreased internal ribosome entry site (IRES)-dependent Myc mRNA translation accounts for the phenotypic changes induced by inhibition of the BCR/ABL-ERK-dependent HNRPK translation-regulatory function.
  • Accordingly, MYC protein but not mRNA levels are increased in the CD34+ fraction of patients with CML in accelerated and blastic phase but not in chronic phase CML patients and in the CD34+ fraction of marrow cells from healthy donors.
  • Thus, BCR/ABL-dependent enhancement of HNRPK translation-regulation is important for BCR/ABL leukemogenesis and, perhaps, it might contribute to blast crisis transformation.

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  • [Cites] Exp Hematol. 1993 Oct;21(11):1460-6 [8405226.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2255-66 [11884611.001]
  • [Cites] Med Oncol Tumor Pharmacother. 1992;9(3):139-47 [1341325.001]
  • [Cites] Nature. 1994 Apr 28;368(6474):867-71 [7512694.001]
  • [Cites] Mol Cell Biol. 1995 Mar;15(3):1324-32 [7862126.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2275-8 [7757976.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2371-8 [7662984.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5531-41 [7565705.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2350-60 [8628302.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3420-7 [8631943.001]
  • [Cites] Leukemia. 1996 May;10(5):751-6 [8656667.001]
  • [Cites] Leuk Res. 1996 Jan;20(1):85-91 [8632682.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1005-12 [8704208.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13137-42 [8917557.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3587-98 [9218800.001]
  • [Cites] J Exp Med. 2001 Aug 6;194(3):275-84 [11489947.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23):6793-804 [11726515.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8249-57 [11781839.001]
  • [Cites] Oncogene. 1997 Nov 6;15(19):2333-42 [9393877.001]
  • [Cites] Blood. 1998 Jan 15;91(2):406-18 [9427693.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4442-55 [9687511.001]
  • [Cites] Oncogene. 1998 Sep 24;17(12):1597-606 [9794237.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6553-8 [10037749.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15101-9 [10329716.001]
  • [Cites] Proteomics. 2005 Feb;5(3):796-804 [15682461.001]
  • [Cites] Cell Death Differ. 2005 Jun;12(6):534-40 [15846378.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6432-40 [16007188.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):355-68 [16286244.001]
  • [Cites] Ann Hematol. 2000 Aug;79(8):424-31 [10985361.001]
  • [Cites] Nat Cell Biol. 2001 Mar;3(3):325-30 [11231586.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9699-704 [11121407.001]
  • [Cites] RNA. 2002 Mar;8(3):265-78 [12003487.001]
  • [Cites] Mol Cell Biol. 2002 Jul;22(13):4535-43 [12052863.001]
  • [Cites] Methods. 2002 Feb;26(2):191-8 [12054896.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7137-46 [12370803.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):346-58 [12800146.001]
  • [Cites] Oncogene. 2003 Sep 11;22(39):8012-20 [12970749.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5716-22 [14522890.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;279:169-97 [14560958.001]
  • [Cites] Oncogene. 2004 Mar 4;23(9):1693-703 [14647428.001]
  • [Cites] Annu Rev Immunol. 2004;22:247-306 [15032571.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3167-74 [15070699.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Cancer Treat Res. 2004;119:239-70 [15164881.001]
  • [Cites] Bioessays. 2004 Jun;26(6):629-38 [15170860.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1314-23 [15142884.001]
  • [Cites] Cancer Genet Cytogenet. 1987 Aug;27(2):349-56 [3474057.001]
  • [Cites] Leuk Res. 1988;12(6):507-16 [3165487.001]
  • [Cites] Cancer. 1988 Sep 15;62(6):1171-8 [3044574.001]
  • [Cites] Cell. 1992 Sep 18;70(6):901-10 [1525828.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:45-6 [8251915.001]
  • (PMID = 16293596.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Ribonucleoproteins; 146410-60-8 / HNRNPK protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1895740
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39. Mondal BC, Majumdar S, Dasgupta UB, Chaudhuri U, Chakrabarti P, Bhattacharyya S: e19a2 BCR-ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases. J Clin Pathol; 2006 Oct;59(10):1102-3
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  • [Title] e19a2 BCR-ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases.
  • This report describes two patients with chronic myeloid leukaemia (CML): one of them developed accelerated phase CML and died 8 years after diagnosis and the other is at the chronic phase.
  • Sequence analysis of reverse transcription-polymerase chain reaction products showed the presence of BCR-ABL fusion transcript e19a2.
  • This finding suggests that CML carrying mu-BCR breakpoint may exhibit a clinical course similar to typical CML.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Disease Progression. Fatal Outcome. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic

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  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Blood. 2000 May 1;95(9):2913-21 [10779439.001]
  • [Cites] Haematologica. 2001 Mar;86(3):320-1 [11255282.001]
  • [Cites] Haematologica. 2002 Aug;87(8):ELT35 [12161380.001]
  • [Cites] Br J Haematol. 1998 Dec;103(4):1104-8 [9886327.001]
  • [Cites] Blood. 1990 Nov 1;76(9):1819-24 [2224129.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2410-4 [8839830.001]
  • [Cites] Blood. 1997 Jun 1;89(11):4239-41 [9166872.001]
  • [Cites] Blood. 2003 Jul 1;102(1):320-3 [12623846.001]
  • (PMID = 17021137.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC1861751
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40. Zang C, Liu H, Waechter M, Eucker J, Bertz J, Possinger K, Koeffler HP, Elstner E: Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines. Cell Cycle; 2006 Oct;5(19):2237-43
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  • [Title] Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines.
  • Despite progress in the treatment of early-stage chronic myeloid leukemia (CML), the accelerated and blastic phases of CML still remain a therapeutic challenge.
  • Persistence of BCR-ABL-positive (bcr-abl(+)) cells or secondary resistance during imatinib therapy frequently occurs.
  • In this study, we investigated the activity of a novel dual ligand specific for peroxisome proliferator-activated receptor alpha and gamma (PPARalpha/gamma) against CML blast crisis cell lines.
  • Exposure of these cell lines (K562, KU812 and KCL22) to TZD18 resulted in a growth inhibition in a dose- and time-dependent manner.
  • Overall, our findings strongly suggest that either TZD18, either alone or in combination with imatinib may be beneficial for the treatment of CML in myeloid blast crisis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Phenyl Ethers / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology. Thiazolidinediones / pharmacology

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  • (PMID = 17102607.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione; 0 / Benzamides; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Phenyl Ethers; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazolidinediones; 8A1O1M485B / Imatinib Mesylate
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41. D'Antonio J: Chronic myelogenous leukemia. Clin J Oncol Nurs; 2005 Oct;9(5):535-8
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  • [Title] Chronic myelogenous leukemia.
  • Chronic myelogenous leukemia (CML) represents about 14% of all leukemias and occurs with a frequency of about 1 in 100,000.
  • CML has three phases: the chronic phase, accelerated phase, and blast phase.
  • Most patients are diagnosed during the chronic phase.
  • Ionizing radiation has been implicated in some cases of CML, but in most individuals no cause is known.
  • The Philadelphia chromosome, an acquired genetic mutation represented by a translocation of chromosome 22 and chromosome 9, drives the leukemic changes in CML.
  • Imatinib mesylate, a tyrosine kinase inhibitor, was approved in 2002 for the treatment of all phases of CML.
  • Because of its effectiveness, imatinib has become the treatment of choice for most patients with CML.
  • It is the only curative treatment for CML.
  • Oncology nurses who are knowledgeable about new therapies for CML can be effective resources for their patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive
  • [MeSH-minor] Age Distribution. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Dasatinib. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Incidence. Leukocyte Count. Mutation / genetics. Nurse's Role. Oncology Nursing. Philadelphia Chromosome. Piperazines / therapeutic use. Polymerase Chain Reaction. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Risk Factors. Stem Cell Transplantation. Thiazoles / therapeutic use. Translocation, Genetic / genetics

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  • [ErratumIn] Clin J Oncol Nurs. 2005 Dec;9(6):672
  • (PMID = 16235580.001).
  • [ISSN] 1092-1095
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 19
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42. Hazarika M, Jiang X, Liu Q, Lee SL, Ramchandani R, Garnett C, Orr MS, Sridhara R, Booth B, Leighton JK, Timmer W, Harapanhalli R, Dagher R, Justice R, Pazdur R: Tasigna for chronic and accelerated phase Philadelphia chromosome--positive chronic myelogenous leukemia resistant to or intolerant of imatinib. Clin Cancer Res; 2008 Sep 1;14(17):5325-31
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  • [Title] Tasigna for chronic and accelerated phase Philadelphia chromosome--positive chronic myelogenous leukemia resistant to or intolerant of imatinib.
  • PURPOSE: This Food and Drug Administration (FDA) approval report describes the data and analyses leading to the approval by the FDA of nilotinib (Tasigna, AMN-107; Novartis Pharmaceuticals Corporation), an inhibitor of Bcr-Abl tyrosine kinase, for the treatment of chronic-phase (CP) and accelerated-phase (AP) chronic myelogenous leukemia (CML) resistant to or intolerant of imatinib.
  • EXPERIMENTAL DESIGN: The FDA approval of the efficacy and safety of nilotinib was based on the results of an ongoing single-arm, open-label, phase 2 clinical trial.
  • The primary end point for CML-CP was unconfirmed major cytogenetic response.
  • The efficacy end point for CML-AP was confirmed hematologic response.
  • The median duration of response has not been reached for both CML-CP and CML-AP responding patients.
  • In CML-CP patients, the common serious drug-related adverse reactions were thrombocytopenia and neutropenia.
  • In CML-AP patients, the common serious drug-related adverse reactions were thrombocytopenia, neutropenia, pneumonia, febrile neutropenia, leukopenia, intracranial hemorrhage, elevated lipase, and pyrexia.
  • Nilotinib prolongs the QT interval and sudden deaths have been reported; these risks and appropriate risk minimization strategies are described in a boxed warning on the labeling.
  • FDA granted accelerated approval to nilotinib (Tasigna) for use in the treatment of CP and AP Philadelphia chromosome positive CML in adult patients resistant to or intolerant of prior therapy that included imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Benzamides. Clinical Trials, Phase II as Topic. Drug Approval. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration

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  • (PMID = 18765523.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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43. Na IK, Kreuzer KA, Lupberger J, Dörken B, le Coutre P: Quantitative RT-PCR of Wilms tumor gene transcripts (WT1) for the molecular monitoring of patients with accelerated phase bcr/abl + CML. Leuk Res; 2005 Mar;29(3):343-5
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  • [Title] Quantitative RT-PCR of Wilms tumor gene transcripts (WT1) for the molecular monitoring of patients with accelerated phase bcr/abl + CML.
  • The tyrosine kinase inhibitor imatinib inhibits the activity of the bcr/abl fusion protein present in patients with chronic myeloid leukemia.
  • Although in chronic phase patients response to therapy can be monitored by quantitative RT-PCR for bcr/abl mRNA transcripts, in advanced disease (accelerated phase or blast crisis) only few patients respond on a molecular level.
  • We investigated Wilms tumor gene (WT1) and bcr/abl mRNA transcripts in 16 accelerated phase CML patients by quantitative real time PCR.
  • In contrast to the bcr/abl mRNA levels the WT1 mRNA levels were indicative for hematologic relapse (n = 6) versus response (n = 10).
  • [MeSH-major] Biomarkers, Tumor / analysis. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. WT1 Proteins / genetics

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  • (PMID = 15661271.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / WT1 Proteins; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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44. Jiang Q, Chen SS, Jiang B, Jiang H, Qiu JY, Liu YR, Zhang Y, Qin YQ, Lu Y, Huang XJ, Lu DP: [The efficacy of imatinib mesylate for 124 patients with chronic myeloid leukemia in accelerated and blastic phase]. Zhonghua Xue Ye Xue Za Zhi; 2007 Nov;28(11):721-6
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  • [Title] [The efficacy of imatinib mesylate for 124 patients with chronic myeloid leukemia in accelerated and blastic phase].
  • OBJECTIVES: To evaluate the efficacy and safety of imatinib mesylate (imatinib) for patients with Philadelphia chromosome-positive (Ph+ ) chronic myeloid leukemia (CML) in accelerated and blastic phase.
  • METHODS: Seventy-five Ph+ CML patients in accelerated phase and 49 in blastic phase were treated with 400 mg or 600 mg of imatinib once daily.
  • RESULTS: For patients in accelerated phase, the cumulative hematological response (HR) rate was 93.3%, including complete HR (CHR) rate 85.3%, and returning to chronic phase (RCP) rate 8% in a median follow-up of 23.0 (1.0 -64.0 ) months.
  • For patients in blastic phase, the cumulative HR rate was 63.3%, including CHR rate 44.9%, and RCP rate 18.4% in a median follow-up of 4.5 (0.3 -63.0) months.
  • CONCLUSIONS: The efficiency of imatinib was decreasing, and severer hematological toxicities increasing with the disease progressing in patients with Ph+ CML.
  • Imatinib improves progression-free survival significantly in most patients in accelerated phase, particularly in those with continuous CCyR or MMoR.
  • The response duration in majority of blastic phase patients is short, and the relapse rate is high.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 18457260.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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45. Talpaz M, Shah NP, Kantarjian H, Donato N, Nicoll J, Paquette R, Cortes J, O'Brien S, Nicaise C, Bleickardt E, Blackwood-Chirchir MA, Iyer V, Chen TT, Huang F, Decillis AP, Sawyers CL: Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med; 2006 Jun 15;354(24):2531-41
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  • [Title] Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias.
  • BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.
  • We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL).
  • METHODS: Patients with various phases of CML or with Ph-positive ALL who could not tolerate or were resistant to imatinib were enrolled in a phase 1 dose-escalation study.
  • RESULTS: A complete hematologic response was achieved in 37 of 40 patients with chronic-phase CML, and major hematologic responses were seen in 31 of 44 patients with accelerated-phase CML, CML with blast crisis, or Ph-positive ALL.
  • Responses were maintained in 95 percent of patients with chronic-phase disease and in 82 percent of patients with accelerated-phase disease, with a median follow-up more than 12 months and 5 months, respectively.
  • Nearly all patients with lymphoid blast crisis and Ph-positive ALL had a relapse within six months.
  • Responses occurred among all BCR-ABL genotypes, with the exception of the T315I mutation, which confers resistance to both dasatinib and imatinib in vitro.
  • CONCLUSIONS: Dasatinib induces hematologic and cytogenetic responses in patients with CML or Ph-positive ALL who cannot tolerate or are resistant to imatinib. (ClinicalTrials.gov number, NCT00064233 [ClinicalTrials.gov].).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062; author reply 1063-4 [16957155.001]
  • [CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062-3; author reply 1063-4 [16960978.001]
  • (PMID = 16775234.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00064233
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR-00865
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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46. Vardiman JW: Chronic myelogenous leukemia, BCR-ABL1+. Am J Clin Pathol; 2009 Aug;132(2):250-60
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  • [Title] Chronic myelogenous leukemia, BCR-ABL1+.
  • Session 1 of the 2007 Workshop of the Society for Hematopathology/European Association for Haematopathology focused on chronic myelogenous leukemia, BCR-ABL1+ (CML).
  • CML is a myeloproliferative neoplasm arising at the level of a pluripotent stem cell and consistently associated with the BCR-ABL1 fusion gene.
  • CML most commonly manifests in a chronic phase of the disease with neutrophilic leukocytosis, and the demonstration of the Philadelphia chromosome is the ultimate confirmation of the diagnosis.
  • However, in select cases, the initial diagnosis remains challenging, and a number of issues pertaining to the manifestations and disease evolution remain unresolved.
  • These issues have been illustrated by the cases submitted to our workshop and include unusual manifestations of CML, including manifestation in the accelerated and/or blast phase, and patterns of disease progression and therapy resistance in the era of protein tyrosine kinase inhibitor therapy.
  • [MeSH-major] Fusion Proteins, bcr-abl. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 19605820.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 59
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47. Plosker GL, Robinson DM: Nilotinib. Drugs; 2008;68(4):449-59; discussion 460-1
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  • Nilotinib is an orally administered BCR-ABL tyrosine kinase inhibitor that has shown good clinical efficacy in imatinib-resistant or -intolerant, Philadelphia chromosome-positive, chronic myeloid leukaemia (CML) in a phase I/II trial.
  • The phase I component of the trial established the dosage regimen used in the phase II part of the trial, which included several arms.
  • Three of these arms, or phase II trials, evaluated nilotinib in each of the three phases of CML (chronic, accelerated or blast crisis).I n the phase II trial in patients with chronic-phase CML, major cytogenetic response (primary endpoint) was achieved in 48% of the 280 patients who received nilotinib and had a follow-up period of > or = 6 months.
  • Major cytogenetic response rates did not differ between imatinib-resistant and -intolerant patients, and nilotinib was effective in patients with BCR-ABL mutations (except T315I).
  • Haematologic response rate (primary endpoint) was 47% in the phase II trial with nilotinib in patients with accelerated-phase CML (n = 119).
  • Complete haematologic response was achieved in 26% of patients and 21% had no evidence of leukaemia or returned to chronic-phase CML.
  • Data from the phase II trial in patients with CML in blast crisis (n = 135) also showed promising results, with 39% of patients achieving haematologic response with nilotinib.
  • [MeSH-minor] Animals. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 18318563.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines
  • [Number-of-references] 36
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48. Cojbasić I, Macukanović-Golubović L: Hematopathologic and cytogenetic findings in imatinib mesylate treated chronic myelogenous leukemia patients: 2.5 years' experience. Vojnosanit Pregl; 2010 Oct;67(10):802-6
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  • [Title] Hematopathologic and cytogenetic findings in imatinib mesylate treated chronic myelogenous leukemia patients: 2.5 years' experience.
  • BACKGROUND/AIM: Imatinib mesylate, a tyrosine kinase inhibitor with specific activity against the breakpoint cluster region--Abelson murine leukemia (BCR-ABL) tyrosine kinase has been developed for treatment of chronic myelogenous leukemia (CML).
  • Its hematologic and cytogenetic effects have been evaluated in a series of clinical trials.
  • The aim of this study was to report hematologic and cytogenetic response in CML patients during the treatment with imatinib mesylate.
  • The median time from CML diagnosis was no more than 12 months, so all the patients received previous treatment with hydroxyurea for which the median time was 3 months.
  • No patients had progressed to accelerated or blastic phase.
  • CONCLUSION: The results obtained in this study confirm that imatinib mesylate induces a complete hematological and cytogenetic response in a high percentage of patients with chronic-phase CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 21061842.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Serbia
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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49. Zhou L, Meng F, Yin O, Wang J, Wang Y, Wei Y, Hu P, Shen Z: Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients. Clin Ther; 2009 Jul;31(7):1568-75
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  • [Title] Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
  • BACKGROUND: Nilotinib, an oral second-generation Bcr-Abi tyrosine kinase inhibitor, is approved in the United States and European Union for the treatment of Philadelphia chromosome-positive (Ph+), chronic-phase (CP) or accelerated-phase (AP) chronic myeloid leukemia (CML) resistant to or intolerant of prior therapy, including imatinib.
  • Information on the pharmacokinetics of nilotinib in Chinese patients with CML is lacking, and regulatory requirements for registration of this drug are needed in China.
  • OBJECTIVES: This study assessed the pharmacokinet-ics of single and multiple oral doses of nilotinib in Chinese patients with CML and compared the pharmacokinetic profiles of nilotinib between the Chinese patients and a subgroup of white patients with CML.
  • METHODS: Chinese patients aged > or =18 years with Ph+ CML-CP, CML-AP, or CML-BC (blast crisis) resistant to or intolerant of imatinib were eligible.
  • RESULTS: Twenty-three patients were enrolled (18 men, 5 women; mean age, 40.0 years; mean weight, 68.3 kg; CML-CP, 22 patients; CML-AP, 1).
  • Steady-state C(max), C(min), AUC(0-tau), and CL/F were not significantly different from those previously reported in a subgroup of white patients with CML who received the same 400-mg BID dose.
  • CONCLUSIONS: In this pharmacokinetic study in Chinese patients with CML resistant to or intolerant of imatinib, nilotinib 400 mg BID was rapidly absorbed after a single dose and multiple doses.
  • The steady-state pharmacokinetic properties in this population were consistent with those reported previously in white patients with CML.
  • [MeSH-minor] Administration, Oral. Adult. Aged. Area Under Curve. Asian Continental Ancestry Group. Benzamides. Blast Crisis / drug therapy. China. Chromatography, Liquid. Drug Administration Schedule. Drug Resistance, Neoplasm. European Continental Ancestry Group. Female. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / drug therapy. Male. Middle Aged. Piperazines / administration & dosage. Tandem Mass Spectrometry. Young Adult


50. Issa JP, Gharibyan V, Cortes J, Jelinek J, Morris G, Verstovsek S, Talpaz M, Garcia-Manero G, Kantarjian HM: Phase II study of low-dose decitabine in patients with chronic myelogenous leukemia resistant to imatinib mesylate. J Clin Oncol; 2005 Jun 10;23(17):3948-56
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  • [Title] Phase II study of low-dose decitabine in patients with chronic myelogenous leukemia resistant to imatinib mesylate.
  • PURPOSE: To determine the activity of decitabine, a DNA methylation inhibitor, in imatinib-refractory or intolerant chronic myelogenous leukemia.
  • MATERIALS AND METHODS: Thirty-five patients were enrolled in this phase II study (12 in chronic phase, 17 in accelerated phase, and six in blastic phase).
  • RESULTS: Complete hematologic responses were seen in 12 patients (34%) and partial hematologic responses in seven patients (20%), for an overall hematologic response rate of 54% (83% in chronic phase, 41% in accelerated phase, and 34% in blastic phase).
  • CONCLUSION: Decitabine induces hypomethylation and has clinical activity in imatinib refractory chronic myelogenous leukemia.
  • [MeSH-major] Azacitidine / administration & dosage. Azacitidine / analogs & derivatives. Drug Resistance, Neoplasm. Enzyme Inhibitors / administration & dosage. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15883410.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 776B62CQ27 / decitabine; 8A1O1M485B / Imatinib Mesylate; EC 2.1.1.- / DNA Modification Methylases; EC 2.7.10.1 / Protein-Tyrosine Kinases; M801H13NRU / Azacitidine
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51. Li ZJ, Qiu LG, Li X, Mai YJ, Wang GR, Yu Z, Wang YF, Li CH, Li Q: [Expression of beta-Catenin Gene in CML and its relationship with bcr/abl]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):931-5
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  • [Title] [Expression of beta-Catenin Gene in CML and its relationship with bcr/abl].
  • This study was aimed to quantitatively detect the expression level of beta-catenin and bcr/abl in different phases of chronic myeloid leukemia (CML) and to analyze their potential relationship and significance in the progression of CML.
  • First, the total RNA isolated from BMMNC of patients with CML and donors was reversely transcribed into cDNA.
  • The real-time quantitative PCR method was used to analyze the expression level of beta-catenin and bcr/abl.
  • The expression level of beta-catenin and bcr/abl in different phases of CML was compared and the correlation was analyzed between the two genes.
  • The results showed that the beta-catenin gene in BMMNC of blast crisis of CML patients was expressed significantly higher than that in chronic phase (p < 0.001) and accelerated phase (p = 0.016) of CML patients and in normal donors (p = 0.004).
  • The expression of bcr/abl in blast crisis of CML was statistically higher than that in chronic phase of CML (p = 0.001).
  • The expression levels of beta-catenin and bcr/abl were correlated with each other in CML patients (r = 0.620, p < 0.001).
  • It is concluded that the beta-catenin gene in blast crisis of CML patients express higher than that in chronic phase and accelerated phase of CML, and its expression level is correlated with the level of bcr/abl expression.
  • The increased expression of beta-catenin may be account partly for the blast crisis of CML.

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  • (PMID = 17956664.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / beta Catenin; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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52. Martin MG, Dipersio JF, Uy GL: Management of the advanced phases of chronic myelogenous leukemia in the era of tyrosine kinase inhibitors. Leuk Lymphoma; 2009 Jan;50(1):14-23
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  • [Title] Management of the advanced phases of chronic myelogenous leukemia in the era of tyrosine kinase inhibitors.
  • Imatinib has revolutionised the management of chronic phase chronic myelogenous leukemia (CML).
  • Unfortunately it has had less of an impact on the management of the advanced phases of CML.
  • These historically difficult-to-treat phases of disease remain largely resistant to therapy.
  • Even when responses are obtained with the tyrosine kinase inhibitors, they are brief, particularly in blast phase (BP) disease.
  • But transplant outcomes are dependent on cytogenetic and gross disease burden at the time of transplant.
  • This review will compare and contrast the various tyrosine kinase- and non-tyrosine kinase inhibitor-based treatments for accelerated and BP CML before allogeneic transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 19117213.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 80
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53. Brazma D, Grace C, Howard J, Melo JV, Holyoke T, Apperley JF, Nacheva EP: Genomic profile of chronic myelogenous leukemia: Imbalances associated with disease progression. Genes Chromosomes Cancer; 2007 Nov;46(11):1039-50
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  • [Title] Genomic profile of chronic myelogenous leukemia: Imbalances associated with disease progression.
  • The expression of the chimeric BCR/ABL1 fusion gene resulting from t(9;22)(q34;q11) in chronic myelogenous leukemia (CML) is necessary for malignant transformation, but not sufficient to maintain disease progression.
  • The appearance of various chromosomal and molecular alterations in the accelerated and terminal phase of CML is well documented, but evidence for causal relationship is largely lacking.
  • We carried out a genome wide screening at a resolution of 1 Mb of 54 samples at different stages of CML together with 12 CML cell lines and found that disease progression is accompanied by a spectrum of recurrent genome imbalances.
  • These genome imbalances are unique to CML cases with clinically manifested or suspected accelerated/blast stage alike, but not seen in chronic phase samples.
  • Previously unrecognized cryptic imbalances occurring within the Ph-chromosome were also detected, although further scrutiny is required to pin-point gene involvement and seek association with disease features.
  • Importantly, some of these imbalances were seen in the CD34(+) cells but not in the whole BM samples of patients in accelerated phase.
  • Taken together, these findings highlight the potential of screening CD34(+) cells for genome wide imbalances associated with disease progression.
  • Finally, the numerous single copy number variations recorded, many unique to this cohort of patients, raise the possible association of genome polymorphism and CML.
  • [MeSH-major] Genome. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Chromosome Mapping. Chromosomes, Artificial, Bacterial. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • [Copyright] Copyright (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17696194.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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54. Agis H, Krauth MT, Böhm A, Mosberger I, Müllauer L, Simonitsch-Klupp I, Walls AF, Horny HP, Valent P: Identification of basogranulin (BB1) as a novel immunohistochemical marker of basophils in normal bone marrow and patients with myeloproliferative disorders. Am J Clin Pathol; 2006 Feb;125(2):273-81
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  • In chronic myeloid leukemia (CML), basophilia is a diagnostic and prognostic variable.
  • We applied the antibasogranulin antibody BB1 on paraffin-embedded BM sections in 21 control samples (normal BM), 45 patients with CML, 9 with chronic idiopathic myelofibrosis, 11 with polycythemia vera, 19 with essential thrombocythemia, and 7 with indolent systemic mastocytosis.
  • BB1+ BM cells were found to be highly elevated in patients with CML compared with normal BM or other MPDs, with maximum counts found in accelerated phase CML (median, 160 cells/mm(2)).
  • In summary, BB1 (basogranulin) is a new immunohistochemical basophil marker that should allow quantification of basophils in CML at diagnosis and during therapy.
  • [MeSH-major] Basophils / chemistry. Bone Marrow / chemistry. DNA-Binding Proteins / analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Phosphoproteins / analysis. Transcription Factors / analysis

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  • (PMID = 16393678.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500729
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human
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55. Copelan EA, Crilley PA, Szer J, Dodds AJ, Stevenson D, Phillips G, Elder P, Nivison-Smith I, Avalos BR, Penza S, Topolsky D, Sobecks R, Kalaycio M, Bolwell BJ: Late mortality and relapse following BuCy2 and HLA-identical sibling marrow transplantation for chronic myelogenous leukemia. Biol Blood Marrow Transplant; 2009 Jul;15(7):851-5
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  • [Title] Late mortality and relapse following BuCy2 and HLA-identical sibling marrow transplantation for chronic myelogenous leukemia.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is the only known curative therapy for chronic myelogenous leukemia (CML).
  • We present mature results in 335 patients with CML who underwent allogeneic bone marrow transplantation (BMT) from HLA-identical siblings following busulfan and cyclophosphamide (BU/Cy2).
  • Two hundred twenty-nine were in chronic phase (CP) and 106 in accelerated or blastic phase at transplantation.
  • The estimated probability of 18-year leukemia-free survival (LFS) for CP patients was 55.6% and for those beyond CP, 10.5%.
  • Of 182 patients who survived leukemia-free at 3 years, the estimated probability of LFS at 18 years was 61.9%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Siblings
  • [MeSH-minor] Adolescent. Adult. Age Factors. Busulfan / administration & dosage. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Histocompatibility Testing. Humans. Male. Middle Aged. Recurrence. Survival Rate. Transplantation, Homologous

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  • (PMID = 19539217.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan; BUCY-2 protocol
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56. Poiré X, Artz A, Larson RA, Kline J, Odenike O, Rich E, Godley L, Stock W, van Besien K: Allogeneic stem cell transplantation with alemtuzumab-based conditioning for patients with advanced chronic myelogenous leukemia. Leuk Lymphoma; 2009 Jan;50(1):85-91
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  • [Title] Allogeneic stem cell transplantation with alemtuzumab-based conditioning for patients with advanced chronic myelogenous leukemia.
  • Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the treatment of choice for patients with chronic myelogenous leukemia (CML) who have failed or are intolerant to tyrosine kinase inhibitors (TKI).
  • Myeloablative conditioning regimens have been associated with high treatment-related mortality (TRM) rate in such patients, and reduced-intensity conditioning (RIC) regimens are often preferred but have high rates of disease recurrence and graft-versus-host-disease (GVHD).
  • We report our experience with nine CML patients (four chronic phase and five with accelerated phase or blast crisis) who failed TKI and underwent allo-HSCT using an alemtuzumab-based RIC regimen.
  • Four patients, all with a history of accelerated phase or blast crisis, died.
  • With a median follow-up of 47 months, five patients, including all those transplanted in first or second chronic phase, are alive and in remission.
  • Allo-HSCT with an alemtuzumab-based conditioning regimen induces remission in patients with CML that have failed TKI therapy and has a low incidence of GVHD.
  • Disease recurrence is frequent but responds to DLI.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / immunology. Antibodies, Neoplasm / therapeutic use. Immunotherapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Transplantation Conditioning
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Combined Modality Therapy. Female. Graft vs Host Disease / immunology. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate. Transplantation, Homologous

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  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5728-38 [16009946.001]
  • [Cites] Blood. 2005 Nov 1;106(9):2969-76 [15998838.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9387-93 [16314618.001]
  • [Cites] Br J Haematol. 2006 Jan;132(1):3-12 [16371014.001]
  • [Cites] Bone Marrow Transplant. 2005 Dec;36(11):1017-8 [16184176.001]
  • [Cites] Bone Marrow Transplant. 2005 Dec;36(11):1009-15 [16205732.001]
  • [Cites] Bone Marrow Transplant. 2006 Feb;37(3):307-10 [16400339.001]
  • [Cites] Haematologica. 2006 May;91(5):663-6 [16627251.001]
  • [Cites] Transplantation. 2006 May 27;81(10):1361-7 [16732169.001]
  • [Cites] Blood. 2006 Jul 1;108(1):28-37 [16522812.001]
  • [Cites] Haematologica. 2006 Nov;91(11):1559-62 [17082014.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1782-9 [17062727.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4686-92 [17317858.001]
  • [Cites] Bone Marrow Transplant. 2007 Sep;40(5):423-30 [17603516.001]
  • [Cites] Br J Haematol. 2007 Oct;139(1):70-80 [17854309.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2828-37 [17626839.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3456-62 [17652620.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4614-7 [17881635.001]
  • [Cites] Leuk Lymphoma. 2007 Dec;48(12):2310-22 [18067005.001]
  • [Cites] Br J Haematol. 2008 Jul;142(3):361-78 [18540942.001]
  • [Cites] Leuk Lymphoma. 2010 Dec;51(12):2240-9 [20919852.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2255-8 [11877308.001]
  • [Cites] Br J Haematol. 2003 Apr;121(1):109-18 [12670340.001]
  • [Cites] Bone Marrow Transplant. 2003 May;31(9):813-6 [12732890.001]
  • [Cites] Blood. 2003 Aug 1;102(3):802-9 [12714524.001]
  • [Cites] Leukemia. 2003 Sep;17(9):1707-12 [12970768.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):685-702, x [15271400.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5065-71 [15297408.001]
  • [Cites] Bone Marrow Transplant. 2004 Nov;34(9):787-94 [15361909.001]
  • [Cites] J Clin Oncol. 1998 Apr;16(4):1498-504 [9552058.001]
  • [Cites] Bone Marrow Transplant. 1998 Apr;21(7):679-86 [9578307.001]
  • [Cites] Bone Marrow Transplant. 1999 May;23(10):1055-60 [10373073.001]
  • [Cites] Bone Marrow Transplant. 1999 Aug;24(3):283-7 [10455367.001]
  • [Cites] Blood. 2004 Dec 15;104(13):3865-71 [15304395.001]
  • [Cites] Eur J Haematol. 2005 Feb;74(2):144-51 [15654906.001]
  • (PMID = 19142796.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24 CA116471; United States / NCI NIH HHS / CA / K24 CA116471
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
  • [Other-IDs] NLM/ NIHMS452872; NLM/ PMC3617055
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57. Kantarjian H, O'Brien S, Talpaz M, Borthakur G, Ravandi F, Faderl S, Verstovsek S, Rios MB, Shan J, Giles F, Cortes J: Outcome of patients with Philadelphia chromosome-positive chronic myelogenous leukemia post-imatinib mesylate failure. Cancer; 2007 Apr 15;109(8):1556-60
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  • [Title] Outcome of patients with Philadelphia chromosome-positive chronic myelogenous leukemia post-imatinib mesylate failure.
  • BACKGROUND: The prognosis of patients with chronic myelogenous leukemia (CML) after failure of imatinib mesylate therapy is not well documented.
  • METHODS: The outcome of 420 patients with CML post-imatinib failure (resistance-recurrence in 374; toxicities in 46) were reviewed in relation to survival, overall, and by different therapies.
  • RESULTS: The estimated 3-year survival rates were 72% in 88 patients who progressed in chronic phase, 30% in 130 patients who progressed in accelerated phase, 7% in 156 patients who progressed in blastic phase, and 75% in 37 patients in chronic phase with imatinib intolerance.
  • Survival in chronic phase was better when subsequent therapy was nilotinib or dasatinib vs allogeneic stem cell transplant vs others (estimated 2-year survival rates 100% vs 72% vs 67%; P = .01), but not in accelerated-blastic phase.
  • CONCLUSIONS: Prognosis post-imatinib failure in chronic phase is reasonable; it is poor if the CML phase post-imatinib failure is accelerated or blastic.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17342766.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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58. Giles FJ, DeAngelo DJ, Baccarani M, Deininger M, Guilhot F, Hughes T, Mauro M, Radich J, Ottmann O, Cortes J: Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia. Semin Oncol; 2008 Feb;35(1 Suppl 1):S1-17; quiz S18-20
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  • [Title] Optimizing outcomes for patients with advanced disease in chronic myelogenous leukemia.
  • The treatment of chronic myelogenous leukemia (CML) has been revolutionized by the development of the small-molecule tyrosine kinase inhibitor imatinib.
  • The primary target for this drug is the oncogenic BCR-ABL kinase.
  • Five-year survival rates for patients in chronic phase CML is now greater than 80%.
  • Patients who have advanced beyond the chronic phase to the accelerated phase or blast crisis, however, have not faired as well.
  • Progression occurs for a variety of reasons, including late diagnosis, slow response to imatinib, and the development of imatinib-resistant clones.
  • Imatinib resistance has, in part, been addressed with the introduction of the new BCR-ABL inhibitors, namely dasatinib and nilotinib.
  • These drugs have shown efficacy in CML patients with wild-type BCR-ABL and some BCR-ABL mutants that are imatinib-resistant.
  • Unfortunately, some BCR-ABL mutations remain resistant to these therapies and will require the development of alternative treatments, and other mechanisms of imatinib resistance besides BCR-ABL mutation exist.
  • More aggressive therapies are being considered for high-risk patients, including increased dosage of the current tyrosine kinase inhibitors, along with combination therapies.
  • Aggressive therapy holds promise, as the data suggest that responses are improved.
  • This is especially important for young CML patients, who hopefully will remain in remission for decades.
  • Polymerase chain reaction analysis has become of primary importance as a means of assessing disease burden, and given the idiosyncrasies of this technique, standards must be established to allow results to be compared across different institutions.
  • Additionally, the nature of advanced disease is being explored.
  • Increased activity of these pathways correlates with poor response and eventual disease progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 18346528.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-jun; 0 / Wnt Proteins; 0 / beta Catenin
  • [Number-of-references] 131
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59. Quintás-Cardama A, Kantarjian H, O'brien S, Borthakur G, Bruzzi J, Munden R, Cortes J: Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure. J Clin Oncol; 2007 Sep 1;25(25):3908-14
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  • [Title] Pleural effusion in patients with chronic myelogenous leukemia treated with dasatinib after imatinib failure.
  • PURPOSE: We investigated the risk factors and management of pleural effusion associated with dasatinib therapy for chronic myelogenous leukemia (CML) after failure of imatinib.
  • PATIENTS AND METHODS: We analyzed 138 patients with CML treated with dasatinib from November 2003 to January 2006 in one phase I (n = 50) and four phase II (n = 88) studies for the development of pleural effusion.
  • RESULTS: Pleural effusion occurred in 48 patients (35%; grade 3/4 in 23 [17%]), including 29% of those treated in chronic phase (CP), 50% in accelerated phase (AP), and 33% in blast phase (BP).
  • By multivariate analysis, history of cardiac disease, hypertension, and use of a twice-daily schedule (v once daily) were identified as factors associated with development of pleural effusions.
  • A twice-daily schedule may result in a higher incidence of pleural effusion.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pleural Effusion / chemically induced. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Thiazoles / adverse effects. Thiazoles / therapeutic use

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  • (PMID = 17761974.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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60. Rice L, Popat U: Every case of essential thrombocythemia should be tested for the Philadelphia chromosome. Am J Hematol; 2005 Jan;78(1):71-3
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  • Essential thrombocythemia (ET) and chronic myelogenous leukemia (CML) usually present with distinctive features.
  • By 4 years, both developed leukocytosis, extreme basophilia, and circulating blasts, typical of accelerated CML.
  • We conclude that CML can present in identical fashion as ET.
  • The mandate for routine Philadelphia chromosome testing is magnified by the availability of targeted therapy and its greater efficacy in early stage disease.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Philadelphia Chromosome. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / genetics
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Female. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15609281.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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61. Jiang Q, Chen SS, Jiang B, Jiang H, Lu Y, Lu DP: [Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions]. Beijing Da Xue Xue Bao; 2005 Dec 18;37(6):612-5
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  • [Title] [Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions].
  • OBJECTIVE: To report disease transformation in 3 imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia (Ph(+)CML) patients who achieved cytogenetic response.
  • METHODS: Hematologic examinations and bone marrow G-banding karyotyping were evaluated at regular intervals in 3 patients with Ph(+)CML who achieved hematologic responses during continuous imatinib therapy, including 1 patient in first chronic phase (case 1), 1 patient in second chronic phase (case 2) and 1 patient in accelerated phase (case 3).
  • Though under continuously imatinib treatment, they developed acute lymphoblastic leukemia, acute myelogenous leukemia and extramedullary blast crisis in the following 12, 6 and 0 months respectively.
  • CONCLUSION: Acute leukemia or extramedullary blast crisis with Ph(-) cells or dominant Ph(-) cells in bone marrow may occur in the patients with Ph(+)CML after imatinib therapy.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Disease Progression. Female. Humans. Imatinib Mesylate. Karyotyping. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction

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  • (PMID = 16378113.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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62. Hoshino T, Tahara K, Miyawaki K, Hatsumi N, Takada S, Miyawaki S, Sakura T: [Clinical profiles of 7 patients with chronic myelogenous leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia treated with dasatinib]. Rinsho Ketsueki; 2010 Mar;51(3):181-8
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  • [Title] [Clinical profiles of 7 patients with chronic myelogenous leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia treated with dasatinib].
  • We retrospectively analyzed the clinical outcome of dasatinib in 7 patients with chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) resistant or intolerant to imatinib.
  • Three patients with chronic phase CML and two patients with Ph+ALL achieved major molecular response, however, two CML patients in accelerated phase (AP)/blast crisis (BC), did not.
  • Among these, two AP/BC-CML patients required interruption/or dose reduction of dasatinib.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Thiazoles / administration & dosage


63. Qin YZ, Liu YR, Li JL, Ruan GR, Zhu HH, Jiang Q, Fu JY, Lu Y, Chang Y, Li LD, Huang XJ, Chen SS, Qiu JY: [Analysis of ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia patients]. Zhonghua Yi Xue Za Zhi; 2005 Nov 30;85(45):3186-9
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  • [Title] [Analysis of ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia patients].
  • OBJECTIVE: To evaluate ABL tyrosine kinase point mutations in imatinib treated chronic myelogenous leukemia (CML) patients.
  • METHODS: A total of 45 bone marrow samples from 30 CML patients were included in this work.
  • The patients were in accelerated/blast phase (AP/BP) or late-chronic phase (CP) at the start of imatinib and usually showed resistance to imatinib.
  • ABL kinase domain of BCR-ABL allele was amplified by nested reverse transcriptase-polymerase chain reaction technique, followed by direct sequencing and sequence homologous analyzing.
  • RESULTS: The ABL point mutation was detected in 13 of 30 patients, 12 of them had progressed to advanced phase, The other patient who was in late chronic phase showed point mutation when she was at 45th months of imatinib treatment, but she was still in complete cytogenetic remission at 50th months and is doing well.
  • 11/12 patients who progressed to advanced disease and showed point mutation were collected samples in advanced stage, 8 patients showed homozygote mutation, and 3 patients had a mixture of wild and mutant type.
  • In advanced stage patients, mutations were detected in a median of 5 months (ranged 0.5-30 months), it appeared much earlier than that in late CP patients (25.5 months, ranged 11-45 months, P < 0.05).
  • In 4/7 followed up patients, the intensity of point mutation increased gradually within 7-15 months before disease progression.
  • 6 patients did not showed ABL point mutation while their disease were in progression.
  • CONCLUSIONS: Abl kinase point mutation is one of the main mechanisms of CML secondary resistance to imatinib.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Point Mutation. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Base Sequence. Benzamides. DNA Mutational Analysis. Female. Follow-Up Studies. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 16405837.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [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
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64. Wright MP, Shepherd JD, Barnett MJ, Nantel SH, Sutherland HJ, Toze CL, Hogge DE, Nevill TJ, Song KW, Abou Mourad YR, Narayanan S, Power MM, Smith CA, Forrest DL: Response to tyrosine kinase inhibitor therapy in patients with chronic myelogenous leukemia relapsing in chronic and advanced phase following allogeneic hematopoietic stem cell transplantation. Biol Blood Marrow Transplant; 2010 May;16(5):639-46
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  • [Title] Response to tyrosine kinase inhibitor therapy in patients with chronic myelogenous leukemia relapsing in chronic and advanced phase following allogeneic hematopoietic stem cell transplantation.
  • Tyrosine kinase inhibitors (TKI) have been used to treat relapse of chronic myelogenous leukemia (CML) after allogeneic stem cell transplant (HSCT), with responses seen predominantly in chronic phase (CP) patients.
  • This study aimed to analyze the response to TKI therapy and overall survival for patients relapsing predominantly in advanced phase.
  • We retrospectively reviewed 22 patients treated with imatinib (n=20) and/or dasatinib (n=6) for relapsed CML after HSCT; 8 patients were in CP, and 14 patients had advanced disease.
  • In advanced phase patients, 11 (79%) achieved CHR, 10 (71%) CCR, and 8 (57%) achieved CMR.
  • TKI therapy is capable of inducing durable molecular responses for CML relapsing after HSCT, both in chronic and advanced phases.
  • The achievement of CMR appears to be crucial in providing long-term disease control for these patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Myeloid, Accelerated Phase / mortality. Leukemia, Myeloid, Accelerated Phase / therapy. Leukemia, Myeloid, Chronic-Phase / mortality. Leukemia, Myeloid, Chronic-Phase / therapy. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Transplantation, Homologous

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  • [Copyright] Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20005967.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
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65. Xue ZK, Jin J, Chen ZM, Lou JY, Yu YB: [Cytogenetic analysis on 135 cases of chronic myelogenous leukemias with non-simple Philadelphia chromosome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Oct;16(5):997-1001
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  • [Title] [Cytogenetic analysis on 135 cases of chronic myelogenous leukemias with non-simple Philadelphia chromosome].
  • The purpose of this study was to investigate 135 cases of chronic myelogenous leukemia with non-simple Philadelphia chromosome and to analyze their cytogenetic date.
  • The results showed that the overall frequency of chronic myelogenous leukemia with non-simple Philadelphia chromosome (based on 1210 cases of chromosome detection in chronic myelogenous leukemia) was 11.16%, which included 87 cases of chronic phase, 21 cases of accelerated phase and 27 cases of blastic phase.
  • Among 87 cases of patients in chronic phase, 14 cases were with simple variant translocation and 22 cases had complex variant translocation while the others were with other chromosomal abnormalities including 4 cases of +8, 4 cases of + Ph and 2 cases of i (17); among 21 cases of patients in accelerated phage, 4 cases were with +8 and 4 cases were with + Ph while 3 cases were with i (17); among 27 cases of patients in blastic phage, 2 cases were with simple variant translocation and 3 cases had complex variant translocation while the others were with other chromosomal abnormalities including 5 cases of +8, 5 cases of + Ph and 2 cases of i (17).
  • It is concluded that karyotype analysis is helpful in diagnosis, prognosis, pathogenesis and treatment selection for chronic myelogenous leukemia.

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  • (PMID = 18928582.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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66. Tong XZ, Li J, Tan EX, Zhang GC, Wu XY, Peng AH, Zheng D, Zou WY, Hong WD, Luo SK: [Effects and prognostic factors of HLA-matched sibling donor allogeneic hematopoietic stem cell transplantation for chronic myelogenous leukemia]. Zhonghua Zhong Liu Za Zhi; 2006 Jul;28(7):545-8
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  • [Title] [Effects and prognostic factors of HLA-matched sibling donor allogeneic hematopoietic stem cell transplantation for chronic myelogenous leukemia].
  • OBJECTIVE: To retrospectively analyze the curative effects and prognostic factors of HLA-matched sibling donor allogeneic hematopoietic stem cell transplantation (allo-HSCT) for chronic myelogenous leukemia patients (CML).
  • METHODS: Of the 35 CML patients, 26 were males and 9 were females, with a median age of 32 (12 - 50) years.
  • 30 patients were in chronic phase of CML, 5 patients were in accelerated phase.
  • Among them, 21 patients (60.0%) had three years disease-free (DFS) survival.
  • Acute graft-versus-host disease (aGVHD) occurred in 18 patients (51.4%), among them 7 patients (20.0%) were of grade III-IV.
  • Chronic GVHD was in 17 patients (48.5%).
  • The 3-year disease-free survival (DFS) was 42.9% in TBI/CY group and 55.6% in BU/CY group (P > 0.05).
  • The 3-year DFS of patients with first chronic phase is higher than patients with advanced diseases (61.3% vs. 40%, P < 0. 05).
  • CONCLUSION: The patients who had transplantation done within 1 year after diagnosis during their first chronic phase of disease and who had low-grade GVHD have better prognosis.
  • Those patients who had III-IV acute GVHD are prone to incorporate severe infection, which was a worse prognostic factor of allo-HSCT for chronic myelogenous leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Adult. Age Factors. Child. Cystitis / etiology. Disease-Free Survival. Female. Follow-Up Studies. Graft vs Host Disease / etiology. Humans. Male. Middle Aged. Recurrence. Retrospective Studies. Siblings. Survival Rate. Transplantation, Homologous

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  • (PMID = 17147125.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
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67. Mughal TI, Goldman JM: Chronic myeloid leukemia: why does it evolve from chronic phase to blast transformation? Front Biosci; 2006;11:198-208
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  • [Title] Chronic myeloid leukemia: why does it evolve from chronic phase to blast transformation?
  • Clinically chronic myeloid leukemia is a biphasic or triphasic disease that is usually diagnosed in the initial 'chronic', 'indolent' or 'stable' phase and then spontaneously evolves after some years into an advanced phase.
  • This advanced phase can sometimes be subdivided into an earlier accelerated phase and a later blast phase or blast transformation--in about one-half of patients the chronic phase transforms unpredictably and abruptly to a blast phase, while in the other half of patients, the disease evolves somewhat more gradually, through an accelerated phase, which may last for months or years, before a blast phase ensues; this may have myeloblastic or lymphoblastic features.
  • Although much is now known about the molecular biology of the disease, the molecular basis of disease progression is still obscure.
  • The popular thinking has been that one or more probably a sequence of additional genetic events occurs in the BCR-ABL positive clone.
  • Here we review what is known of the mechanisms underlying the evolution of chronic myeloid leukemia from a chronic phase to a blast transformation.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation
  • [MeSH-minor] Animals. Apoptosis. Biological Evolution. Blast Crisis. Cytogenetics. Cytokinesis. DNA Repair. Disease Progression. Fusion Proteins, bcr-abl / chemistry. Humans. Janus Kinase 1. Lymphocytes / metabolism. Models, Biological. Mutation. Philadelphia Chromosome. Phosphatidylinositol 3-Kinases / metabolism. Proteasome Endopeptidase Complex / metabolism. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-myc / metabolism. RNA, Messenger / metabolism. Recombinant Fusion Proteins / metabolism. STAT5 Transcription Factor / metabolism. Time Factors

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  • (PMID = 16146725.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Janus Kinase 1; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 95
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68. Szabo SM, Levy AR, Davis C, Holyoake TL, Cortes J: A multinational study of health state preference values associated with chronic myelogenous leukemia. Value Health; 2010 Jan-Feb;13(1):103-11
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  • [Title] A multinational study of health state preference values associated with chronic myelogenous leukemia.
  • OBJECTIVES: Chronic myelogenous leukemia (CML) is a progressive, largely fatal cancer.
  • The purpose was to estimate preference weights from the general population in four developed countries for standardized health states experienced by persons with CML.
  • METHODS: Time trade-off preferences with a 10-year time horizon were elicited for CML-related health states using an interviewer-administered survey from convenience samples in Canada (n=103), the United States (n=74), the UK (n=97), and Australia (n=79).
  • Standardized descriptions of seven CML-related health states (characterizing chronic, accelerated and blast phases, each with responding and nonresponding state, and adverse events of treatment) were derived in consultation with oncologists.
  • Mean unadjusted preference values of CML-related health states ranged from 0.84 for "Chronic phase responding to treatment" to 0.21 for "Blast phase, not responding to treatment."
  • For each phase, preferences were lower for the nonresponding state.
  • CONCLUSION: These data quantify the deteriorating impact of CML disease progression and the impact of nonresponse to treatment.
  • The study results add to evidence from other disease areas that systematic differences exist in preference values between countries.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Patient Preference
  • [MeSH-minor] Adolescent. Adult. Aged. Cost-Benefit Analysis. Cross-Cultural Comparison. Disease Progression. Female. Humans. Male. Middle Aged. Quality-Adjusted Life Years. Treatment Outcome. Young Adult

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  • (PMID = 19659707.001).
  • [ISSN] 1524-4733
  • [Journal-full-title] Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research
  • [ISO-abbreviation] Value Health
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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69. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with CML and other MPD.
  • METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with CML (chronic phase, n = 37; accelerated phase, n = 9), and other MPD (chronic idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
  • 2D7(+) bone marrow cells were found to increase in CML compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2): CML, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
  • The highest basophil counts were recorded in accelerated phase CML (115/mm(2)).
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • [Cites] J Allergy Clin Immunol. 2002 Feb;109(2):287-93 [11842299.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3784-92 [11739187.001]
  • [Cites] Scand J Haematol. 1977 Jan;18(1):25-38 [265093.001]
  • [Cites] J Clin Invest. 1980 Feb;65(2):390-9 [6965379.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Cancer. 1981 May 15;47(10):2470-7 [6944141.001]
  • [Cites] Blood. 1982 Jul;60(1):113-20 [6952947.001]
  • [Cites] Fed Proc. 1983 May 15;42(8):2504-9 [6301890.001]
  • [Cites] Blood. 1984 Jul;64(1):78-83 [6234038.001]
  • [Cites] Am J Clin Pathol. 1984 Jul;82(1):1-14 [6588747.001]
  • [Cites] Prog Clin Biol Res. 1984;154:3-17 [6382299.001]
  • [Cites] J Immunol. 1986 May 1;136(9):3447-54 [3007619.001]
  • [Cites] Blood. 1987 Dec;70(6):1872-9 [3118989.001]
  • [Cites] Br J Haematol. 1987 Nov;67(3):281-4 [3479996.001]
  • [Cites] Cancer. 1988 Apr 1;61(7):1441-6 [3162181.001]
  • [Cites] Leukemia. 1988 Mar;2(3):141-3 [3258049.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2288-92 [3258425.001]
  • [Cites] J Med. 1987;18(5-6):293-303 [3505257.001]
  • [Cites] Blood. 1989 Feb 15;73(3):777-81 [2644988.001]
  • [Cites] Blood. 1989 May 15;73(7):1763-9 [2469498.001]
  • [Cites] Int Arch Allergy Appl Immunol. 1990;91(2):198-203 [1971264.001]
  • [Cites] Crit Rev Oncol Hematol. 1990;10(4):327-52 [2278641.001]
  • [Cites] Adv Immunol. 1992;52:333-423 [1332448.001]
  • [Cites] J Pathol. 1993 Oct;171(2):83-98 [7506771.001]
  • [Cites] Allergy. 1994 Dec;49(10):861-5 [7709996.001]
  • [Cites] J Immunol. 1995 Jun 15;154(12):6548-55 [7759888.001]
  • [Cites] Immunology. 1996 Apr;87(4):535-43 [8675206.001]
  • [Cites] Leuk Lymphoma. 1996 Jul;22(3-4):187-204 [8819068.001]
  • [Cites] Sao Paulo Med J. 1996 Jan-Feb;114(1):1083-90 [8984584.001]
  • [Cites] Int Rev Cytol. 1998;180:87-236 [9496635.001]
  • [Cites] J Allergy Clin Immunol. 1998 Mar;101(3):354-62 [9525452.001]
  • [Cites] J Natl Cancer Inst. 1998 Jun 3;90(11):850-8 [9625174.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1132-40 [9737247.001]
  • [Cites] Lab Invest. 1999 Jan;79(1):27-38 [9952108.001]
  • [Cites] Prog Histochem Cytochem. 1998;33(3-4):III-IX, 169-320 [10319376.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2343-56 [10498606.001]
  • [Cites] Acta Med Scand. 1963 Aug;174:249-54 [14051143.001]
  • [Cites] Haematologica. 1999 Nov;84(11):978-87 [10553157.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4028-38 [11110670.001]
  • [Cites] Adv Immunol. 2001;77:93-122 [11293121.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3484-90 [11369641.001]
  • [Cites] Hum Pathol. 2001 May;32(5):545-52 [11381374.001]
  • [Cites] J Allergy Clin Immunol. 2001 Aug;108(2):205-11 [11496235.001]
  • [Cites] Clin Exp Allergy. 2001 Nov;31(11):1705-13 [11696046.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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70. Steinberg M: Dasatinib: a tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia. Clin Ther; 2007 Nov;29(11):2289-308
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  • [Title] Dasatinib: a tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia and philadelphia chromosome-positive acute lymphoblastic leukemia.
  • The resulting gene product, BCR-ABL, encodes for an abnormal tyrosine kinase (TK) that is a factor in the pathology of chronic myelogenous leukemia (CML).
  • Use of targeted therapy that inhibits BCR-ABL kinase activity may lead to hematologic and cytogenetic responses in affected individuals.
  • The oral TK inhibitor dasatinib was approved in 2006 for use in patients with CML or Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL) who are unable to tolerate or have not responded to other treatments.
  • METHODS: Pertinent information was identified through searches of MEDLINE (1966-May 2007), EMBASE (1980-first quarter 2007), and International Pharmaceutical Abstracts (1970-May 2007) using the terms dasatinib, BMS-354825, chronic myelogenous leukemia, Sprycel, Philadelphia chromosome, and acute lymphoblastic leukemia.
  • RESULTS: Observed mutations in the amino acid sequence of BCR-ABL cause the failure of treatment with existing TK inhibitors.
  • Dasatinib has shown in vitro and in vivo activity against BCR-ABL, including mutations that are resistant to other available TK inhibitors.
  • The 5 phases of START (SRC/ABL Tyrosine kinase inhibition Activity Research Trials of dasatinib) represent the largest and most comprehensive evaluation of dasatinib in the treatment of patients in all stages of CML or Philadelphia chromosome-positive ALL who had undergone previous treatment for leukemia.
  • Dasatanib had the greatest benefit in patients in the chronic phase of CML, with complete hematologic responses in 90% of patients, 52% of whom achieved a major hematologic response.
  • Compared with those in the chronic phase, patients in the accelerated phase or blast crisis of CML, or with Philadelphia chromosome-positive ALL had lower responses.
  • CONCLUSIONS: Dasatinib has a wider spectrum of activity against a broader range of BCR-ABL forms than existing TK inhibitors.
  • It has shown clinical benefit and tolerability in patients in all phases of CML, as well as in those with Philadelphia chromosome-positive ALL.
  • Dasatinib illustrates the potential for targeted drug development based on an understanding of the genetic alterations leading to CML and the development of resistance to treatment.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Clinical Trials as Topic. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dasatinib. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Models, Chemical. Mutation. Piperazines / therapeutic use. Proto-Oncogene Proteins c-bcr / genetics. Randomized Controlled Trials as Topic. Receptors, Purinergic P2 / genetics

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  • [Copyright] Copyright (c) 2007 Excerpta Medica, Inc.
  • (PMID = 18158072.001).
  • [ISSN] 0149-2918
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Receptors, Purinergic P2; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr; RBZ1571X5H / Dasatinib
  • [Number-of-references] 52
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71. Quintás-Cardama A, Kantarjian H, Ravandi F, O'Brien S, Thomas D, Vidal-Senmache G, Wierda W, Kornblau S, Cortes J: Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy. Cancer; 2009 Jun 1;115(11):2482-90
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  • [Title] Bleeding diathesis in patients with chronic myelogenous leukemia receiving dasatinib therapy.
  • BACKGROUND: The most frequent nonhematologic side effects associated with dasatinib therapy in patients with chronic myeloid leukemia (CML) are gastrointestinal, rash, and fluid retention syndromes.
  • In the current study, the authors investigated the risk factors and management of bleeding associated with dasatinib therapy for CML after imatinib failure.
  • METHODS: The bleeding episodes associated with dasatinib therapy in 138 patients with CML who were consecutively treated at the study institution in clinical trials were evaluated.
  • RESULTS: Bleeding occurred in 32 (23%) patients (grade >or=3 in 9 [7%] patients [according to National Cancer Institute Common Toxicity Criteria]), including in 12% of patients treated in chronic phase, 31% of patients treated in accelerated phase (AP), and 35% of patients treated in blast phase (BP) (P = .02).
  • Although 37% of episodes occurred with platelet counts >100 x 10(9)/L, multivariate analysis identified thrombocytopenia and advanced phase CML as risk factors for bleeding.
  • CONCLUSIONS: Bleeding occurs during dasatinib therapy, particularly in patients with AP or BP disease and low platelet counts.
  • [MeSH-major] Hemorrhagic Disorders / chemically induced. Leukemia, Myeloid, Chronic-Phase / complications. Leukemia, Myeloid, Chronic-Phase / drug therapy. Pyrimidines / adverse effects. Thiazoles / adverse effects

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  • [Copyright] (c) 2009 American Cancer Society.
  • [Cites] Science. 2000 Sep 15;289(5486):1938-42 [10988075.001]
  • [Cites] J Natl Cancer Inst. 2008 Jul 2;100(13):926-39 [18577747.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Blood. 2003 Jan 15;101(2):690-8 [12509383.001]
  • [Cites] N Engl J Med. 2003 Mar 13;348(11):994-1004 [12637609.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):672-7 [14744784.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] J Biol Chem. 2004 Aug 13;279(33):34227-39 [15175350.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Development. 1999 Jun;126(14):3047-55 [10375497.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Mol Pharmacol. 2006 May;69(5):1527-33 [16436588.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Drug Metab Dispos. 2008 Jul;36(7):1357-64 [18420784.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3204-12 [18541900.001]
  • [Cites] Blood. 2001 Apr 1;97(7):1990-8 [11264163.001]
  • (PMID = 19280591.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS629436; NLM/ PMC4180711
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72. Takagi Y, Aota Y, Gotoh A, Sakurai M: [Effect of low-dose dasatinib in an elderly patient with chronic myelogenous leukemia (CML)]. Gan To Kagaku Ryoho; 2010 Nov;37(11):2213-5
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  • [Title] [Effect of low-dose dasatinib in an elderly patient with chronic myelogenous leukemia (CML)].
  • We experienced a case of chronic myelogenous leukemia (CML) treated successfully with low-dose dasatinib (20 mg/day).
  • An 87-year-old man was diagnosed with CML in January 2003 and was given imatinib (200 mg/day).
  • However, since the blood count was poorly controlled with HU, treatment with dasatinib, one of the second-generation tyrosine kinase inhibitors, was started at the accelerated phase (AP) in June 2009.
  • Dasatinib was given in a daily dose of 20 mg, intending dose escalation after confirmation of its safety.
  • Low-dose dasatinib might be a useful treatment in the control of selected patients with CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • (PMID = 21084830.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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73. Jiang Q, Chen SS, Jiang B, Jiang H, Lu Y, Qiu JY, Lu DP: [Clonal evolution of abnormal Philadelphia chromosome-negative cells after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jan;26(1):23-6
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  • [Title] [Clonal evolution of abnormal Philadelphia chromosome-negative cells after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia].
  • OBJECTIVE: To investigate clonal evolution of abnormal Philadelphia chromosome-negative cells (Ph- CE) after imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (Ph+ CML).
  • METHODS: Bone marrow cells G-banding karyotype was evaluated every 3 months in 100 patients with Ph+ CML after achieving hematologic responses on the course of imatinib therapy.
  • There were 54 patients in chronic phase (CP), 37 in accelerated phase (AP) and 9 in blast phase (BP).
  • CONCLUSION: Ph- CE occurred in about 11% of the patients with Ph+ CML who achieved major or minor cytogenetic responses on imatinib therapy.
  • After a median follow-up of more than 2 years, most of the patients with Ph- CE were in a stable status with no disease progression.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / drug therapy. Philadelphia Chromosome. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15946504.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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74. Huang M, Hu Z, Chang W, Ou D, Zhou J, Zhang Y: The growth factor independence-1 (Gfi1) is overexpressed in chronic myelogenous leukemia. Acta Haematol; 2010;123(1):1-5
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  • [Title] The growth factor independence-1 (Gfi1) is overexpressed in chronic myelogenous leukemia.
  • The activation of ABL tyrosine kinase in BCR/ABL-positive chronic myelogenous leukemia (CML) leads to a diversity of biological changes related to the pathogenesis of the disease.
  • In CML patients, we determined the expression of growth factor independence-1 (Gfi1), a transcription repressor with weak oncogenic activity.
  • Our data demonstrated that the Gfi1 mRNA level in both the mononuclear cells and purified CD34(+) cells from CML were significantly higher as measured by quantitative real-time PCR.
  • Using flow cytometry and Western blot, we also showed that the Gfi1 protein content was increased in CML CD34(+) cells.
  • The expression of Gfi1 was correlated with BCR/ABL significantly.
  • Gfi1 may be implicated in the pathogenesis of CML and can serve as a potential target for the management of the disease.
  • [MeSH-major] DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism
  • [MeSH-minor] Antigens, CD34 / metabolism. Base Sequence. Benzamides. Blast Crisis / genetics. Blast Crisis / metabolism. DNA Primers / genetics. Gene Expression. Genes, abl. Hematopoietic Stem Cells / immunology. Hematopoietic Stem Cells / metabolism. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / genetics. Leukemia, Myeloid, Accelerated Phase / metabolism. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / metabolism. Neoplastic Stem Cells / immunology. Neoplastic Stem Cells / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Stem Cell Transplantation

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  • [Copyright] Copyright (c) 2009 S. Karger AG, Basel.
  • (PMID = 19887785.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Benzamides; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
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75. Sanz J, Montesinos P, Saavedra S, Lorenzo I, Senent L, Planelles D, Larrea L, Martín G, Palau J, Jarque I, Martínez J, de la Rubia J, Moscardó F, Martinez D, Gómez I, López M, Sanz MA, Sanz GF: Single-unit umbilical cord blood transplantation from unrelated donors in adult patients with chronic myelogenous leukemia. Biol Blood Marrow Transplant; 2010 Nov;16(11):1589-95
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  • [Title] Single-unit umbilical cord blood transplantation from unrelated donors in adult patients with chronic myelogenous leukemia.
  • Clinical studies focused on outcomes of umbilical cord blood transplantation (UCBT) for patients with chronic myelogenous leukemia (CML) in need of allogeneic stem cell transplantation and lacking an HLA-matched adult donor are limited.
  • We analyzed the outcome of 26 adults with CML receiving single-unit UCBT from unrelated donors after myeloablative conditioning at a single institution.
  • At the time of transplantation, 7 patients (27%) were in first chronic phase (CP), 11 (42%) were in second CP, 2 (8%) were in accelerated phase (AP), and 6 (23%) were in blast crisis (BC).
  • The cumulative incidence (CI) of myeloid engraftment was 88% at a median time of 22 days and was significantly better for patients receiving higher doses of CD34(+) cells.
  • The CI of acute graft-versus-host disease (GVHD) grade II-IV was 61%, that of acute GVHD grade III-IV was 39%, and that of chronic extensive GVHD was 60%.
  • After a median follow-up of 8 years, none of the patients relapsed, giving an overall disease-free survival (DFS) at 8 years of 41%.
  • These results demonstrate that UCBT from unrelated donors can be a curative treatment for a substantial number of patients with CML.
  • [MeSH-major] Blood Donors. Cord Blood Stem Cell Transplantation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Cause of Death. Disease-Free Survival. Female. Graft Rejection / epidemiology. Graft Survival. Graft vs Host Disease / diagnosis. Graft vs Host Disease / epidemiology. Histocompatibility. Humans. Leukocyte Count. Male. Middle Aged. Neutrophils / cytology. Platelet Count. Recurrence. Retrospective Studies. Transplantation Chimera. Treatment Outcome. Young Adult

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  • [Copyright] Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20553927.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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76. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
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  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Described here are five cases of CML associated with del(15q): four men and one woman.
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • Of the three patients who did not receive ASCT, one died, one was in persistent blast phase, and one was in clinical remission with molecular evidence of residual disease at 16, 6, and 34 months, respectively, after identification of the del(15q).
  • Of the two patients who had ASCT, one died and one was in clinical remission with molecular evidence of disease at 15 and 64 months, respectively, after identification of the del(15q).
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • Del(15q) appears to be associated with a poor prognosis in CML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

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  • [Cites] Mod Pathol. 2004 Jan;17(1):96-103 [14657955.001]
  • [Cites] Cancer Genet Cytogenet. 2009 Jan 15;188(2):118-23 [19100517.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jun;151(2):146-51 [15172752.001]
  • [Cites] Am J Clin Pathol. 2004 Jun;121(6):836-42 [15198355.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):671-84, x [15271399.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] Cancer. 1999 Dec 15;86(12):2632-41 [10594858.001]
  • [Cites] Cancer Res. 2000 Jan 1;60(1):70-3 [10646855.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] Arch Pathol Lab Med. 2001 Mar;125(3):437-9 [11231500.001]
  • [Cites] Cancer. 2002 Feb 15;94(4):1102-10 [11920481.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1266-72 [12481006.001]
  • [Cites] Int J Cancer. 2003 Aug 10;106(1):74-7 [12794759.001]
  • [Cites] Cancer Genet Cytogenet. 2003 Jul 1;144(1):1-5 [12810248.001]
  • [Cites] Scand J Haematol. 1976 Jul;17(1):17-28 [1066809.001]
  • [Cites] Cancer. 1979 Apr;43(4):1350-7 [445335.001]
  • [Cites] Hum Genet. 1981;58(3):285-93 [6948765.001]
  • [Cites] Cancer. 1985 Feb 1;55(3):535-41 [3965107.001]
  • [Cites] Leuk Res. 1991;15(8):683-91 [1654480.001]
  • [Cites] Cancer Genet Cytogenet. 1991 Aug;55(1):35-8 [1913605.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:11-5 [8251885.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Feb;86(2):124-8 [8603337.001]
  • [Cites] Baillieres Clin Haematol. 1997 Jun;10(2):223-31 [9376661.001]
  • [Cites] Leuk Res. 1998 Sep;22(9):845-7 [9716017.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):302-8 [9747637.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Am J Clin Pathol. 2005 Nov;124(5):807-14 [16203287.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1730-8 [16532439.001]
  • [Cites] J Cell Biochem. 2007 Apr 15;100(6):1376-86 [17131381.001]
  • [Cites] Cancer. 2008 May 15;112(10):2112-8 [18348294.001]
  • [Cites] Cancer. 2008 Oct 1;113(7 Suppl):1933-52 [18798533.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
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77. Kast RE, Focosi D: Three paths to better tyrosine kinase inhibition behind the blood-brain barrier in treating chronic myelogenous leukemia and glioblastoma with imatinib. Transl Oncol; 2010 Feb;3(1):13-5
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  • [Title] Three paths to better tyrosine kinase inhibition behind the blood-brain barrier in treating chronic myelogenous leukemia and glioblastoma with imatinib.
  • Chronic myelogenous leukemia (CML) can be controlled for years with the tyrosine kinase inhibitor imatinib but because imatinib poorly penetrates the blood-brain barrier (BBB), on occasion, the CML clone will thrive and evolve to an accelerated phase in the resulting imatinib sanctuary within the central nervous system.
  • In this, CML resembles glioblastoma in that imatinib, which otherwise may be effective, cannot get to the tumor.
  • 1) Pharmaceutical methamphetamine may have a useful role in treating both CML and glioblastoma by allowing higher imatinib concentrations behind the BBB.
  • 2) The old antidepressant and monoamine oxidase inhibitor selegiline, used to treat Parkinson disease, is catabolized to methamphetamine.

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  • [Cites] J Infect Dis. 2007 Aug 1;196(3):361-70 [17597450.001]
  • [Cites] J Neurooncol. 2007 Nov;85(2):217-22 [17594055.001]
  • [Cites] J Exp Clin Cancer Res. 2007 Sep;26(3):353-9 [17987795.001]
  • [Cites] Int J Oncol. 2008 Apr;32(4):829-39 [18360710.001]
  • [Cites] Neuropathology. 2008 Oct;28(5):507-15 [18410277.001]
  • [Cites] AAPS J. 2008;10(1):166-77 [18446517.001]
  • [Cites] Rev Recent Clin Trials. 2006 Sep;1(3):265-81 [18473979.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1005-12 [18477770.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Nov 7;376(1):86-90 [18765229.001]
  • [Cites] Nat Biotechnol. 2009 Jan;27(1):77-83 [19098899.001]
  • [Cites] Mol Cancer Ther. 2009 Feb;8(2):394-406 [19190119.001]
  • [Cites] Clin Cancer Res. 2009 Feb 15;15(4):1222-31 [19190128.001]
  • [Cites] Cancer. 2009 May 15;115(10):2188-98 [19248046.001]
  • [Cites] Cell Signal. 2009 Jul;21(7):1143-50 [19275932.001]
  • [Cites] Cell Mol Neurobiol. 2009 Sep;29(6-7):845-58 [19288188.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3173-9 [19318569.001]
  • [Cites] J Neurooncol. 2009 Sep;94(2):163-7 [19322519.001]
  • [Cites] Cancer Lett. 2009 Sep 8;282(1):35-42 [19346066.001]
  • [Cites] Addiction. 2009 Jul;104(7):1085-99 [19426289.001]
  • [Cites] J Neurooncol. 2009 Nov;95(2):151-63 [19436954.001]
  • [Cites] J Psychoactive Drugs. 2009 Mar;41(1):11-7 [19455905.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1698-707 [19474800.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):1132-5 [19484755.001]
  • [Cites] J Clin Oncol. 2009 Jul 20;27(21):3472-9 [19487385.001]
  • [Cites] Intern Med J. 2009 Jun;39(6):408-11 [19580620.001]
  • [Cites] Semin Hematol. 2009 Apr;46(2 Suppl 3):S22-6 [19621546.001]
  • [Cites] Semin Hematol. 2009 Apr;46(2 Suppl 3):S27-33 [19621547.001]
  • [Cites] Br J Neurosurg. 2009 Aug;23(4):351-63 [19637006.001]
  • [Cites] Leukemia. 2009 Sep;23(9):1628-33 [19641527.001]
  • [Cites] J Neurovirol. 2001 Feb;7(1):66-71 [11519485.001]
  • [Cites] Br J Haematol. 2002 Oct;119(1):106-8 [12358909.001]
  • [Cites] Lancet Oncol. 2003 Apr;4(4):198 [12681250.001]
  • [Cites] J Anal Toxicol. 2003 Apr;27(3):135-41 [12731653.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Apr;53(4):313-23 [14658008.001]
  • [Cites] J Anal Toxicol. 2006 May;30(4):232-7 [16803660.001]
  • [Cites] J Neurooncol. 2007 Aug;84(1):103-5 [17318411.001]
  • [Cites] Pharm Res. 2007 Sep;24(9):1720-8 [17380257.001]
  • [Cites] J Neurooncol. 2007 Oct;85(1):109-10 [17464448.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jul 6;358(3):908-13 [17512905.001]
  • [Cites] J Neural Transm Suppl. 2007;(72):165-73 [17982891.001]
  • (PMID = 20165690.001).
  • [ISSN] 1936-5233
  • [Journal-full-title] Translational oncology
  • [ISO-abbreviation] Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2822451
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78. Hosoya N, Sanada M, Nannya Y, Nakazaki K, Wang L, Hangaishi A, Kurokawa M, Chiba S, Ogawa S: Genomewide screening of DNA copy number changes in chronic myelogenous leukemia with the use of high-resolution array-based comparative genomic hybridization. Genes Chromosomes Cancer; 2006 May;45(5):482-94
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  • [Title] Genomewide screening of DNA copy number changes in chronic myelogenous leukemia with the use of high-resolution array-based comparative genomic hybridization.
  • Chronic myelogenous leukemia (CML) evolves from an indolent chronic phase (CP) characterized by the Philadelphia chromosome.
  • Without effective therapy, it progresses to an accelerated phase (AP) and eventually to a fatal blast crisis (BC).
  • To identify the genes involved in stage progression in CML, we performed a genomewide screening of DNA copy number changes in a total of 55 CML patients in different stages with the use of the high-resolution array-based comparative genomic hybridization (array CGH) technique.
  • Our data suggests that at least a proportion of CML patients carry still-unknown cryptic genomic alterations that could affect a gene or genes of importance in the disease progression of CML.
  • [MeSH-major] DNA, Neoplasm / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Nucleic Acid Hybridization / methods. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adult. Aged. Chromosomes, Artificial, Bacterial. Disease Progression. Female. Humans. Male. Middle Aged

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  • [Copyright] 2006 Wiley-Liss, Inc
  • (PMID = 16425296.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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79. Udvardy M: [Chronic myeloid leukemia]. Orv Hetil; 2005 Feb 6;146(6):243-7
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  • [Title] [Chronic myeloid leukemia].
  • [Transliterated title] Krónikus myeloid leukaemia.
  • Chronic myeloid leukemia is still the most characteristic entity of the chronic myeloproliferative diseases.
  • The tumor promoter role of able-dependent tyrosine kinase activation, which is enhanced by bcr/abl rearrangement (due the classical translocation of Philadelphia chromosomal abnormality) has been quite well clarified.
  • The better understanding of the role of altered cell signalling pathways in the pathogenesis of chronic myeloid leukaemia opened new areas for extensive and fruitful pharmacological research.
  • The first, non-myelosuppressive agent, which was able to reduce the number of Philadelphia positive clonal cells was the interferon group, which drug could substantially prolong the chronic phase and mortality of chronic myeloid leukaemia.
  • Imatinib is also a powerful agent in the accelerated or blastic phased of chronic myeloid leukaemia.
  • With the advent of these new drugs the therapeutic algorithm of chronic myeloid leukaemia and allogenous bone marrow transplantation seems to be reconsidered, too.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Diagnosis, Differential. Enzyme Activation / drug effects. Humans. Imatinib Mesylate. Interferons / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Signal Transduction / drug effects

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  • (PMID = 15779811.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 9008-11-1 / Interferons; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 19
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80. Wang JX, Huang XJ, Wu DP, Hu JD, Liu T, Hu Y, Meng FY, Chen XQ, Hou M, Li Y, Wang SJ, Wang JM, Ren HY, Yu L, Chen FY, Qiu LG, Jiang B, Sun AN, Liu TB, Zhu HL, Guo T, Xu D, Ji CY, Lü XY, Jiao L, Song XM, Huang HH: [Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.]. Zhonghua Xue Ye Xue Za Zhi; 2009 Nov;30(11):721-5
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  • [Title] [Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.].
  • OBJECTIVE: To explore demographic characteristics, current diagnosis and treatment patterns of chronic myelogenous leukemia (CML) patients in China.
  • METHODS: Data of hospitalized CML patients in 2005 whole year and outpatient information (July 1 through September 30, 2006) from 15 hospitals throughout China were analyzed.
  • RESULTS: A total of 1824 CML cases were analyzed, including 722 inpatients and 1102 outpatients.
  • The median age at diagnosis was 40.02 (2.45 - 83.29) years old, 90.41% of the patients were diagnosed at chronic phase.
  • Proportion of accelerated phase or blast crisis patients increased to 21.66% during study period.
  • 93.20% of the patients received blood routine and bone marrow morphologic examination at diagnosis and in monitoring; 70.29% were performed cytogenetic analysis and 51.54% performed molecular measurement in addition.
  • The most common therapy for CML treatment was hydroxycarbamide.
  • The proportions of accelerated phase and blast crisis patients treated with imatinib were 48.28% and 48.42%, respectively, being significantly higher than that of chronic phase patients (35.9%) (P < 0.05).
  • CONCLUSIONS: CML in China tends to afflict younger population than in Western countries.
  • Most patients were diagnosed in the chronic phase.
  • Due to restriction of financial support, only one third of CML patients were treated with imatinib, and the majority of the treated were not monitored in time.
  • Clinicians should pay attention to resistance and intolerance to imatinib treatment in accelerated phase or blast crisis patients.
  • [MeSH-minor] Benzamides / therapeutic use. China. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 20137304.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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81. Weisser M, Tischer J, Schnittger S, Schoch C, Ledderose G, Kolb HJ: A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation. Haematologica; 2006 May;91(5):663-6
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  • [Title] A comparison of donor lymphocyte infusions or imatinib mesylate for patients with chronic myelogenous leukemia who have relapsed after allogeneic stem cell transplantation.
  • Imatinib mesylate is highly effective in relapsed chronic myelogenous leukemia (CML) after allogeneic hematopoetic stem cell transplantation (HSCT).
  • The outcome of CML patients transplanted at our center who had received only imatinib for relapse after HSCT was compared with that of patients treated with donor lymphocyte infusions (DLI).
  • Imatinib therapy resulted in a higher incidence of relapse and inferior leukemia-free survival (p=0.006 and p=0.016, respectively).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Lymphocyte Transfusion. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Salvage Therapy
  • [MeSH-minor] Adult. Benzamides. Biomarkers, Tumor / biosynthesis. Disease-Free Survival. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / biosynthesis. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase / surgery. Leukemia, Myeloid, Chronic-Phase / surgery. Living Donors. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16627251.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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82. Sessions J: Chronic myeloid leukemia in 2007. Am J Health Syst Pharm; 2007 Dec 15;64(24 Suppl 15):S4-9
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  • [Title] Chronic myeloid leukemia in 2007.
  • PURPOSE: Chronic myeloid leukemia (CML), a hematopoietic stem cell cancer representing 15-20% of adult leukemias, is discussed.
  • SUMMARY: CML is a myeloproliferative disorder that affects all lineages of hematopoiesis.
  • Final confirmation of CML comes with detection of the Philadelphia Chromosome (Ph) or BCR-ABL transcripts.
  • The disease presents in one of three phases: chronic phase, accelerated phase, or blast crisis.
  • Progression from chronic phase to accelerated phase usually involves the accumulation of additional cytogenetic aberrations and the arising of resistance to therapy.
  • Although at one point mortality associated with CML was high, new kinase inhibitor therapies have markedly extended the life-span of these patients.
  • These inhibitors were derived through the initial observation of the association of the Ph with CML and the eventual identification of the BCR-ABL oncogene which arises from this translocation.
  • Analysis of the mechanism by which BCR-ABL transforms cells identified this protein as a tyrosine kinase and led to the targeting of this activity.
  • The majority of patients present in chronic phase, which is where these kinase inhibitors have their greatest efficacy.
  • Monitoring of disease progression is of critical importance as the prognosis drops significantly for patients with advanced disease.
  • Blood counts, cytogenetics, and polymerase chain reaction (PCR) are currently used to assess disease.
  • CONCLUSION: Our understanding of BCR-ABL has allowed the development of therapies, which may keep patients with CML in chronic phase indefinitely.
  • This has created a situation in which patient monitoring is essential for detecting changes in the status of CML.
  • The tests described here provide a comprehensive assessment of disease status allowing for effective patient management.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis
  • [MeSH-minor] Clinical Trials as Topic. Drug Resistance, Neoplasm. Humans. Leukemia, Myeloid, Chronic-Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / therapy. Neoplasm Staging


83. Piazza RG, Magistroni V, Franceschino A, Andreoni F, Tornaghi L, Colnaghi F, Corneo G, Pogliani EM, Gambacorti-Passerini C: The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years. Blood Cells Mol Dis; 2006 Sep-Oct;37(2):111-5
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  • [Title] The achievement of durable complete cytogenetic remission in late chronic and accelerated phase patients with CML treated with Imatinib mesylate predicts for prolonged response at 6 years.
  • Despite the positive results achieved by Imatinib mesylate (Imatinib) in the treatment of chronic myeloid leukemia (CML), over the past several years, Imatinib does not eradicate the leukemic clone.
  • Long-term follow-up of CML patients treated with Imatinib will ultimately define the durability of such treatment and the frequency of reemergence of progressive disease.
  • We present the results of a 6-year follow-up of 40 CML patients either in chronic or accelerated phase who obtained a durable (>6 months) complete cytogenetic remission (CCyR) after treatment with Imatinib in a single center.
  • No progressions to more advanced phases of disease have been detected during the follow-up period.
  • Cytogenetic relapse was predicted by either a decrease in the amount of BCR-ABL transcript of less than 2 logs after the achievement of CCyR (p=0.0041) or a time-to-CCyR of more than 12 months (p<0.0001).
  • This 6-year follow-up of the efficacy of Imatinib therapy in CML patients who obtained a durable CCyR indicates that the relapses rate is low over this period of observation and that the rate of relapse does not increase over time.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16908206.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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84. Moen MD, McKeage K, Plosker GL, Siddiqui MA: Imatinib: a review of its use in chronic myeloid leukaemia. Drugs; 2007;67(2):299-320
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib: a review of its use in chronic myeloid leukaemia.
  • Imatinib (Gleevec, Glivec) is a synthetic tyrosine kinase inhibitor used in the treatment of chronic myeloid leukaemia (CML).
  • It is specifically designed to inhibit the breakpoint cluster region (BCR)-Abelson (ABL) fusion protein that results from the chromosomal abnormality known as the Philadelphia chromosome.
  • CML is characterised by this abnormality, which leads to abnormalities of the peripheral blood and bone marrow including an increase in the number of granular leukocytes.
  • Imatinib is approved in numerous countries worldwide for the treatment of newly diagnosed Philadelphia chromosome-positive (Ph+) chronic-phase CML, Ph+ accelerated-phase or blast-crisis CML, and in patients with Ph+ chronic-phase CML who have failed to respond to interferon-alpha therapy.
  • It is also indicated in paediatric patients with newly diagnosed Ph+ chronic-phase CML, in accelerated-phase or blast-crisis CML, or in chronic-phase CML after failure of interferon-alpha therapy or when the disease has recurred after haematopoietic stem cell transplantation (HSCT).
  • Imatinib is effective and generally well tolerated in patients with Ph+ CML.
  • In patients with newly diagnosed chronic-phase CML, imatinib was more effective than interferon-alpha plus cytarabine in preventing progression of the disease and in achieving haematological and cytogenetic responses.
  • Patients with accelerated-phase or blast-crisis CML, or those who have not responded to prior interferon-alpha therapy also benefit from imatinib treatment.
  • The introduction of imatinib has had a marked impact on outcomes in patients with CML.
  • It remains a valuable treatment for all stages of the disease, especially initial treatment of newly diagnosed Ph+ chronic-phase CML, and is endorsed by European and US treatment guidelines as a first-line option.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17284091.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 90
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85. Tóthová E, Kafková A, Fricová M, Benová B, Kirschnerová G, Tóthová A: Imatinib mesylate in Philadelphia chromosome-positive, chronic-phase myeloid leukemia after failure of interferon alpha. Neoplasma; 2005;52(1):63-7
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  • [Title] Imatinib mesylate in Philadelphia chromosome-positive, chronic-phase myeloid leukemia after failure of interferon alpha.
  • The introduction of imatinib has chanced the philosophy of mechanisms of cancer therapy and already changed current management of patients with chronic myeloid leukemia (CML).
  • A total of 49 patients with later chronic phase CML in whom previous therapy with interferon alpha had failed were treated with 400 mg of oral imatinib daily.
  • After a median follow-up of 18 months, CML had not progressed to the accelerated or blast phases in an estimated 98% of patients, and 100 percent of the patients were alive.
  • The results of current study indicate that imatinib has a significant therapy benefit in CML patients in whom treatment with IFN alpha had failed.
  • Therefore, has favorably changed the prognosis for patients with chronic myelogenous leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use


86. Hughes T, Saglio G, Branford S, Soverini S, Kim DW, Müller MC, Martinelli G, Cortes J, Beppu L, Gottardi E, Kim D, Erben P, Shou Y, Haque A, Gallagher N, Radich J, Hochhaus A: Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. J Clin Oncol; 2009 Sep 1;27(25):4204-10
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  • [Title] Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase.
  • PURPOSE: Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase (CP; CML-CP) and accelerated phase (AP; CML-AP) who are resistant to or intolerant of prior imatinib therapy.
  • In this subanalysis of a phase II study of nilotinib in patients with imatinib-resistant or imatinib-intolerant CML-CP, the occurrence and impact of baseline and newly detectable BCR-ABL mutations were assessed.
  • PATIENTS AND METHODS: Baseline mutation data were assessed in 281 (88%) of 321 patients with CML-CP in the phase II nilotinib registration trial.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use


87. Conte E, Stagno F, Guglielmo P, Scuto A, Consoli C, Messina A: Survivin expression in chronic myeloid leukemia. Cancer Lett; 2005 Jul 8;225(1):105-10
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  • [Title] Survivin expression in chronic myeloid leukemia.
  • In this study, we investigated the expression of survivin (SVV) in 44 patients with typical Ph-positive chronic myeloid leukemia (CML) in different phases of the disease as well as in 20 matched healthy donors.
  • We found a very high SVV expression in a predominant percentage of CML patients.
  • We also observed a significantly increased SVV expression in patients in accelerated/blastic phase of the disease compared to patients in chronic phase.
  • Moreover, SVV expression levels correlated in all CML patients with % of Ph-chromosome positive cells, with Bcr-Abl expression levels and with WBC-count.
  • Based on this finding we suggest that SVV detection and monitoring in CML could represent both a useful biomarker and attractive candidate for devising new targeted and combined therapies in CML.
  • [MeSH-major] Biomarkers, Tumor / blood. Gene Expression Profiling. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / blood

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  • (PMID = 15922862.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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88. Phan TX, Hoang AV, Huynh VM, Nguyen KT, Nguyen TB, Huynh N, Pham QT, Tran VB, Tran VB, Tokunaga K, Sato Y: Unique secondary chromosomal abnormalities are frequently found in the chronic phase of chronic myeloid leukemia in southern Vietnam. Cancer Genet Cytogenet; 2006 Jul 1;168(1):59-68
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  • [Title] Unique secondary chromosomal abnormalities are frequently found in the chronic phase of chronic myeloid leukemia in southern Vietnam.
  • Although we have observed much shorter survival in southern Vietnamese chronic myeloid leukemia (CML) patients, the cause remains to be clarified.
  • Here, we report cytogenetic and molecular findings for 47 CML patients.
  • Cytogenetically, the Philadelphia (Ph) chromosome was found in 44 patients (93.6%); of the remaining 3 patients with Ph-negative CML, 2 exhibited BCR/ABL transcripts but no BCR/ABL FISH fusion signals, suggesting the existence of two clones, with and without the BCR/ABL fusion gene.
  • Surprisingly, in 17 patients (36.2%) (4 at diagnosis, 11 during chronic phase, and 2 in accelerated phase), we found several unique secondary chromosome abnormalities including trisomy 13, partial trisomy 13, and abnormalities of 1p, 3p, 6p, 7p, 10p, and 11p, which are different from the so-called additional chromosome abnormalities (extra Ph, +8, i(17q), +19, and +21) observed in blastic phase CML.
  • Of these, 2 had two clones, with and without der(9) deletion, suggesting that der(9) deletion would occur in a subset of patients during disease progression.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 13 / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Deletion. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Male. Middle Aged. Philadelphia Chromosome. RNA, Messenger / analysis. Translocation, Genetic / genetics. Trisomy / genetics. Vietnam

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  • (PMID = 16772122.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / abl-bcr fusion protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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89. Xiao-Jun H, Lan-Ping X, Kai-Yan L, Dai-Hong L, Huan C, Wei H, Yu-Hong C, Jing-Zhi W, Yao C, Xiao-Hui Z, Hong-Xia S, Dao-Pei L: HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase. Ann Med; 2008;40(6):444-55
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  • [Title] HLA-mismatched/haploidentical hematopoietic stem cell transplantation without in vitro T cell depletion for chronic myeloid leukemia: improved outcomes in patients in accelerated phase and blast crisis phase.
  • BACKGROUND: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only proven curative therapy for chronic myeloid leukemia (CML), but lack of human leukocyte antigen (HLA)-matched sibling or unrelated donors has restricted its application.
  • AIM: To evaluate the outcomes of CML patients who underwent haploidentical allo-HSCT.
  • RESULTS: Our data showed that the cumulative incidence of acute graft-versus-host disease (GVHD) was 64.52%, and grade III-IV was 26.45%, 61.79% had chronic GVHD, and 28.93% had extensive chronic GVHD.
  • Probability of 1-year and 4-year leukemia-free survival was similar in chronic phase (CP) 1, CP2/CR2, accelerated phase, and blast crisis patients.
  • Probability of 4-year overall survival varied as 76.5% (CP1), 85.7% (CP2/CR2), 73.3% (accelerated phase), and 61.5% (blast crisis).
  • Multivariate analysis indicated that factors affecting transplantation outcomes were HLA-B+DR mismatches versus others for II-III acute GVHD and III-IV acute GVHD, the stage of disease at transplantation for relapse, and the time from diagnosis to transplantation for leukemia-free survival, overall survival, and transplantation-related mortality.
  • In our protocol, survival of HSCT for advanced CML was similar to stable stage.
  • [MeSH-major] Blast Crisis / therapy. Hematopoietic Stem Cell Transplantation / methods. Histocompatibility Testing. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Directed Tissue Donation. Female. Graft Survival. Graft vs Host Disease. Humans. Male. Middle Aged. Opportunistic Infections. Survival Analysis. Transplantation Conditioning. Transplantation, Homologous. Young Adult


90. Imataki O, Shintani T, Waki F, Ohnishi H, Ishida T: [Tolerability of imatinib for patients with chronic myelogeneous leukemia (CML)]. Gan To Kagaku Ryoho; 2008 Nov;35(11):1863-7
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  • [Title] [Tolerability of imatinib for patients with chronic myelogeneous leukemia (CML)].
  • We reviewed a patients' cohort treated with imatinib in our hospital in 2007 for chronic myelogeneous leukemia (CML).
  • The disease status at onset was chronic phase in 13 patients and accelerated phase in 1.
  • In 4 of these 6 intolerant cases, CR was maintained 2 years after the start of imatinib therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Tolerance. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Disease Progression. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Stem Cell Transplantation. Survival Rate. Young Adult

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  • (PMID = 19011333.001).
  • [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
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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91. Perrotti D, Jamieson C, Goldman J, Skorski T: Chronic myeloid leukemia: mechanisms of blastic transformation. J Clin Invest; 2010 Jul;120(7):2254-64
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  • [Title] Chronic myeloid leukemia: mechanisms of blastic transformation.
  • The BCR-ABL1 oncoprotein transforms pluripotent HSCs and initiates chronic myeloid leukemia (CML).
  • Patients with early phase (also known as chronic phase [CP]) disease usually respond to treatment with ABL tyrosine kinase inhibitors (TKIs), although some patients who respond initially later become resistant.
  • In most patients, TKIs reduce the leukemia cell load substantially, but the cells from which the leukemia cells are derived during CP (so-called leukemia stem cells [LSCs]) are intrinsically insensitive to TKIs and survive long term.
  • LSCs or their progeny can acquire additional genetic and/or epigenetic changes that cause the leukemia to transform from CP to a more advanced phase, which has been subclassified as either accelerated phase or blastic phase disease.
  • Here, we discuss what is known about the molecular mechanisms leading to blastic transformation of CML and propose some novel therapeutic approaches.

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  • [Cites] Leuk Lymphoma. 2008 Apr;49(4):610-4 [18398719.001]
  • [Cites] Cancer Res. 2008 Apr 15;68(8):2576-80 [18413724.001]
  • [Cites] Cancer Metastasis Rev. 2008 Jun;27(2):159-68 [18213449.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Genes Dev. 2008 Jun 1;22(11):1411-5 [18519632.001]
  • [Cites] Cancer Cell. 2008 Jun;13(6):496-506 [18538733.001]
  • [Cites] Nature. 2008 Jun 19;453(7198):1072-8 [18469801.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1413-23 [18524993.001]
  • [Cites] Antioxid Redox Signal. 2008 Oct;10(10):1813-48 [18593226.001]
  • [Cites] Mol Cell. 2001 Oct;8(4):795-806 [11684015.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] Gene. 2003 Mar 13;306:1-12 [12657462.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):10002-7 [12890867.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2632-7 [12829601.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):675-86 [14701740.001]
  • [Cites] Leukemia. 2004 Apr;18(4):727-33 [14961028.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3167-74 [15070699.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(14):6172-83 [15226421.001]
  • [Cites] Hematol Oncol Clin North Am. 2004 Jun;18(3):671-84, x [15271399.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13312-7 [15326310.001]
  • [Cites] Am J Med. 1977 Oct;63(4):542-7 [269664.001]
  • [Cites] EMBO J. 1994 Feb 1;13(3):504-10 [8313895.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2013-6 [7718873.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2371-8 [7662984.001]
  • [Cites] Stem Cells. 1995 Jul;13(4):445-52 [7549904.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):154-8 [8563753.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13137-42 [8917557.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] J Biol Chem. 1997 Aug 8;272(32):19633-6 [9289489.001]
  • [Cites] Methods Mol Biol. 1998;93:59-66 [9664527.001]
  • [Cites] Oncogene. 1998 Oct 15;17(15):1889-92 [9788431.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):3931-4 [10463586.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3746-53 [15304390.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]
  • [Cites] J Exp Med. 2004 Dec 20;200(12):1689-95 [15611295.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Feb;157(1):53-61 [15676148.001]
  • [Cites] J Biol Chem. 2005 Feb 18;280(7):5361-9 [15574429.001]
  • [Cites] Br J Haematol. 2006 May;133(4):400-2 [16643447.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2794-9 [16477019.001]
  • [Cites] Blood. 2006 May 15;107(10):4080-9 [16418324.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 9;103(19):7444-9 [16651519.001]
  • [Cites] Cell Cycle. 2006 May;5(9):994-1000 [16687921.001]
  • [Cites] Blood. 2006 Jul 1;108(1):319-27 [16527898.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6082-93 [16880519.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1353-62 [16670262.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Cell Cycle. 2006 Dec;5(24):2862-6 [17172863.001]
  • [Cites] EMBO J. 2007 Mar 7;26(5):1456-66 [17318191.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4594-9 [17360569.001]
  • [Cites] Clin Cancer Res. 2007 Mar 15;13(6):1638-42 [17363515.001]
  • [Cites] Blood. 2007 May 1;109(9):4016-9 [17213283.001]
  • [Cites] Leukemia. 2007 May;21(5):926-35 [17330101.001]
  • [Cites] J Natl Cancer Inst. 2007 May 2;99(9):680-93 [17470736.001]
  • [Cites] Blood. 2007 May 15;109(10):4399-405 [17284533.001]
  • [Cites] Nat Rev Cancer. 2007 Jun;7(6):441-53 [17522713.001]
  • [Cites] Haematologica. 2007 Jun;92(6):834-7 [17550857.001]
  • [Cites] J Pathol. 2007 Aug;212(4):402-10 [17503411.001]
  • [Cites] Cell. 2007 Jul 13;130(1):51-62 [17632056.001]
  • [Cites] Blood. 2007 Aug 1;110(3):994-1003 [17475908.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2408-21 [17717597.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Nov;46(11):1039-50 [17696194.001]
  • [Cites] Blood. 2007 Oct 15;110(8):2991-5 [17625066.001]
  • [Cites] Biochem Soc Trans. 2007 Nov;35(Pt 5):1347-51 [17956348.001]
  • [Cites] Lancet Oncol. 2007 Nov;8(11):1018-29 [17976612.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4005-11 [17785585.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):528-41 [18068630.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2076-81 [18250304.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2843-53 [18156496.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3735-41 [18202228.001]
  • [Cites] Blood. 2009 Mar 12;113(11):2517-25 [19141860.001]
  • [Cites] Cancer Cell. 2009 Apr 7;15(4):341-52 [19345332.001]
  • [Cites] Oncogene. 2009 Apr 9;28(14):1669-81 [19234487.001]
  • [Cites] Nature. 2009 Apr 9;458(7239):776-9 [19169242.001]
  • [Cites] J Clin Invest. 2009 May;119(5):1109-23 [19363292.001]
  • [Cites] Nat Med. 2009 May;15(5):566-71 [19363496.001]
  • [Cites] Leukemia. 2009 May;23(5):892-9 [19158832.001]
  • [Cites] Cell Stem Cell. 2009 Jun 5;4(6):559-67 [19497284.001]
  • [Cites] Leukemia. 2009 Jun;23(6):1054-61 [19282833.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):783-92 [19503090.001]
  • [Cites] Am J Hematol. 2009 Aug;84(8):517-22 [19544476.001]
  • [Cites] Best Pract Res Clin Haematol. 2009 Jun;22(2):181-90 [19698927.001]
  • [Cites] Cancer Cell. 2009 Sep 8;16(3):232-45 [19732723.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3299-308 [19625708.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3292-8 [19654405.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1862-6 [15528314.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Mar;157(2):104-8 [15721630.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1659-69 [15747376.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4893-4 [15933063.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4100-9 [15867198.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1573-8 [15990860.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2128-37 [15914554.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6432-40 [16007188.001]
  • [Cites] Cancer Res. 2005 Oct 1;65(19):8912-9 [16204063.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):355-68 [16286244.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1118-24 [16205638.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2507-16 [16293596.001]
  • [Cites] Haematologica. 2006 Apr;91(4):513-21 [16533723.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6338-43 [16606850.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93 [16618932.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1758-66 [10688835.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Cancer Res. 2008 Sep 1;68(17):6884-8 [18757400.001]
  • [Cites] Cancer Cell. 2008 Sep 9;14(3):238-49 [18772113.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1806-7 [18668129.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Dec;47(12):1110-7 [18767145.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3847-55 [18650450.001]
  • [Cites] Leukemia. 2008 Nov;22(11):1975-89 [19002192.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 18;105(46):17967-72 [19004799.001]
  • [Cites] Cancer Res. 2008 Dec 1;68(23):9624-33 [19047139.001]
  • [Cites] Cancer Cell. 2008 Dec 9;14(6):485-93 [19061839.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2008;:436-42 [19074122.001]
  • [Cites] Mol Cancer Res. 2008 Dec;6(12):1830-40 [19074828.001]
  • [Cites] Mol Cancer Ther. 2008 Dec;7(12):3834-41 [19056677.001]
  • [Cites] Leukemia. 2009 Feb;23(2):279-86 [19020542.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3925-9 [19237556.001]
  • [Cites] Blood. 2009 Dec 10;114(25):5191-200 [19855080.001]
  • [Cites] Blood. 2010 Feb 4;115(5):1049-53 [19965645.001]
  • [Cites] Cell. 2010 Mar 5;140(5):652-65 [20211135.001]
  • [Cites] Leukemia. 2010 Mar;24(3):638-40 [19865111.001]
  • [Cites] Haematologica. 2010 Apr;95(4):582-8 [20015884.001]
  • [Cites] Leukemia. 2010 Aug;24(8):1445-9 [20520635.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1969-72 [18401418.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Blood. 2002 Jan 1;99(1):319-25 [11756187.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8236-48 [11781838.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2255-66 [11884611.001]
  • [Cites] Acta Haematol. 2002;107(2):76-94 [11919388.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7622-7 [12032333.001]
  • [Cites] Mutat Res. 2002 Jun;511(2):145-78 [12052432.001]
  • [Cites] Cancer. 2002 Jun 1;94(11):2996-9 [12115389.001]
  • [Cites] Leuk Res. 2002 Nov;26(11):1011-6 [12363470.001]
  • [Cites] Blood. 2003 Jan 15;101(2):655-63 [12393654.001]
  • [Cites] Blood. 2003 Jan 15;101(2):690-8 [12509383.001]
  • (PMID = 20592475.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA123014; United States / NCI NIH HHS / CA / R21 CA133646; United States / NCI NIH HHS / CA / R01 CA123014; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA133646; United States / NCI NIH HHS / CA / CA095512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 144
  • [Other-IDs] NLM/ PMC2898591
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92. Shen Q, Zhou JW, Zhu GR, Yang YY, Qiu HR, Zhu GR, Xia W, Jiang PJ: [Chronic myeloid leukemia onset with marked thrombocythemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):247-51
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  • [Title] [Chronic myeloid leukemia onset with marked thrombocythemia].
  • This study was aimed to investigate the clinical, pathological and biological features of a special case of chronic myeloid leukemia (CML) with marked thrombocythemic onset.
  • The morphological changes of cells were analyzed by using bone marrow smear and biopsy; Ph chromosome, a specific marker of CML, was assayed by conventional chromosomal analysis and fluorescence in situ hybridization, bcr/abl fusion gene was detected by reverse transcription-polymerase chain reaction.
  • The results indicated that CML mimicked essential thrombocythemia (ET) at presentation was relatively rare and might be misdiagnosed as ET, bone marrow smear and biopsy revealed, marked thrombocytosis and moderate leukocytosis; RT-PCR, FISH and conventional chromosomal analysis demonstrated the existence of Ph chromosome and bcr/abl fusion gene.
  • This special CML could progress into accelerated phase or blast crisis.
  • Patients diagnosed as Ph+ ET might progress into CML and showed a high tendency to myelofibrosis and blastic transformation.
  • It is concluded that the value of routine cytogenetical and molecular biological analysis in diagnosis for potential CML cases, which mimicked ET as in this presentation, is very distinctive, and the importance is magnified by the recent availability of imatinib, a specific inhibitor of the bcr/abl tyrosine kinase produced by the Philadelphia chromosome.
  • Every case of "ET" should be tested for the Philadelphia chromosome and bcr/abl transcript.

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  • (PMID = 16638190.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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93. Nicolini FE, Corm S, Lê QH, Sorel N, Hayette S, Bories D, Leguay T, Roy L, Giraudier S, Tulliez M, Facon T, Mahon FX, Cayuela JM, Rousselot P, Michallet M, Preudhomme C, Guilhot F, Roche-Lestienne C: Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP). Leukemia; 2006 Jun;20(6):1061-6
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  • [Title] Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospective analysis from the French intergroup of CML (Fi(phi)-LMC GROUP).
  • The emergence of ABL point mutations is the most frequent cause for imatinib resistance in chronic myelogenous leukemia (CML) patients and can occur during any phase of the disease; however, their clinical impact remains controversial.
  • In this study, we retrospectively analyzed the predictive impact of 94 BCR-ABL kinase domain mutations (18 T315I, 26 P-loop, 50 in other sites) found in 89 imatinib-resistant CML patients.
  • At imatinib onset, 64% of patients (57/89) were in chronic phase (CP), 24% (21/89) in accelerated phase (AP) and 12% (11/89) in blastic phase (BP).
  • T315I and P-loop mutations were preferentially discovered in accelerated phase of BP CML, and other types of mutations in CP (P=0.003).
  • Therefore, P-loop and T315I mutations selectively impair the outcome of imatinib-resistant CML patients, in contrast to other mutations, which may benefit from dose escalation of imatinib, able to improve or stabilize disease response.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Point Mutation. Pyrimidines / therapeutic use

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  • (PMID = 16642048.001).
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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94. Sakamaki H, Ishizawa K, Taniwaki M, Fujisawa S, Morishima Y, Tobinai K, Okada M, Ando K, Usui N, Miyawaki S, Utsunomiya A, Uoshima N, Nagai T, Naoe T, Motoji T, Jinnai I, Tanimoto M, Miyazaki Y, Ohnishi K, Iida S, Okamoto S, Seriu T, Ohno R: Phase 1/2 clinical study of dasatinib in Japanese patients with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia. Int J Hematol; 2009 Apr;89(3):332-41
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  • [Title] Phase 1/2 clinical study of dasatinib in Japanese patients with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • A phase 1/2 study was conducted to assess the safety and efficacy of dasatinib in Japanese patients with chronic myelogenous leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) resistant or intolerant to imatinib.
  • In phase 1, 18 patients with chronic phase (CP) CML were treated with dasatinib 50, 70, or 90 mg twice daily to evaluate safety.
  • In phase 2, dasatinib 70 mg was given twice daily to CP-CML patients for 24 weeks and to CML patients in accelerated phase (AP)/blast crisis (BC) or Ph(+) ALL for 12 weeks.
  • In the CP-CML group (n = 30) complete hematologic response was 90% and major cytogenetic response (MCyR) 53%.
  • In the AP/BC-CML group (n = 11) major hematologic response (MaHR) was 64% and MCyR 27%, whereas in the Ph(+) ALL group (n = 13) MaHR was 38% and MCyR 54%.
  • Dasatinib therapy resulted in high rates of hematologic and cytogenetic response, suggesting that dasatinib is promising as a new treatment for Japanese CML and Ph(+) ALL patients resistant or intolerant to imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Asian Continental Ancestry Group. Dasatinib. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Middle Aged. Mutation / genetics


95. Deremer DL, Ustun C, Natarajan K: Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia. Clin Ther; 2008 Nov;30(11):1956-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib: a second-generation tyrosine kinase inhibitor for the treatment of chronic myelogenous leukemia.
  • BACKGROUND: Nilotinib, a second-generation tyrosine kinase inhibitor (TKI) formerly known as AMN107, was approved by the US Food and Drug Administration (FDA) on October 29, 2007, for the treatment of adult patients with chronic-phase (CP) and accelerated-phase (AP) Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) resistant to or intolerant of prior treatment that included imatinib.
  • OBJECTIVE: The purpose of this review was to evaluate the pharmacology, pharmacokinetic properties, and pharmacodynamic properties of nilotinib; results of clinical trials in patients with CML, Ph+ acute lymphoblastic leukemia (ALL), and gastrointestinal stromal tumors (GISTs); and potential drug interactions.
  • Search terms included, but were not limited to, nilotinib, AMN107, chronic myelogenous leukemia, acute lymphoblastic leukemia, bcr-abl, imatinib resistance, adverse events, pharmacology, and clinical trials.
  • RESULTS: Nilotinib is an orally bioavailable derivative of imatinib with improved specificity toward the breakpoint cluster region-Abelson murine leukemia (bcr-abl) viral protooncogene.
  • In preclinical studies, nilotinib was found to have activity against 32 of 33 imatinib-resistant bcr-abl mutations, but not against the T3151 mutation.
  • In 2 Phase II, open-label, single-arm clinical studies, nilotinib was found to be beneficial in patients with CML that was imatinib resistant or intolerant.
  • Overall, 58% of patients with CML-CP achieved a major cytogenetic response; 42%, a complete cytogenetic response; and 77%, a complete hematologic response (CHR).
  • Of patients whose disease had progressed to AP, nilotinib was associated with major cytogenetic response in 32%; complete cytogenetic response in 19%; and CHR in 30%.
  • At 12 months, an estimated 56% of patients lacked progression of disease, and the estimated overall survival rate was 82%.
  • CONCLUSIONS: Nilotinib is an oral second-generation bcr-abl TKI indicated for the treatment of imatinib resistant or -intolerant Ph+ CML-CP and -AP in adults.
  • Positive clinical activity and tolerability have been reported in clinical trials.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Fusion Proteins, bcr-abl. Gastrointestinal Stromal Tumors / drug therapy. Humans. Models, Biological. Molecular Structure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


96. Klyuchnikov E, Kröger N, Brummendorf TH, Wiedemann B, Zander AR, Bacher U: Current status and perspectives of tyrosine kinase inhibitor treatment in the posttransplant period in patients with chronic myelogenous leukemia (CML). Biol Blood Marrow Transplant; 2010 Mar;16(3):301-10
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  • [Title] Current status and perspectives of tyrosine kinase inhibitor treatment in the posttransplant period in patients with chronic myelogenous leukemia (CML).
  • Following the introduction of tyrosine kinase inhibitors (TKIs) in chronic myelogenous leukemia (CML), allogeneic stem cell transplantation (SCT) took a shift toward high-risk patients.
  • Imatinib was shown to be effective in patients with molecular or hematologic relapse of chronic or accelerated phase posttransplant (CP, AP), whereas outcomes in blast phase were more unfavorable.
  • The combination of imatinib with donor lymphocytes did not result in increased toxicity or graft-versus-host disease (GVHD).
  • In conclusion, TKIs of the first- and second-generation are promising options for the posttransplant period of patients with CML, but algorithms for dosage, intervals from SCT, duration of application, and the combination with donor lymphocytes still have to be developed.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Stem Cell Transplantation

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  • [Copyright] Copyright (c) 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
  • (PMID = 19744571.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 65
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97. Fava C, Kantarjian HM, Jabbour E, O'Brien S, Jain N, Rios MB, Garcia-Manero G, Ravandi F, Verstovsek S, Borthakur G, Shan J, Cortes J: Failure to achieve a complete hematologic response at the time of a major cytogenetic response with second-generation tyrosine kinase inhibitors is associated with a poor prognosis among patients with chronic myeloid leukemia in accelerated or blast phase. Blood; 2009 May 21;113(21):5058-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Failure to achieve a complete hematologic response at the time of a major cytogenetic response with second-generation tyrosine kinase inhibitors is associated with a poor prognosis among patients with chronic myeloid leukemia in accelerated or blast phase.
  • Second-generation tyrosine kinase inhibitors are effective in Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) and chronic myeloid leukemia (CML).
  • Occasionally, patients with Ph(+) ALL, or accelerated phase (AP) or blast phase (BP) CML achieve a major cytogenetic response (MCyR) but not a complete hematologic response (CHR).
  • We analyzed 126 patients with CML in AP or BP, or with Ph(+) ALL treated with dasatinib or nilotinib after imatinib failure.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Blast Crisis. Cytogenetic Analysis. Dasatinib. Female. Humans. Imatinib Mesylate. Leukemia, Myeloid, Accelerated Phase. Male. Middle Aged. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Prognosis. Pyrimidines / administration & dosage. Remission Induction / methods. Survival Analysis. Thiazoles / administration & dosage. Treatment Failure. Young Adult

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  • [Cites] Blood. 2006 Sep 15;108(6):1809-20 [16709930.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Blood. 2007 May 15;109(10):4143-50 [17264298.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2309-15 [17496201.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Br J Haematol. 1998 Apr;101(1):111-8 [9576191.001]
  • [Cites] Clin Adv Hematol Oncol. 2008 Feb;6(2):113-7 [18347562.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1200-6 [18401416.001]
  • [Cites] Semin Hematol. 2003 Jan;40(1):79-86 [12563614.001]
  • [Cites] Cancer. 2003 Feb 15;97(4):1033-41 [12569603.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3097-9 [12842982.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1834-9 [18048643.001]
  • (PMID = 19282457.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC4081366
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98. Gucluler G, Baran Y: Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells. Hematology; 2009 Jun;14(3):139-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel enhances the cytotoxic effects of imatinib on Philadelphia positive human chronic myeloid leukemia cells.
  • Chronic myelogenous leukemia (CML) results from a translocation between chromosomes 9 and 22 which generates BCR/ABL fusion protein and characterized by uncontrolled proliferation of immature white blood cells.
  • Imatinib, a molecularly targeting anticancer agent, is used widely for the treatment of CML and showed significant activity in chronic and accelerated phases but much less in blast crisis phase.
  • The resistance to imatinib especially in blast crisis phase is recognized as a major problem in the treatment of CML patients.
  • Docetaxel is shown to arrest cells in G2/M phase of the cell cycle which makes cells more sensitive to chemo- and radiotherapy.
  • In this study, we aimed to increase chemosensitivity of human K562 CML cells to imatinib in combination with docetaxel.
  • Taken together, our results showed that the combination of imatinib and docetaxel decreased cellular proliferation and increased apoptosis in human K562 chronic myeloid leukemia cells as compared to any agent alone.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology. Radiation-Sensitizing Agents / pharmacology. Taxoids / pharmacology

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  • (PMID = 19490758.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Radiation-Sensitizing Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 8A1O1M485B / Imatinib Mesylate; EC 3.4.22.- / Caspase 3
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99. Brave M, Goodman V, Kaminskas E, Farrell A, Timmer W, Pope S, Harapanhalli R, Saber H, Morse D, Bullock J, Men A, Noory C, Ramchandani R, Kenna L, Booth B, Gobburu J, Jiang X, Sridhara R, Justice R, Pazdur R: Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate. Clin Cancer Res; 2008 Jan 15;14(2):352-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate.
  • Food and Drug Administration approved dasatinib (Sprycel; Bristol-Myers Squibb), a new small-molecule inhibitor of multiple tyrosine kinases, for the treatment of adults with chronic phase, accelerated phase, or myeloid or lymphoid blast phase chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) with resistance or intolerance to prior therapy including imatinib.
  • The primary efficacy end point in chronic phase CML was major cytogenetic response.
  • The primary end point in accelerated phase, myeloid phase, and lymphoid blast phase CML, and Ph(+) ALL was major hematologic response.
  • In patients with chronic phase CML, the major cytogenetic response rate was 45% with a complete cytogenetic response rate of 33%.
  • Major hematologic response rates in patients with accelerated phase CML, myeloid CML, lymphoid blast CML, and Ph(+) ALL were 59%, 32%, 31%, and 42%, respectively.
  • Median response durations in chronic phase, accelerated phase, and myeloid phase CML had not been reached.
  • The median durations of major hematologic response were 3.7 months in lymphoid blast CML and 4.8 months in Ph(+) ALL.
  • CONCLUSIONS: This report describes the Food and Drug Administration review supporting the approval of dasatinib for CML and Ph(+) ALL based on the rates and durability of cytogenetic and hematologic responses.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Benzamides. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dasatinib. Drug Approval. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Multicenter Studies as Topic. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration


100. Burke MJ, Trotz B, Luo X, Weisdorf DJ, Baker KS, Wagner JE, Verneris MR: Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients. Bone Marrow Transplant; 2009 Aug;44(3):169-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib use either pre- or post-allogeneic hematopoietic cell transplantation (allo-HCT) does not increase cardiac toxicity in chronic myelogenous leukemia patients.
  • Since the introduction of imatinib mesylate, the role of allogeneic hematopoietic cell transplantation (allo-HCT) for CML has essentially been reserved for patients with advanced disease or imatinib resistance.
  • We investigated the outcome of 61 patients with CML who received a myeloablative allo-HCT at the University of Minnesota between 1999 and 2006.
  • Thirty-seven patients were in first chronic phase and twenty-four patients in a second chronic or accelerated phase at the time of HCT.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Heart Diseases / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / adverse effects. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects
  • [MeSH-minor] Adolescent. Adult. Benzamides. Child. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome. Young Adult






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