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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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2. 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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  • (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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3. 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


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4. 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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5. 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


6. 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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7. 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


8. Breccia M, Muscaritoli M, Cannella L, Stefanizzi C, Frustaci A, Alimena G: Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib. Leuk Res; 2008 Oct;32(10):1626-8
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  • [Title] Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blood Glucose / analysis. Diabetes Complications / drug therapy. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 18321570.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [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 / Blood Glucose; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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9. 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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  • [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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10. 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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  • [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


11. Kantarjian H, Giles F, Bhalla K, Pinilla J, Larson RA, Gattermann N, Ottmann OG, Gallagher NJ, Baccarani M, leCoutre P: Nilotinib in chronic myeloid leukemia patients in chronic phase (CML-CP) with imatinib (IM) resistance or intolerance: Longer follow-up results of a phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):7029

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib in chronic myeloid leukemia patients in chronic phase (CML-CP) with imatinib (IM) resistance or intolerance: Longer follow-up results of a phase II study.
  • : 7029 Background: Nilotinib is a potent and highly selective BCR-ABL inhibitor approved for the treatment of Ph+ CML patients (pts) in CP or accelerated phase who are resistant or intolerant to prior therapy including IM.
  • This study evaluated the efficacy and safety of nilotinib (400 mg bid) in CML-CP pts resistant or intolerant to IM.
  • RESULTS: CML-CP pts (n = 321, 70% IM-resistant, 30% IM-intolerant with resistance) with a minimum follow-up of 19 months (mos) were evaluated; 72% were treated with ≥600 mg/day IM prior to enrollment.
  • CONCLUSIONS: These results demonstrate that nilotinib was highly effective, with rapid and durable responses in CML-CP pts failing prior therapy due to resistance or intolerance.

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  • (PMID = 27961402.001).
  • [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] Journal Article
  • [Publication-country] United States
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12. Ghadyalpatil N, Banawali S, Kurkure P, Arora B, Bansal S, Amare P, Choughule A, Soy L, Singh R: Efficacy and tolerability of imatinib mesylate in pediatric chronic myeloid leukemia in a large cohort: Results from a tertiary care referral center in India. J Clin Oncol; 2009 May 20;27(15_suppl):10047

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy and tolerability of imatinib mesylate in pediatric chronic myeloid leukemia in a large cohort: Results from a tertiary care referral center in India.
  • : 10047 Background: Chronic myeloid leukemia (CML) is a rare disease in children and there is limited data of safety and efficacy of imatinib mesylate (IM) in this age group.
  • METHODS: We analyzed the outcomes of 48 consecutive children (September 1998 to December 2008) in chronic phase (CP) or accelerated phase (AP) CML not eligible for Allo-SCT and were treated with IM [Glivec (Novartis), through patient assistance programme GIPAP or Veenat (NATCO), generic brand for GIPAP ineligible patients] within 12 months of diagnosis.
  • RESULTS: The median age at the time of diagnosis was 12 years (range 3-18 years).
  • One patient had secondary IM resistance and had progressive disease even on dose escalation.
  • Two patients in AP at diagnosis achieved CCR at 5 and 7 months and continue to be in CCR.
  • CONCLUSIONS: Results from this largest single center study indicate that outcome of children with CML receiving IM is similar to adults.

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  • (PMID = 27962473.001).
  • [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] Journal Article
  • [Publication-country] United States
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13. Martinelli G, Castagnetti F, Poerio A, Breccia M, Palandri F, Alimena G, Pane F, Saglio G, Baccarani M, Rosti G: Molecular responses with nilotinib 800 mg daily as first-line treatment of chronic myeloid leukemia in chronic phase: Results of a phase II trial of the GIMEMA CML WP. J Clin Oncol; 2009 May 20;27(15_suppl):7074

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular responses with nilotinib 800 mg daily as first-line treatment of chronic myeloid leukemia in chronic phase: Results of a phase II trial of the GIMEMA CML WP.
  • To investigate the efficacy and the safety of nilotinib 400 mg BID in untreated, early chronic phase (ECP) CML patients (pts), the GIMEMA CML WP is conducting a multicentric, phase II study trial (ClinicalTrials.gov NCT00481052 ).
  • One patient progressed at 6 months to accelerated-blastic phase with the T315I mutation.
  • CONCLUSIONS: In ECP Ph-pos CML pts both cytogenetic and molecular responses to nilotinib are substantially faster than the responses to IM.

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  • (PMID = 27961457.001).
  • [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] Journal Article
  • [Publication-country] United States
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14. Verma D, Kantarjian H, Jones D, Borthakur G, Garcia-Manero G, Thomas DA, Verstovsek S, Rios M, Cortes J: Chronic myeloid leukemia (CML) with e1a2 BCR-ABL fusion transcript type: Analysis of characteristics, outcomes, and prognostic significance. J Clin Oncol; 2009 May 20;27(15_suppl):7030

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukemia (CML) with e1a2 BCR-ABL fusion transcript type: Analysis of characteristics, outcomes, and prognostic significance.
  • : 7030 Background: The most common BCR-ABL fusion transcripts in CML are e13a2 (b2a2) and e14a2 (b3a2).
  • Currently, there is no published series of data on efficacy of imatinib or other tyrosine kinase inhibitors (TKIs) in CML with e1a2.
  • METHODS: We analyzed records of 1,292 CML patients treated with TKI at our institution between January 2000 and November 2008.
  • RESULTS: 14 CML patients with e1a2 transcripts were identified, 9 in chronic phase (CP), 1 in accelerated phase (AP), and 4 in blast phase (BP).
  • Median age at diagnosis was 60 (range 28-86) years, median follow-up 39.5 (range 2-109) months.
  • 5 patients (2 post-interferon failure - 1 in CHR, 1 in PCyR; 3 frontline imatinib - 1 in CHR, 1 in CCyR, 1 non-responder) progressed to advanced phases (3 myeloid BP, 1 lymphoid BP, 1 AP) at a median 48 (range 4-92) months after CML diagnosis; with only 1 alive and in CMR after allogeneic SCT.
  • Six patients (5 CP, 1 AP) were alive at a median 39 (range 2-85) months after initial diagnosis: 4 with CHR (2 on imatinib, 1 nilotinib, 1 bosutinib), 1 with MCyR on imatinib, and 1 with CMR after allogeneic SCT.
  • CONCLUSIONS: CML with e1a2 BCR-ABL fusion transcripts is rare and is associated with an inferior outcome to therapy with TKI, with responses being usually short-lived.

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  • (PMID = 27961392.001).
  • [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] Journal Article
  • [Publication-country] United States
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15. Lima L, Assouline SE, Saxe D, Mann K, McLemore M, Souza L, Arellano M, Winton EF, Bernal-Mizrachi L, Khoury HJ: Does pre-imatinib (IM) fluorescence in situ hybridization (FISH) predict myelosuppression and outcomes in chronic myeloid leukemia (CML)? J Clin Oncol; 2009 May 20;27(15_suppl):7071

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does pre-imatinib (IM) fluorescence in situ hybridization (FISH) predict myelosuppression and outcomes in chronic myeloid leukemia (CML)?
  • : 7071 Background: IM-associated myelosuppression occurs in 4-40% of CML patients (pts) vs. 1-16% in GIST.
  • In the absence of clinically applicable methods to quantitate Ph+/Ph- progenitor ratio, we hypothesized that the pre-IM percentage of BCR-ABL+ cells measured by FISH predicts myelosuppression.
  • METHODS: FISH pre-IM was available in 58 CML pts with chronic phase (CP, n=52), or advanced phase (AP, accelerated =3, blast =3) at 2 institutions.
  • Myelosuppression AP pts expired (CML=2, GVHD=1); 1 after complete hematologic (CHR) and minor cytogenetic response (CTGR), 1 after partial HR, and 1 resistant disease.
  • CONCLUSIONS: Higher FISH pre-IM identifies a group of CML pts who develop myelosuppression and are less likely to respond to IM.

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  • (PMID = 27961454.001).
  • [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] Journal Article
  • [Publication-country] United States
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16. Prabhash K, Vora T, Ghadyalpatil NS, Rangarajan B, Hingmire SS, Menon H, Jain P, Kurkure PA, Parikh PM: Patterns of imatinib resistance mutation analysis in chronic myeloid leukemia (CML) patients on imatinib at the time of loss of response to the drug in Asian Indian subjects. J Clin Oncol; 2009 May 20;27(15_suppl):7079

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of imatinib resistance mutation analysis in chronic myeloid leukemia (CML) patients on imatinib at the time of loss of response to the drug in Asian Indian subjects.
  • : 7079 Background: The treatment of (CML) has undergone major changes in the past decade with the introduction of tyrosine kinase inhibitors (TKI).
  • METHODS: We identified 17 males and 8 female patients with median age 40 yrs (range 9-55 years) with CML who were on imatinib at the time of loss of hematologic response (HR), cytogenetic (CyR), or molecular response (MR) and performed imatinib-resistance mutation analysis.
  • RESULTS: This group included 22 patients with chronic phase (CP) disease, 2 patients with accelerated phase (AP), and 1 patient with extramedullary blast crisis (BC).
  • Fourteen patients received treatment with agents other than imatinib as the first-line therapy due to either nonavailability of the drug at the time of diagnosis in India, but were started on imatinib when drug became available.

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  • (PMID = 27961486.001).
  • [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] Journal Article
  • [Publication-country] United States
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17. Cortes JE, Khoury HJ, Corm S, Nicolini F, Schenk T, Jones D, Hochhaus A, Craig AR, Humphriss E, Kantarjian H, Omacetaxine 202 Study Group: Subcutaneous omacetaxine mepesuccinate in imatinib-resistant chronic myeloid leukemia (CML) patients (Pts) with the T315I mutation: Data from an ongoing phase II/III trial. J Clin Oncol; 2009 May 20;27(15_suppl):7008

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous omacetaxine mepesuccinate in imatinib-resistant chronic myeloid leukemia (CML) patients (Pts) with the T315I mutation: Data from an ongoing phase II/III trial.
  • : 7008 Background: Omacetaxine (OM), a first-in-class cetaxine shows clinical activity against Ph+ CML with a mechanism independent of tyrosine kinase inhibition.
  • METHODS: Adult Pts with T315I+ CML following TKI failure received OM induction at 1.25 mg/m<sup>2</sup> subcutaneous (SC) twice daily (BID) for 14 days every 28 days followed by maintenance at 1.25 mg/m<sup>2</sup> SC BID for 7 days every 28 days (maintenance after at least one induction cycle and achievement of hematologic response).
  • RESULTS: 66 pts (39 chronic [CP], 16 accelerated [AP] and 11 blast phase [BP]) have been enrolled.
  • Median disease duration is 58 mos.
  • CONCLUSIONS: Omacetaxine in T315I+ CML Pts results in de-selection of the T315I clone and induces hematologic and cytogenetic responses.

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  • (PMID = 27961380.001).
  • [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] Journal Article
  • [Publication-country] United States
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18. Le Coutre PD, Giles F, Hochhaus A, Apperley JF, Ossenkoppele G, Haque A, Gallagher NJ, Baccarani M, Cortes J, Kantarjian H: Nilotinib in chronic myeloid leukemia patients in accelerated phase (CML-AP) with imatinib (IM) resistance or intolerance: Longer follow-up results of a phase II study. J Clin Oncol; 2009 May 20;27(15_suppl):7057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib in chronic myeloid leukemia patients in accelerated phase (CML-AP) with imatinib (IM) resistance or intolerance: Longer follow-up results of a phase II study.
  • : 7057 Background: Nilotinib is a potent and highly selective BCR-ABL inhibitor approved for the treatment of Ph+ CML patients (pts) in chronic phase or AP who are resistant or intolerant to prior therapy including IM.
  • This study evaluated the efficacy and safety of nilotinib (400 mg bid) in CML-AP pts resistant or intolerant to IM.
  • RESULTS: 137 CML-AP pts (80% IM-resistant; 20% IM-intolerant with resistance) with minimum follow-up of 11 months (mos) (median age, 57 years; median duration of prior IM treatment, 28 mos) were included.
  • CONCLUSIONS: These long-term follow-up results confirm that nilotinib induces rapid and durable responses in CML-AP pts who failed prior IM due to intolerance or resistance, with a favorable risk/benefit.

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  • (PMID = 27961447.001).
  • [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] Journal Article
  • [Publication-country] United States
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19. Wetzler M, Hellmann A, Lipton J, Roy L, Jones D, Schenk T, Hochhaus A, Benichou A, Kantarjian H, Cortes J, Omacetaxine 203 Study Group: Subcutaneous omacetaxine mepesuccinate in chronic myeloid leukemia (CML) patients resistant or intolerant to two or more tyrosine kinase inhibitors (TKIs): Data from an ongoing phase II trial. J Clin Oncol; 2009 May 20;27(15_suppl):7027

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous omacetaxine mepesuccinate in chronic myeloid leukemia (CML) patients resistant or intolerant to two or more tyrosine kinase inhibitors (TKIs): Data from an ongoing phase II trial.
  • : 7027 Background: Omacetaxine (OM), a first-in-class cetaxine, shows clinical activity against Ph+ CML with a mechanism of action independent to tyrosine kinase inhibition.
  • Patients (Pts) who have failed multiple TKIs may benefit from an alternative therapy for CML.
  • METHODS: Pts include adult CML following resistance or intolerance to at least 2 TKIs.
  • T315I+ Pts are enrolled in a separate trial.
  • RESULTS: 60 pts (30 chronic phase [CP], 14 accelerated phase [AP], and 16 blast phase [BP] have been enrolled with 51% having failed at least 3 prior TKIs.
  • Median disease duration: 74 months.
  • At baseline, 38.5% of pts had Bcr-Abl mutations including 9.6% with compound mutations.
  • Efficacy data are available for 30 Pts: Conclusions: Omacetaxine in multi-TKI resistant or intolerant CML is well tolerated and has achieved hematologic and cytogenetic responses in these heavily pre-treated Pts.

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  • (PMID = 27961400.001).
  • [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] Journal Article
  • [Publication-country] United States
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20. Khoury HJ, Lima L, Saxe D, Mann KP, Arellano M, Heffner L, Bernal-Mizrachi L, McLemore M, Langston A, Winton E: Monitoring chronic myeloid leukemia (CML) response to tyrosine kinase inhibitors (TKI) and homoharringtonine (HHT) using peripheral blood (PB) fluorescence in situ hybridization (FISH) and quantitative RT-PCR (Q-PCR): Are bone marrow biopsies still needed? J Clin Oncol; 2009 May 20;27(15_suppl):7064

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring chronic myeloid leukemia (CML) response to tyrosine kinase inhibitors (TKI) and homoharringtonine (HHT) using peripheral blood (PB) fluorescence in situ hybridization (FISH) and quantitative RT-PCR (Q-PCR): Are bone marrow biopsies still needed?
  • : 7064 Background: The purpose of this study is to compare simultaneously obtained PB and bone marrow (BM) BCR-ABL FISH and Q-PCR to monitor response to TKI and HHT in CML.
  • METHODS: Between January 2005 and December 2008, 52 patients (pts) with chronic (n = 37, 80%), accelerated (n = 6, 7%), and blast phase (n = 9, 14%) CML had 112 simultaneous PB and BM FISH and Q-PCR before and/or after start of imatinib (IM, n = 27), dasatinib (n = 9), nilotinib (n = 1), bosutinib (n = 13), or HHT (n = 2) for newly diagnosed (n = 27), IM resistant (n = 20), or IM intolerant (n = 5) CML.
  • 13 (26%) had chromosomal abnormalities in addition to the Philadelphia chromosome, and 10 (20%) had a detectable BCR-ABL mutation including the T315I in 2 pts.
  • Correlation was not affected by the presence of additional chromosomal abnormalities, phase of the disease, treatment (TKI or HHT), or the number of prior therapies.
  • CONCLUSIONS: FISH and Q-PCR are reliable methods to monitor CML response to TKI and HHT in patients with CML and may render the need for BM biopsy monitoring obsolete.

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  • (PMID = 27961440.001).
  • [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] Journal Article
  • [Publication-country] United States
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21. 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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  • [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


22. 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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  • [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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23. 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

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  • (PMID = 19938637.001).
  • [ISSN] 0564-3783
  • [Journal-full-title] T︠S︡itologii︠a︡ i genetika
  • [ISO-abbreviation] Tsitol. Genet.
  • [Language] ukr
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Ukraine
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24. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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25. 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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  • [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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26. 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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27. 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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  • [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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28. 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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29. 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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  • [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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30. 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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31. 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


32. 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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33. 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


34. 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


35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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36. 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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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


38. 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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39. 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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  • [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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40. 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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  • [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

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  • (PMID = 18223208.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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41. 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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  • [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.
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  • (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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42. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


43. 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


44. 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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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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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46. 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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47. 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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48. 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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49. 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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50. 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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  • (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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51. 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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52. Kumar L: Chronic myelogenous leukaemia (CML): an update. Natl Med J India; 2006 Sep-Oct;19(5):255-63
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  • [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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53. 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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54. 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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  • [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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55. 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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56. 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


57. 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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58. Kantarjian H, Shah NP, Hochhaus A, Cortes J, Shah S, Ayala M, Moiraghi B, Shen Z, Mayer J, Pasquini R, Nakamae H, Huguet F, Boqué C, Chuah C, Bleickardt E, Bradley-Garelik MB, Zhu C, Szatrowski T, Shapiro D, Baccarani M: Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med; 2010 Jun 17;362(24):2260-70
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  • [Title] Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia.
  • BACKGROUND: Treatment with dasatinib, a highly potent BCR-ABL kinase inhibitor, has resulted in high rates of complete cytogenetic response and progression-free survival among patients with chronic myeloid leukemia (CML) in the chronic phase, after failure of imatinib treatment.
  • We assessed the efficacy and safety of dasatinib, as compared with imatinib, for the first-line treatment of chronic-phase CML.
  • METHODS: In a multinational study, 519 patients with newly diagnosed chronic-phase CML were randomly assigned to receive dasatinib at a dose of 100 mg once daily (259 patients) or imatinib at a dose of 400 mg once daily (260 patients).
  • The rate of major molecular response was higher with dasatinib than with imatinib (46% vs. 28%, P<0.0001), and responses were achieved in a shorter time with dasatinib (P<0.0001).
  • Progression to the accelerated or blastic phase of CML occurred in 5 patients who were receiving dasatinib (1.9%) and in 9 patients who were receiving imatinib (3.5%).
  • Since achieving complete cytogenetic response within 12 months has been associated with better long-term, progression-free survival, dasatinib may improve the long-term outcomes among patients with newly diagnosed chronic-phase CML. (ClinicalTrials.gov number, NCT00481247. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Dasatinib. Disease Progression. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Young Adult

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  • [Copyright] 2010 Massachusetts Medical Society
  • [CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]
  • [CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]
  • (PMID = 20525995.001).
  • [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/ NCT00481247
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; 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; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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59. Ding JH, Ma Y, Chen BA, Zhao G, Wang J, Sun YY, Cheng J, Su AL, Dong WM, Zhang Y: [Nonmyeloablative peripheral blood stem cell transplantation for chronic myeloid leukemia in chronic and accelerated phases]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Apr;16(2):373-6
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  • [Title] [Nonmyeloablative peripheral blood stem cell transplantation for chronic myeloid leukemia in chronic and accelerated phases].
  • The aim of this study was to investigate the effect of nonmyeloablative peripheral blood stem cell transplantation in treatment of chronic myeloid leukemia in chronic phase (CML-CP) and accelerated phase (CML-AP).
  • 24 patients with CML including 16 in CML-CP and 8 in CML-AP were treated with nonmyeloablative conditioning regimen for peripheral blood stem cell transplantation (PBHSCT).
  • 2 cases died of severe acute GVHD and 1 case died of chronic GVHD, 2 cases died of interstitial pneumonia and 1 case died of relapsed.
  • In conclusions, nonmyeloablative peripheral blood stem cell transplantation is an effective therapeutic method for CML patients in chronic phase and accelerated phase.


60. Kantarjian HM, Larson RA, Guilhot F, O'Brien SG, Mone M, Rudoltz M, Krahnke T, Cortes J, Druker BJ, International Randomized Study of Interferon and STI571 (IRIS) Investigators: Efficacy of imatinib dose escalation in patients with chronic myeloid leukemia in chronic phase. Cancer; 2009 Feb 01;115(3):551-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of imatinib dose escalation in patients with chronic myeloid leukemia in chronic phase.
  • BACKGROUND: Imatinib mesylate given orally at a daily dose of 400 mg is the standard of care as initial therapy for patients with chronic myeloid leukemia (CML) in chronic phase (CML-CP).
  • Treatment guidelines propose dose escalation based on clinical assessments of disease response.
  • METHODS: Response and survival were analyzed in a cohort of patients (n = 106) with newly diagnosed CML-CP who were enrolled on the International Randomized Study of Interferon and STI571 (IRIS) trial, who began treatment with imatinib at a dose of 400 mg daily, and who subsequently underwent dose escalation to either 600 mg or 800 mg daily.
  • RESULTS: Among all 106 patients who underwent dose escalation, the rates of freedom from progression to accelerated phase or blast phase and overall survival were 89% and 84% at 3 years after dose increase, respectively.
  • CONCLUSIONS: The results from this retrospective analysis supported imatinib dose escalation as an appropriate initial option for patients with CML-CP who were experiencing suboptimal cytogenetic response or resistance.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Benzamides. Clinical Trials as Topic. Disease-Free Survival. Drug Administration Schedule. Imatinib Mesylate. Survival Analysis. Treatment Outcome

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  • [Copyright] (c) 2008 American Cancer Society.
  • [ErratumIn] Cancer. 2010 Aug 1;116(15):3750. Santini, Valeria [added]
  • (PMID = 19117345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00006343
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632
  • [Publication-type] 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
  • [Other-IDs] NLM/ NIHMS676524; NLM/ PMC4445370
  • [Investigator] Durant S; Schwarer A; Joske D; Seymour J; Grigg A; Ma D; Arthur C; Bradstock K; Joshua D; Louwagi A; Martiat P; Bosly A; Shistok C; Lipton J; Forrest D; Walker I; Roy DC; Rubinger M; Bence-Bruckler I; Stewart D; Kovacs M; Turner AR; Birgens H; Bjerrum O; Facon T; Harousseau JL; Tulliez M; Guerci A; Blaise D; Maloisel F; Michallet M; Andreesen R; Nerl C; Freund M; Gattermann N; Ehninger G; Deininger M; Ottmann O; Peschel C; Fruehauf S; Neubauer A; le Coutre P; Aulitzky W; Fanin R; Rosti G; Mandelli F; Lazzarino M; Morra E; Carella A; Petrini M; Nobile F; Liso V; Ferrara F; Rizzoli V; Fiortoni G; Martinelli G; Ossenkoppele G; Browett P; Gedde-Dahl T; Tangen JM; Dahl I; Odrizoala J; Hernandez Boulda JC; Steegman JL; Canizo C; Diaz J; Grenena A; Fernandez MN; Stenke L; Paul C; Bjoreman M; Malm C; Wadenvik H; Nilsson PG; Turesson I; Hess U; Solenthaler M; Clark RE; Green AR; Holyoake TL; Lucas GS; Smith G; Milligan DW; Rule SJ; Burnett AK; Moroose R; Wetzler M; Bearden J; Cataland S; Robinowitz I; Meisenberg B; Thompson K; Graziano S; Emanuel P; Gross H; Cobb P; Bhatia R; Dakhil S; Irwin D; Issell B; Pavletic S; Kuebler P; Layhe E; Butra P; Glass J; Moore J; Grant B; Neill H; Herzig R; Burris H; Petersen B; Kalaycio M; Stirewalt D; Samlowski W; Berman E; Limentani S; Seay T; Shea T; Akard L; Smith G; Becker P; Devine S; Hart R; Veith R; Wade J; Brunvad M; Kalman L; Strickland D; Shurafa M; Bashey A; Shadduck R; Safah H; Rubenstein M; Collins R; Keller A; Tallman M; Pecora A; Agha M; Homes H; Guidice R; Santini V
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61. Chen Y, Peng C, Li D, Li S: Molecular and cellular bases of chronic myeloid leukemia. Protein Cell; 2010 Feb;1(2):124-32
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  • [Title] Molecular and cellular bases of chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the overproduction of granulocytes, which leads to high white blood cell counts and splenomegaly in patients.
  • Based on clinical symptoms and laboratory findings, CML is classified into three clinical phases, often starting with a chronic phase, progressing to an accelerated phase and ultimately ending in a terminal phase called blast crisis.
  • Blast crisis phase of CML is clinically similar to an acute leukemia; in particular, B-cell acute lymphoblastic leukemia (B-ALL) is a severe form of acute leukemia in blast crisis, and there is no effective therapy for it yet.
  • CML is induced by the BCR-ABL oncogene, whose gene product is a BCR-ABL tyrosine kinase.
  • Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML.
  • However, the inability of BCR-ABL kinase inhibitors to completely kill leukemia stem cells (LSCs) indicates that these kinase inhibitors are unlikely to cure CML.
  • In addition, drug resistance due to the development of BCRABL mutations occurs before and during treatment of CML with kinase inhibitors.
  • In this review, we will focus on LSCs in CML by summarizing and discussing available experimental results, including the original studies from our own laboratory.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / enzymology. Neoplastic Stem Cells / pathology. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] 5-Lipoxygenase-Activating Proteins / metabolism. Animals. Benzamides. Disease Models, Animal. Humans. Imatinib Mesylate. Male. Mice. PTEN Phosphohydrolase / metabolism. Philadelphia Chromosome. Piperazines / therapeutic use. Point Mutation. Protein Structure, Tertiary. Pyrimidines / therapeutic use

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  • (PMID = 21203982.001).
  • [ISSN] 1674-8018
  • [Journal-full-title] Protein & cell
  • [ISO-abbreviation] Protein Cell
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 5-Lipoxygenase-Activating Proteins; 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; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC4875160
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62. 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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63. 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.


64. 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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65. 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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66. 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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67. Irfan SM, Bhurgri Y: Clinico-pathological features and outcomes in chronic phase chronic myeloid leukemia patients treated with hydroxyurea. Asian Pac J Cancer Prev; 2009 Oct-Dec;10(4):591-4
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  • [Title] Clinico-pathological features and outcomes in chronic phase chronic myeloid leukemia patients treated with hydroxyurea.
  • OBJECTIVE: To study the clinico-pathological features and major outcomes in patients with chronic myeloid leukemia, chronic phase, treated with hydroxyurea.
  • The median age at diagnosis was 39 years (range 11 to 66 years).
  • The median delay in diagnosis was 156 days (range 30 to 360 days).
  • LDH values above 1,000 ug/l were observed in 38 (21.5%) cases and creatinine above 1.5 ug/l in 21 (12%) cases.
  • All patients tested, were positive for Philadelphia chromosome and bcr-abl transcripts.
  • At the close of the study, disease advancement was observed in 76 (43.2%) cases, of which 35 (20%) transformed to acute leukemia.
  • One hundred and two (58.4%) patients were in chronic phase, 22 (12.5%) in accelerated phase and 19 (10.7%) in blast crisis.
  • Disease progression remained the major cause of death and was seen in 29 (16.4%) patients.
  • CONCLUSION: In the study population, CML was observed in a younger age group with significant delay in definitive diagnosis.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hydroxyurea / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / pathology

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  • (PMID = 19827875.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea
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68. 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


69. 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 / / MRC/ G0500729
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human
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70. 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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71. 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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72. Yin OQ, Gallagher N, Li A, Zhou W, Harrell R, Schran H: Effect of grapefruit juice on the pharmacokinetics of nilotinib in healthy participants. J Clin Pharmacol; 2010 Feb;50(2):188-94
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  • Nilotinib (Tasigna; Novartis Pharmaceuticals) is a second-generation BCR-ABL tyrosine kinase inhibitor newly approved for the treatment of imatinib-resistant or imatinib-intolerant Philadelphia chromosome positive (Ph+) chronic myeloid leukemia in chronic phase or accelerated phase.
  • All participants underwent 2 study periods during which they received a single oral dose of 400 mg nilotinib with 240 mL double-strength grapefruit juice or 240 mL water in a crossover fashion.
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacokinetics. Beverages. Cross-Over Studies. Fusion Proteins, bcr-abl / metabolism. Headache / chemically induced. Humans. Male. Middle Aged. Protein-Tyrosine Kinases / metabolism. Vomiting / chemically induced. Young Adult

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  • (PMID = 19948946.001).
  • [ISSN] 1552-4604
  • [Journal-full-title] Journal of clinical pharmacology
  • [ISO-abbreviation] J Clin Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; 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 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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73. 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


74. Boma PO, Durosinmi MA, Adediran IA, Akinola NO, Salawu L: Clinical and prognostic features of Nigerians with chronic myeloid leukemia. Niger Postgrad Med J; 2006 Mar;13(1):47-52
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  • [Title] Clinical and prognostic features of Nigerians with chronic myeloid leukemia.
  • AIMS AND OBJECTIVES: Chronic myeloid leukemia (CML).
  • PATIENTS AND METHODS: CML patients confirmed at the OAUTHC, Ile-Ife between June 1986 and December 1999 were studied prospectively until death or the last visit to the clinic.
  • Stages of the disease at diagnosis, presenting clinical features and laboratory parameters, as well as the drug history were noted for each patient.
  • Survival of each patient was computed from the date of diagnosis until the date of death.
  • Philadelphia chromosome was positive in the five patients (12.0%) that underwent cytogenetic analysis.
  • Thirty-three of the patients (78.6%) presented in treatable chronic phase and the other 9 (21.4%) were seen in advanced stages (7 in accelerated & 2 in blastic phase).
  • The median survival of patients that presented in chronic phase was 31.7 months compared to 0.16 months in patients presenting in advanced stages, the difference was statistically significant (log rank=7.8, p-value=0.005).
  • Significant positive correlation was obtained between spleen size and total white cell count at diagnosis (r=0.36, p=0.02).
  • Univariate regression analysis showed negative relationship between survival and ages of patients at diagnosis, haematocrit value, spleen and liver sizes, and blast count.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 16633379.001).
  • [ISSN] 1117-1936
  • [Journal-full-title] The Nigerian postgraduate medical journal
  • [ISO-abbreviation] Niger Postgrad Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Nigeria
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75. Verma D, Kantarjian HM, Jones D, Luthra R, Borthakur G, Verstovsek S, Rios MB, Cortes J: Chronic myeloid leukemia (CML) with P190 BCR-ABL: analysis of characteristics, outcomes, and prognostic significance. Blood; 2009 Sep 10;114(11):2232-5
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  • [Title] Chronic myeloid leukemia (CML) with P190 BCR-ABL: analysis of characteristics, outcomes, and prognostic significance.
  • The most common BCR-ABL transcripts in chronic myeloid leukemia (CML) are e13a2(b2a2) and e14a2(b3a2).
  • We analyzed 1292 CML patients and identified 14 with only e1a2 transcripts, 9 in chronic phase (CP), 1 in accelerated phase (AP), and 4 in blast phase (BP).
  • Five patients progressed to myeloid BP (3), lymphoid BP (1), or AP (1).
  • P190(BCR-ABL) CML is rare and is associated with an inferior outcome to therapy with TKI.
  • [MeSH-major] Blast Crisis / genetics. Blast Crisis / mortality. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Benzamides. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Dasatinib. Dexamethasone / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Imatinib Mesylate. Male. Middle Aged. Piperazines / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Retrospective Studies. Survival Rate. Thiazoles / administration & dosage. Vincristine / administration & dosage


76. 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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77. Michor F: Chronic myeloid leukemia blast crisis arises from progenitors. Stem Cells; 2007 May;25(5):1114-8
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  • [Title] Chronic myeloid leukemia blast crisis arises from progenitors.
  • Chronic myeloid leukemia (CML) progresses through three distinct clinical stages: chronic phase, accelerated phase, and blast crisis.
  • The progression to accelerated phase and blast crisis is driven by activation of oncogenes, inactivation of tumor suppressor genes, and/or amplification of the BCR-ABL fusion gene, which causes the chronic phase of the disease.
  • Here, I develop a simple mathematical model of CML blast crisis to investigate whether blasts arise from leukemic stem cells or more differentiated leukemic cells.
  • Therefore, CML blasts are likely to arise from leukemic progenitors.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Benzamides. Disease Progression. Humans. Imatinib Mesylate. Models, Immunological. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use


78. Ahmed R, Naqi N, Hussain I, Khattak BK, Nadeem M, Iqbal J: Presentating phases of chronic myeloid leukaemia. J Coll Physicians Surg Pak; 2009 Aug;19(8):469-72
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  • [Title] Presentating phases of chronic myeloid leukaemia.
  • OBJECTIVE: To determine the frequency of three phases of chronic myeloid leukaemia at first presentation.
  • METHODOLOGY: Forty-five patients of either gender with Chronic Myeloid Leukaemia (CML) at their first presentation in outpatient department were included in the study by consecutive sampling technique.
  • Each phase was defined on the basis of World Health Organization (WHO) criteria.
  • The pattern of presentation revealed 35 (77.8%) in Chronic Phase (CP), 7 (15.5%) in Accelerated Phase (AP) and 3 (6.7%) in Blast Crisis (BC).
  • CONCLUSION: CML presented at a younger age in the chronic phase.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Philadelphia Chromosome
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Blast Crisis / diagnosis. Blast Crisis / epidemiology. Blast Crisis / genetics. Blast Crisis / pathology. Female. Humans. Leukemia, Myeloid, Accelerated Phase / diagnosis. Leukemia, Myeloid, Accelerated Phase / epidemiology. Leukemia, Myeloid, Accelerated Phase / genetics. Leukemia, Myeloid, Accelerated Phase / pathology. Leukemia, Myeloid, Chronic-Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / epidemiology. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / pathology. Male. Middle Aged. Pakistan / epidemiology. Risk Assessment. Risk Factors. Sex Factors. Young Adult

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  • (PMID = 19651006.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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79. Wang XR, Kang HY, Cen J, Li YH, Wang LL, Yu L: [Methylation status of id4 gene promoter in patients with chronic myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Dec;18(6):1402-4
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  • [Title] [Methylation status of id4 gene promoter in patients with chronic myeloid leukemia].
  • This study was purposed to investigate the methylation status of id4 gene promoter in patients with chronic myeloid leukemia (CML) and explore the relationship between methylation of the id4 gene and progress of CML.
  • The methylation status of id4 gene in 48 chronic myeloid leukemia patients and 10 healthy individuals was detected by using methylation-specific polymerase chain reaction (MS-PCR).
  • The results showed that id4 gene was unmethylated in bone marrow samples from both healthy individuals and CML patients in chronic phase (CP).
  • The rate of id4 gene methylation in both CML patients in accelerated phase (AP) and blast crisis (BC) was 66%, and was higher than those of CML patients in CP phase.
  • In one CML patient who received a serial observations, the status of id4 was unmethylated in CP, but it was methylated in AP and BC phase.
  • It is concluded that the id4 gene in CML patients is unmethylated in CP, while it is methylated in AP or BC.
  • The detection of id4 gene methylation status may be useful for monitoring disease advance in CML and may be used as a marker of disease progression in CML.

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  • (PMID = 21176338.001).
  • [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 / DNA Primers; 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins
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80. Syed NN, Usman M, Khaliq G, Adil SN, Khurshid M: Clinico-pathologic features of chronic myeloid leukemia and risk stratification according to Sokal score. J Coll Physicians Surg Pak; 2006 May;16(5):336-9
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  • [Title] Clinico-pathologic features of chronic myeloid leukemia and risk stratification according to Sokal score.
  • OBJECTIVE: To compile the clinical and haematological parameters of chronic myeloid leukemia (CML) and risk stratification according to Sokal score in our population.
  • SUBJECTS AND METHODS: All patients with diagnosis of chronic myeloid leukemia treated as outpatient in haematology clinic, or admitted in haem-oncology wards in The Aga Khan University Hospital were included.
  • RESULTS: During the 8 years study period, 245 patients with chronic myeloid leukemia were analyzed, the median age of presentation was 35 years (range 11-73); with male to female ratio 1.69:1.
  • At the time of diagnosis, 178 patients (72.6%), 48 (19.7%) and 17 (7.8%) of patients were in chronic, accelerated and blast phase of the disease respectively.
  • CONCLUSION: CML occurred more commonly at younger age in this series.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • [CommentIn] J Coll Physicians Surg Pak. 2007 Mar;17(3):182; author reply 182 [17374310.001]
  • (PMID = 16756777.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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81. 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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  • [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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82. 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


83. Labussière H, Hayette S, Tigaud I, Michallet M, Nicolini FE: [Treatment of chronic myeloid leukemia in 2007]. Bull Cancer; 2007 Oct;94(10):863-9
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  • [Title] [Treatment of chronic myeloid leukemia in 2007].
  • [Transliterated title] Le traitement de la leucémie myéloïde chronique en 2007.
  • The treatment of chronic myeloid leukemia (CML) has considerably evolved since imatinib mesylate has been introduced as a new therapeutic weapon for this disease.
  • The 5-year updated results of the IRIS study confirmed that imatinib mesylate is the best first line therapy for chronic phase CML with an overall survival of 90%.
  • However, despite these remarkable improvements, new problems arise as sub-optimal responses, imatinib-resistances with recently identified BCR-ABL protein point mutations, responsible for a variety of therapeutic consequences : imatinib dose increase, alternative treatments with second generation tyrosine kinase inhibitors (TKIs : dastinib, nilotinib) or allogeneic stem cell transplantation.
  • The treatment of accelerated and blastic phases relies on imatinib +/- conventional chemotherapy, ideally followed by allogeneic stem cell transplantation, as newly developed TKIs are currently evaluated within this frame.
  • Finally, BCR-ABL(T315I) mutations remain a new therapeutic critical challenge as none of the three TKIs (imatinib, nilotinib, dasatinib) can efficiently control such diseases.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Leukemia, Myeloid, Chronic-Phase / drug therapy


84. Bhattacharyya J, Mihara K, Yasunaga S, Tanaka H, Hoshi M, Takihara Y, Kimura A: BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of chronic myeloid leukemia. Ann Hematol; 2009 Apr;88(4):333-40
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  • [Title] BMI-1 expression is enhanced through transcriptional and posttranscriptional regulation during the progression of chronic myeloid leukemia.
  • Patients with chronic myeloid leukemia (CML) are at a risk of developing blastic crisis (BC) even after the emergence of imatinib mesylate.
  • In this study, to determine the relevance of BMI-1 to BC, we investigated the expression of BMI-1 in CD34(+) cells at each of the chronic phase (CP), the accelerated phase (AP), and BC by flow cytometry.
  • Interestingly, the level of BMI-1 expression was significantly higher in CP than in controls and was further increased during the course of the disease progression (control--5.66%; CP--36.93%; AP and BC--76.41%).
  • Curiously, mRNA levels for BMI-1 were almost consistent during the disease progression from CP to BC (control--2.21; CP--9.77; AP and BC--9.70 (BMI-1/glyceraldehyde-3-phosphate dehydrogenase ratio)).
  • Since we further found that overexpression of BCR-ABL in human embryonic kidney-293 cells enhanced BMI-1 expression and that BMI-1 expression was increased in K562 cells, derived from patients with BC, in the presence of proteasomal inhibitors, BMI-1 was presumed to be positively regulated by BCR-ABL and further by posttranscriptional modification in the course of the disease progression.
  • We suggest the usefulness of BMI-1 expression in CD34(+) cells as a molecular marker for monitoring patients with CML.
  • [MeSH-major] Blast Crisis / pathology. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Nuclear Proteins / analysis. Proto-Oncogene Proteins / analysis. Repressor Proteins / analysis. Transcription, Genetic
  • [MeSH-minor] Antigens, CD34. Cell Line, Tumor. Disease Progression. Fusion Proteins, bcr-abl / physiology. Humans. Neoplastic Stem Cells / pathology. Polycomb Repressive Complex 1. RNA Processing, Post-Transcriptional

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  • (PMID = 18781299.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BMI1 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 6.3.2.19 / Polycomb Repressive Complex 1
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85. Singh RK, Tripathi AK, Tripathi P, Singh S, Singh R, Ahmad R: Studies on biomarkers for oxidative stress in patients with chronic myeloid leukemia. Hematol Oncol Stem Cell Ther; 2009;2(1):285-8
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  • [Title] Studies on biomarkers for oxidative stress in patients with chronic myeloid leukemia.
  • BACKGROUND: Chronic myeloid leukemia (CML) is a myeloproliferative disorder with a unique genetic rearrangement, the Philadelphia chromosome.
  • The aim of this study was to evaluate the products of protein oxidation and lipid peroxidation in plasma as biomarkers of oxidative stress in CML patients.
  • PATIENTS AND METHODS: The study included 40 CML patients and 20 age- and sex-matched healthy volunteers.
  • Of 40 CML patients, 28 were in chronic phase (CML-CP) and 12 in accelerated phase (CML-AP).
  • RESULTS: There were significant differences (P < .05) in plasma levels of PC, TBARS and LOOH in CML, CML-CP and CML-AP patients as compared to controls.
  • CONCLUSION: PC, TBARS and LOOH might reflect oxidative stress in CML patients and might be used as biomarkers in such patients.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Oxidative Stress / physiology


86. Ahmad R, Tripathi AK, Tripathi P, Singh R, Singh S, Singh RK: Oxidative stress and antioxidant status in patients with chronic myeloid leukemia. Indian J Clin Biochem; 2008 Oct;23(4):328-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxidative stress and antioxidant status in patients with chronic myeloid leukemia.
  • Chronic myeloid leukemia is a myeloproliferative disorder with a unique rearrangement, the Philadelphia chromosome.
  • The aim of this study was to evaluate the role of oxidative stress in pathophysiology of Chronic myeloid leukemia by measuring the circulating plasma lipid peroxide levels in terms of malonyldialdehyde, total lipid hydroperoxide and oxidized proteins as protein carbonyl whereas antioxidant status were estimated in terms of reduced glutathione and total thiol in plasma of Chronic myeloid leukemia patients.
  • The present study included 47 Chronic myeloid leukemia patients and 20 age-and sex-matched healthy subjects.
  • Out of 47 Chronic myeloid leukemia patients, 31 were in chronic phase (CML-CP) and 16 in accelerated phase (CML-AP).
  • The median age of Chronic myeloid leukemia patients was 33 years and that of controls was 32 years.
  • There was a significant increase (p<0.05) in plasma malonyldialdehyde, total lipid hydroperoxide and protein carbonyl levels in Chronic myeloid leukemia patients as compared to healthy subjects.
  • Our results also showed that plasma malonyldialdehyde and protein carbonyl levels were markedly elevated (p<0.05) in both chronic phase (CML-CP) and accelerated phase (CML-AP) as compared to healthy volunteers.
  • Antioxidant status was found to be significantly decreased (p<0.05) in Chronic myeloid leukemia patients and its phases as compared to healthy participants.
  • It could be concluded that oxidative stress may be associated with the pathophysiology of Chronic myeloid leukemia.

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  • (PMID = 23105780.001).
  • [ISSN] 0970-1915
  • [Journal-full-title] Indian journal of clinical biochemistry : IJCB
  • [ISO-abbreviation] Indian J Clin Biochem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453137
  • [Keywords] NOTNLM ; Antioxidants / Chronic myeloid leukemia / Malonyldialdehyde / Oxidative stress / Protein carbonyl / Total lipid hydroperoxide
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87. Babicka L, Zemanova Z, Pavlistova L, Brezinova J, Ransdorfova S, Houskova L, Moravcova J, Klamova H, Michalova K: Complex chromosomal rearrangements in patients with chronic myeloid leukemia. Cancer Genet Cytogenet; 2006 Jul 1;168(1):22-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex chromosomal rearrangements in patients with chronic myeloid leukemia.
  • During progression of chronic myeloid leukemia (CML) from the chronic to the accelerated phase and/or blast crisis, clonal evolution with nonrandom secondary aberrations such as +8, +Ph, i(17q), +19, -Y, +21, +17, and -7 is frequently observed.
  • The aim of this study was to determine the chromosomes and chromosomal regions which are involved in CCR during progression of the disease and the frequency of nonrandom changes.
  • Conventional cytogenetics, FISH, and multicolor FISH (mFISH) were used to study karyotypes of 18 CML patients with CCR ascertained by G-banding.
  • Precise determination of breakpoints involved in CCR can give new dimension to the understanding of genetic mechanisms which play role in progression of malignant disease.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Chromosome Banding. Chromosome Breakage / genetics. Chromosomes, Human, Pair 2 / genetics. Female. Fusion Proteins, bcr-abl / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Philadelphia Chromosome. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 16772117.001).
  • [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; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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88. Radich JP: Optimizing timing of secondary tyrosine kinase therapy in chronic myeloid leukemia. Clin Lymphoma Myeloma; 2008 Mar;8 Suppl 3:S89-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optimizing timing of secondary tyrosine kinase therapy in chronic myeloid leukemia.
  • The tyrosine kinase inhibitor (TKI) imatinb has radically changed the treatment of chronic myeloid leukemia (CML).
  • Most patients treated in chronic phase can be expected to achieve a complete cytogenetic remission (CCyR).
  • However, primary imatinib therapy fails in a number of patients initially, or relapse occurs later after a good cytogenetic response.
  • Treatment of accelerated phase and blast crisis yields disappointing results and is rarely associated with long-term disease control.
  • This review will define the types of tests used to monitor the disease, provide clinically relevant endpoints, and outline guidelines for monitoring patients with CML on imatinib therapy.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 19254886.001).
  • [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; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 27
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89. 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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  • [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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  • (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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90. Ahmad R, Tripathi AK, Tripathi P, Singh S, Singh R, Singh RK: Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia. In Vivo; 2008 Jul-Aug;22(4):525-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia.
  • However, evidence for this association has often been lacking because of a lack of specific biomarkers and methods available to evaluate oxidative stress status in humans with disease conditions.
  • The aim of this study was to investigate the plasma levels of malondialdehyde (MDA) and protein carbonyl (PC) as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia (CML).
  • MATERIALS AND METHODS: The study included 20 CML patients and 10 age-and sex-matched healthy control volunteers.
  • The mean age of CML patients was 37.11+/-11.36 years and that of controls was 31.07+/-7.60 years.
  • RESULTS: There was a significant increase (p<0.05) in plasma MDA and PC levels in CML patients as compared to healthy volunteers.
  • Our results also showed that plasma MDA and PC levels were significantly higher (p<0.001) in both chronic phase (CML-CP) and accelerated phase (CML-AP) as compared to healthy volunteers.
  • During the follow-up of 12 months, two patients of CML-CP progressed to the accelerated phase.
  • The mean plasma levels of MDA and PC in patients with CML-CP who progressed to CML-AP were found to be higher than in patients with CML-CP who did not progress to the accelerated phase.
  • CONCLUSION: Plasma MDA and PC appears to reflect the oxidative stress status and disease progression in CML and can be used as biomarkers for oxidative stress and disease progression.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Accelerated Phase / metabolism. Leukemia, Myeloid, Chronic-Phase / metabolism. Malondialdehyde / metabolism. Oxidative Stress. Protein Carbonylation. Proteins / metabolism
  • [MeSH-minor] Adult. Case-Control Studies. Disease Progression. Humans. Time Factors


91. Hochhaus A, Druker B, Sawyers C, Guilhot F, Schiffer CA, Cortes J, Niederwieser DW, Gambacorti-Passerini C, Stone RM, Goldman J, Fischer T, O'Brien SG, Reiffers JJ, Mone M, Krahnke T, Talpaz M, Kantarjian HM: Favorable long-term follow-up results over 6 years for response, survival, and safety with imatinib mesylate therapy in chronic-phase chronic myeloid leukemia after failure of interferon-alpha treatment. Blood; 2008 Feb 1;111(3):1039-43
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  • [Title] Favorable long-term follow-up results over 6 years for response, survival, and safety with imatinib mesylate therapy in chronic-phase chronic myeloid leukemia after failure of interferon-alpha treatment.
  • Imatinib mesylate, a targeted inhibitor of BCR-ABL tyrosine kinase, is the standard of care for chronic myeloid leukemia (CML).
  • A phase 2 trial of imatinib in late chronic-phase (CP) CML after interferon-alpha (IFNalpha) failure enrolled 532 patients, 454 with a confirmed diagnosis of CP CML.
  • Median time from diagnosis was 34 months; median duration of imatinib treatment was 65 months.
  • Estimated rates of freedom from progression to accelerated phase (AP) and blastic phase (BP) and overall survival at 6 years were 61% and 76%, respectively.
  • Imatinib continues to be an effective and safe therapy for patients with CP CML after failure of IFN.
  • [MeSH-major] Drug-Related Side Effects and Adverse Reactions. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / pathology. Piperazines / adverse effects. Piperazines / therapeutic use. Pyrimidines / adverse effects. Pyrimidines / therapeutic use. Salvage Therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Disease Progression. Follow-Up Studies. Humans. Imatinib Mesylate. Middle Aged. Survival Rate. Time Factors. Treatment Outcome


92. Aleem A, Siddiqui N: Chronic myeloid leukemia presenting with extramedullary disease as massive ascites responding to imatinib mesylate. Leuk Lymphoma; 2005 Jul;46(7):1097-9
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  • [Title] Chronic myeloid leukemia presenting with extramedullary disease as massive ascites responding to imatinib mesylate.
  • Patients with chronic myeloid leukemia (CML) can develop extramedullary involvement during the course of the illness.
  • This usually occurs during the accelerated phase or blast crisis.
  • We describe a patient who presented with massive ascites probably due to mesenteric/peritoneal infiltration during chronic phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Ascites / drug therapy. Ascites / etiology. Blast Crisis / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Cytogenetic Analysis. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Remission Induction


93. Zhu ZH, Qian J, Lin J, Qian Z, Yao DM, Wang YL, Chen Q, Xiao GF: [Quantification of prame gene transcript in chronic myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):855-8
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  • [Title] [Quantification of prame gene transcript in chronic myeloid leukemia].
  • This study was purposed to analyze the expression level of preferentially expressed antigen of melanoma (prame) transcript in the patients with chronic myeloid leukemia (CML) and explore its clinical significance.
  • Real-time quantitative PCR (RQ-PCR) assay was used to detect the level of prame gene transcript in the bone marrow samples from 30 patients with CML and 15 patients with iron deficiency anemia (IDA).
  • The results showed that CML patients had significantly higher prame mRNA level (0% - 772.25%, median 8.28%) than IDA cases (0% - 1.46%, median 0.19%) (p < 0.001).
  • The level of prame gene transcript was significantly correlated with that of bcr-abl fusion gene transcript (r = 0.708, p < 0.001) in CML patients.
  • Furthermore, 6 patients in blastic crisis (BC) and accelerated phase (AP) had significantly higher prame gene transcript than that of 24 cases in chronic phase (CP) (p = 0.007).
  • In 2 CML patients with sequential samples, prame gene transcript increased in AP and BC, compared with in CP, and was consistent with the altering tendency of bcr-abl transcript.
  • It is concluded that the level of prame gene transcript increases in CML which associates with the progression of the disease, prame gene transcript level can be used for monitoring the disease state.


94. Vidović A, Janković G, Colović M, Tomin D, Perunicić M, Bila J, Marković O, Bosković D: The proto-oncogene expression varies over the course of chronic myeloid leukemia. Hematology; 2008 Feb;13(1):34-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The proto-oncogene expression varies over the course of chronic myeloid leukemia.
  • The chronic phase (CP) of chronic myeloid leukemia (CML) is characterized by the expression of chimeric BCR/ABL gene, extended survival, and profligate growth of maturing granulocyte stemline.
  • The accelerated phase (AP) and blast crisis (BC) of CML are usually manifested by additionally acquired oncogene aberrations, resistance to therapy, advancing anaplasia, progressive organomegaly, and increased blast count.
  • Abnormal expression of some proto-oncogenes may accompany or even precede AP or BC of CML.
  • Our objective was to follow-up oncogene expression over time covering different clinical phases of CML.
  • Temporal variation in expression (percentage positivity per 1000 analyzed cells) of c-kit, c-myc, H-Ras, cyclin A1, p53, bcl-2 and VEGF oncogenic proteins in CP, AP, and BC of CML was studied by immunohistochemical procedures.
  • This was then correlated with parameters of clinical disease (organomegaly, duration of CP, AP, and BC) and laboratory (Hb, WBC and platelet counts, and the percentage of blasts) data.
  • The level of c-kit expression differed significantly over the course of disease (x(2), p = 0 x 025).
  • Antiapoptotic bcl-2 protein increased significantly with the progression of CML (x(2), p = 0 x 005).
  • There was no significant difference in the level of expression of H-Ras, cyclin A1 and p53 over the course of disease.
  • CONCLUSION: The changes in oncogene expression, assessed by immunohistochemical approach over the course of CML may have clinical relevance in deciding on and timing of therapy.
  • Temporal distribution of changes in oncoprotein expression in CML requires further study at the molecular level.
  • [MeSH-major] Blast Crisis / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Proto-Oncogene Proteins c-myc / metabolism


95. Saglio G, Kim DW, Issaragrisil S, le Coutre P, Etienne G, Lobo C, Pasquini R, Clark RE, Hochhaus A, Hughes TP, Gallagher N, Hoenekopp A, Dong M, Haque A, Larson RA, Kantarjian HM, ENESTnd Investigators: Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia. N Engl J Med; 2010 Jun 17;362(24):2251-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib versus imatinib for newly diagnosed chronic myeloid leukemia.
  • BACKGROUND: Nilotinib has been shown to be a more potent inhibitor of BCR-ABL than imatinib.
  • We evaluated the efficacy and safety of nilotinib, as compared with imatinib, in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia (CML) in the chronic phase.
  • METHODS: In this phase 3, randomized, open-label, multicenter study, we assigned 846 patients with chronic-phase Philadelphia chromosome-positive CML in a 1:1:1 ratio to receive nilotinib (at a dose of either 300 mg or 400 mg twice daily) or imatinib (at a dose of 400 mg once daily).
  • Patients receiving either the 300-mg dose or the 400-mg dose of nilotinib twice daily had a significant improvement in the time to progression to the accelerated phase or blast crisis, as compared with those receiving imatinib (P=0.01 and P=0.004, respectively).
  • No patient with progression to the accelerated phase or blast crisis had a major molecular response.
  • CONCLUSIONS: Nilotinib at a dose of either 300 mg or 400 mg twice daily was superior to imatinib in patients with newly diagnosed chronic-phase Philadelphia chromosome-positive CML. (ClinicalTrials.gov number, NCT00471497. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Blast Crisis / prevention & control. Disease Progression. Female. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Young Adult

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  • [Copyright] 2010 Massachusetts Medical Society
  • [CommentIn] N Engl J Med. 2010 Jun 17;362(24):2314-5 [20525994.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672; author reply 1673-5 [20961253.001]
  • [CommentIn] Expert Opin Pharmacother. 2011 Jan;12(1):157-63 [21108601.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973146.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1673; author reply 1673-5 [20973145.001]
  • [CommentIn] N Engl J Med. 2010 Oct 21;363(17):1672-3; author reply 1673-5 [20973144.001]
  • (PMID = 20525993.001).
  • [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/ NCT00471497
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; 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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Investigator] Moiraghi B; Perez M; Greil R; Valent P; Bosly A; Martiat P; Noens L; André M; Verhoef G; Conchon M; Souza C; Nonino A; Hungria V; Zanichelli MA; Colturato V; Forrest D; Lipton JH; Savoie ML; Delage R; Lalancette M; Quintero G; Gomez M; Klamova H; Faber E; Bjerrum OW; Fredriksen H; Vestergaard H; Marcher C; Kamel H; Elzawam H; Porkka K; Remes K; Reiffers J; Guilhot F; Facon T; Tulliez M; Guerci-Bresler AP; Nicolini FE; Charbonnier A; Rea D; Johnson-Ansah A; Legros L; Harousseau JL; Rigal-Huguet F; Escoffre M; Gardembas M; Guyotat D; Cahn JY; Gattermann N; Ottmann O; Niederwieser D; Stegelmann F; Schafhausen P; Brümmendorf T; Duyster J; Blumenstengel K; Scheid C; Kneba M; Kwong YL; Masszi T; Petrini M; Alimena G; Di Raimondo F; Rosti G; Rotoli B; Pane F; Pungolino E; Amadori S; Abruzzese E; Fioritoni G; Lauria F; Bosi A; Martelli M; Rambaldi A; Ferrara F; Nobile F; Gobbi M; Carella AM; Orlandi EM; Leoni P; Tiribelli M; Levis A; Imamura M; Takahashi N; Tsukamoto N; Chiba S; Nagai T; Okamoto S; Miura O; Kurokawa M; Ohnishi K; Toba K; Nakao S; Tomita A; Miyamura K; Hino M; Maeda Y; Kimura A; Kawaguchi T; Miyazaki Y; Nakaseko C; Jinnai I; Matsuda A; Matsumura I; Ishikawa J; Ohyashiki K; Okada M; Usuki K; Kobayashi Y; Ohishi K; Imai K; Miyawaki S; Kanda Y; Park SY; Kim HJ; Sohn SK; Lee KH; Jung CW; Ong TC; Gómez Almaguer D; Kassack J; Ossenkoppele GJ; Gedde-Dahl T; Hjorth-Hansen H; Jedrzejczak W; Dmoszynska A; Starzak-Dwozdz J; Holowiecki J; Kyrcz-Krzemieñ S; Kuliczkowski K; Zaritsky A; Turkina A; Pospelova T; Goh YT; Koh LP; Demitrovicova L; Mistrik M; Ruff P; Louw V; Dreosti LM; Novitzky N; Cohen G; Cervantes F; Cañizo C; de Paz R; del Castillo S; Perez Encinas M; Sanz Alonso M; Marin F; Pérez-López R; Hernandez Boluda J; Echeveste Gutierrez MA; Odriozola J; Herrera P; Steegman JL; Conde E; Lopez P; Giraldo P; Boque C; Heredia B; Font AJ; Rodriguez RF; Rodriguez MJ; Batlle J; Stenke L; Lehmann S; Wadenvik H; Simonsson B; Markevärn B; Själander A; Richter J; Bjoreman M; Eriksson KM; Chalandon Y; Shih LY; Yao M; Wang MC; Jootar S; Bunworasate U; Ulkü B; Haznedar R; Undar B; Sahin B; Marin D; Smith G; Byrne J; Holyoake T; Kalaycio M; Akard L; Heaney M; Al-Janadi A; Goldberg S; Powell B; Harker WG; Shea T; Gingrich R; Glass J; Paquette R; Siegrist C; Woodson M; Fehrenbacher L; Koh H; Flinn I; Arrowsmith E; Ervin T; Guerra M; Wallach H; Berry W; Burke J; Edenfield W; Guzley G; Davis J; Richards D; Schlossman D; Kolibaba K; Alemany C; Savin M; Robbins G; Lopez J; Goldman JM; Camm J; Schiffer CA; Sargent DJ
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96. Sailaja K, Surekha D, Rao DN, Rao DR, Vishnupriya S: Association of the GSTP1 gene (Ile105Val) polymorphism with chronic myeloid leukemia. Asian Pac J Cancer Prev; 2010;11(2):461-4
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  • [Title] Association of the GSTP1 gene (Ile105Val) polymorphism with chronic myeloid leukemia.
  • We here assessed the impact of the GSTP1 codon 105 polymorphism in chronic myeloid leukemia (CML) development and therapy response.
  • Two hundred and sixty patients with CML and 248 healthy, age and sex matched controls were included in the study of associations with patient characteristics and treatment outcome.
  • The GSTP1 Ile105Val polymorphism was significantly associated with CML development (?2 = 9.57; df = 2; p = 0.0084).
  • With respect to clinical phase, CML patients in advanced phase (accelerated and blast crisis) had higher frequency of heterozygous (Ile/Val) genotype (47.62%) compared to chronic phase (36.5%).
  • Further 54.5% of patients in blast crisis carried valine allele as compared to those in chronic phase (36.5%).
  • Hence the present study suggests that GSTP1 Ile105Val polymorphism with reduced GSTP1 enzyme activity might influence CML development, progression and response rates.
  • [MeSH-major] Glutathione S-Transferase pi / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Polymorphism, Single Nucleotide / genetics

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  • (PMID = 20843134.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.7.10.1 / Protein-Tyrosine Kinases
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97. Radich JP, Dai H, Mao M, Oehler V, Schelter J, Druker B, Sawyers C, Shah N, Stock W, Willman CL, Friend S, Linsley PS: Gene expression changes associated with progression and response in chronic myeloid leukemia. Proc Natl Acad Sci U S A; 2006 Feb 21;103(8):2794-9
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  • [Title] Gene expression changes associated with progression and response in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a hematopoietic stem cell disease with distinct biological and clinical features.
  • The biologic basis of the stereotypical progression from chronic phase through accelerated phase to blast crisis is poorly understood.
  • We used DNA microarrays to compare gene expression in 91 cases of CML in chronic (42 cases), accelerated (17 cases), and blast phases (32 cases).
  • Three thousand genes were found to be significantly (P < 10(-10)) associated with phase of disease.
  • A comparison of the gene signatures of chronic, accelerated, and blast phases suggest that the progression of chronic phase CML to advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step process, with new gene expression changes occurring early in accelerated phase before the accumulation of increased numbers of leukemia blast cells.
  • Studies of CML patients who relapsed after initially successful treatment with imatinib demonstrated a gene expression pattern closely related to advanced phase disease.

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  • (PMID = 16477019.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE4170
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA-18029; United States / NCI NIH HHS / CA / CA-85053
  • [Publication-type] 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 / DNA-Binding Proteins; 0 / Kruppel-Like Transcription Factors; 0 / MZF1 protein, human; 0 / Peptide Elongation Factor 1; 0 / Piperazines; 0 / Pyrimidines; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1413797
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98. Valent P, Agis H, Sperr W, Sillaber C, Horny HP: Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia. Leuk Lymphoma; 2008 Apr;49(4):635-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic and prognostic value of new biochemical and immunohistochemical parameters in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a stem-cell disease characterized by multilineage expansion of clonal BCR/ABL+ cells.
  • Transformation from chronic into accelerated and blast phase of CML is usually associated with drug resistance and is accompanied by typical clinical and/or laboratory features, such as splenomegaly, increase in precursor cells, disturbed megakaryopoiesis, basophilia or marrow fibrosis.
  • Because of new treatment options, early recognition of disease-acceleration is of importance.
  • These tests are useful to quantitate basophil-lineage cells in the peripheral blood in CML, to determine and quantify basophilia in the bone marrow, and to detect focal accumulations of blast cells and megakaryocytes as well as increased angiogenesis and fibrosis in bone marrow sections.
  • Application of these markers may assist in determining the phase of disease and may help to better predict the prognosis in individual patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis


99. Baran Y, Ural AU, Gunduz U: Mechanisms of cellular resistance to imatinib in human chronic myeloid leukemia cells. Hematology; 2007 Dec;12(6):497-503
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of cellular resistance to imatinib in human chronic myeloid leukemia cells.
  • A major advancement in the treatment of chronic myeloid leukemia (CML) has been the development of imatinib, which has shown striking activity in the chronic phase and the accelerated phase, but less so in the blast phase of the disease.
  • Despite high rates of hematologic and cytogenetic responses to therapy, the emergence of resistance to imatinib has been recognized as a major problem in the treatment of patients with CML.
  • In this study, mechanisms of resistance to imatinib-induced apoptosis in human Meg-01 CML cells were examined.
  • There was an increased expression of BCR/ABL, Bcl-2 and an increase in mitochondrial membrane potential (MMP) detected in resistant cells comparing to parental sensitive cells.
  • In this study, it has been shown that the degree of BCR/ABL expression appears to be directly proportional to the levels of imatinib resistance.
  • In addition, there have been BCR/ABL-independent mechanisms reported for deriving resistance against imatinib.
  • Our results revealed that besides BCR/ABL overexpression, imatinib resistance also depends on the inhibition of apoptosis as a result of up-regulation of anti-apoptotic stimuli and down-regulation of pro-apoptotic stimuli through MMP but does not depend on any mutation on imatinib binding site of ABL kinase.
  • [MeSH-major] Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacokinetics. Pyrimidines / pharmacokinetics
  • [MeSH-minor] Apoptosis. Apoptosis Regulatory Proteins / genetics. Benzamides. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Fusion Proteins, bcr-abl / analysis. Gene Expression Regulation, Neoplastic. Humans. Imatinib Mesylate

  • Genetic Alliance. consumer health - Chronic Myeloid Leukemia.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
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  • (PMID = 17852433.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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100. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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






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