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Items 1 to 75 of about 75
1. 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

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  • (PMID = 19487385.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC4979080
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2. 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


3. 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

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  • (PMID = 17264298.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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4. 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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5. 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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  • [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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6. 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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7. 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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8. 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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9. 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


10. 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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11. Mondal BC, Majumdar S, Dasgupta UB, Chaudhuri U, Chakrabarti P, Bhattacharyya S: e19a2 BCR-ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases. J Clin Pathol; 2006 Oct;59(10):1102-3
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  • [Title] e19a2 BCR-ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases.
  • This report describes two patients with chronic myeloid leukaemia (CML): one of them developed accelerated phase CML and died 8 years after diagnosis and the other is at the chronic phase.
  • Sequence analysis of reverse transcription-polymerase chain reaction products showed the presence of BCR-ABL fusion transcript e19a2.
  • This finding suggests that CML carrying mu-BCR breakpoint may exhibit a clinical course similar to typical CML.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Disease Progression. Fatal Outcome. Humans. Male. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic

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

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  • [Copyright] (c) 2010 American Cancer Society.
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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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13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. 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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15. Li X, Yang J, Chen X, Liu J, Li H, Zheng J, He Y, Chen Z, Huang S: A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript. Cancer Genet Cytogenet; 2007 Jul 15;176(2):166-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.
  • The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.
  • However, our knowledge about its therapeutic effect on CML patients with rare BCR/ABL fusion transcripts e19a2(u-bcr) remains sparse.
  • Here, we report on two CML patients with e19a2 transcripts who rapidly progressed into the accelerated phase, further confirming the possibility that 19a2 might be associated with an unfavorable prognosis in CML.
  • [MeSH-major] Gene Expression Regulation, Leukemic / drug effects. Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Disease Progression. Exons. Female. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Time Factors. Translocation, Genetic. Treatment Outcome

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

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  • (PMID = 20302388.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Number-of-references] 30
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19. 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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20. Moen MD, McKeage K, Plosker GL, Siddiqui MA: Imatinib: a review of its use in chronic myeloid leukaemia. Drugs; 2007;67(2):299-320
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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21. 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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22. 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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23. 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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24. 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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25. 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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26. 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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27. Quintás-Cardama A, Kantarjian H, Garcia-Manero G, O'Brien S, Faderl S, Estrov Z, Giles F, Murgo A, Ladie N, Verstovsek S, Cortes J: Phase I/II study of subcutaneous homoharringtonine in patients with chronic myeloid leukemia who have failed prior therapy. Cancer; 2007 Jan 15;109(2):248-55
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  • [Title] Phase I/II study of subcutaneous homoharringtonine in patients with chronic myeloid leukemia who have failed prior therapy.
  • Intravenous HHT has demonstrated activity in patients with chronic myeloid leukemia (CML) after failure with interferon.
  • METHODS: A Phase I study was completed of subcutaneous (s.c.
  • ) HHT in patients with CML in accelerated or blast phases and demonstrated efficacy and good tolerance at the same doses used by intravenous (i.v.) administration.
  • The cohort was then expanded to treated at the MTD to include patients in late chronic phase CML after imatinib failure.
  • The 2 patients with BCR-ABL kinase domain mutations at the start of therapy with HHT had a CG response and in both instances the mutations became undetectable.
  • CONCLUSIONS: Subcutaneous HHT is well tolerated and may have clinical activity in patients with CML after imatinib failure.
  • [MeSH-major] Harringtonines / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • [ErratumIn] Cancer. 2007 Jun 15;109(12):2625. Dosage error in article text
  • (PMID = 17154172.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Benzamides; 0 / Harringtonines; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 6FG8041S5B / homoharringtonine; 8A1O1M485B / Imatinib Mesylate
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28. 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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29. Kantarjian H, Talpaz M, O'Brien S, Giles F, Faderl S, Verstovsek S, Garcia-Manero G, Shan J, Rios MB, Champlin R, de Lima M, Cortes J: Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience. Cancer; 2005 May 15;103(10):2099-108
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  • [Title] Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience.
  • BACKGROUND: The effect of imatinib mesylate on survival in the accelerated phase of chronic myelogenous leukemia (CML) is unknown.
  • The objectives of this study were to update the long-term experience with imatinib in patients who had accelerated-phase CML and to compare outcomes with historic experience.
  • METHODS: The outcomes of 176 patients who received treatment with imatinib were reviewed and compared with the outcomes of 213 historic control patients with accelerated-phase CML who received treatment with interferon-alpha or with other modalities.
  • This may have implications in relation to subsequent therapy, because, according to the outcomes of patients who underwent allogeneic transplantation in accelerated phase at the authors' institution and from literature reports, the estimates of 5-year survival were 25-30%.
  • CONCLUSIONS: The current results suggest that imatinib improved survival compared with other therapies in patients with accelerated-phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Anemia / chemically induced. Benzamides. Bone Marrow Transplantation. Cohort Studies. Cytogenetic Analysis. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Hemoglobins / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Longitudinal Studies. Male. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 15830345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hemoglobins; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. 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

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  • (PMID = 19695406.001).
  • [ISSN] 1879-114X
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00302016
  • [Publication-type] Controlled Clinical Trial; Journal Article; 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
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32. Joske DJ: Chronic myeloid leukaemia: the evolution of gene-targeted therapy. Med J Aust; 2008 Sep 1;189(5):277-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukaemia: the evolution of gene-targeted therapy.
  • Chronic myeloid leukaemia (CML) was the first human cancer linked to an acquired chromosomal abnormality, subsequently shown to be a reciprocal translocation between chromosomes 9 and 22.
  • The resulting fusion gene product, BCR-ABL, was shown to be the causative agent of the disease.
  • CML has an incidence of around 1-2 cases per 100,000; in Australia, there are probably more than 200 new cases per year and more than 1300 prevalent cases.
  • Treatment of CML with imatinib has been a powerful vindication of the concept of rational, gene-targeted drug design.
  • Five-year published experience with imatinib at 400 mg orally daily demonstrates 89% overall survival and an estimated 93% freedom from disease progression.
  • Up to 28% of patients may have to stop imatinib because of intolerance or disease resistance, mostly due to point mutations of BCR-ABL.
  • Management of CML patients should involve close monitoring, especially in the first 2 years, with regular cytogenetics and quantitative polymerase chain reaction to optimise response and identify suboptimal responders as early as possible.
  • Bone marrow transplantation remains the only known cure, but is reserved for patients whose kinase inhibitor therapy has failed, or who have advanced disease (accelerated phase or blastic transformation).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Australia. Benzamides. Drug Approval. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. United States

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  • (PMID = 18759727.001).
  • [ISSN] 0025-729X
  • [Journal-full-title] The Medical journal of Australia
  • [ISO-abbreviation] Med. J. Aust.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 41
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33. Raza S, Ullah K, Ahmed P, Khan B, Kamal MK: Post-transplant outcome in chronic myeloid leukaemia. J Coll Physicians Surg Pak; 2008 Oct;18(10):615-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Post-transplant outcome in chronic myeloid leukaemia.
  • OBJECTIVE: To determine post-transplant survival in chronic myeloid leukaemia patients undergoing allogeneic stem cell transplant.
  • METHODOLOGY: All patients of chronic myeloid leukaemia in chronic phase having HLA identical donor and age under 55 years, normal hepatic, renal and cardiac functions with good performance status were selected.
  • Patients in accelerated phase or blast crisis, poor performance status, impaired hepatic, renal, cardiac functions or pregnancy were excluded.
  • RESULTS: Thirty seven patients with chronic myeloid leukaemia underwent allogeneic stem cell transplant from HLA identical sibling donors.
  • All patients and donors were CMV positive.
  • Post-transplant complications encountered were acute GvHD (Grade II-IV) (n=13, 35.1%), chronic GvHD in 18.9% (n=7), Veno Occlusive Disease (VOD) in 5.4% (n=2), acute renal failure in 2.7% (n=1), haemorrhagic cystitis in 2.7% (n=1), bacterial infections in 40.5% (n=15), fungal infections in 16.2% (n=6), CMV infection in 5.4% (n=2), tuberculosis in 5.4% (n=2), Herpes Zoster infection 2.7% (n=1) and relapse in 2.7% (n=1).
  • Overall Disease Free Survival (DFS) was 73% with a median duration of follow-up of 47.4 +/-12 months.
  • CONCLUSION: Results of allogeneic stem cell transplant in standard risk group CML patients were good and comparable with other international centres, however, results in high-risk CML patients need further improvement, although, number of patients in this group is small.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Disease-Free Survival. Female. Humans. Longitudinal Studies. Male. Middle Aged. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 18940118.001).
  • [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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34. Mauro MJ: Tailoring tyrosine kinase inhibitor therapy in chronic myeloid leukemia. Cancer Control; 2009 Apr;16(2):108-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. 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


36. Jørgensen HG, Holyoake TL: Characterization of cancer stem cells in chronic myeloid leukaemia. Biochem Soc Trans; 2007 Nov;35(Pt 5):1347-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of cancer stem cells in chronic myeloid leukaemia.
  • CML (chronic myeloid leukaemia) is a myeloproliferative disease that originates in an HSC (haemopoietic stem cell) as a result of the t(9;22) translocation, giving rise to the Ph (Philadelphia chromosome) and bcr-abl oncoprotein.
  • The disease starts in CP (chronic phase), but as a result of genomic instability, it progresses over time to accelerated phase and then to BC (blast crisis), becoming increasingly resistant to therapy. bcr-abl is a constitutively active tyrosine kinase that has been targeted by TKIs (tyrosine kinase inhibitors), including IM (imatinib mesylate), nilotinib and dasatinib.
  • We have developed various flow cytometry techniques to enable us to isolate candidate CML stem cells from CP patients at diagnosis that efflux Hoechst dye, express CD34, lack CD38 and are cytokine-non-responsive in culture over periods of up to 12 days in growth factors.
  • These stem cells have been shown to regenerate bcr-abl-positive haemopoiesis in immunocompromised mice upon transplantation.
  • We previously demonstrated that IM was antiproliferative for CML stem cells but did not induce apoptosis.
  • Clinical experience now confirms that IM may not target CML stem cells in vivo with few patients achieving complete molecular remission and relapse occurring rapidly upon drug withdrawal.
  • Our recent efforts have focused on understanding why CML stem cells are resistant to IM and on trying to find novel ways to induce apoptosis of this population.
  • We have shown that CML stem cells express very high levels of functional wild-type bcr-abl; no kinase domain mutations have been detected in the stem cell population.
  • Dasatinib, a more potent multitargeted TKI than IM, inhibits bcr-abl activity more efficiently than IM but still does not induce apoptosis of the stem cell population.
  • Most recently, we have tested a number of novel drug combinations and found that FTIs (farnesyl transferase inhibitors) have activity against CML.
  • BMS-214662 is the most effective of these and induces apoptosis of phenotypically and functionally defined CML stem cells in vitro, as a single agent and in combination with IM or dasatinib.
  • The effect against CML stem cells is selective with little effect on normal stem cells.
  • The drug is also effective against BC CML stem cells and equally effective against wild-type and mutant bcr-abl, including the most resistant mutant T315I.
  • Our intentions are now to explore the activity of BMS-214662 in other cancer stem cell disorders and to move this preclinical work to a clinical trial combining dasatinib with BMS-214662 in CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Neoplastic Stem Cells / cytology

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  • (PMID = 17956348.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Imidazoles; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 12794-10-4 / Benzodiazepines; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Number-of-references] 16
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37. 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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38. Keller G, Brassat U, Braig M, Heim D, Wege H, Brümmendorf TH: Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy. Hematol Oncol; 2009 Sep;27(3):123-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.
  • Due to the end replication problem, each cell division results in a loss of telomeric repeats in normal somatic cells.
  • However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia.
  • Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders.
  • In CML, telomere shortening correlates with disease stage, duration of chronic phase (CP), prognosis measured by the Hasford risk score and the response to disease-modifying therapeutics such as the tyrosine kinase inhibitor Imatinib.
  • In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC).
  • Here, we review the current state of knowledge of the role of telomere and telomerase biology in CML and discuss the possible impact of novel treatment approaches.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / pathology
  • [MeSH-minor] Animals. Disease Progression. Humans

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  • (PMID = 19569255.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 67
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39. 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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40. Vidović A, Janković G, Tomin D, Perunicić-Jovanović M, Djunić I, Djurasinović V, Colović M: [Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of chronic myeloid leukaemia]. Srp Arh Celok Lek; 2009 Jul-Aug;137(7-8):379-83
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  • [Title] [Prognostic significance of cellular vascular endothelial growth factor (VEGF) expression in the course of chronic myeloid leukaemia].
  • INTRODUCTION: Increased angiogenesis in bone marrow is one of the characteristics of chronic myeloid leukaemia (CML), a clonal myeloproliferative disorder that expresses a chimeric bcr/abl protein.
  • The impact of elevated VEGF expression on the course of chronic myeloid leukaemia is unknown.
  • OBJECTIVE: The aim of this study was the follow-up of VEGF expression during the course of CML.
  • METHODS: We studied VEGF expression of 85 CML patients (median age 50 years, range 16-75 years).
  • At the commencement of the study, 29 patients were in chronic phase (CP), 25 in an accelerated phase (AP), and 31 in the blast crisis (BC).
  • The temporal expression (percentage positivity per 1000 analysed cells) VEGF proteins over the course of CML were studied using the immunohistochemical technique utilizing relevant monoclonal antibodies.
  • It was correlated with the laboratory (Hb, WBC and platelet counts, and the percentage of blasts) and clinical parameters (organomegaly, duration of CP, AP, and BC) of disease progression.
  • CONCLUSION: Immunohistochemically confirmed significance of the expression of VEGF in dependence of the CML stage could be of clinical importance in deciding on the timing therapy.
  • These data suggest that VEGF plays a role in the biology of CML and that VEGF inhibitors should be investigated in CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 19764591.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A
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41. 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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42. Campbell LJ, Fidler C, Eagleton H, Peniket A, Kusec R, Gal S, Littlewood TJ, Wainscoat JS, Boultwood J: hTERT, the catalytic component of telomerase, is downregulated in the haematopoietic stem cells of patients with chronic myeloid leukaemia. Leukemia; 2006 Apr;20(4):671-9
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  • [Title] hTERT, the catalytic component of telomerase, is downregulated in the haematopoietic stem cells of patients with chronic myeloid leukaemia.
  • Telomere shortening is associated with disease progression in chronic myeloid leukaemia (CML).
  • To investigate the biology and regulation of telomerase in CML, we evaluated expression of the telomerase components, its regulators and several telomeric-associated proteins.
  • Quantitative real-time-polymerase chain reaction (PCR) was used to compare gene expression in the CD34+/leukaemic blast cells of 22 CML patient samples to the CD34+ cell population of healthy individuals. hTERT, the catalytic component of telomerase, was downregulated in eight of 12 chronic phase (CP) patients (P = 0.0387).
  • Furthermore, hTERT was significantly downregulated in two of three patients in accelerated phase (AP) and seven of seven patients in blast crisis (BC), P = 0.0017.
  • With the exceptions of TEP1 and hTR, expression of these factors was highest in CP and decreased during disease progression.
  • Expression of c-Myc, a positive regulator of hTERT transcription, correlated with hTERT expression and decreased with disease progression, falling below control levels in BC. hTERT levels were increased in CP patients following successful treatment with imatinib, relative to untreated CP patients.
  • We suggest that reduced hTERT expression directly causes the shortened telomeres observed in CML.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic / genetics. Hematopoietic Stem Cells / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Telomerase / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD34 / biosynthesis. Benzamides. Carrier Proteins / biosynthesis. Disease Progression. Down-Regulation / genetics. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Piperazines / pharmacology. Piperazines / therapeutic use. Proto-Oncogene Proteins c-myc / biosynthesis. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. RNA / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tankyrases / biosynthesis. Telomeric Repeat Binding Protein 1 / biosynthesis. Telomeric Repeat Binding Protein 2 / biosynthesis. Transcription, Genetic. Tumor Suppressor Proteins / biosynthesis

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  • (PMID = 16498395.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Benzamides; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / PINX1 protein, human; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyrimidines; 0 / TEP1 protein, human; 0 / Telomeric Repeat Binding Protein 1; 0 / Telomeric Repeat Binding Protein 2; 0 / Tumor Suppressor Proteins; 0 / telomerase RNA; 63231-63-0 / RNA; 8A1O1M485B / Imatinib Mesylate; EC 2.4.2.30 / Tankyrases; EC 2.4.4.30 / TNKS protein, human; EC 2.7.7.49 / Telomerase
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43. Plosker GL, Robinson DM: Nilotinib. Drugs; 2008;68(4):449-59; discussion 460-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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44. 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


45. Grzybowska-Izydorczyk O, Góra-Tybor J, Robak T: [Tyrosine kinase inhibitors in the therapy of chronic myeloid leukaemia]. Postepy Hig Med Dosw (Online); 2006;60:490-7
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  • [Title] [Tyrosine kinase inhibitors in the therapy of chronic myeloid leukaemia].
  • Chronic myeloid leukemia (CML) is a malignant clonal disorder of hematopoietic stem cells resulting in increased myeloid and erythroid cells and platelets, and marked hyperplasia in the bone marrow.
  • The natural history of CML is progression from a benign chronic phase, often through an accelerated phase, to a rapidly fatal blast crisis within 3-5 years.
  • The constitutively activated ABL tyrosine kinase domain of the chimeric BCR-ABL oncoprotein is responsible for the transformation of hematopoietic stem cells and the symptoms of CML.
  • Imatinib mesylate (Glivec), a specific small-molecule inhibitor of BCR-ABL, has become the standard drug therapy in all phases of the disease.
  • Imatinib has greatly improved the outcome for patients with CML.
  • Considerable progress has recently been made in understanding the structural biology of ABL and the molecular basis for resistance, facilitating the discovery and development of second- generation drugs designed to combat mutant forms of BCR-ABL.
  • The first of these compounds to enter clinical development were dasatinib (BMS-354825) and AMN107 and, from phase I results, both of these promise a breakthrough in the treatment of imatinib-resistant CML.

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  • (PMID = 17013368.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 51
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46. Imatinib: a second look. Longer follow-up in chronic myeloid leukaemia: clear advantages. Prescrire Int; 2008 Dec;17(98):226-8
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  • [Title] Imatinib: a second look. Longer follow-up in chronic myeloid leukaemia: clear advantages.
  • (1) In 2002/2003, the clinical evaluation of imatinib, a tyrosine kinase inhibitor, in the treatment of chronic myeloid leukaemia left many questions unanswered.
  • (3) As second-line treatment for patients in the chronic phase, we now have non-comparative follow-up data on 532 patients in whom interferon had failed.
  • (4) As second-line treatment for patients in the accelerated phase, we now have non-comparative follow-up data on 235 patients.
  • (9) In practice, imatinib seems to increase survival time when used as a first-line or second-line treatment for patients in different phases of chronic myeloid leukaemia.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19415889.001).
  • [ISSN] 1167-7422
  • [Journal-full-title] Prescrire international
  • [ISO-abbreviation] Prescrire Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines
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47. Fausel CA: Novel treatment strategies for chronic myeloid leukemia. Am J Health Syst Pharm; 2006 Dec 1;63(23 Suppl 8):S15-20; quiz S21-2
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  • [Title] Novel treatment strategies for chronic myeloid leukemia.
  • PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma.
  • Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.
  • SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants.
  • Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.
  • Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.
  • Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials.
  • CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.
  • [MeSH-major] Drug Therapy / methods. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy

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  • (PMID = 17106016.001).
  • [ISSN] 1079-2082
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors
  • [Number-of-references] 23
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48. Shi P, Chandra J, Sun X, Gergely M, Cortes JE, Garcia-Manero G, Arlinghaus RB, Lai R, Amin HM: Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells. J Cell Mol Med; 2010 Jun;14(6B):1777-92
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  • [Title] Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.
  • Chronic myeloid leukaemia (CML) is the most common subtype of chronic myeloproliferative diseases.
  • Typically, CML evolves as a chronic phase (CP) disease that progresses into accelerated (AP) and blast phase (BP) stages.
  • In this study, we show that IGF-IR is universally expressed in four CML cell lines.
  • Increased expression levels of IGF-IR with CML progression was supported by quantitative real-time PCR that demonstrated significantly higher levels of IGF-IR mRNA in BP patients.
  • Inhibition of IGF-IR decreased the viability and proliferation of CML cell lines and abrogated their growth in soft agar.
  • Importantly, inhibition of IGF-IR decreased the viability of cells resistant to imatinib mesylate including BaF3 cells transfected with p210 BCR-ABL mutants, CML cell lines and primary neoplastic cells from patients.

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  • (PMID = 19508387.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA114395; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS405889; NLM/ PMC3444523
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49. Kim SH, Kim D, Kim DW, Goh HG, Jang SE, Lee J, Kim WS, Kweon IY, Park SH: Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent. Hematol Oncol; 2009 Dec;27(4):190-7
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  • [Title] Analysis of Bcr-Abl kinase domain mutations in Korean chronic myeloid leukaemia patients: poor clinical outcome of P-loop and T315I mutation is disease phase dependent.
  • Despite durable responses to imatinib in chronic myeloid leukaemia (CML), mutations in Bcr-Abl kinase domain (KD) are known to induce imatinib resistance and cause poor clinical outcome.
  • We characterized Bcr-Abl KD mutations in 137 Korean CML patients with imatinib resistance (n = 111) or intolerance (n = 26) using allele specific oligonucleotide polymerase chain reaction (PCR) and direct sequencing.
  • Seventy (51%) patients harboured 81 mutations of 20 different types with increasing prevalence in advanced phase.
  • T315I was the most common mutation and P-loop was the hottest spot in Bcr-Abl KD.
  • Survival analysis according to disease phase of mutation being detected and type of mutations provided correlation between P-loop or T315I mutation and poor overall survival in blast crisis, but not in accelerated phase (AP) or chronic phase (CP), indicating poor clinical outcome of particular mutations depends on disease phase.
  • CML patients with imatinib resistance showed high rate (63%) of mutations in Bcr-Abl KD and therefore CML patients who do not respond to imatinib should be the candidates for mutation screening as molecular monitoring.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Benzamides. DNA Mutational Analysis. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Korea / epidemiology. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Survival Rate. Treatment Outcome. Young Adult

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  • [Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19274615.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 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
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50. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with CML and other MPD.
  • METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with CML (chronic phase, n = 37; accelerated phase, n = 9), and other MPD (chronic idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
  • 2D7(+) bone marrow cells were found to increase in CML compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2): CML, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
  • The highest basophil counts were recorded in accelerated phase CML (115/mm(2)).
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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51. 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


52. Amin HM, Hoshino K, Yang H, Lin Q, Lai R, Garcia-Manero G: Decreased expression level of SH2 domain-containing protein tyrosine phosphatase-1 (Shp1) is associated with progression of chronic myeloid leukaemia. J Pathol; 2007 Aug;212(4):402-10
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  • [Title] Decreased expression level of SH2 domain-containing protein tyrosine phosphatase-1 (Shp1) is associated with progression of chronic myeloid leukaemia.
  • Chronic myeloid leukaemia (CML) is characterized by t(9;22)(q34;q11) and the aberrant expression of the fusion protein Bcr-Abl that leads to constitutive activation of c-Abl kinase.
  • Bcr-Abl plays a major role in the development and progression of CML through chronic, accelerated, and blast phases.
  • The interaction between Bcr-Abl and other oncogenic molecules has been extensively documented.
  • Nonetheless, negative regulatory mechanisms of Bcr-Abl are not completely defined.
  • In the present study, we demonstrate that Shp1 levels are markedly decreased in advanced stage CML patients compared with those in chronic phase.
  • Furthermore, we did not detect mutations in the Shp1 gene in CML cell lines or patient samples.
  • These data suggest that the decrease in Shp1 in advanced stage CML patients is due to post-transcriptional modifications.
  • Our findings suggest that the decrease in Shp1 expression levels plays a role in the progression of CML.
  • Also, the decrease in Shp1 and subsequently its inhibitory effect on Bcr-Abl could provide an explanation for imatinib resistance seen in advanced stage CML patients.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism
  • [MeSH-minor] Adult. Aged. DNA Methylation. DNA Mutational Analysis / methods. DNA, Complementary / genetics. DNA, Neoplasm / genetics. Disease Progression. Female. Humans. Male. Middle Aged. Protein Phosphatase 1. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17503411.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100067; United States / NCI NIH HHS / CA / CA105771; United States / NCI NIH HHS / CA / CA114395
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6
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53. DeAngelo DJ, Attar EC: Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice. Leuk Lymphoma; 2010 Mar;51(3):363-75
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  • [Title] Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.
  • The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).
  • The mechanisms underlying resistance are multifactorial and may include mutations in the kinase domain of BCR-ABL, increased production of BCR-ABL, or activation of BCR-ABL-independent pathways.
  • Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.
  • Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.
  • Nilotinib, an analogue of imatinib, is approved for the treatment of imatinib-resistant or -intolerant patients with chronic or accelerated phase CML.
  • Both agents have shown significant clinical activity in patients with imatinib-resistant or -intolerant CML, and their approval represents a major advancement in the treatment options available.
  • The presence of certain disease characteristics (e.g. specific BCR-ABL mutations) or patient comorbidities may facilitate more effective treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20038231.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 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; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
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54. Bryant BJ, Alperin JB, Elghetany MT: Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia. Am J Hematol; 2007 Feb;82(2):150-4
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  • [Title] Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia.
  • Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML).
  • They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder.
  • Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia.
  • Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia.
  • This is the first case report of paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed CML.
  • The CBC revealed a leukocyte count of 238,300/microl and a differential consistent with CML.
  • Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML.
  • Although extramedullary blast crises herald the accelerated phases in approximately 10% of CML cases, megakaryoblastic blast transformation of CML accounts for less than 3% of these cases.
  • The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation. Paraplegia / pathology. Spinal Cord Compression / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Combined Modality Therapy. Female. Humans. Middle Aged. Splenic Neoplasms / diagnosis. Splenic Neoplasms / pathology. Splenic Neoplasms / secondary. Splenic Neoplasms / therapy

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17019692.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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55. Shepherd P, Dhanapala C, Maguire C, White J, Drummond M, Holyoake T, Johnson PR: Successful use of National Cancer Registry data to monitor the effective use of imatinib for treating chronic myeloid leukaemia. Scott Med J; 2008 Aug;53(3):8-12
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  • [Title] Successful use of National Cancer Registry data to monitor the effective use of imatinib for treating chronic myeloid leukaemia.
  • Imatinib is a tyrosine kinase inhibitor, which selectively antagonises the BCR-ABL molecular pathway which causes chronic myeloid leukaemia (CML).
  • METHODS: All imatinib usage since its first prescription in Scotland in September 2000 to July 2003 was audited through pharmacy records and through the Scotland Leukaemia Registry (SLR), an existing national registry of patients with CML.
  • RESULTS: One hundred and four patients in Chronic Phase (CP), 36 in Accelerated Phase (AP) and five in Blast Phase (BP) received imatinib.
  • CONCLUSIONS: We believe such data collection should be an important ongoing resource for assessing outcomes in a rare form of leukaemia but one which already has major implications for health economics and will continue to do so given the future development of dual tyrosine kinase inhibitors for imatinib resistant cases.
  • [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 = 18780518.001).
  • [ISSN] 0036-9330
  • [Journal-full-title] Scottish medical journal
  • [ISO-abbreviation] Scott Med J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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56. 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

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  • (PMID = 17091608.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Platelet Aggregation Inhibitors; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Quinazolines; 0 / anagrelide; 8A1O1M485B / Imatinib Mesylate
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57. 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


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

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062; author reply 1063-4 [16957155.001]
  • [CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062-3; author reply 1063-4 [16960978.001]
  • (PMID = 16775234.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00064233
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR-00865
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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59. 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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60. 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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61. Agis H, Krauth MT, Böhm A, Mosberger I, Müllauer L, Simonitsch-Klupp I, Walls AF, Horny HP, Valent P: Identification of basogranulin (BB1) as a novel immunohistochemical marker of basophils in normal bone marrow and patients with myeloproliferative disorders. Am J Clin Pathol; 2006 Feb;125(2):273-81
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  • In chronic myeloid leukemia (CML), basophilia is a diagnostic and prognostic variable.
  • We applied the antibasogranulin antibody BB1 on paraffin-embedded BM sections in 21 control samples (normal BM), 45 patients with CML, 9 with chronic idiopathic myelofibrosis, 11 with polycythemia vera, 19 with essential thrombocythemia, and 7 with indolent systemic mastocytosis.
  • BB1+ BM cells were found to be highly elevated in patients with CML compared with normal BM or other MPDs, with maximum counts found in accelerated phase CML (median, 160 cells/mm(2)).
  • In summary, BB1 (basogranulin) is a new immunohistochemical basophil marker that should allow quantification of basophils in CML at diagnosis and during therapy.
  • [MeSH-major] Basophils / chemistry. Bone Marrow / chemistry. DNA-Binding Proteins / analysis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood. Phosphoproteins / analysis. Transcription Factors / analysis

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  • (PMID = 16393678.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500729
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Transcription Factors; 148814-46-4 / BNC1 protein, human
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62. 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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63. Bee PC, Gan GG, Teh A, Haris AR: Imatinib mesylate in the treatment of chronic myeloid leukemia: a local experience. Med J Malaysia; 2006 Dec;61(5):547-52
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  • [Title] Imatinib mesylate in the treatment of chronic myeloid leukemia: a local experience.
  • This study was done to assess the overall response rate of imatinib mesylate in local patients with chronic myeloid leukaemia.
  • Of the 69 patients; 35% were in the chronic phase, 41% were in the accelerated phase, 17% were in blast crisis and the remaining 7% were after stem cell transplantation.
  • Complete haematological response rates of patients in chronic phase, accelerated phase and blast crisis were 95.8%, 96.4% and 41.7% respectively.
  • The cytogenetic response rates were 80%, 41.7% and 18.2% in chronic, accelerated and blast crisis phase respectively (p < 0.005).
  • This was affected by the different phases of disease (chronic phase was better than accelerated and blast crisis) (p < 0.001).
  • In conclusion, our local CML patients did well on treatment with imatinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Treatment Outcome
  • [MeSH-minor] Benzamides. Cytogenetics. Disease Progression. Female. Humans. Imatinib Mesylate. Malaysia. Male. Prognosis. Prospective Studies


64. 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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65. 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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66. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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67. Holzerová M, Faber E, Veselovská J, Urbánková H, Balcárková J, Rozmanová S, Voglová J, Muzík J, Chroust K, Indrák K, Jarosová M, CAMELIA-Chronic Myeloid Leukaemia Project: Imatinib mesylate efficacy in 72 previously treated Philadelphia-positive chronic myeloid leukemia patients with and without additional chromosomal changes: single-center results. Cancer Genet Cytogenet; 2009 May;191(1):1-9
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  • [Title] Imatinib mesylate efficacy in 72 previously treated Philadelphia-positive chronic myeloid leukemia patients with and without additional chromosomal changes: single-center results.
  • Reported here are 72 previously treated Philadelphia chromosome-positive (Ph+) CML patients on imatinib (IM) therapy, with a focus on patients with additional chromosomal aberrations (CAs).
  • Patients in accelerated phase had significantly worse overall survival on IM, regardless of additional CAs.
  • The present results confirm that the majority of previously treated Ph+ CML patients benefit from starting IM therapy, including patients with defined additional changes.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19389502.001).
  • [ISSN] 1873-4456
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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68. Kumar L, Gangadharan VP, Rao DR, Saikia T, Shah S, Malhotra H, Bapsy PP, Singh K, Rao R: Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India. Natl Med J India; 2005 Mar-Apr;18(2):66-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety and efficacy of an indigenous recombinant interferon-alpha-2b in patients with chronic myelogenous leukaemia: results of a multicentre trial from India.
  • BACKGROUND: Compared to hydroxyurea, treatment with interferon-alpha (IFN-alpha) is known to prolong survival in patients with chronic phase of chronic myelogenous leukaemia (CML) and was considered as first-line therapy till recently.
  • We conducted a multicentre trial using an indigenous recombinant IFN-alpha-2b to evaluate its efficacy and toxicity in chronic phase CML.
  • METHODS: Between September 2000 and August 2001, patients with chronic phase CML were recruited within 8 weeks of diagnosis at 7 centres in India.
  • All patients were given the study drug in a dose of 5 million units daily subcutaneously.
  • Nineteen patients had progression (blast crisis n=15, accelerated phase n=4) while on treatment.
  • Currently, 95 patients are alive, 91 in the chronic phase and 4 in the accelerated phase.
  • Four patients were lost to follow up and all 15 patients with blast crisis died of progressive disease at a median Interval of 6.5 months (range 1-15 months).
  • CONCLUSION: This study confirms the efficacy of the indigenous recombinant IFN-alpha-2b in chronic phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interferon-alpha / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • [ErratumIn] Natl Med J India. 2005 May-Jun;18(3):130
  • (PMID = 15981440.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b
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69. 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
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. Hu Z, Pan XF, Wu FQ, Ma LY, Liu DP, Liu Y, Feng TT, Meng FY, Liu XL, Jiang QL, Chen XQ, Liu JL, Liu P, Chen Z, Chen SJ, Zhou GB: Synergy between proteasome inhibitors and imatinib mesylate in chronic myeloid leukemia. PLoS One; 2009;4(7):e6257
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergy between proteasome inhibitors and imatinib mesylate in chronic myeloid leukemia.
  • BACKGROUND: Resistance developed by leukemic cells, unsatisfactory efficacy on patients with chronic myeloid leukemia (CML) at accelerated and blastic phases, and potential cardiotoxity, have been limitations for imatinib mesylate (IM) in treating CML.
  • METHODS AND FINDINGS: We tested the therapeutic efficacies as well as adverse effects of low dose IM in combination with proteasome inhibitor, Bortezomib (BOR) or proteasome inhibitor I (PSI), in two CML murine models, and investigated possible mechanisms of action on CML cells.
  • Consistently, BOR and PSI enhanced IM-induced inhibition of long-term clonogenic activity and short-term cell growth of CML stem/progenitor cells, and potentiated IM-caused inhibition of proliferation and induction of apoptosis of BCR-ABL+ cells.
  • While exerting suppressive effects on BCR-ABL, E2F1, and beta-catenin, IM/BOR and IM/PSI inhibited proteasomal degradation of protein phosphatase 2A (PP2A), leading to a re-activation of this important negative regulator of BCR-ABL.
  • CONCLUSION: These data suggest that combined use of tyrosine kinase inhibitor and proteasome inhibitor might be helpful for optimizing CML treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protease Inhibitors / therapeutic use. Proteasome Inhibitors. Pyrimidines / therapeutic use


71. Yin OQ, Gallagher N, Tanaka C, Fisher D, Sethuraman V, Zhou W, Lin TH, Heuman D, Schran H: Effects of hepatic impairment on the pharmacokinetics of nilotinib: an open-label, single-dose, parallel-group study. Clin Ther; 2009;31 Pt 2:2459-69
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Nilotinib is a second-generation BCR-ABL tyrosine kinase inhibitor approved for the treatment of patients who have imatinib-resistant Philadelphia chromosome-positive chronic myeloid leukemia in the chronic or accelerated phase or who are unable to tolerate imatinib.
  • The mean (SD) t(1/2) was 15.1 (4.97) and 16.0 (9.13) hours in the mild-impairment and control groups, respectively, but was 21.6 (7.77) and 32.4 (10.7) hours in the moderate- and severe-impairment groups, respectively, reflecting the decrease in CL/F and/or increase in Vz/F in the latter 2 groups.
  • [MeSH-minor] Adult. Aged. Area Under Curve. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • [Copyright] Copyright 2009 Excerpta Medica Inc. All rights reserved.
  • (PMID = 20110053.001).
  • [ISSN] 1879-114X
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00418626
  • [Publication-type] Clinical Trial; Journal Article; 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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72. Cunningham MT, Ganguly S: Chronic myeloid leukemia in accelerated phase with basophilic transformation of the bone marrow. Am J Hematol; 2006 May;81(5):380-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myeloid leukemia in accelerated phase with basophilic transformation of the bone marrow.
  • [MeSH-major] Basophils / pathology. Bone Marrow / pathology. Cell Transformation, Neoplastic / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 16628736.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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73. Sonmez M, Ovali E, Omay SB: Tumor lysis syndrome during treatment with AMN107 (Nilotinib) in a patient with chronic myelogenous leukemia accelerated phase. J Clin Pharm Ther; 2008 Feb;33(1):91-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor lysis syndrome during treatment with AMN107 (Nilotinib) in a patient with chronic myelogenous leukemia accelerated phase.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Accelerated Phase / drug therapy. Pyrimidines / adverse effects. Tumor Lysis Syndrome / etiology

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  • (PMID = 18211624.001).
  • [ISSN] 1365-2710
  • [Journal-full-title] Journal of clinical pharmacy and therapeutics
  • [ISO-abbreviation] J Clin Pharm Ther
  • [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 / Pyrimidines
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74. 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
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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75. Huang Q: Chronic myelogenous leukemia in accelerated phase. Arch Pathol Lab Med; 2005 May;129(5):710
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic myelogenous leukemia in accelerated phase.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fusion Proteins, bcr-abl / genetics. Leukemia, Myeloid, Accelerated Phase. Philadelphia Chromosome. Translocation, Genetic

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  • (PMID = 15859653.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Benzamides; 0 / Oxides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; S7V92P67HO / arsenic trioxide; X6Q56QN5QC / Hydroxyurea
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